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OB FINALS 2014 REVIEWER  Chest pain related to effort or exertion

CLINICAL FINDINGS
MODULE 1  Cyanosis
 Clubbing of the fingers
CARDIOVASCULAR DISEASES IN PREGNANCY  Persistent neck vein engorgement
 Systolic murmur greater than Gr III/VI
Circulatory changes during pregnancy  Diastolic murmur
Parameter Change  Cardiomegaly
Plasma Volume 6 weeks AOG-32 weeks, increase an  Sustained arrhythmia
average of 50% over baseline  Persistently split S2
Red Cell Volume After 1st trimester, increases 20%  Loud P2 (criteria for pulmonary hypertension)
over baseline by term  Loud P2 (criteria for pulmonary hypertension)
Blood Volume 6weeks: increases an average 40%
by 32weeks Predicting Cardiac Complications during Pregnancy
- Prior heart failure, transient ischemic attack, arrhythmia, or stroke
Changes in Diagnostic Tests Findings during Pregnancy - Baseline NYHA Class III or greater or cyanosis
 normal pregnancy, - Left-sided heart obstruction defined as mitral valve area below 2
 functional systolic heart murmurs are common; respiratory effort cm2, aortic valve area below 1.5 cm2, or peak ventricular outflow
is accentuated and at times suggests dyspnea; edema in the lower tract gradient above 30 mm Hg by echocardiography
extremities after midpregnancy is common; and fatigue and - Ejection fraction less than 40%
exercise intolerance develop in most women - most important predictors of complications were prior congestive
1. Cardiac Physical Examination heart failure, depressed ejection fraction, and smoking
 Increase in the intensity of first heart sound with exaggerated
splitting Signs and Symptoms of Congestive Heart Failure
- persistent rales at the lung bases – first warning sign of CHF
 May have systolic ejection flow murmurs
- sudden diminution of the capacity to work
 Diastolic murmurs are rare and would warrant further study
- increasing dyspnea on exertion
2. Chest X-ray Film
- hemoptysis (usually associated with pulmonary hypertension)
 Lordosis can create straightening of the left upper cardiac border,
- progressive dyspnea, edema and tachycardia
mimicking left atrial enlargement
- Presence of any of these symptoms warrants admission. Much of
 Elevation of the diaphragm causes more horizontal position of
the load on patients occurs at around the second half of
the heart
pregnancy
 Pulmonary vasculature appears more prominent
3. Electro-cardiogram
 Horizontal position of the heart causes left or right shift of QRS
Group 1 Minimal Risk 01-%
 Transient ST-segment an t-wave changes are common
 Right axis deviation, RBBB, or ST depression of 1 mm on left
precordial leads
 Q waves in lead III, T wave inversion in III, V2 and V3
 Small decreases of PR and QT
 Rotation of =/- of 15 degrees (QRS axis) ve
 Atrial and ventricular premature contractions are relatively
frequent
 Pregnancy does not alter voltage findings Group 2A Moderate Risk 5-15%
4. Echocardiogram
 allows noninvasive evaluation of structural and functional cardiac
factors Aortic coartation without valvular involvement
 Increase in end-diastolic and end-systolic ventricular
measurements with no increase in wall thickness
 Mild tricuspid regurgitation may be due to increase volume arfan syndrome, normal aorta
 Increased Trivial tricuspid regurgitation (43 to 94% at term)
 Pulmonary regurgitation (94% at term)
 Increased left atrial size by 12 to 14% Group 2B Moderate Risk 5-15%
 Increased LV end diastolic dimensions by 6-10%
 Inconsistent increase in LV thickness / left ventricular mass
 Pericardial effusions
5. Pulmonary artery catheterization – no change Group 3 Major Risk 25-50%

Heart diseases in Pregnancy


ic involvement
 Coronary- Rare
 Rheumatic- Common
 Congenital- Variable MITRAL STENOSIS
- Rheumatoid endocarditis – causes ¾ of mitral stenosis
Clinical Finding in Heart Disease - Contracted valve impedes blood flow from the left atrium to the
SYMPTOMS right ventricle
 Severe or progressive dyspnea - 8% develop congestion,
 Nocturnal cough - 6 % experience symptomatic atrial arrhythmia
 Hemoptysis - 1-2% may have embolism.
 Syncope with exertion
- About less than half develop pulmonary hypertension, which is a - Epidural anesthesia : may not be tolerated
poor prognostic factor - During labor : if cyanosis develops = R to L shunting
- Supplemental O2 + measures to inc. vascular resistance + invasive
Indications for surgical treatment: hemodynamic monitoring
1. Non-responsive pulmonary edema
2. History of pulmonary edema, even with good medical treatment ATRIAL SEPTAL DEFECT
3. Profuse and profound hemoptysis - Common in adults
- Most common RHD in pregnant patients - Most common form : Ostium secundum defect
- Primary symptom : Easy fatigability - asymptomatic until the third or fourth decade
- Patients (ideally) should undergo surgical correction prior to - Assoc. with mitral valve prolapse or regurgitation
pregnancy - R sided failure and arrhythmias : 4th or 5th decade of life
Features : - potential to shunt blood right to left makes possible a paradoxical
- fixed CO , embolism—entry of a venous thrombus through the septal defect
- shortened diastolic filling time, and into the systemic circulation embolic stroke
- elevated left atrial and Management:
- pulmonary capillary pressure - During pregnancy : well tolerated and requires no specific
Management therapy in most gravidas
- Limit activity + diuretic therapy + dietary sodium restricted - Invasive monitoring : rarely needed
- (+) atrial enlargement : anticoagulation is indicated - Epidural anesthesia : preferred
- Valvuloplasty or valve replacement may be necessary if medical - Compression stockings+prophylactic heparin in othe presence of
therapy fails immobility
During Labor and Delivery : - Bacterial endocarditis prophylaxis
- invasive hemodynamic monitoring may be helpful
- Epidural anesthesia, control of HR , supplemental O2 , semi- TETRALOGY OF FALLOT
fowler’s positioning , avoidance of Valsalva , and assisted forceps a. RV outflow obstruction
delivery are advisable. b. VSD
- Puerperium : most hazardous time c. RV hypertrophy
- May need diuretics to prevent pulmonary edema d. Aorta overriding the VSD

AORTIC REGURGITATION/ INSUFFICIENCY - R to L shunting : usually present


- flow of blood from the aorta into the left ventricle - Uncorrected lesions :
- Causes: RF, connective-tissue abnormalities, congenital lesions  reduced life expectancy
- With Marfan Syndrome  aortic root may dilate, resulting in  Pregnancy is rare
regurgutation  If (+) pregnancy =spontaneous abortion , IUGR ,
- Aortic and mitral valve insufficiency have been linked to the cardiac failure
appetite suppressants fenfluramine and dexfenfluramine and to - Corrected lesions :
ergot-derived dopamine agonists  Pregnancy : well tolerated
- Rarely causes LV failure until the 4th or 5th decade of life  Inc. risk of IUGR
- Complicates pregnancy in <10% of cases During Labor and Delivery :
Management Goals : reduction in afterload - Supplemental O2 + efforts to maintain venous return
- restrict activity - Narcotics or pudendal block : vaginal delivery
- (+) Heart failure : digoxin + diuretics - General anesthesia : CS delivery
- Epidural anesthesia : recommended - Vaginal delivery preferred
- Bradycardia inc. regurgitation across the valve and is poorly
tolerated. COARCTATION OF THE AORTA
- Bacterial endocarditis prophylaxis may be recommended - Usually corrected during infancy
- Clinical : BP gradient between upper and lower extremity
CONGENITAL HEART DISEASES - Isolated HPN in the R upper arm
 ASD - atrial septal defects, without pulmonary hypertension - Fixed stroke volume
 VSD - ventricular septal defects, without pulmonary hypertension or - Cerebral berry aneurysms : common
left-to-right shunts - Patients with prior repair should be reevaluated for aortic
 PDA - patent ductus arteriosus which was corrected in childhood. If it is narrowing
not corrected, or if it is with a large left-to-right shunt, pregnancy can
result in left ventricular overload and failure MITRAL VALVE PROLAPSE
 Pulmonary and Tricuspid valvular lesions, unless, severely compromised - Dx: presence of a pathological connective tissue disorder—often
predating pregnancy termed myxomatous degeneration—which may involve the valve
Two most common congenital problems are VSD and ASD leaflets themselves, the annulus, or the chordae tendineae
- Both are abnormal holes in the wall between the side of the heart that - Most common cardiac lesion in women
pumps oxygen-poor blood to the lungs, and the side that pumps - Incidence : ~ 12%
oxygen-rich blood out to the body. - Most patients are asymptomatic and have uneventful pregnancies
- Complication occurs if with pulmonary hypertension - B-blockers - given to decrease sympathetic tone, relieve chest pain
and palpitations, and reduce the risk of life-threatening
VENTRICULAR SEPTAL DEFECT arrhythmias
- Small VSDs : well tolerated - Endocarditis prophylaxis is not indicated unless there is a
- if the defect is less than 1.25 cm2, pulmonary hypertension and coexistent mitral insufficiency
heart failure do not develop
- Other Cardiac Conditions
shunting with cyanosis occurs - Coronary Artery Disease
- When pulmonary arterial pressures reach systemic levels, - Peripartal Cardiomyopathy
however, there is reversal or bidirectional flow—Eisenmenger  cardiomegaly
syndrome (Eisenmenger syndrome)  presence of S3
 jugular distention perform any physical activity
 mitral or tricuspid regurgitation without discomfort. Symptoms are
 diastolic or late systolic murmurs present at rest and are increased
 cool extremities with any physical activity.
Treat the decompensation, and
NEW YORK HEART ASSOCIATION CLASSIFICATION then manage any obstetric
Management problem. This is associated with
Class I Uncompromised, with no high maternal mortality rate. Close
limitation of cardiac activity. No persons who have coordination with the cardiologist
symptoms of cardiac insufficiency respiratory infections is made. Counseling on the risk of
or anginal pain. Pneumococcal and pregnancy is made.
These patients usually go influenza vaccines
through pregnancy well . But Cigarette smoking is
should still watch out for any prohibited ENDOCARDITIS PROPHYLAXIS
complication which may push them NSD preferred Indication Regimen
into failure During labor, kept in Labor and Delivery Ampicillin 2 gm IV + Gentamicin
semirecumbent position 1.5mg/kg IV during active phase of
with lateral tilt labor, repear after 3 hours
Epidural analgesia for Patients with beta lactam allergies Replace ampicillin with vancomycin
NSD minimize 1gm IV (above regimen)
intrapartum CO Alternative regimen for low risk Amoxicillin 3gm po prior to
fluctuations and allows procedure or indication procedure and 1.5gm every 6 hr
forceps or vacuum assisted later
delivery
High Risk Patient 1. Prosthetic cardiac valves
SE conduction analgesia: (bioprosthetic and homograft)
maternal hypotension 2. Previous bacterial endocarditis
Tubal sterilization and 3. Complex cyanotic congenital heart
contraception best after disease (Fallot or TGA)
vaginal delivery and 4. Surgically corrected systemic
woman is stable, afebrile, pulmonary shunts or conduits
not anemic, ambulates Moderate Risk Category 1. Other congenital heart disease
normally 2. Acquired valvular dysfunction
3. MVP with regurgitation or
Class II Slightly compromised, with slight -same to class I thickened leaflets
limitation of physical activity. Negligible risk
Comfortable at rest, but with
ordinary or usual physical activity, Management Principles during Post-Partum Period
the patient experiences excessive - Maintain on hospital confinement for at least another week
fatigue, palpitation, dyspnea or
- Avoid extra exertion, maintain on bed rest
anginal pain. - Massage uterus to avoid atony
Management is the same as that
for Class I, but more vigilance in
Questions Problems Management
watching out for complications is
Rheumatic Mitral Dec diastolic filling Dec HR, dec IV volume
made because of the higher
Stenosis
incidence of complications.
ASD, VSD No problem Conservative
Tetralogy Corrected No problem Conservative
Class III Markedly compromised, with Management
marked limitation of physical Impt question whether Eisenmenger Pulmo HPN, IC shunt Avoid dec BP
activity.Comfortable at rest but pregnancy should be Syndrome
symptomatic with less than undertaken Marfan Syndrome Dilated aortic root Surgical reconstruction
ordinary activity. If women make that Cardiomyopathy Biventricular failure Supportive care
These patients must be co- choice, they must
managed with an internist- understand the risks and
cardiologist. These patients may cooperate fully with HYPERTENSIVE DISEASES OF PREGNANCY
have to be admitted, as one-third planned care. Definition of terms:
of them will decompensate to class  Hypertension- BP of at least 140 mmhg systolic and 90 mmhg
IV. Labor must be in the hospital. If feasible, women with diastolic (to be able to diagnose it you must have at least 2 values
Counseling on the risk of pregnancy some types of severe taken on 6 hours apart)
must be made. cardiac disease should  Korotkoff phase V is used to define diastolic pressure
consider pregnancy  Proteinuria- at least 300 mg/240
interruption.  At least 1000 mg / random sample of urine taken 60
If the pregnancy is apart.
continued, prolonged  Dipstick values: mild (trace to +1)
hospitalization or bed rest Heavy (+2-+4)
is often necessary.  Edema is also no longer used as a diagnostic criterion
because it is too common in normal pregnancy to be
NSD preferred discriminant

Class IV -same to class III


Severely compromised. Unable to
Table 34-1. Diagnosis of Hypertensive Disorders Complicating Pregnancy Severe Preeclampsia
Gestational Hypertension:  SBP ≥160 mmHg or DBP ≥110 mmHg
 Systolic BP >/=140 or diastolic BP >/=90 mm Hg for first time  Proteinuria: ≥4 gms/ day or ≥+2 on dipstick
during pregnancy  Oliguria <400 cc/day due to decreased renal blood flow and GFR
 Severe headache or visual disturbance- (+) Cerebral edema
 No proteinuria
 Pulmonary edema or cyanosis- hemodynamic changes increase in
 BP returns to normal before 12 weeks postpartum afterload
 Final diagnosis made only postpartum  Intrauterine Growth Restriction- due to decreases uteroplacental
 May have other signs or symptoms of preeclampsia, for example, blood flow.
epigastric discomfort or thrombocytopenia  This means that the fetal weight for that AOG is below
Preeclampsia: 10%
Minimum criteria:  RUQ or epigastric pain- due to ischemia or necrosis leading to the
 BP >/=140/90 mm Hg after 20 weeks' gestation distention of the Glisson’s capsule of the liver.
 Worst case would be hepatic rupture
 Proteinuria >/=300 mg/24 hours or >/=1+ dipstick
 Williams 22nd: result form hepatocellular necrosis, ischemia and
Increased certainty of preeclampsia:
edema that stretches the Glisson capsule the characteristic pain is
 BP >/=160/110 mm Hg accompanied by elevated serum hepatic transaminase.
 Proteinuria 2.0 g/24 hours or >/=2+ dipstick  The pain foretell hepatic infarction and hemorrhage or
 Serum creatinine >1.2 mg/dL unless known to be previously the catastrophic rupture of the subcapsular hematoma
elevated which is rare
 Platelets < 100,000/<uL  Hemolysis- manifests as inc. serum LDH, hemoglobinuria or (+)
schistocytes
 Microangiopathic hemolysis—increased LDH  Elevated liver enzymes- hepatocellular necrosis
 Elevated serum transaminase levels—ALT or AST  Low platelet count: ≤ 100,000/mm3
 Persistent headache or other cerebral or visual disturbance  Williams 22nd: caused by platelet activation and
 Persistent epigastric pain aggregation as well as microangiopathic hemolysis
Eclampsia: induced by severe vasospasm
HELLP syndrome
 Seizures that cannot be attributed to other causes in a woman
 Triad of
with preeclampsia
 Hemolysis,
Superimposed Preeclampsia On Chronic Hypertension:
 Elevated Liver Enzymes,
 New-onset proteinuria >/=300 mg/24 hours in hypertensive  Low platelet count
women but no proteinuria before 20 weeks' gestation  Williams 22nd the lower the platelet count the higher the
 A sudden increase in proteinuria or blood pressure or platelet maternal and fetal morbidity and mortality
count < 100,000/uL in women with hypertension and proteinuria
before 20 weeks' gestation Management of PIH:
Chronic Hypertension:  Guiding Principles:
 BP >/=140/90 mm Hg before pregnancy or diagnosed before 20  Prevent or control convulsions
weeks' gestation not attributable to gestational trophoblastic
disease  DOC: Mg SO4
or  magnesium sulfate administered parenterally is an
 Hypertension first diagnosed after 20 weeks' gestation and effective anticonvulsant that avoids producing central
persistent after 12 weeks postpartum nervous system depression in either the mother or the
infant
Table 34.2: Indicators for the Severity of Gestational Hypertensive Disorders  women with preeclampsia-eclampsia usually are given
magnesium sulfate during labor and for 24 hours
postpartum
 Magnesium sulfate is not given to treat hypertension
 Loading dose:
 4-6 gm slow IV over 15-20 min in 100 ml
fluid or
 10 gm deep IM (5 gm IM into each buttock)
 the mother stops convulsing
after the initial 4-g loading dose.
 By an hour or two, she regains
consciousness sufficiently to be
oriented to place and time
 Maintenance:
 2 gms/ hr controlled IV infusion or
 5 gms deep IM every 4-6hrs
 Maintenance magnesium sulfate
therapy is continued for 24 hours
after delivery
 For eclampsia that develops postpartum, magnesium
sulfate is administered for 24 hours after the onset of
convulsions
 MOA: cerebral vasodilator, inc uterine blood flow,
reduces levels of plasma endotheline-1 and inc renal
excretion of prostacyclin, central anticonvulsant effect o Maternal serum concentration of thyroid-binding globulin ---
and inc EDRF precursors increased concomitantly with total or bound thyroid hormone
 Therapeutic plasma levels: 4-7 mEq/L levels
 Discontinued 24 hrs after delivery due to post partum o Thyrotropin, or thyroid-stimulating hormone (TSH---plays a
eclampsia central role in screening and diagnosis of many thyroid disorders
 Monitor o Serum thyrotropin levels in early pregnancy decrease because of
 adequate patellar reflex, thyroid stimulation from the weak TSH effects of human
 adequate urine output (≥ 30 cc/hr), chorionic gonadotropin (hCG)
 no respiratory depression o TSH does not cross the placenta
o hCG serum levels---are maximal for the first 12 weeks, free
Clinical Correlated of serum MgSO4 thyroxine levels increase to suppress pituitary thyrotropin
Clinical response mEq/L secretion
Loss of patellar reflex 10 o thyrotropin-releasing hormone (TRH) ----is undetectable in
maternal serum.
Somnolence 10-12
o Fetal serum TRH--- is detectable beginning at midpregnancy, but
Slurred speech 10-12
does not increase
Respiratory difficulty 10
o Maternal thyroxine--- for brain development
Respiratory arrest ≥12
o fetal gland begins concentrating iodine and synthesizing thyroid
Cardiac arrest 30-35 hormone after 12 weeks

Management of MgSO4 toxicity: EVALUATING THE THYROID


 Calcium Gluconate 1 gm IV
 Severe Respiratory Depression/ Arrest: prompt tracheal
intubation, mechanical ventilation SENSITIVE TSH

Control of BP
 Goal: is to lower BP gradually because drastic reduction of BP
may compromise placental perfusion.
 Emergency parenteral therapy for severe HPN: HIGH NORMAL LOW
 Hydralazine(Aprasoline): direct vasodilator-
 5 mg IV initial dose,
 may be repeated q 10-20min up to a
loading dose of 20 mg (fastest way to lower FT4
BP)
 Labetalol: non- selective β1 and £1 blocker, LOW NORMAL
 20 mg initial IV bolus,
 may give another 40 mg after 10 min if BP
response is inadequate followed by another
80 mg q10 min x 2 doses. HYPOTHYROID SUBCLINICAL
HYPOTHYROIDISM
 Total dose should not exceed 220 mg
 Nifedipine: Ca channel blocker
 10 mg orally may be repeated after 30 min.  If the TSH is high, and FT4 is low  hypothyroid
 drawback: difficult to control;  If TSH is high and FT4 is normal  subclinical hypothyroidism
 may cause severe hypotension
 Na Nitroprusside/ Nitroglycerine
 seldom used: causes fetal cyanide toxicity SENSITIVE TSH
 Verapamil – IV infusion at 5-10 mg/hr
 Ketanserin – a selective serotonergic (5HT2A)
 Goal: BP 140-150/90-100 mmHg

THYROID DISEASE IN PREGNANCY HIGH NORMAL LOW

NORMAL THYROID PHYSIOLOGY DURING PREGNANCY

Increase in GFR FT4



Increase renal excretion of iodine

Plasma iodine levels decrease
NORMAL

 Plasma inorganic iodine levels > 0.08µg/dl  Goiters sec to


iodine deficiency not likely
 Clinical significance : Only pxs with plasma inorganic iodine levels
 If TSH is normal and FT4 normal  normal thyroid
that are borderline before pregnancy show an increased incidence
of goiter during pregnancy.
 Prevention : Inorganic iodine supplementation using 250 µg/day

Thyroid Physiology and Pregnancy


SENSITIVE o Labor
TSH o CS
o non-compliance with meds
 Maternal mortality : > 25%
 Clinical Symptoms :
NORMAL LOW o Hyperthermia
HIGH
o Marked Tachycardia
o Perspiration
o Severe Dehydration
FT4  Treatment Plan:
FT3 o Blocking β-adrenergic activity with Propanolol 20-80 mg q 6
NORMAL hrs
o Blocking secretion of thyroid hormone with sodium iodide
NORMAL
HIGH o Blocking synthesis of thyroid hormone and conversion of T4
HIGH
to T3 with 1200-1800 mg of PTU given in divided doses
o Blocking of deamination of T4 to T3 with Dexamethasone 8
SUBCLINICAL mg/day
HYPOTHYROIDISM HYPERTHYROID o Replacing fluid losses with at least 5 L of fluid
o Rapidly lowering Temp with hypothermic techniques
 If TSH is low and FT4 and FT3 is normal  subclinical NEONATAL THYROTOXICOSIS :
hypothyroidism
 If TSH is low and FT4 is normal but FT3 is high  hyperthyroid THERAPY :
 If TSH is low and FT4 is high  hyperthyroid  DOC : Levothyroxine 0.15 mg/day
 Goal : keep TSH levels within normal range
MATERNAL HYPERTHYROIDISM
 Incidence : 1 per 500 pregnancies Monitoring :
 Monthly TSH levels
 Causes :  Pregestational Thyroid Tx : TSH and free T4 levels at initial visit ,
1. Grave’s Disease (most common) 16-20 weeks and 28-32 weeks AOG
 Triad of
o hyperthyroidism, NEONATAL HYPOTHYROIDISM (Cretinism)
o exophthalmos,  Incidence of congenital hypothyroidism : 1 in 4000 births
o pretibial myxedema  Most common cause of neonatal goiter :
 Autoantibodies that have TSH properties  maternal ingestion of iodides present in cough syrup
 Menorrhagia, amenorrhea
 Symptoms: nervousness, heat intolerance,
PULMONARY DISORDERS OF PREGANACY
weight loss
2. Hydatidiform mole
VC, IC, TV, minute ventilation
3. Toxic Nodular Goiter
Physiological changes induced by pregnancy:
1. Vital capacity and inspiratory capacity increase by approximately 20 %
DIAGNOSIS :
by late pregnancy
 Serum free T4 : elevated (NV 2.5-3.5ng/dl)
2. Expiratory reserve volume decreases from 1300 mL to approximately
 TSH assay : decreased
1100 mL
 Thyroid Stimulating Antibody (TsAb) : increased
3. Tidal volume increases approximately 40 % as a result of the
respiratory stimulant properties of progesterone
THERAPY
4. Minute ventilation increases about 30 to 40 percent due to increased
 Radioactive iodine : contraindicated during pregnancy,
tidal volume. Arterial pO2 also increases from 100 to 105 mm Hg
can ablate fetal thyroid  cretinism
5. Carbon dioxide production increases approximately 30 percent, but
diffusion capacity also increases, and with alveolar hyperventilation,
 Mainstay :
the pCO2 decreases from 40 to 32 mm Hg
o Prophylthiouracil (PTU)
6. Residual volume decreases approximately 20 percent from 1500 mL to
o Methimazole : aplasia cutis
approximately 1200 mL
7. The expanding uterus and increased abdominal pressure cause chest
 PTU : preferred oral therapy
wall compliance to be reduced by a third. Thus, the functional residual
o also blocks conversion of T4T3
capacity—the sum of expiratory reserve and residual volumes—
o Starting dose : 100-150 mg q 8 hrs
decreases by 10 to 25 percent.
o Goal : use the lowest dose to maintain free T4 levels
in the upper normal range
 The sum of these changes is substantively increased ventilation due to
 Only 1-5% of pxs using high dose PTU develop fetal goiter and deeper but not more frequent breathing.
hypothyroidism  *These changes presumably are induced by basal oxygen
consumption, which increases incrementally by 20 to 40 mL/min in the
 Mother can safely breastfeed postpartum second half of pregnancy.
 The kidney increases bicarbonate excretion and serum levels decrease
 Surgical Tx : only if medical tx fails to approximately 15 to 20 meq/L, while pH is slightly alkalotic at 7.45.
o subtotal thyroidectomy  delayed until 2nd trimester
ASTHMA
THYROID STORM  Asthma is seen frequently during pregnancy
 Major risk of Thyrotoxicosis in pregnancy  *chronic inflammatory airway disorder with a major hereditary
 Precipitating factors : component
o Infection
 *The hallmarks of asthma are reversible airway obstruction from Pregnancy Outcome
bronchial smooth muscle contraction, vascular congestion, tenacious  *unless there is severe disease, pregnancy outcomes are generally
mucus, and mucosal edema. excellent
 *There is airway inflammation and increased responsiveness to a  increased morbidity is linked to progressively more severe disease,
number of stimuli including irritants, viral infections, aspirin, cold air, poor control, or both
and exercise.  *Life-threatening complications from status asthmaticus include
 *Genetics – Chromosome 5,11,12 muscle fatigue with respiratory arrest
 Inflammation is caused by response of mast cells, eosinophils,
lymphocytes, and bronchial epithelium. Fetal Effects
 * A number of inflammatory mediators by these and other cells include The fetal response to maternal hypoxemia:
histamine, leukotrienes, prostaglandins, cytokines, and many others. Decreased umbilical blood flow,
 IgE also plays a central role in pathophysiology Increased systemic and pulmonary vascular resistance
 *Because F-series prostaglandins and ergonovine exacerbate asthma, Decreased cardiac output.
these commonly used obstetrical drugs should be avoided if possible. Monitoring the fetal response is, in effect, an indicator of maternal status

Clinical Course Clinical Evaluation


The functional result of acute bronchospasm is airway obstruction and *Inaccurate predictors of severity
decreased airflow The subjective severity of asthma frequently does not correlate with
 The work of breathing progressively increases objective measures of airway function or ventilation(clinical evaluation)
 Patients present with chest tightness wheezing Clinical signs:
 Breathlessness  labored breathing
 ventilation–perfusion mismatching  Tachycardia
 Pulsus paradoxus
 prolonged expiration
 Use of accessory muscles
Pneumomediastinum
Acute cor pulmonale
Cardiac arrhythmias
Signs of a potentially fatal attack include central cyanosis and altered
consciousness
*Arterial blood gas analysis provides objective assessment of maternal
oxygenation, ventilation, and acid–base status
pCO2 >35 mm Hg with a pH < 7.35 is consistent with hyperventilation
and CO2 retention
*Sequential measurement of the FEV1 or the peak expiratory flow
rate—PEFR—are the best measures of severity
*FEV1 less than 1 L, or less than 20 percent of predicted value,
correlates with severe disease defined by hypoxia, poor response to
therapy, and a high relapse rate
* The PEFR correlates well with the FEV1, Normal Value: 380-550
L/min, component

Management of Acute Asthma


1. First-line therapy for acute asthma includes a B- adrenergic agonist:
terbutaline, albuterol, isoetharine, epinephrine, isoproterenol, or
metaproterenol,
 Which is given subcutaneously, taken orally, or inhaled.
 MOA: modulate bronchial smooth muscle relaxation
 *Regimens recommended for out-patient management:
For mild asthma: inhales B-agonist as needed are usually
sufficient.
For persistent asthma: inhaled Corticosteroids are administered
every 3-4 hours
The goal is to reduce the use of B-agonist for symptomatic relief
 *Treatment of acute asthma during pregnancy is similar to that for the
non-pregnant asthmatic. An exception is a significantly lowered
threshold for hospitalization.
 *Intravenous hydration may help clear pulmonary secretions, and
supplemental oxygen is given by mask
 *The therapeutic aim is to maintain the pO2 greater than 60 mm Hg,
and preferably normal, along with 95-percent oxygen saturation.

Status Asthmaticus and Respiratory Failure


 Severe asthma of any type not responding after 30 to 60 minutes of
intensive therapy is termed status asthmaticus
 Consideration should be given to early intubation when maternal
respiratory status worsens despite aggressive treatment
 Fatigue, carbon dioxide retention, and hypoxemia are indications for
mechanical ventilation
Labor and Delivery  Because most adult pneumonias are caused by pneumococci,
 Maintenance medications are continued through delivery. mycoplasma, or chlamydophilia, monotherapy initially is with a
 The usual dose is 100 mg of hydrocortisone given intravenously every 8 macrolide—azithromycin, clarithromycin, or erythromycin
hours during labor and for 24 hours after delivery
 The PEFR or FEV1 should be determined on admission, and serial For women with severe disease
measurements are taken if symptoms develop. (1) A respiratory fluoroquinolone—levofloxacin, moxifloxacin, or
gemifloxacin;
Epidural is ideal (2) B-lactam plus a macrolide—high-dose amoxicillin or amoxicillin-
Avoid tracheal intubation clavulanate are preferred B-lactams, and alternatives include ceftriaxone,
Oxytocin and PGE2- ok cefpodoxime, or cefuroxime. Levofloxacin is also acceptable.
PGF2α and ergotamine derivatives- NOT OK
 Clinical improvement is usually evident in 48 to 72 hours with
PNEUMONIA resolution of fever in 2 to 4 days,
Types:  Radiographic abnormalities may take up to 6 weeks to completely
1. Community-acquired pneumonia (CAP) is typically encountered in resolve
otherwise healthy young women, including during pregnancy.  Recommended for a minimum of 5 days
2. Healthcare-associated pneumonia (HCAP) develops in patients in  Treatment failure may occur in up to 15 percent of cases, and a wider
outpatient care facilities and more closely resembles hospital-acquired microbial antibiotic regimen is warranted in these cases.
pneumonia (HAP)
3. Nursing home-acquired pneumonia (NHAO) and Pregnancy Outcome with Pneumonia
4. Ventilator-associated pneumonia (VAP). Common complications:
 Prematurely ruptured membranes
*Any pregnant woman suspected of having pneumonia should undergo chest  Preterm delivery
radiograph  Low-birth weight infants

*Bacterial Pneumonia *Fungal Pneumonia


 Many bacteria that cause community-acquired pneumonia, such as  Seen in women with HIV infection or who are otherwise
Streptococcus pneumoniae, are part of the normal resident flora immunocompromised
 Some factors that perturb the symbiotic relationship between  Usually mild and self-limited.
colonizing bacteria and mucosal phagocytic defenses include  Characterized initially by cough and fever, and dissemination is
acquisition of a virulent strain or bacterial infections following a viral infrequent.
infection  Pregnant women with symptomatic infection- better prognosis if there
 Cigarette smoking and chronic bronchitis favor colonization with S. was associated erythema nodosum
pneumoniae, Haemophilus influenzae, and Legionella species.  Treatment: disseminated fungal infection: amphotericin B or
 Other risk factors include asthma, binge drinking, and human ketoconazole
immunodeficiency virus (HIV) infection  Caspofungin, micafungin, and anidulafungin— effective for invasive
candidiasis
*Incidence and Causes
 Pregnancy itself does not predispose to pneumonia TUBERCULOSIS
 More than half of adult pneumonias are bacterial, and S. pneumoniae is  Infection is via inhalation of Mycobacterium tuberculosis, which incites
the most common cause agranulomatous pulmonary reaction.
Manifestations:
Diagnosis Cough with minimal sputum production
 Typical symptoms include cough, dyspnea, sputum production,and Low-grade fever hemoptysis
pleuritic chest pain. Weight loss
 Chest radiography is essential for diagnosis but does not accurately Evaluation
predict the etiology  Sputum examination for acid fast bacilli
 The responsible pathogen is identified in less than half of cases.  Bronchoscopy
 Chest X-ray – infiltrative patterns and mediastinal lymphadenopathy
 Liver function test – because some treatment drugs are hepatotoxic

Treatment
DOTS: Directly Observed Therapy

 Isoniazid
o 5mg/kg,not to exceed 300 mg daily
 Pyridoxine
o 50 mg daily
 Rifampicin
o 10mg/kg ,not to exceed 600 mg daily
 Ethambutol
o 5-25mg/kg, not to exceed 2.5 g daily
Figure 46-2 Chest radiographs in a pregnant woman with right lower lobe
pneumonia. A. Complete opacification of the right lower lobe (arrows) is MDR-TB: Multidrug Resistant TB
consistent with the clinical suspicion of pneumonia. B. Opacification (arrows)  Four-drug regimen for initial empirical treatment of patients with
is also seen on the lateral projection. symptomatic tuberculosis
 Isoniazid, rifampin, pyrazinamide, and ethambutol
Management  given until susceptibility studies are performed
 Antimicrobial treatment is empirical.  Standard treatment with pregnancy: RIPE
 AntiTB drugs: chemotherapeutic drugs; just give if there is a high MODULE 2
probability of TB
 Therapy maintained for a minimum of 9 months RENAL DISEASES IN OBSTETRICS
 If evidence of resistance occurs with any of the three first line
drugs, Pyrazinamide may be considered.
INFECTIONS
 Streptomycin, although a first line drug is avoided in pregnancy
o Congenital deafness • asymptomatic bacteriuria: most common
• symptomatic infection
Tuberculosis and Pregnancy – Cystitis: bladder
Without antituberculosis therapy, pregnancy likely has adverse effects on the – Pyelonephritis: renal calyces, pelvis, parenchyma
course of active tuberculosis Etiology
• Escherichia coli strains
Outcomes are dependent on the site of infection and timing of diagnosis in
– nonobstructive pyelonephritis
relation to delivery.
– Adhesins: P- & S-fimbriae  enhanced virulence
Effect on pregnancy • promote binding: vaginal and uroepithelial cells
preterm delivery • urinary stasis & vesicoureteral reflux
low-birthweight and growthrestricted
– symptomatic upper urinary infections
• Diabetics: susceptible to pyelonephritis
infants, and perinatal mortality

Effect of pregnancy ASYMPTOMATIC BACTERIURIA


Development of maternal respiratory impairment due to pregnancy
unlikely Diagnosis: > 100,000 organisms/mL
– TREAT! even if lower
Extrapulmonary tuberculosis is less common. Complications
 associated with preterm or low-birthweight infants
Diagnosis Recurrence?
Purified protein derivative (PPD) • 30 percent
 Intermediate strength of 5 tuberculin units.
• covert upper tract infection
 If negative- no further evaluation is needed.
• longer therapy
 Positive skin test- measures > 5 mm in diameter and requires evaluation
for active disease, including a chest radiograph
• nitrofurantoin 100 mg orally at bedtime x 21 days
 For very high-risk patients-those who are HIV- positive, those with • persistent or frequent bacteriuria recurrences
abnormal chest radiography, or those who have a recent contact with – suppressive therapy
an active case— – nitrofurantoin 100 mg orally at bedtime
5 mm or greater is considered treatable. – AE: rarely causes an acute pulmonary reaction

Active Infection CYSTITIS AND URETHRITIS


 Recommended initial treatment for active tuberculosis in pregnant • May develop anytime
patients is a three-drug • Dysuria, urgency, and frequency
 Regimen with isoniazid, rifampin, and ethambutol. – few associated systemic findings
 Isoniazid-resistant tuberculosis- pyrazinamide is added to the initial
regimen until susceptibility testing is completed. Treatment: LUT symptoms + pyuria + sterile culture
 If the organism is susceptible, the regimen is given for 9 months.
 Breast feeding- not prohibited during antituberculous therapy. – Chlamydia trachomatis
Pregnant women receiving isoniazid should also be given pyridoxine, 25 – (+) Mucopurulent cervicitis  erythromycin
mg/day orally, to decrease hepatic toxicity.
 HIV-infected women- the use of rifampin or rifabutin may be Acute Pyelonephritis
contraindicated if certain protease inhibitors or nonnucleoside reverse • Leading cause of septic shock during pregnancy
transcriptase inhibitors are being administered. • Second trimester: common
 If there is resistance to rifabutin or rifampin, then pyrazinamide therapy • Nulliparity, young age: risk factors
is given.
 Second-line regimens- the aminoglycosides— streptomycin, kanamycin, Evidence of the sepsis syndrome is common
amikacin, and capreomycin—are ototoxic to the fetus and are
contraindicated • Clinical evidence of acute infection
• Hyperthermia or hypothermia
*NEONATAL TUBERCULOSIS • Tachycardia
 Tubercular bacillemia can infect the placenta, but in only a few of • Tachypnea
these, the fetus is also infected to cause congenital tuberculosis.
 The term also applies to newborns who are infected by aspiration of Treatment
infected secretions at delivery.
Cornerstone: Intravenous hydration
 Neonatal infection is unlikely if the mother with active disease has been
– adequate urinary output
treated before delivery or if her sputum culture is negative.
Antimicrobials
**GDM NO SOFT COPY – initially worsen endotoxemia
– bacterial lysis
Serial determinations
– urinary output
– Vital signs
High fever: cooling blanket or acetaminophen
– teratogenic effects of hyperthermia • Acute INC serum creatinine: renal ischemia
Antimicrobial therapy • Oliguria: acutely impaired renal function
• Empirical • Prerenal and intrarenal factors (Ex. severe hypovolemia - massive
• ampicillin plus gentamicin hemorrhage, superimposed preeclampsia - oliguria)
• cefazolin or ceftriaxone • Early dialysis: reduces MMR
• extended-spectrum antibiotic • TIME  normal renal function
• Serum creatinine
– Monitored HEMATOLOGICAL DISORDERS IN PREGNANCY
– nephrotoxic drugs Thalassemia

Discharge  These genetically determined hemoglobinopathies are characterized


• oral therapy for a total of 7 to 10 days by:
o Impaired production of one or more of the normal globin peptide
Chronic renal disease chains.
 Abnormal synthesis rates may result in ineffective erythropoiesis,
hemolysis, and varying degrees of anemia.
Categories Of Renal Function
 Thalassemias are classified according to the globin chain that is
• Serum creatinine deficient, and several hundred syndromes have been identified. The
• Normal/mild impairment: < 1.5 mg/dL two major forms involve impaired production or instability either of α-
• Moderate impairment: 1.5 to 3.0 mg/dL peptide chains—causing α-thalassemia or of β-chains—causing β-
• Severe renal insufficiency: > 3.0 mg/dL thalassemia.

Glomerulopathies
• Single stimulus (ex poststreptococcal GN)
• Multisystem disease (ex SLE or DM)
• glomerulopathic syndromes:
– acute nephritic
– pulmonary-renal
– Nephrotic
– basement membrane, glomerulovascular, and infectious-
disease syndromes
• Young women, childbearing  pregnancy

ACUTE NEPHRITIC SYNDROME


• Acute glomerulonephritis
– IgA Nephropathy (Berger disease)
• Hypertension, hematuria, red-cell casts, pyuria, and proteinuria
α-Thalassemia
• Renal insufficiency and salt and water retention, which causes
edema, hypertension, and circulatory congestion
• Renal biopsy
– determine etiology
– management
• Pregnancy outcome  degree of renal insufficiency and hypertension
• Normal renal function
– overall fetal loss: 25 %

Pregnancy
• HPN: 50% of women
– Severe

• Proteinuria: worsened in 60 %
• Worst perinatal outcomes:
– impaired renal function
– early or severe hypertension
– nephrotic-range proteinuria

ACUTE RENAL FAILURE


 Because there are four α-globin genes, the inheritance of α-
aka ACUTE KIDNEY INJURY thalassemia is more complicated than for β-thalassemia For each,
• Rapid decrease in the GFR a close correlation has been established between clinical severity
– minutes to days and the degree of α-globin chains synthesis impairment.
• Significant source of obstetrical morbidity  In most populations, the α-globin chain “cluster” or gene loci are
• Most often associated with severe preeclampsia-eclampsia doubled on chromosome 16. Thus, the normal genotype for
– develops postpartum diploid cells can be expressed as αα/αα. There are two main
groups of α-thalassemia determinants: α-thalassemia is β-thalassemia
characterized by the deletion of both loci from one chromosome
(– –/αα), whereas α+-thalassemia is characterized by the loss of a
single locus from one allele (–α/αα heterozygote) or a loss from
each allele alleles (–α/–α homozygote).
 There are two major phenotypes. The deletion of all four α-globin
chain genes (– –/– –) characterizes homozygous α- thalassemia.
Because α chains are contained in fetal hemoglobin, the fetus is
affected. With none of the four genes expressed, there are no α-
globin chains, and instead, hemoglobin Bart (γ4) and hemoglobin
H (β4) are formed as abnormal tetramers
 Hemoglobin Bart has an appreciably increased affinity for oxygen,
and hemoglobin Bart disease is a common cause of stillbirths in
Southeast Asia
o The fetus dies either in utero or very soon after birth
and demonstrates the typical features of nonimmune
hydrops fetalis
 Fetal anemia can be detected using Doppler flow measurement of
middle cerebral artery velocity
These are the consequences of impaired production of β –globin chains or
 The compound heterozygous state for α- and α+-thalassemia
instability of chains:
results in the deletion of three of four genes (– –/–α).
 Most are single-nucleotide substitutions that produce
 hemoglobin H disease: only one functional α-globin gene per
transcription or translation defects, RNA splicing or modification,
diploid genome and is compatible with extrauterine life.
or frameshifts that result in highly unstable hemoglobins. Thus,
deletional and nondeletional mutations affect -globin RNA.
 The -gene “cluster” is on chromosome 11
 In beta-thalassemia, there is:
o Decreased beta-chain production, and
o excess alpha chains precipitate to cause cell
membrane damage.
o In addition, beta-thalassemia may be due to alpha-
chain instability.
 hemoglobin-stabilizing protein (AHSP)-a molecular chaperone
that regulates -globin subunit stability, which forms a stable
complex with free α–globin and prevents precipitation. Mutations
in the AHSP gene may modify the clinical picture of β-
thalassemia.
o an overexpression of AHSP may convert β-
thalassemia major to β-thalassemia intermedia.

 These basic defects lead to the panorama of pathology that


 The neonate appears well at birth but soon develops hemolytic characterizes homozygous β-thalassemia, so called thalassemia
anemia. Most of the hemoglobin Bart present at birth is replaced major or Cooley anemia.
postnatally by hemoglobin H.  With heterozygous thalassemia minor, hypochromia,
o The disease is characterized by hemolytic anemia, microcytosis, and slight to moderate anemia develop without
which may be severe and similar to β-thalassemia the intense hemolysis that characterizes the homozygous state.
major in children and adults.  The hallmark of the common β-thalassemias is an elevated
 Anemia in these women usually is worsened during pregnancy. hemoglobin A2 level.
 In α-thalassemia minor- A deletion of two genes which is
characterized by minimal to moderate hypochromic microcytic  In the typical case of thalassemia major, the neonate is healthy at
anemia. birth, but as the hemoglobin F level falls, the infant becomes
 Other than mild anemia, there are no associated clinical severely anemic and fails to thrive
abnormalities with α-thalassemia minor, and it often goes  A child who is entered into an adequate transfusion program
unrecognized. develops normally until the end of the first decade.
 Hemoglobin Bart is present at birth, but as its levels drop, it is not o Then, effects of iron loading become apparent.
replaced by hemoglobin H. o Prognosis is improved by iron chelation therapy with
o Red cells are hypochromic and microcytic, and the deferoxamine
o hemoglobin concentration is normal to slightly o Pregnancy is recommended only if there is normal
depressed. maternal cardiac function and prolonged
 Women with α-thalassemia minor tolerate pregnancy well. hypertransfusion to maintain the hemoglobin
 The single gene deletion (–α/αα) is the silent carrier state. No concentration at 10 g/dL.
clinical abnormality is evident in the individual with a single gene o Withβ -thalassemia minor, hemoglobin A2, which is
deletion. composed of two α- and two δ-globin chains, is
increased to more than 3.5 percent.
o Simultaneously, hemoglobin F, which is composed of
two α- and two γ-globin chains, is usually increased to
more than 2 percent.
 Anemia is mild, and the red cells are hypochromic and microcytic.
 There is usually pregnancy induced augmentation of • Ig in the 3rd tri
erythropoiesis, and using erythrocytes tagged with chromium-51 • Splenectomy
 There is no specific therapy for β-thalassemia minor during • Fetal thromocytopenia, Ig G crosses placenta
pregnancy. • fetal scalp platelet determinations
o Prophylactic iron and folic acid are given. • Acute ITP is most often a childhood disease that follows a viral
o Fetal-growth restriction and oligohydramnios were infection.
increased twofold in affected women. • Most cases resolve spontaneously, although perhaps
 Prenatal diagnosis of β-thalassemia major is more difficult than 10 percent become chronic.
detecting abnormal hemoglobins because of the large number of • In adults, immune thrombocytopenia is primarily a chronic
mutations. disease of young women and rarely resolves spontaneously.
 To diagnose a particular mutation, targeted mutation analysis is • Secondary forms of chronic thrombocytopenia appear in
done that requires prior identification of the disease-causing association with:
mutation for that particular family • systemic lupus erythematosus,
o Most of these are done using samples obtained by • lymphomas,
CVS. • leukemias,
o Preimplantation blastomere biopsy has been • a number of systemic diseases.
described • For example, about 2 percent of thrombocytopenic patients have
o Isolation of single nucleated red blood cells from positive serological tests for lupus, and in some cases, there are
maternal circulation is being explored for prenatal high levels of anticardiolipin antibodies.
diagnosis of β-thalassemia.
Treatment:
POLYCYTHEMIA Who are treated?
 Those whose platelet counts remain less than 30,000/L
 those with significant bleeding at higher levels.
 Prednisone: 1 to 2 mg/kg orally daily,
o Increases the platelet count in approximately 2/3
of cases.
o Relapse is common.
 Glucocorticoids:
o Suppress the phagocytic activity of the splenic
monocyte-macrophage system.
 Intravenous immunoglobulin (IVIG)
o TOTAL DOSE:2 g/kg over 2 to 5 days is usually
effective
o If there is no response to corticosteroid therapy
in 2 to 3 weeks  splenectomy
 Immunosuppressive drugs, including:
o azathioprine,
 Excessive erythrocytosis during pregnancy is usually related to
o cyclophosphamide, and
chronic hypoxia due to maternal congenital cardiac disease or a
o cyclosporine,
pulmonary disorder.
 Danazol, vinca, alkaloids, plasma exchange, and high-dose
 Occasionally, it is from heavy cigarette smoking.
dexamethasone pulse therapy have also been described.
o There are healthy young pregnant women who were
 Thrombopoietin agonists (eltrombopa) have shown promise
heavy smokers with chronic bronchitis and with a
but are considered experimental
hematocrit from 55 to 60 volumes percent
 a woman with persistent erythrocytosis associated with a
Immune Thrombocytopenia and Pregnancy
placental site tumor.
Treatment is considered if the platelet count is less than 30,000 to
 If polycythemia is severe, the probability of a successful
50,000/L
pregnancy outcome is low.
 Prednisone: 1 mg/kg orally/day and
o Require for improvement and most likely
Polycythemia vera treatment will have to be continued throughout
 a myeloproliferative hemopoietic stem cell disorder characterized pregnancy.
by excessive proliferation of erythroid, myeloid, and  Corticosteroid therapy
megakaryocytic precursors.  high-dose immunoglobulin
 It is uncommon and likely an acquired genetic disorder of stem o With steroid-refractory disease given
cells intravenously
 Measurement of serum erythropoietin by radioimmunoassay o may be considered as first-line therapy in the
differentiates polycythemia vera—low values—from secondary third trimester
polycythemia—high values.
 Symptoms are related to: Von Willebrand Disease (Types I, II, and III)
o Increased blood viscosity, and o factor VIII complex and platelet dysfunction
o thrombotic complications o rapid onset of subcutaneous bruising or mucous
 Fetal loss has been reported to be high in women with membrane bleeding
polycythemia vera and pregnancy outcome may be improved o Acquired vWD  Etiologies include benign and
with aspirin therapy malignant hematological conditions, solid tumors,
autoimmune disorders, and medications
IMMUNE THROMBOCYTOPENIC PURPURA o Desmopressin; cryoprecipitate
• IgG antibodies directed against one or more platelet glycoproteins
• In pregnancy
• Treat when platelet is <30,000 to 50,000/L
• Steroids
Other Inherited Coagulation Factor Deficiencies EFFECTS ON THE MOTHER:postpartum hge
• Factor VII deficiency
• Factor X or Stuart-Prower factor EFFECTS ON THE FETUS:
• Factor XI—plasma thromboplastin antecedent—  both parents have disorder: homozygous offspring develop a
deficiency serious bleeding disorder
• Factor XII deficiency  periventricular hemorrhage in a 32-week fetus who inherited
• Factor XIII deficiency type IIa vW disease
• Dysfibrinogenemias, hypofibrinogenemia,
afibrinogenemia, hypodysfibrinogenemia MANAGEMENT:Desmopressin

GASTROINTESTINAL DISORDERS IN PREGNANCY


Hyperemesis gravidarum
Pathogenesis • Most women, mild to moderate nausea an vomiting usually disappears at
The von Willebrand factor is a series of large plasma multimeric around 16 weeks AOG. In some women, however, it is severe and
glycoproteins that form part of the factor VIII complex. It is essential for unresponsive to simple dietary modification and Antiemetics.
normal platelet adhesion to subendothelial collagen and formation of a
 Nausea and vomiting of varying severity usually commence between the
primary hemostatic plug at the site of blood vessel injury. It also plays a
1st and 2nd missed menstrual period and continue until 14 to 16weeks.
major role in the stabilization of the coagulant properties of factor VIII. The
procoagulant component
Diaphragmatic Hernia
is the antihemophilic factor or factor VIII:C, which is a glycoprotein
synthesized by the liver. Conversely, von Willebrand precursor, which is Defect or hole in the diaphragm that allows abdominal contents to move into
present in platelets as well as plasma, is synthesized by endothelium and the thoracic cavity.
megakaryocytes under the control of autosomal genes on chromosome 12. • The Bochdalek hernia, also known as a postero- lateral diaphragmatic
The von Willebrand factor antigen (vWF:Ag) is the antigenic determinant hernia accounts for more than 95% of cases. The majority of Bochdalek
measured by immunoassays. hernias (80-85%) occur on the left side of the diaphragm.
• This rare anterior defect of the diaphragm is variably referred to as
Von Willebrand Disease Morgagni, retrosternal, or parasternal hernia.
 most commonly inherited bleeding disorders
 inherited as autosomal dominant traits  types I and II, Upper Gastrointestinal Bleeding
which are the most common variants Occasionally, persistent vomiting is accompanied by worrisome upper
 Type III, which is the most severe, is phenotypically recessive gastrointestinal bleeding.
 S/Sx: rapid onset of subcutaneous bruising or mucous Occasionally, there is a bleeding peptic ulceration.
membrane bleeding in those with no prior personal or family However, most of these women have small linear mucosal tears near the
history of clotting abnormalities gastroesophageal junction— Mallory-Weiss tears

ETIOLOGY: Management:
 aberrations of factor VIII complex and platelet dysfunction 1. Iced saline irrigations, topical antacids, and intravenously administered H2-
 benign and malignant hematological conditions, solid blockers.
tumors, autoimmune disorders, and medications 2. Transfusions may be needed, and if there is persistent bleeding, then
endoscopy is indicated With persistent retching, the less common, but
Pathogenesis more serious, esophageal rupture—Boerhaave syndrome—may develop
 von Willebrand factor series of large plasma multimeric from greatly increased esophageal pressure
glycoproteins that form part of the factor VIII complex.
 essential for normal platelet adhesion to Ulcerative Colitis and Pregnancy
subendothelial collagen and formation of a primary Inflammation is confined to the superficial luminal layers of the colon,
hemostatic plug at the site of blood vessel injury. typically beginning at the rectum and extending proximally for a variable
 plays a major role in the stabilization of the coagulant distance.
properties of factor VIII. • Endoscopic findings include mucosal granularity and friability interspersed
 The procoagulant component is the antihemophilic with mucosal ulcerations and a mucopurulent exudate.
factor or factor VIII:C, which is a glycoprotein • Bloody diarrhea is the cardinal presenting finding.
synthesized by the liver. • Management: 5-aminosalicyclic acid (5-ASA) or mesalamine are used for
 von Willebrand precursor, which is present in platelets active colitis as well as maintenance therapy. For recalcitrant disease,
as well as plasma, is synthesized by endothelium and proctocolectomy is performed.
megakaryocytes under the control of autosomal genes There is no evidence to suggest that pregnancy has any significant effects on
on chromosome 12. ulcerative colitis.
 The von Willebrand factor antigen (vWF:Ag) is the
antigenic determinant measured by immunoassays. Ulcerative colitis quiescent at conception worsened in approximately a third
of pregnancies
Clinical Manifestations:
 considered in women with bleeding suggestive of a chronic Management:
disorder of coagulation  Most part is the same as for nonpregnancy
 Type Ieasy bruising; epistaxis; mucosal hemorrhage; and  Flares may be caused by psychogenic stress and reassurance is
excessive bleeding with trauma, including surger important.
 Calcium supplementation is provided because osteoporosis is
DIAGNOSIS: common.
 prolonged bleeding time, prolonged partial thromboplastin  Maintenance of colitis is continued with 5-ASA derivatives, and
time flares are treated with corticosteroids.
 dec. vWF antigen; decreased factor VIII  Recalcitrant disease is treated with immunomodulators
 Leukocytapheresis
 Parenteral nutrition may be necessary for women with prolonged  Preinvasive intraepithelial lesions
exacerbations.  Diagnosis via biopsy
 Colorectal endoscopy is performed as indicated  Clinically staged: PE, CXR, intravenous pyelography (IVP) or CT
 Colectomy for fulminant colitis may be lifesaving, and it has been and stage does not change based on operative findings
performed during each trimester.  “cervical ca=clinically staged;
 Most women underwent partial or complete colectomy  ovarian/endometrial ca= surgically staged”
decompression colostomy with ileostomy- 10 and 16-week  “cervical ca obstruct the kidneys, most px die not because of
pregnancy. cervical ca but with renal problems”
 Proctocolectomy improves sexual function and fertility
 Women who have had a colectomy and ileal pouch– anal HPV causing cervical CA
anastomosis can safely deliver vaginally.  HPV, double stranded DNA viruses replicate w/in the epithelium
 Cesarean delivery should be for obstetrical indications  Transmission may be by sexual activity
 Pouchitis is an inflammatory condition of the ileoanal pouch,  Most detected infections cleared w/in a few months although
probably due to bacterial proliferation, stasis, and endotoxin some may persist for as long as 36 months
release. It usually responds to cephalosporins or metronidazole.  Compromised immune system may increase risk of infection
 Smoking increases risk of CIN3
Ulcerative colitis has minimal adverse effects on pregnancy outcome.  2 vaccines are available and ideally given prior to sexual activity
(Cervarix & Gardasil)
Perinatal outcomes were not substantively different from those in the  “Young exposed females to HPV can still remove the virus is the
general obstetrical population. system” at 20’s to 30’s. You can get the virus at an early age but
still can able to remove it s. But with constant contact with
Specifically, the incidences of spontaneous abortion, preterm delivery, and affected male partners until you reach 40’s, virus cannot be
stillbirths were remarkably low. removed anymore”

Inexplicably increased incidence of congenital malformations. PAP SMEAR: every year in the Phil. but in other countries its different

Increased rate of caesarean delivery. Philippine Society of Cervical Pathology and Colposcopy
“based on studies done abroad”:
Crohns Disease  Screening should begin approx 3 years after the onset of vaginal
intercourse, but not earlier than 21y/o (applicable in Phil)
Crohn Disease and Pregnancy o “16 y/o sexually active- do not do pap smear”
 No evidence that pregnancy affects Crohn disease. o “22 y/o, first sexual intercourse- do pap smear”
 One report suggested that disease activity might even be decreased  For women aged 21-29 years, screening w/ cytology alone every 3
(Agret and colleagues, 2005). In general, disease activity is related to its years is recommended. Despite the high prevalence of HPV
status around the time of conception. infection in this age group, HPV testing is not recommended due
Management: to the transient nature of the HPV infection (applicable abroad)
 Maintenance therapy is similar to that for nonpregnant women.  Women aged 35-65 years should be screened with cytology alone
 Oral or topical 5-ASA derivatives, usually with azathioprine, 6- every 3 years, or cytology and HPV testing (“co-testing”) every 5
mercaptopurine, or cyclosporine, are continued as they appear to be years. Studies of screening intervals in women with history of
safe during pregnancy negative cytology results show increased risk of cancer after 3
 Methotrexate is contraindicated, and recently mycophenolate mofetil year (applicable abroad)
and mycophenolic acid havebeen reported to cause serious congenital  Due to the disease burden and low sensitivity of cytology in local
anomalies setting, either screening using conventional cytology (every year)
 Monoclonal antibody infliximab- treatment was given in the first or biennial screening with liquid based cytology (every 3 years) is
trimester with no adverse sequelae. recommended (applicable in Phil)
 Calcium supplementation is given to combat osteoporosis.
 Parenteral hyperalimentation has been used successfully during severe Cervical cytology reporting: The Bethesda System
recurrences. 1. Adequacy of sample
 Endoscopy or surgery is performed as indicated. a. Satisfactory
 Crohn disease is associated with increased adverse perinatal b. Unsatisfactory
 Outcomes usually related to disease activity 2. Squamous cell abnormalities
a. Atypical squamous cells (ASC)
 ↑ Preterm birth .
i. ASC of undetermined significance
 LBW – 2ndary absorption
ii. ASC cannot exclude high grade lesion
b. Low grade squamous intraepithelial lesion
MODULE 3 c. High grade squamous intraepithelial lesion
d. Squamous carcinoma
PREVENTIVE GYNECOLOGY 3. Glandular cell abnormalities
Cervical Cancer a. Atypical glandular cells, specify site or origin, if possible
 Abnormal bleeding or brownish discharge b. Atypical glandular cells, favor neoplastic
c. Adenocarcinoma in situ
Signs and Symptoms of Cervical CA d. Adenocarcinoma
 Patient presents with abnormal bleeding or brownish foul- 4. Other cancers (ex. Lymphoma, metastatic, sarcoma)
smelling discharge frequently noted following douching or
intercourse and also occurring spontaneously between menstrual FIRST STEP IN EVALUATION OF A WOMAN WITH AN ABNORMAL CERVICAL
periods CYTOLOGY REPORT
 Other symptoms: back pain, loss of appetite, weight loss (10%)
are late manifestations Squamous lesions
 History of not having Pap smear for years  ASC-US: HPV DNA testing for HR types; repeat pap test in 6
 40s to 60s median age of 52 years months; colposcopy
 ASC-H: colposcopy o Speculum exam
 LSIL: colposcopy or HPV DNA testing; ff up cytology in 12 months o Rectovaginal exam
o “Low grade can be pathologic or can be easily o Palpation
removed” o Ultrasound
o In menopause, HPV DNA testing or repeat cytology in
6-12 months is preferred to cytology in some Endometrial Cancer
consensus  50-60 years old
 HSIL: colposcopy  Compl ex atypical hyperplasia results from increased
estrogenic stimulation of the endometrium and is a precursor to
“COLPOSCOPY – another modality aside from pap smear, just like a big endometrioid endometrial cancer
microscope, uses magnifying lens that can pinpoint pathologies with smallest  Some CA develop w/o previous hyperplasia w/c are more poorly
lesion” differentiated and more aggressive
 Obesity is a strong risk factor (BMI > 30)
Once you see a lesion, do a biopsy  Unopposed estrogen stimulation is strongly associated with
endometrial cancer; risk could be decreased with use of
Glandular lesions: all reports require colposcopy and further evaluation if progestins
negative  OCP decreases the risk; protective effect starts after 1 year of use
and lasts approx 15 years after discontinuation
Cervical Biopsy  PCOS may also increase risk
(“punch”): small  SERM (selective estrogen receptor modulator) also increases risk
tissue samples  Most endometrial CA that develop from tamoxifen were
are taken from endometrioid histology and low endometrial CA grade and
the cervix & endometrial CA stage
examined for  Screen for endometrial ca: Endometrial biopsy by aspiration or
disease or other endometrial curettage
problems
Role of ultrasound on endometrial CA
“CIN: precancerous lesions of cervical ca. Do not mistake CIN diagnosis with
pap smear. CIN is only done after a biopsy” Cut-off >40mm??? for
post menopausal
Natural history of CIN women, aside from
 CIN1 or mild dysplasia result from an infection w/ HPV; may mass seen in UTZ,
resolve spontaneously (benign, can still wait, assess the px after 3- endometrial lining has
6mos, if still persistent do another modality) more contrast??
 CIN2 one half to two thirds of the thickness of the epithelium;
reversible, resolve spontaneously in 40%
Endometrial CA risk factors
 CIN3 full thickness of the epithelium involved in neoplastic
Increases the risk:
process; severe dysplasia and carcinoma in situ; precursor of
 Unopposed estrogen stimulation
invasive CA; 1/3 spontaneously resolve
Treatment  Unopposed menopausal estrogen replacement therapy (4-8x)
 CIN1  Menopause after 52 yrs (2.4x)
o Treatment is no longer preferred method except in  Obesity (2-5x)
patients with lesions that persist >12 month;  Nulliparity (2-3x)
treatment < 21 y/o is not recommended except if  Diabetes (2.8x)
lesion >24 months  Feminizing ovarian tumors
o Manifestation of a transient HPV  PCOS
o Require follow up and to ensure patient that lesion will  Tamoxifen therapy for breast CA
regress Decreases the risk:
 CIN2  Ovulation
o 40% regress spontaneously  Progestin therapy
o Follow up patient; if it progress to CIN3 then treat  Combination oral contraceptives
patient  Menopause before 49 years of age
o <21 y/o no need to treat, follow up  Normal weight
 CIN3  Multiparity
o Treat and long term follow up
o More related to cervical ca Ovarian CA
 Ultrasound remains to be the most helpful imaging examination
CASE for ovarian CA diagnosis with the highest sensitivity (92%)
19 year old
 Case in due to vaginal discharge Features highly suggestive of ovarian CA:
 Plan of management  Complex mass with both solid and cystic components
o Ask for sexual activity o Solid mass= malignant
o Screening modality: Gram stain: get a sample of  Papillary excrescences and projections
discharge  Internal echoes and septations
o Bacterial Vaginosis- clue cells seen histologically o Mass is probably malignant
36 year old  Ascites
 Case in due to intermenstrual bleeding o Advanced forms of ovarian ca, for tumors who have
o Do a biopsy metastasized
39 year old  Peritoneal metastasis
 Case in due to prolonged menses
 Plan of management
 ACS: every 5 years combined with FOBT is preferable to
sigmoidoscopy alone
Solid tumor
within a cystic Colonoscopy
mass with  More specific and sensitive
septations
 More expensive
 Screening: every 10 years for average risk person
 Patients who undergo colonoscopy do not require annual FOBT
 Addition of Doppler studies can help in preoperative evaluation
by providing better vascular characteristics of the ovarian masses Double Contrast Barium Enema
o Doppler studies are UTZ that can note the flow of  Alternative to Colonoscopy
blood within and outside the mass  Less expensive and more readily available
o Higher resistance=benign; Lower resistance= seen  Less sensitive and specific than colonoscopy
neovascularization, tumors that are more malignant  Abnormalities on DCBE need follow-up with colonoscpoy
have more neovascularization
 For epithelial ovarian CA, the combination of CA 125 and Human PEDIATRIC AND ADOLESCENT GYNECOLOGY
epididymal protein 4 (HE-4) provides highest sensitivity in GYNECOLOGIC EXAM IN A CHILD
predicting whether a pelvic mass is benign or malignant  components of a complete pediatric examination
 For epithelial ovarian CA, the risk of ovarian malignancy algorithm o history
(ROMA) presents a predictive index with different cut-offs for o inspection with visualization of the vulva, vagina, and
premenopausal and postmenopausal women using both CA-125 cervix
and HE-4 o if necessary, a rectal examination
o Premenopausal: ROMA value > 7.4 = high risk; < 7.4% =  History = child often ramble, many unrelated facts much- from
low risk parents.
o Postmenopausal: ROMA value >25.3% = high risk; <  Young children define their symptomatology on direct
25.3% = low risk questioning.
 The risk for malignancy index (RMI) in a woman w/ a pelvic mass  Educate = genital area call them “private areas”
includes a scoring system using UTZ, menopause status and CA  counsel= age appropriate and potential sexual abuse
125 serum measurements  reassure = examination will not hurt.
 sense of control and divert the child‘s attention
Ca125 o place the child‘s hand on top of the physician‘s hand
 Glycoprotein found on the surface of epithelial cells derived from o give her some choices = doll or toy with her
coelomic epithelium  Emphasize = most important part is just looking and theres
 Epithelial cells lining the fallopian tube, __?__ (sorry, blurred on conversation during the entire process.
trans), bronchus normally produces Ca125  To successfully examine a child=cooperation of the patient and a
 Poor sensitivity medical assistant.
 Abnormal in only 50% of women with Stage 1 disease  Child‘s reaction - depend on age, emotional maturity, and
 High false positive __?__ (sorry, blurred on trans) previous experience with health care providers allowed to
visualize and handle instruments to be used
Colorectal Cancer  Primary contact - immunizations= assure that no “shots” involved
 Colorectal cancer is a disease in which cells in the colon or rectum  assure that adult speculums are not part of the examination
become abnormal and divide without control, forming a mass  Occasionally pelvic examination done only until the second visit.
called a tumor. Difficult decision because in the field of pediatric gynecology,
o Risk factor: high meat diet and patients with many errors are errors of omission rather than of commission.
POLYPOSIS  Never restrain
 The exact causes of colorectal cancer are not known. However,  Reassurance and sometimes delay = best approach.
studies show that certain factors increase a person's chance of
 Rapport = feel safe to allow a gynecologic exam
developing colorectal cancer.
 rarely sedation or general anesthesia to complete an exam
 Health care providers may suggest one or more tests for
 to ensure cooperation = child as partner and assure her that shots
colorectal cancer screening, including a fecal occult blood test
are not involved.
(FOBT); sigmoidoscopy; regular, or standard, colonoscopy; virtual
colonoscopy; or double contrast barium enema (DCBE).
***Draping = may produce more anxiety
 People should talk with their health care provider about when to
begin screening for colorectal cancer, what tests to have, the
 handheld mirror = help when discussing specifics of genital
benefits and risks (potential harms) of each test, and how often to
anatomy.
schedule appointments.
 have all tools, culture tubes, and equipment within easy reach
 New methods, such as the genetic testing of stool samples, to
screen for colorectal cancer are under study.
First phase of the pelvic examination is evaluation of the external genitalia.
Fecal Occult Blood Testing
 Not adequate as a screening method Infant - examined on her mother‘s lap
 Regular FOBT can reduce mortality by 15-33% Young children = frog leg position
 ACS: yearly FOBT with sigmoidoscopy every 5 years is preferable Children 2 to 3 years of age = lithotomy with stirrups.
to FOBT alone Lithotomy = 4 to 5 years of age and older

Sigmoidoscopy  Once positioned, the vulvar area and Introitus is inspected


 Periodic sigmoidoscopy can reduce mortality by _?_% (sorry,  Introitus will gape open with gentle pressure downward and
blurred on trans) outward on
 Lowest cost compared to colonoscopy  The lower thigh or undeveloped thigh or labia majora area .
 Asking the child to pretend to blow out candles on a birthday cake o pelvic pain
may o suspicion of a foreign body
 Facilitate the process. o pelvic mass
 warned - rectal examination will feel pressure of a bowel
Second phase of the examination involves evaluation of the vagina. movement
 prepubertal uterus and ovaries = non-palpable on rectal exam
 Without the use of any insertion of instruments.  ratio of cervix to uterus = 2 to 1 in child, opposite in adult
 Utilize the knee chest position  Except for the cervix, any mass discovered on rectal examination
 Assistant pulls upward and outward on the labia majora on one  In a prepubertal exam should be considered abnormal.
side
 Examiner does the same with the non-dominant hand on the VULVOVAGINITIS
contralateral labia.  most common gynecologic problem
 An oto/ophthalmoscope = illuminate the vulvar area,used as  80% to 90% involve the classic symptoms of vulvovaginitis
magnifying  introital irritation(discomfort/pruritus)or discharge .
 Instrument light source ; not inserted into the vagina.  prepubertal vagina neutral or slightly alkaline
 The light from the oto ophthalmoscope is shone into the vagina as  on puberty vagina becomes acidic = bacilli dependent on a
the examiner evaluates the vaginal walls. glycogenated estrogen-dependent vagina.
 Cervix appears as transverse ridge or flat button that is redder  Breast budding is a reliable sign that the vaginal pH is shifting to
than the vagina. an acidic environment.
 Generally successful in cooperative children unless there is a very  severity of symptoms varies
high crescent-shaped hymen, too difficult to shine light into small  pathophysiology = involves primary irritation of the vulva, may be
aperture at the vaginal introitus. accompanied by secondary involvement of the lower third of the
 foreign object and the cervix may be visualized using this vagina.
technique.  Most cases involve an irritation of vulvar epithelium by normal
 Following inspection, vaginal secretions = microscopic rectal flora or chemical irritants == nonspecific vulvovaginitis.
examination and culture.  predisposing vulvar irritations perfumed soaps, tight seams of
blue jeans, which creates denudation, allowing the rectal flora to
NORMAL FINDINGS - HYMEN OF A PREPUBERTAL CHILD infect the irritated epithelium.
 crescent-shaped, annular or ring-like in configuration.  vagina cultures = normal rectal flora or Escherichia coli
 no reported cases - congenital absence of the hymen.  Nonspecific vulvovaginitis accounts for the majority of
 mounding of hymeneal tissue is called a bump which are normal vulvovaginitis cases.
 variant, often attached to longitudinal ridges in the vagina.
 Hymens in newborns are estrogenized have thick elastic Physiologic Reasons why children are more susceptible
redundancy.  lack of labial fat pad, pubic hair
 Older unestrogenized girls have thin non-elastic hymens  anatomical proximity of vagina and anus
 complete transections of the hymeneal tissue between 3 o‘clock  thin labia minora
and 9 o‘clock are not congenital but acquired  no estrogen
 Noncongenital ―bumps‖ may be present near hymeneal  alkaline pH
transections.  lack glycogen, lactobacilli, sufficient antibodies

NORMAL FINDINGS -VAGINA OF A PREPUBERTAL CHILD Behavioral Reasons-child prone


 Vaginal epithelium = redder and thinner  major factor is poor perineal hygiene
 Vagina is 4 to 6 cm long; narrower, and lacks the distensibility  anatomic proximity of the rectum and vagina
 Secretions = neutral or slightly alkaline pH.  after toilet training, unsupervised when defecating
 Indications for Vaginoscopy  wipe anus from posterior to anterior
 Recurrent vulvovaginitis  minor vulvar irritation scratch-itch cycle, secondary seeding
 Persistent bleeding occurs
 Suspicion of a foreign body or neoplasm  because children don‘t wash their hands
 Congenital anomalies  tight fitting & nonabsorbent clothes= vulvar skin irritated, warm
 Vaginoscopy requires inhalation-anesthesia, and moist
 Narrow-diameter endoscopes Kelly air cystoscope contact
hysteroscopes, pediatric cystoscopes, small-diameter Etiologic Factors of Premenarcheal Vulvovaginitis
laparoscopes, plastic vaginoscopes, and special virginal speculums  Nonspecific Vulvovaginitis
byHuffman and Pederson. o rectal normal flora /
 Ideal pediatric endoscope - cystoscope or hysteroscope because o chemical irritants
the accessory channel facilitates lavage of the vagina. o poor perinal hygiene
 Nasal speculum or otoscope is too short has advantage of having  Specific
built-in light sources. o Group A-ß hemolytic Strep
 Local anesthesia 2% topical viscous lidocaine (Xylocaine) o Strep pneumoniae
lidocaine/prilocaine. o H.influenza
o E.coli ; other enterics
 Divert the child‘s attention by simultaneously compressing one of
o Shigella
the patient‘s buttocks, an extinction technique.
o Chlamydia
o N.gonorrhea
Last step in the pelvic examination may be a rectal examination.
 Helminthiasis: Enterobius Vermicularis
o nocturnal vulvar and perianal itching
 most distressing part; may be omitted, depending on the child‘s o discovered by flashlight or by dabbing of clear
symptoms. cellophane adhesive tape
 reasons for rectal exam:  mycotic not common = alkaline pH dont support fungal growth
o genital tract bleeding o immunosuppressed
o Systemic dse  denuded epith-agglutinates and fuses tog
o Systemic skin dse  thin,narrow line in a vertical direction-pathognomonc
o lichen sclerosus  diff : imperforate hymen,vaginal agensis
 Other specific causes of vulvovaginitis  2-6 years old-nadir of estrogen
o systemic diseases = chicken pox, and herpes simplex  Spontaneous sepration : 6-18 months
infection  symptomatic
S/S of Vulvovaginitis  voiding difficulties
 variable and not diagnostic  recurrent vulvovaginitis
 mother becomes aware :  discomfort from labia pulling at the line of adhesion
 staining of the child‘s underwear  bleeding from the line of adhesion
 child complains of itching or burning  treatment - topical estrogen cream
 wide color ranges, quantity of discharge,  separates in 2-8 weeks
 bloody and purulent discharge = from a foreign body
 patients infected Shigella boydii = present with a bloody or URETHRAL PROLAPSE
 blood-tinged discharge.  presentation - prepubertal bleeding
 vulvar erythema, edema, and excoriation  sliding out of the urethral mucosa thru the ext meatus
 red donut-like annular mass-can becomes necrotic
Differential Diagnosis of Persistent or Recurrent Vulvovaginitis  Diff Dx : sarcoma botryoides grapelike mass
 Not responsive to treatment include :  Treatment
o foreign body o conservative and noninteventional.
o primary vulvar skin disease o estrogen creams and antibiotic ointments.
o ectopic ureter o Surgery - necrosis ,persistent s/s despite medical tx
o child abuse
o predominant symptom is pruritus = pinworms or LICHEN SCLEROSUS / LICHEN SCLEROSUSATROPHICUS
irritant/ nonspecific vulvitis are the most likely  skin dystrophy - occur in epithelium that is irritated.
diagnosis  commonly - postmenopausal women , prepubertal children.
o vulvar skin affected by systemic skin diseases-- lichen  cause - unclear, may be autoimmune
sclerosus,
 Histology - thinning of vulvar epithelium with loss of rete pegs.
o seborrheic dermatitis, psoriasis, and atopic dermatitis.
 lesions - always limited by the labia majora
o classic perianal ―figure-8‖ or ―hourglass‖ rash is
lichens
S/Sx :
o scleroses with white patches
 pruritus and vulvar discomfort.
o ectopic ureter emptying to vagina may intermittently
 other : prepubertal bleeding, constipation, and dysuria.
o release
 hourglass or figure-8 formation of genital and perianal area,
o small amount of urine
lichenified with a parchment-like appearance.
Treatment of Vulvovaginitis  Secondary changes - excoriation = blood blisters and breaks in the
 foundation of treatment = improvement of local perineal hygiene. skin w/c presents as prepubertal bleeding. And usually
misdiagnose as sexual abuse
 vulvar skin should be kept clean, dry, and cool
 diagnosis is unclear = punch biopsy to confirm
 avoid irritants (bubble bath)
 acute weeping lesions, wet compresses of Burrow‘s solution
Treatment
 void with knees spread wide apart
 avoiding irritation or trauma
 wipe from front to back after defecation
 avoid straddle activities when
 Loose-fitting cotton undergarments
 symptomatic
 avoid harsh soapsMost cured solely = improved local hygiene
 sitz baths
 (hygienic changes and sitz baths)
 Tight clothing
 Relief of vulvar irritation
 avoid scrubbing with soap - exacerbate the disease
 bland cream- zinc oxide creams or cod liver oil creams
 mature reproductive women - clobetasol = treatment of choice
 very low, low or medium potency steroid creams
 short duration-complication= adrenal suppression
 oral antibiotics for 10 to 14 days, = for recalcitrant cases
 safety not established in children < 12 years old, response-2-week
 If the problem is hygiene, broad-spectrum antibiotics only offer
interval
temporary relief
 LS improves with puberty ; resolution sometimes occur
 Vaginal cultures determine choice of oral antibiotic
 recurrent cases = broad spectrum to decrease E. coli inoculums.
VULVAR TRAUMA
 obtaining a vaginal culture
 common cause - straddle injury
 nasopharyngeal small swab moistened with nonbacteriostatic
 unilateral and superficial injury rarely involving the hymen
saline
 hymen is transected from accidental trauma= history of
 using a catheter within a catheter- uses a No. 12 red rubber
penetrating injury (falling onto a stick horse or broom) = confirm
bladder catheter for the outer catheter and the hub end of an
that object has not penetrated into the vaginal wall
intravenous butterfly catheter for the inner catheter. The outer
 dangerous hematoma
catheter serves as an insulator, and the inner catheter is used to
 perforation into the cul-de-sac
instill a small amount of saline and aspirate into the vaginal fluid.
 perforation of the abdominal cavity
 presence of sexually transmitted organisms =sexual abuse ;
 with potential visceral damage
appropriate referral and follow-up is necessary
 A vaginoscopy or laparoscopy- to rule out these possibilities
 perineal hygiene
 In children presenting with trauma and genital bleeding
 bland creams - zinc oxides,cod lier creams
 site, extent, and amount of bleeding
 steroid cream
 topical anesthesia
 antibiotics
LABIAL ADHESION/ADHESIVE VULVITIS  wash- irrigate with sterile warmed water
 labia minora adhered tog  Typical lacerations- denudation around urethra or labia
 posterior fourchette is less commonly involved  complete interview by mental health provider
 give booster tetanus toxoid if last immunization > 5 years o minimizes repetitive questioning
 superficial lacerations (first-degree obstetric lacerations) no repair o allow rapport to begin
 treated - applying oxidized cellulose or similar products to stop o relationship can transit into therapy if indicated.
the bleeding.  also consider sexual abuse based on historical complaints or PE
 Slightly deeper lacerations can be repaired with small Steri-Strips  critical for the provider to query the guardian or parent in a
 deeper lacerations - suturing to stop substantial bleeding nonthreatening manner
o inferior aspect of the labia minora o approach is ―we are all on the same team and we
 General anesthesia both want to ensure the safety of your child.
o for diagnosis and treatment of deep & extensive  Queries to the child = open ended and nonjudgmental
lacerations
o children- unable to tolerate repair Legal Issues in Reporting Possible Sexual Abuse
 after anesthesia, laceration is irrigated and debrided, the vessels  Every state requires that suspected and known child abuse be
ligated, and the injuries repaired reported.
 laparoscopy or an exploratory celiotomy - retroperitoneal  suspected = Isolated complaints that may be associated with
 hematoma or intraabdominal injury suspected sexual abuse (e.g., nightmares or genital bleeding)often do not
require a report.
VULVAR HEMATOMA  Clinicians may suspect sexual abuse based historical complaints
 blunt object - hematoma results and physical exam findings
 sharp object - laceration  If a provider is unsure= discuss the situation with local child
 potential for penetration of perineum protective services or a social worker.
 injury to internal pelvic organs.  They can help providers avoid filing vague unnecessary reports
 Others : sexual abuse, automobile and  They also aid in filing reports in borderline cases that justify
 bicycle accidents, kicks sustained in a exploration to obtain safety of children.
 fight, and self-inflicted wounds  discussion with agencies - help protect providers from
 Initially - bleeding into loose connective tissue prosecution for failure to report.
 pressure from expanding hematoma exceeds venous pressure=  important to document discussions in patient charts.
stop  Providers should not be hesitant to file because of fear of liability
 extent of hematoma - determined by visualization and palpation for an alleged false report = states generally ensure immunity
 treatment of nonexpanding hematomas – majority  there have been successful malpractice actions against providers
o observation by serial examination who have failed to diagnose or report sexual abuse
o ice pack or cool sitz bath
o pain medications Hymens in the Evaluation of Sexual Abuse
 surgical exploration if expanding over 1 to 2 min = arterial  transverse diameter of hymen was previously used as a marker of
laceration abuse
 state of the hymen is not a reliable marker of abuse.
SEXUAL ABUSE  Complete transections of the hymen and clefts that extend to the
 extremely common junction of the hymen between 3 o‘clock and 9 o‘clock are not
 20% - involved in some type of sexual activity during childhood. congenital, but if present they could be from abuse or a child
 Most perpetrators are male acquaintances known and trusted by inserting an object.
the families.  Controversies exist as to the significance of incomplete
 Fathers- 21% transections
 other male relatives - 19%
OVARY AND ADNEXA
 mothers involved 4% to 8%
 Babysitting -common reason - gain access to children.
Corpus luteum cysts
 child or family presents with potential sexual abuse as the chief
 Management is similar to that in mature reproductive women,
complaint
 observation ; unless signs of malignancy are present.
 child is seen for another complaint but provider considers the
 Consideration if theres both solid and cystic components.
possibility of sexual abuse based on historical information or
o dermoids
physical examination.
o germ cell tumors
 Telephone calls regarding potential sexual abuse are a challenge
 rare cases of intersex such as mixed gonadal dysgenesis, suspicion
for practitioners.
of malignancy should be high.
 Urgent evaluation is necessary
 A rare presentation of hypothyroidism is pediatric ovarian cysts.
o abuse occurred within 72 hours (for forensic evidence)
o child is in a danger of repeated abuse or self-harm
Ovarian Tumors in Childhood and Adolescents
o obvious injuries such as lacerations require treatment
 can be benign and malignant
 If none of these criteria = evaluated on a nonurgent basis.
 considered if with solid ovarian masses or cystic and solid
 specially trained personnel /sexual abuse team/other community
components on ultrasound.
 resources/qualified mental health provider (such as a social
 if functional ovarian cysts do not resolve during serial monitoring.
worker or
 Germ cell tumors = most common gynecologic neoplasm
 psychologist) who is experienced in evaluating sexual abuse
 most are benign ovarian teratomas
 Unless medical reasons, interview is performed prior to a genital
exam  most common malignant germ cell tumor = dysgerminoma
1. children may not be able to separate exam from followed by endodermal sinus tumors.
touching involved in abuse= history more difficult  Bilaterality - 10% to 15% of dysgerminomas, but it is rare in all of
2. majority of abused children - exam is completely the other germ cell tumors of the ovary except for immature
normal. teratomas.
 important not to rely on exam to seek counseling or intervention  Sex cord tumors, such as granulosa and thecal cell tumors =
that would keep their child safe. produce steroids.
 gonadoblastomas, a germ cell and sex cord tumor, seen in  with onset of gonarche and reactivation of HPO axis, level of
patients with intersex disorders such as mixed gonadal estrogen becomes cyclic resulting to menstruation.
dysgenesis.  menstrual bleeding-anovulatory in first 2 years after menarche
 most common clinical manifestation of an ovarian tumor  ovulatory or regular cycles only after maturation of the biphasic
o Recurrent abdominal pain = ovaries are abdominal positive feedback system
organs  rise in estrogen at the late follicular phase triggers luteinizing
o presence of a mass homone surge and ovulation at mid cycle
 increasing abdominal girth=symptom ovarian enlargement.  sequence of physiologic events
 Some -only vague discomfort, abdominal fullness or bloating. o begins - somatic change: an increase in growth velocity
 adnexal masses in children - more frequently associated with o followed by appearance of secondary sexual
acute complications characteristics
o torsion  breast development (thelarche)
o hemorrhage  appearance of pubic hair (adrenarche),
o rupture o followed by - period of maximal growth
 1% of all neoplasms in premenarcheal children. velocity(approximately 9 cm/year)
 Ultrasound o menarche
o to establish the origin of mass
o cystic or solid TYPES OF DISORDERS
o presence of ascites  GnRH-dependent (complete, true)
o Calcifications - appear toothlike = ovarian teratoma.  GnRH-independent (incomplete, pseudo)
 abdominal computed tomography (CT)  isosexual and heterosexual disorders.
 magnetic resonance imaging (MRI)  pathophysiology- divided into two distinct categories
 preoperative workup = tumor markers o normal physiologic process (involving GnRH secretion
o a-fetoprotein with an integrated hypothalamic–pituitary axis) occurs
o human chorionic gonadotropin (HCG; both alpha and at an abnormal time
beta) o physiologic process independent of an integrated
o inhibin hypothalamic-pituitary-ovarian axis.
o lactate dehydrogenase  GnRH-dependent precocious puberty
o stradiol o premature maturation of theHPO axis
o testosterone o normal menses, ovulation, and the possibility of
 in preadolescent females, both benign and malignant, are usually pregnancy.
unilateral.  GnRH-independent precocious puberty involves
 conservative management - opposite ovary to protect future o premature female sexual maturation
fertility. o estrogen-induced uterine stimulation and bleeding
 During surgery -opposite ovary inspected and palpated. o without any normal ovarian follicular activity.
 unnecessary to biopsy a normal-appearing contralateral ovary  Both have increased levels of estrogen
 exceptions in malignancies where bilaterality usual  Prolonged follow-up= to rule out subtle, slowgrowing lesions of
o dysgerminoma the brain, ovary, or adrenal gland.
o immature teratoma  70% develop a GnRH-dependent process
 referred to specialists o cause= unknown (constitutional)
o proper staging procedures,  30% are secondary to CNS disease.
o lymph node sampling and omentectomy  Kisspeptin, a hypothalamic peptide that stimulates the release of
o for adjuvant chemotherapy in nondysgerminomas GnRH, is involved in the initiation of puberty.
 in premenarcheal adolescent o Two activating mutations of the Kisspeptin receptor
o 75% to 85% in that necessitate surgery are benign have been described in girls with central precocios
o 15% to 25% are malignant neoplasms puberty.
 two goals in surgical therapy:  definitive diagnosis is established more often for
o appropriate surgical procedure including lymph nodes pseudoprecocious puberty, usually related to ovarian or adrenal
o preservation of future fertility disorder.
 hysterectomy not necessary even in bilateral childhood or  secondary sex characteristics are discordant with the genetic and
adolescent ovarian malignancy. phenotypic gender, =heterosexual precocious puberty.
o for future fertility - artificial reproductive
technology/use of donor eggs Hypothyroidism
 usually associated with delayed pubertal development
PRECOCIOUS PUBERTY  rare cases, untreated hypothyroidism results in isosexual, GnRH-
Changes during Puberty dependent, or GnRHindependent precocious puberty.
1. Appearance of secondary sexual characteristic  caused = primary thyroid insufficiency, usuallyHashimoto‘s
 zona reticularis of the adrenal glands grows at 6- 8 yo and thyroiditis
secretes dehydroepiandrosterone,its sulfate and  pathophysiology = diminished negative feedback of thyroxine,
androstenedione.= devt of acne vulgaris,body odor,pubic and increased production of TSH and gonadotropins
axillary hair  ONLY cause of PP where bone age is retarded.
 at 8 y/o= thelarche /breast development noted  observed = 6 to 8 years old
2. Growth Spurt
 peak height velocity is reached 6 months before menstruation Iatrogenic or factitious precocious puberty
 hormonal control of puberty growth  when a young female used hormone cream or ingested adult
o sex steroids medications ( oral estrogen or birth control pills)
o growth hormone  secondary sexual characteristics regress after discontinuation of
o insulin growth factor 1(IGF 1) medication
o thyroid hormone DIAGNOSIS
3. Menstruation  begins with history and physical examination
 primary emphasis = to rule out life-threatening neoplasms of the  Insulin Resistance/ hyperinsulinema
ovary, adrenal gland, or CNS. o Acanthosis nigricans
 secondary emphasis = to delineate the speed of the maturation o Abdominal obesity
process, o Glucose intolerance
 The height of girl and exact stage of pubertal development,Tanner  Polycystic ovaries on ultrasound
stage, is recorded. o Enlarged ovaries
 long list of causes, a number of tests, including imaging studies of
the brain, serum estradiol level, FSH level, and thyroid function Screen for metabolic abnormalities
tests, may need to be carried out to establish the diagnosis  Age 6 – 10 years
 With this acceleration of development, sex steroid and adrenal o Obesity if >90th percentile waist circumference
androgen (DHEAS) levels are elevated  Age 10 – 16 years
 Acceleration of growth is one of the earliest clinical features of o Waist circumference >90th percentile
precocious puberty. o Adult criteria for triglycerides. HDL – C
 bone age is determined by hand-wrist films and o Blood pressure elevation
 compared with standards for a patient‘s age o Blood glucose

Normal Menstrual Cycle Metabolic sequelea of PCOS


 mean interval between menses = 28 days (7 days).  hyperinsulinemia stimulates both ovarian and adrenal androgen
 mean duration of menstrual flow = 4-7 days secretion
 mean cycle interval = 21-45 days  Suppresses SHBG from the liver resulting in an increase in free,
 average menstrual blood loss = 35 mL biologically active androgens.
 accurate method used in predicting blood loss = alkaline hematic  The excess in local ovarian androgen production augmented but
method, which measures hematin hyperinsulinemia causes premature follicular atresia anovulation.

Polycystic Ovarian Syndrome Goals of therapy in adolescents with PCOS


 Presents during adolescence  Short term – amelioration of hirsutism, acne and irregular
 Anovulation (amenorrhea, oligomenorrhea, irregular cycles) menstruation.
 Symptoms of androgen excess (hirsutism, acne, alopecia)  Long term – prevention of long term sequelae from anovulation
 Polycystic ovaries and hyperinsulinemia

Etiology Management of PCOS in adolescent


 genetic disorder  Treat obesity, hirsutism and irregular menses
o Familial clustering of cases  Combined oral contraceptive pills
o Greater concordance of symptoms in identical twins  Minor lipid pattern
compared to non-identical twins  Metformin plus a change of diet-obese adolescent
o Heritability of endocrine and metabolic features o Diminish insulin resistance, total cholesterol and
o Mode of inheritance remains unclear triglycerides
 Environmental factors can influence clinical and biochemical o Resumption of normal menses
phenotype
 Prenatal Androgen excess is linked to developmental of PCOS Managemant of Hirsutism in the adolescent
later in life.  Physical methods of hair removal
 Insulin resistance in association with premature pubarche  Oral contraceptive pill
increase risk of development of PCOS.  Antiandrogenin combination with OCS
o Spironolactone
Mechanism o Flutamide
 Peripheral insulin resistance o Cyproterone acetate
 Consequent compensatory hyperinsulinemia
ABNORMAL UTERINE BLEEDING
Rotterdam criteria in adolescents Definitions
 Oligomenorrhea or amenorrhea present for at least 2 years after Normal menses
menarche  Every 28 days +/- 7 days
 Polycystic ovaries on ultrasound including ovarian size of >10cm2  Mean duration is 4 days.
 Hyperandrogenemia: not just the sign of androgen exces  More than 7 days is abnormal.
 Hyperandrogenemia: maybe a more consistent marker for PCOS  Average blood loss with menstruation is 35-50cc.
during the teenage years  95% of women lose <60cc

Identifying teenage groups at risk for PCOS Menorrhagia:


 Obese  Prolonged menstrual bleeding
 Hirsute  > 7 days or > 80 cc occurring at regular intervals.
 Irregular menses
 Diagnosis should include all 3 elemnts of Rotterdam Criteria Frequency of AUB
 Confirmed only if hyperandrogenism, oligoamenorrhea, and  Menorrhagia occurs in 9-14% of healthy women.
polycystic ovaries on ultrasound  Most common Gynecological disorder of reproductive age
women
Alternative method for diagnosis of PCOS in adolescents
 Oligomenorrhea or amenorrhea two years after amenarche Metrorrhagia:
 Clinical hyperandrogenism : persistent acne, severe hirsutism  Uterine bleeding occurring at irregular but frequent intervals. (<
 Biological hyperandrogenism, 21 days) but the duration and amount is normal
o Plasma testosterone >50 ng/dl  May regular interval kaso nga lng may intermenstrual bleeding.
o increased : LH/FSH ratio >2 May normal cycle pa rin.
Reproductive Tract Causes
Menometrorrhagia: 1. Gestational events
 Prolonged uterine bleeding occurring at irregular intervals. >7  Abortions
days and irregular  Ectopic pregnancies: Why? Because the endometrium always
 Most problematic because it is unpredictable in interval, duration decidualize when you get pregnant, pag d sya nagimplant sa
and amount. endometrium decidualized parin sya, thickened so it has the
capacity to bleed
Oligomenorrhea:  Trophoblastic disease (H-mole) more profuse bleeding
 Reduction in frequency of menses  IUP
 Between 35 days and 6 months. 2. Malignancies
 >6 months= amenorrhea  Endometrial
 > 1 year (esp. pag matanda na)= menopause  Ovarian
 Cervical
Amenorrhea:  Vaginal
 Absence of menses 3. Benign
 Primary amenorrhea- no menses since birth  Atrophy
 Secondary amenorrhea  Infections
o No menses for 3-6 months  Uterine
o Pregnancy
Hypomenorrhea o Leiomyomas
 Reduction on number of days( 1-2 days) o Polyps
 Reduction in amount of flow o Hyperplasia
 Regular interval o Carcinoma
 Vaginal or labial lesions
Menarche (12-13 y/o) o Carcinoma
 average age 12.43 years o Sarcoma
 First menstrual flow o Adenosis
 Signifies Start of reproductive potential o Lacerations
 Doc: it does not signify the start of the reproductive capability. It o Foreign body
is only an EVENT in a woman’s life! Because the first 3 years of  Cervical lesions
menstruation is usually anovulatory and irregular so there is still o Polyps
no capacity to reproduce. o Condyloma
o Cervicitis
Reproductive years (Lasts 360 cycles) o Neoplasia
 Monthly menstrual flow  Urethral
 Signifies period of reproductive potential o Caruncle
 15-45 y/o regular bleeding o Infected diverticulum
 GI
Menopause o Hemorrhoids because the anus and vaginal canal are in
 Perimenopause- abnormal bleeding before menopause bec of close proximity minsan akala vaginal bleeding pero
anovulation. galling pala sa anus
 average age 51.4 years
 Last menstrual flow
 Signifies end of reproductive potential
 Doc: end of bleeding. 1 year without bleeding

Ovulatory cycles for 30 years

Most Common Causes of Reproductive Tract AUB ENDOMETRIOSIS AND ADENOMYOSIS


 Pre-menarchal ENDOMETRIOSIS
o Foreign body
 Reproductive age Pathogenesis:
o Gestational event(always) 1. Implantation Theory/ Retrograde Menstruation Theory (Sampson,
o pregnancy related 1921)
 Post-menopausal 2. Lymphatic and Vascular Dissemination Theory (Javert, 1952)
o Atrophy 3. Coelomic Theory (Meyer)
o Not cancer! 4. Genetic Theory
5. Immune System Dysfunction (immunologic theory)
6. Iatrogenic Dissemination
Most popular: retrograde Symptoms are
 Very variable
Pathology  Vary with the focus location
A. Appearance  Often bear no relation to the extent of the disease
 The most common sites:  Quite often deposits are found incidentally in women who have
1. Ovary (chocolate cyst) no symptoms.
2. Peritoneum of the recto–vaginal cul–de–sac of the Pouch of  (25% have no symptoms)
Douglas  Often bear no relation to the extent of the disease--‐pts may be
3. Utero–sacral ligaments severe but with minimal presentation. May be related to pain
4. Sigmoid colon threshold
5. Broad ligament
**Not all non chocolate cyst would mean not an endometriosis. It is affected Diagnosis
by the cycle. During postmenstrualtion, may appear as  History
yellowish,brownish,white.  Pelvic/Internal examination
**Common factor:all within the pelvic area  Laparoscopy (gold standard)
**Chocolate cyst- ovaries enlarged into 12cm demonstrated with cystic  Ultrasonography (transvaginal/transabdominal)
cavity. Cut section blood filled, aberrant endometrial tissue that is affected
 CA–125↑(< 200U/ml;normal value 35U/ml)
by the hormonal tissue
 MRI
 Less common sites:
**Hx:painandinfertilityUTZ--‐unlessthereiscystitisinconclusive
1. Cervix
Increased CA125(>200U/ml ; normal value 35U/ml elevated in pts with
2. Round ligament
cancer, infection intraabdominaly, because it is a measure of intrabdominal
3. Urinary system(bladder, ureter)
irritation.
4. Umbilicus Laparoscopic-‐is both diagnostic and therapeutic
5. Appendix
6. Laparotomy scars Staging Systems
 Multiple Appearances of endometrial implants  Points are assigned for severity of endometriosis based on the
o Raised,reddish,superficial nodules size and depth of the implant and for the severity of adhesions.
o Fibrotic,whitish nodules  The points are summed and the patients are assigned to one to
o Raised,glossy,translucent blobs four stages:
o Reddish or bluish ovarian cysts Stage
o Appearance dependent on age I Minimal disease 1-5 points
**Grossly, in areas of endometriosis the blood is darker and gives the small
II Mild disease 6-15points
foci of endometriosis the gross appearance of "powder burns". Areas of
III Moderate disease 16-40points
endometriosis can be seen and obliterated by cauterization via laparoscopy)
IV Severe disease >40points
**Powder burn lesions and some implants. - Why remove because of the
severe pain. **More adhesions you have the bigger the size of lesions the greater the
**Before radical surgery, try medical management (first--‐>fails--‐>surgery or depth scoring is higher ergo stage is higher
neoadjuvant effect)

B. Microscopic Appearance
 Histomorphologically similar to endometrium
 Four major components:
1. endometrial glands
2. endometrial stroma
3. fibrosis
4. hemorrhage

Clinical Manifestations
 Symptoms
o Pain
o progressive dysmenorrhea
o dyspareunia
o Menstrual disturbance
o Infertility
o **Most common- pain and infertility
o Younger age group: pain, dyspareunia. Uterus is fixed:
uncomfortable during sex, because it is adherent to
uterine peritoneum.
o Another hallmarks :adhesions—non patent fallopian
tubes leading to infertility
 Signs
o Enlargement of the ovaries, fixed
o Fixed retroversion of the uterus
o Tender nodules within the pelvis
o Cannot be diagnosed by PE/IE alone.
o Should always be considered when patients have
symptoms referable to the pelvic cavity.
**retroversion of the uterus uterus facing down Treatment
25% of pts are asymptomatic and if single infertility is not yet a complain Goal:
Goldstandard: Laparoscopy  Relief of PAIN
 Restore FERTILITY (Fertility work-up, semen analysis..) o Hyperestrogenemia
 Prevent RECURRENCE o Viral transmission
Expectant Therapy: Pathology
 Indications: with very limited disease (whose symptoms are  Gross Appearance:
minimal or nonexistent) o Globular uterus- bleeds- uterus balloons
 If trying to get pregnant, the best way is to do laparoscopic o Usually hyperemic with thickened walls
therapy as early as possible. o The foci are frequently scattered diffusely throughout
Medical Therapy: the myometrium.
 Indications: chronic pelvic pain o Occasionally,may be more circumscribed,with the
o severe dysmenorrhea formation of a distinct nodule,an adenomyoma
o no desire to get pregnant  Adenomyosis- no distinct nodule
o no ovarian cyst formation  Adenomyoma- nodule but with no capsule, no clear border
 Hormone–inhibition therapy
 GOAL: induction of amenorrhea Clinical Symptoms
 Pain Reliever only +infertility drugs- wants to get pregnant  Symptomatic adenomyosis occurs primarily in parous women
Drugs: over the age of 40. (30-50y/o)
 Danazol:pseudomenopause therapy: (800mg/day)high-dose  Classic symptoms:
progestin: 2.5-7.5mg/wk) o secondary dysmenorrhea
 GnRH–agonist: medical oophorectomy o abnormal uterine bleeding
o leuprolide acetate 3.75mg IM/mo or 11.25mg IM/3mo  Most common physical sign:
o nafarelin acetate 800ug/day o a diffusely enlarged uterus (rarely exceeds 12 weeks
o goserelin acetate 3.6mg/28d SCimplant gestation in size)
 add – back therapy : o particularly tender during menstruation
o to reduce vasomotor symptoms, vaginal atrophy,  Secondary dysmenorrheal- before wala, ngayon meron na dahil sa
demineralization of bone trauma
 30pg/ml estradiol  Tender during menstruation
 Progestogens:pseudopregnancy therapy  Best time to do physical exam- Menstruation (3rd-5th day)
Surgical Therapy (1) (goal: preserve function, to reproduce) ** (+) reproductive age group, secondary dysmenorrhea – dysmenorrhea 3-4
 Indications: days prior to onset or after the menses; abnormal uterine bleeding –
o adnexal mass prolonged bleeding, menorrhagia, bleed in the middle of the cycle
o pelvic pain
o infertility Diagnosis
 Approaches:  History
o trans – abdominal  Pelvic examinations
o laparoscopic (advantage is faster recovery)  Ultrasonography – large, thick, small cystic s
Surgical Therapy (2)  Serum markers:CA-125↑
 Methods: **Elicit the symptoms usually seen
o Conservative surgery **IE: slight enlarged uterus and tender
o preserve the fecundity
o preserve the ovarian function Treatment
 Definitive surgery:  Hormone therapy
o hysterectomy + salpingo–oophorectomy  Hysterectomy, the only uniformly successful treatment for
Combination of Medical and Surgical Treament: 3 Step Approach (recurrence adenomyosis, is necessary
are is very high)  Uterine Artery Embolization
**rarely will the uterus enlarge for about 14 weeks; if ?  do surgery
**Ligate the uterine artery by introducing an emboli, is variably successful
**the only definitve surgery: hysterecomy

MODULE 4

INFECTIONS OF THE LOWER GENITAL TRACT


Infections of the Vagina
- normal pH: 4.0
- normal flora: Lactobacillus vaginalis
It is important to individualize the choice of therapy. - normal secretions: white, floccular or curdy, and odourless
 Therapy must be tailored to - - vaginal discharge is the most common symptom in gynecology
o the degree of symptomatology associated symptoms of vaginal infection include:
o the patient’s age  superficial dyspareunia
o her desire to maintain fertility  dysuria
ADENOMYOSIS  odor
 A benign uterine condition in which endometrial glands and  vulvar burning and pruritus
stroma are found deep in the myometrium - three common infections of the vagina are produced by:
 A type of endometriosis  fungus (candidiasis)
 protozoon (Trichomonas)
Etiology  synergistic bacterial infection (bacterial vaginosis)
 Basal endometrial hyperplasia invading a hyperplastic myometrial
stroma. A. TRICHOMONIASIS
 Four primary theories: - Caused by Trichomonas vaginalis ( flagellated protozoa )
o Heredity - Sexually Transmitted
o Trauma - curettage
- Can inhabit vagina and male urethra - Terconazole
- 25 % of infected pxs are asymptomatic
- Clinical Features : C. BACTERIAL VAGINOSIS
1. Thin , frothy , pale greenish or grayish - Formerly called non-specific vaginitis or Gardnerella vaginitis
2. vaginal discharge - Presence of anaerobes : Bacteroides sp. Peptococcus spp.
3. Foul rancid odor - Not classified as Sexually Transmitted Disease
4. Erythema and edema of vulva/vagina - Clinical Features :
5. Petechiae of cervix (“strawberry cervix”)  Profuse , thin , grayish , foul-smelling discharge+ KOH
- Diagnosis : Wet mount smear or Culture Pear-shaped motile  release of amines  “Fishy Odor”
protozoa with flagella  Profuse, Thin Homogenous Discharge
- Recommended Treatment :  Vulvovaginal itching and irritation (~ 20 %)
a. Metronidazole 2 gms orally single dose or 500 mg BID x - Amsell’s Criteria for diagnosis of BV : 3 oUt of 4:
7 days 1. (+) homogenous vaginal discharge
b. Both partners have to be treated to prevent reinfection 2. pH of vaginal discharge ≥ 4.5
3. (+) Whiff test
Thin , Frothy 4. (+) Clue cells > 20 % more than vaginal epithelial cells on wet
Discharge smear/mount

Profuse, Thin
Homogenous
Strawberry Discharge
Cervix

Clue Cells

Trichomonads

Recommended Treatment :
 Metronidazole 500 mg BID x 7 days
B. CANDIDIASIS  Metronidazole gels
- Caused by a yeast : Candida albicans ,glabrata ,tropicalis  Clindamycin creams
- High-risk factors :
o Pregnancy GENITAL ULCERS
o Diabetes A. HERPES GENITALIS
o Oral Contraceptives - Venereal disease caused by : Herpes simplex type II (90% of cases)
o Antibiotic abuse and type I (10% of cases)
- Normal inhabitant of the vagina - Primary infection : s/sxs appear within 3-7days after exposure
- Opportunistic infection - May be asymptomatic
- Clinical Features: - Evolution of HSV Lesions :
o Whitish to yellowish , thick , “cheese-like” or “ curd- Clear vesicles (labia, vulva, perineal area ,vagina and ectocervix ) Vesicles
like” discharge rupture (within 7 days) Ulcer formation (shallow , painful with red borders
o Vulvar pruritus, edema , or erythema ) Secondary infection ( necrosis )
o Dysuria
o Dyspareunia
o Vaginal pH : ~ 4.5
- Diagnosis: KOH wet mount
- Identification of pseudo-hyphae and spores of C. albicans
- Others : Nickerson’s / Sabouraud’s medium; Latex Agglutination
Test ( for nonalbicans sp.)
Thick , Cheese-like
Discharge
Multinucleated
Giant Cell

Pseudohyphae

Recommended Treatment :
- Oral : Fluconazole 150 mg single dose
- Intravaginal Agents : creams , ointments, vaginal tablets or
suppositories
Diagnosis :
Others:
- Usually done clinically +Tsanck or Paps smear
- Butoconazole
- Multinucleated giant cells with nuclear inclusions
- Clotrimazole
- Others : Direct Immunoflourescence of ulcer scrapings
- Miconazole
Viral culture
- Nystatin
- Tioconazole
Recommended Treatment  Polymerase or Ligase Chain Reaction
1st episode - Valacyclovir 1 gm PO BID x 7 days
: - Acyclovir 200 mg 5x daily or 400mg TID for 7-10 - Recommended Treatment:
days  Doxyxcycline 100 mg BID x 7 days
- Famciclovir 250 mg TID for 7-10 days  Alternative Regimens :
Recurrent - Valacyclovir 500 mg PO bID x 5 days - Azithromycin 1 gm PO single dose
Episode - Acyclovir 400 mg TID for 5 days or 800mg BID for - Erythromycin base 500 mg PO QID x 21 days
5 days or 800 mg TID for 3 days - Ciprofloxacin 750 mg PO BID x 3 weeks
- Famciclovir 125 mg BID for 5 days or 1 gm BID for
1 day
Daily - Valacyclovir 500 mg daily (≤ 8 recurrences/yr) or
Suppressive - 1 gm daily or 250 mg BID (> 9 recurrences /yr)
Therapy - Acyclovir 400mg BID
- Famciclovir 250 mg BID

B. CHANCROID
- Caused by : Hemophilus ducreyi bacillus , gm (-) rod in chain
- More frequent in tropical / subtropical countries

- Clinical feature : Groove Sign


1. Painful suppurative ulcers with a grayish base and foul
odor
2. Lymphadenopathy
3. Inguinal Buboes (pus-filled lymph node bulge 
drain thru the skin )
- Diagnosis : Clinical Culture of H. ducreyi
- Treatment :
D. GRANULOMA INGUINALE
 Azithromycin 1 gm PO single dose or
- Aka Donovanosis
 Ceftriaxone 250 mg IM single dose or
- Caused by Calymmatobacterium granulomatis , gm (-) rod with
 Ciprofloxacin 500 mg PO x 3 days
bipolar staining
- More common in African-Americans
- Clinical Feature :
1. Painless , “ beefy red “ ulcers with irregular borders
2. Inguinal lymphadenopathy
3. Pseudo-bubo formation (inguinal inflammation but no
lymphatic involvement)
Soft Chancre
- Diagnosis :
Giemsa – Wright stain
o Enlarged mononuclear cells with cytoplasmic vacoules
packed with bipolar-staining bacteria
 (“Safety pin ” appearance)
Inguinal Buboe  DONOVAN BODIES (Pathognomonic)
 Recommended Treatment :
 Doxycycline 100 mg BID x 3 weeks

- Alternative Regimens
o Trimethoprim-Sulfamethoxazole 80/400 mg BID x 3
weeks or
o Ciprofloxacin 750 mg BID x 3 weeks or
C. LYMPHOGRANULOMA VENEREUM o Erythromycin base 500 mg QID x 3 weeks or
- Caused by Chlamydia trachomatis o Azithromycin 1gm PO q week x 3 weeks
- Sexually transmitted
- Affects males 20x more than females
- Clinical feature :
1. Painless vulvovaginal ulcer
2. Adenitis
3. Inguinal buboes
- Chronic progression
1. ulceration Donovan Body
2. elephantiasis
3. sinus tract formation
4. rectovaginal fistula
5. abscesses
6. rectal strictures
Clinical Features:
- Diagnosis : Clinical + lab tests :  syphilis is divided into primary, secondary, and tertiary stages
 Biopsy and Culture of Cyclohexamide treated tissues
 Complement fixation- Direct Immunoflourescence for Primary syphilis
antibodies  A papule, which is usually painless, appears at the site of
 Enzyme Immuno-assay inoculation 2 to 3 weeks after exposure.
PROLIFERATIVE INFECTIONS diaphragm
A. Condyloma Acuminatum  Nonoxynol 9 - A chemical detergent used in spermicidal preparations
 Papillomatous “ cauliflower-like ” lesions on the perianal area, that is also bactericidal and viricidal.
vulva , vagina , or cervix
 Synonyms for vulvar condylomata acuminata include genital, ENDOMETRITIS
venereal, or anogenital warts

 Caused by Human Papilloma Virus ( type 6 and 11 )


 Often occur with Trichomonas and Bacterial Vaginosis
 Sexually Transmitted
 Diagnosis is clinical
 Paps smear : koilocytosis

Management :
1. Podophyllin 0.5% solution BID x 3 days
- may be repeated after 4 days for 4 cycles
Pelvic inflammatory disease
2. Imiquimod cream 5% TID at bedtime for 16 weeks
 an infection in the upper genital tract not associated with pregnancy or
3. Cryotheraphy
intraperitoneal pelvic operations
4. Trichloroacetic acid 80-90%
 may include infections of: endometrium (endometriris), oviducts
5. Surgical removal
(salpingitis), ovary (oophoritis), uterine wall (myometriris), uterine
6. Laser surgery
serosa and broad ligament (parametriris) and pelvic peritoneum
 Salpingitis – most characteristic and the most common component of
PID
o most long-term sequelae of PID result from destruction of the
tubal architecture by the infection
 Etiology
o usually a polymicrobial infection caused by organisms
ascending from the vagina and cervix along the mucosa of the
endometrium to infect the mucosa of the oviduct
o two classic STD organisms involved:
 N. Gonorrhoeae
 C. Trachomatis
 atypical or silent PID – an asymptomatic or
relatively asymptomatic,inflammation of the
upper genital tract often associated with
chlamydial infection
With
poikilocytosis  Mycoplasma
o role: unclear
o agents: Mycoplasma hominis and Ureaplasma urealyticum
 obtained from the majority of young, sexually
active women
o route of spread: via the parametria
 the primary upper genital tract infection is in the
parametria and the tissue surrounding the tubes,
NOT in the tubal lumen
AZITHROMYCIN DOXYCYCLINE  low success rate of direct tubal cultures
CHANCROID GRANULOMA INGUINALE o histology: does not appear to produce damage to the tubal
METRONIDAZOLE FLUCONAZOLE mucosa
TRICHOMONADS CANDIDIASIS o not highly pathogenic
o may colonize or persist in the endometrial cavity after
INFECTIONS OF THE UPPER GENITAL TRACT complete recover from acute PID
o may be a commensal bacterium rather than a
pathogen in the oviducts
o M. Genitalium
 Nonculturable
 identified by PRC
 associated with cervicitis, endometritis, and
tubal factor infertility
 Tuboovarian complexes – more common in women with concurrent
 Fitz-Hugh–Curtis Syndrome - A syndrome of perihepatic inflammation bacterial vaginosis or HIV infection
that develops in 5% to 10% of women with acute pelvic inflammatory
disease, originating from transperitoneal or vascular dissemination of
either Neisseria gonorrhoeae or Chlamydia trachomatis.
o diagnosis: laparoscopy
 liver capsule will
appear inflamed, with
classic “violin string”
adhesions to the
parietal peritoneum
beneath the
Barriers
o Condom
 Protects partnerfrom direct contact with semen, urethral
discharge, or penile lesion
 Effective in vitro barrier to Chlamydia, CMV, and HIV, partial
protection with HSV
 Protects wearer from direct contact with partner’s mucosal
secretions
 Appears to decrease risk of acquiring urethral/cervical GC,
PID, and male urethral Ureaplasma colonization; partial HPV
protection
 Effects on risk of acquiring NGU not established
o Spermicide
 Chemically inactivates infectious agents
 Inactivates gonococci, syphilis spirochetes, trichomonads,
HSC, ureaplasmas, and HIV in vitro.
o Diaphragm
 Mechanical barrier covers cervix used with spermicides
 Appears to decrease risk of acquiring cervical GC and PID

PELVIC TB
 Rare
 Chronic salpingits and chronic endometritis
 Usually premenopausal (10% postmenopausal)
 Immigrants (Asia, Middle East, Latin America).

 Organisms:
o Mycobacterium tuberculosis
 Primary site: Lungs
 Hematogenous spread.
o Mycobacterium bovis.
 Oviduct – primary site (GIT – for bovine TB)

 Predominant presentation : Infertility and AUB.


 Other S/sx:
o Mild-to-moderate chronic abdominal pelvic pain (35%).
o Ascites – advance cases
o Mild adnexal tenderness.

 Diagnosis of Pelvic TB
o (+) Tuberculin test.
o Endometrial biopsy (secretory phase): Culture and histologic
exam.
 Gross Findings : Eversion of
the ends of the oviduct 
“ Tobacco pouch ”
o Confirmatory of the Dx: giant
cells and caseation necrosis.

 Treatment of Pelvic TB
o Medical (Multi-drug regimen).  Outlet resistance is increased by reflex stimulation of the alpha-
 INH adrenergic receptors within the smooth muscle of the bladder
 Rifampicin neck & proximal urethra.
 Streptomycin  Stimulation of the striated external urethral sphincter via the
 PZA pudendal nerve.
* TB infection should be suspected in women who do not respond to
antibiotic treatment for Acute PID ANATOMY & PHYSIOLOGY OF MICTURITION
o Surgical  To maintain URINARY CONTINENCE at the level of the bladder
 Reserved for women with: neck & urethra, IUP > IVP (during rest & with stress)
1. Persistent pelvic masses  In CONTINENT women: increased IAP (coughing, lifting, straining)
2. Some women with resistant organisms increases IUP equally to the r
3. Women older than 40 other allowing closure pressure to be maintained.
4. Women whose endometrial cultures remain positive.
DIAGNOSTIC PROCEDURES
Methods of Preventing PID 1. Phase I - Provides information to establish diagnosis in 75-80% of
Behavioral : Monogamy patients.
Reduce number of sexual Partners 2. Phase II - More sophosticated urodynamic testing needed in 20-
Barriers Condoms 20% of patients.
Spermicides
Diaphragms BONNEY Test
Vaccines : Hep B  Part of phase I
Research in progress : HIV , HSV ,  indicated in case of a positive stress test associated with a
Gonococcal cystocoele – may manifest as a vaginal mass
Oral Antibiotics : PCN  To know if incontinence is due to descent of bladder neck or
Sulfathioazole weakness of the sphincter.
Tetracycline  The index and middle fingers are placed on both sides of the
Local Postcoital urination urethra to elevate the bladder neck upwards.
Postcoital washing  If no urine escapes on stress it means that the incontinence is due
Postcoital antisepsis to descent of the bladder neck, but if urine still escapes it means
weakness of the sphincter
ACTINOMYCOSIS
o Etiology LOWER URINARY TRACT INFECTIONS
 Actinomyces – is rare cause of upper genital tract infection  Bacteriuria is quite common in women who are on chronic
 agent: Actinomyces israelii catheterization and in women in nursing homes who are chronically
o A. israelii is discovered either by histologic examination or culture from incontinent.
women with tuboovarian abscesses o Asymptomatic bacteriuria is no longer treated, even in the
o risk factor: chronic use of IUD (ave. 8 years) elderly, unless they are undergoing an invasive procedure.
o progression to upper tract infection is highly unlikely to be related o The presence of at least 100,000 organisms per milliliter of
o the decision to remove the IUD to treat a patient is influenced by the urine is generally accepted as evidence for a clinical
presence or absence of clinical symptoms infection.
A. CYSTITIS
 Most common UTI in outpatient settings
UROGYNECOLOGY
 (+)100,000/ml bacteria concentration in a clean-catch urine specimen
Bladder capacity = 400 – 500 cc
B. URETHRAL DIVERTICULITIS
 majority of diverticula seem to occur between the ages of 30 and 50.
 Etiology:
o Congenital
o acute/ chronic inflammatory
o Urethral trauma from multiple catheterizations or from
childbirth
o The infectious origin is probably the most common and
the prevalence in women with recurrent UTIs may be
as high as 40%.
 s/sx:
o urgency
o frequency
o three “Ds” = dysuria, dyspareunia, postvoid dribbling
o hematuria
o incontinence
o Occasionally, patients have urinary stones within the
diverticula or discharge or pus from the urethra.
PHYSIOLOGIC BLADDER FILLING:  Dx: Diagnosis is generally suggested by physical examination.
 Little or no increase in IVP is observed, despite large increases in  Tx: marsupialization
urine volume.
 As filling increases, detrusor muscle contractility is inhibited by URINARY INCONTINENCE
activation of a spinal sympathetic reflex. Types
 Results in inhibition of parasympathetic ganglion transmission &  Genuine stress incontinence
stimulation of beta-adrenergic receptors in the bladder body.  Detrusor instability
 Mixed (GSI and DI)
 Overflow
 Fistulae (True Incontinence) SURGICAL TREATMENT
 It is the primary treatment of stress incontinence.
Genuine stress incontinence  The operation is done vaginally, abdominally, or abdominovaginally.
 Is the involuntary loss of urine in the absence of a detrusor contraction,
the intravesical pressure exceeds the urethral pressure. INFERTILITY
 There is not an associated desire to void.  Primary infertility : identified in couples in whom a pregnancy has
never been established.
Detrusor instability  Secondary infertility : identified in couples who have previously
 Involuntary detrusor contractions either spontaneous or provoked conceived but are currently unable to do so.
which cannot be suppressed and may cause incontinence.
 It is associated with a strong desire to void.  Examples of some of the principal dysfunctions for each component of
 Abnormal nerve supply to bladder (spinal cord injury, spina bifida) - the reproductive system are :
detrusor hyperreflexia. o Sperm :
 childhood mumps
MIXED INCONTINENCE: GSI +DI  testicular injury/sexually transmitted diseases
 Presence of both GSI & DI  varicocele
 Address foremost one component, preferable the worse one.  sexual dysfunction
 exposure to toxins endocrinopathies
Overflow incontinence  CAUSES OF INFERTILITY:
 Is an involuntary loss of urine associated with over distension of the 1. Anovulation
bladder 2. Fallopian tube is non functional or not patent
 May present as SI or dribble. 3. Spermatozoa are not present or not functional
 Due to bladder outlet obstruction or impaired detrusor contraction. 4. Coitus is either not timely or is not performed properly
 More common in males. 5. Unfavorable cervical mucus
6. Unreceptive endometrium
True incontinence
 In this case, urine escapes continuously by day and by night.  Hysterosalpingogram
 It is caused by: o Fluoroscopic and radiographic visualization of the interior of
a. Urinary fistulae as vesicovaginal fistula – MOST COMMON the female upper genital tract after instillation of
b. Ectopia vesica. radiopaque dye.
o Schedule the HSG during the week following the end of
MANAGEMENT menses to avoid irradiating a possible pregnancy
1. Prophylactic o can assess proximal or distal occlusion of an oviduct by
2. Conservative (non-surgical) outlining internal anatomy through infusion of a radio-
3. Surgical opaque medium.
o Patency is confirmed by extrusion of media into the cul-de-
PROPHYLACTIC TREATMENT sac.
1. During labor, the bladder should be kept empty. o Often, performing an HSG results in pregnancy; the
2. Episiotomy is performed if necessary. procedure may break fimbrial adhesions.
3. Physiotherapy. o Premedication with prophylactic doxycycline and
prostaglandin synthetase inhibitors can prevent
* Pelvic floor exercises are started after delivery. exacerbation of previous PID and stimulation of painful
* These include repeated stoppage of the urinary stream during micturition uterine cramping.
and repeated contractions of the pelvic floor muscles.

CONSERVATIVE TREATMENT
Indications:
1. Mild stress incontinence.
2. The patient not completed her family as vaginal delivery may
damage a bladder neck repair
3. Patient is unfit for surgery or refuses surgery.
4. When stress incontinence is combined with detrusor instability.

* The latter should be treated at first before surgery is done for stress
incontinence.  Luteal phase deficiency
o Deficient progesterone secretion or action resulting in a
 Physiotherapy: Kegel perineometer delay of normal endometrial development.
 Faradic current stimulation of the levator ani muscles  Ovarian hyperstimulation syndrome
 Vaginal cones: 5-9 o Mild – abdominal pain, distention, and weight gain
 Estrogen therapy for menopausal patients o Moderate – >10 cm ovarian enlargement, ascites, nausea,
 Alpha-adrenergic stimulants vomiting
 Large vaginal diaphragms, Hodge pessary - to elevate and support the o Severe – hemoconcentration, oliguria, elevated serum
bladder neck creatinine. Pleural effusion and ascites can be present.
 Reduction of weight in obese patients to reduce intra-abdominal  Post-coital test – examination of the cervical mucus to evaluate the
pressure. presence of sperm several hours after sexual intercourse.
 Stop caffeine (to avoid diuresis) and smoking (to avoid coughing) o 20 forwardly progressive sperm should be seen per high-
 Injection of Teflon or bovine collagen in the submucosal layer in the power field.
region of the bladder neck.
o This leads to narrowing of the urethral lumen and increased
urethral resistance.
Dx of ANOVULATION
a) A basal body temperature (BBT) is based on the thermogenic effect of
progesterone. The BBT should remain increased 0.5° to 0.8°F for at
Management is based on the following abnormal findings: least 11 days during the luteal phase.
1. If sperm are absent, coital technique (e.g., use of sexual lubricants, b) Serum progesterone > 3 ng/ml provides indirect evidence of ovulation.
post-coital douching) should be investigated. c) Endometrial biopsy may reveal a luteal phase defect, which is a
 The woman should difference of 2 or more days on endometrial histology compared with
be advised to remain the known cycle day.
supine for 15
minutes after coitus Intrauterine Insemination (IUI)
with her knees bent  Placement of spermatozoa that
to enhance cervical have been separated from the
mucus contact with seminal fluid into the
the seminal pool. endometrial cavity through
2. If the mucus is of poor quality, small catheter.
and the sperm have poor  Effective for couples in which
motility but adequate numbers, the male has a low sperm
the timing within the cycle should be assessed. Mid-cycle exogenous count.
estrogen may improved mucus quality.  Donor insemination is a last resort.
3. If the mucus is of good quality, and there are adequate sperm numbers,
the woman should be evaluated for sperm antibodies. Immunobead Test
 Type of male fertility test that can help assess common male fertility
 If the woman is having regular menstrual cycles, a serum progesterone problems.
level should be measured in the mid-luteal phase to provide indirect  This preliminary male fertility test looks for the presence of antisperm
evidence of ovulation as well as normal luteal function. antibodies, which can have a negative effect on the reproductive
o A se prog level of 10 ng/ml = indicative of adequate luteal health of both men and women, thereby reducing fertility.
function.
 Serum motility begins to decline 2 hours after ejaculation, and it is best Management
to examine the specimen within this time period. 1. Clomiphene citrate is the usual initial agent used
Documentation of anovulation: TV UTZ
Characteristic Value Done on 10th day of cycle every 2 days
Observe for: Mature ovarian follicle
Semen volume 2 – 5 ml
Sperm count > 20 million / ml Px does not ovulate on her own.
Sperm motility > 50% Day 3-7: clomiphine citrate
Normal forms > 30% Increase in dosage every cycle until ovulation is achieved
Forward progression >2 (scale 0-4)
Normal morphology >50% normal 2. Human menopausal gonadotropin (hMG) stimulation
 which triggers ovulation
 used for patients who are resistant to clomiphene.
 Measurement of TSH and Prolactin in ovulatory women
 Ovarian response must be monitored closely by:
o If women with anovulation have hypothyroidism or
o serum estrogen levels and
hyperprolactinemia, tx with thyroid replacement or
o sonographic assessment of follicle number
dopamine agonists
 Ovulation is successful in 90% of women
 Luteal deficiency
o pregnancy rate of 50%.
o Diagnosis of luteal deficiency can be determined by finding
Very expensive
serum progesterone levels consistently below 10 ng/ml a
Starts at day 6 until the px has a mature follicle at a size of 1.6- 1.8
week before menses
Seen via transvaginal ultrasound
*eto yung galing sa mga nun. Wala silang sexual intercourse kaya yung
Most Couples Will Achieve Conception Within :
sa kanila ang kinukuha.
 1 month : 25%
 6 months : 60% 3. Hyperstimulation
 9 months : 75%  Excessive stimulation can produce large theca lutein cysts with
 1 year : 80% transudation of ovarian fluid, resulting in ascites and
 18 months : 90% hemoconcentration (OHSS).
o Treatment is conservative, allowing spontaneous
involution. Uncomplicated Gonococcal Infections of the Cervix, Urethra, and Rectum* :
4. Assisted reproductive technology (ART) CDC 2010
 refers to all techniques, in lab or hospital, involving direct retrieval Recommended Ceftriaxone 250 mg IM in a single dose
of oocytes from the ovary. Regimens or
Cefixime 400 mg orally in a single dose or 400 mg by
 They may be used when conventional infertility therapy has suspension (200 mg/5ml)
failed. or
Single dose Cephalosporin regime IM
*More prone to multifetal pregnancy: implantation of multiple fertilized PLUS
ovum are all successful Azithromycin 1 gm oral single dose or
In-Vitro Fertilization (IVF) Doxicycline 100 mg orally BID x 7 days
 Involves extraction of Alternative Spectinomycin 2 g in a single intramuscular (IM)
oocytes, fertilization on the Regimens dose
laboratory, and transcervical OR
transfer of embryos into the Single-dose cephalosporin regimens
uterus.
Uncomplicated Gonococcal Infections of the Pharynx* : CDC 2010
Recommended Regimens Ceftriaxone 250 mg IM in a single dose
PLUS
Azithromycin 1 gm single oral dose or
Doxicycline 100 mg BID x 7 days
Gamete intrafallopian transfer
(GIFT)
 Placement of human ova and
Disseminated Gonococcal Infection(DGI) : CDC 2010
sperm into the distal end of
Recommended Regimens Ceftriaxone 1 g IM or IV every 24 hours
the oviduct.
 Refers to placement of
oocytes and sperm directly
into the fallopian tube. Alternative Regimens Cefotaxime 1 g IV every 8 hours
 Used if the infertile woman OR
has a functioning oviducts Ceftizoxime 1 g IV every 8 hours
 Modifications include zygote Fitz- Hugh- Curtis Syndrome:
intrafallopian transfer (ZIFT)  Transperitoneal or vascular dissemination of Neisseria or
and tubal embryo stage Chlamydia- perihepatic inflammation-
transfer (TEST)  “violin strings”
 ZIFT the oocytes are
fertilized in vitro and
transferred 24 hours later.
 (TET)  is similar to ZIFT
except the embryos are
transferred 8 to 72 hours
after fertilization 
 Symptoms:
o PID sxs (abdominal tenderness, cervical motion
Intracytoplasmic sperm injection tenderness, adnexal tenderness) + RUQ pain+ pleuritic
(ICSI) pain
 Sperm (single spermatozoa) o Treatment same as PID
is placed inside the egg by Management Guidelines for PID
microinjection
 Partners of women with PID should also be given tx  250 mg
Ceftriaxone IM plus Doxyxycline 100 mg BID for 7 days OR
 A single spermatozoon is
Azithromycin 1 gm PO single dose
injected into the cytoplasm of
 25 % recurrence within 10 weeks if male partner is not treated
an ovum.
Oral Treatment for Acute PID
(CDC 2010)
UPPER GENITAL TRACT INFECTIONS
Ceftriaxone 250 mg IM in a single dose
Risk factors for PID: PLUS
 Young Menstruating Female Doxycycline 100 mg orally twice a day for 14 days
 Multiple Sex partners WITH or WITHOUT
 No Contraceptive use: Metronidazole 500 mg orally twice a day for 14 days
o OCP’s Decrease risk of STD’s due to: OR
 Thicker cervical mucus Cefoxitin 2 g IM in a single dose and Probenecid, 1 g orally administered
 Shorter duration and amount of menstrual concurrently in a single dose
flow PLUS
o Condoms, diaphragms and spermicides Doxycycline 100 mg orally twice a day for 14 days
 Provide mechanical and chemical barriers
WITH or WITHOUT
Metronidazole 500 mg orally twice a day for 14 days
OR
Other parenteral third-generation cephalosporin (e.g., ceftizoxime or
cefotaxime)  CIN is graded in three steps:
PLUS a) CIN 1 – little or no clinical consequence as it usually
Doxycycline 100 mg orally twice a day for 14 days result of a transient HPV infection only. In the past,
WITH or WITHOUT referred to as mild dysplasia.
Metronidazole 500 mg orally twice a day for 14 days b) CIN 2 – cellular changes are more extensive and include
one-half to 2/3 of the thickness of the epithelium
c) CIN 3 – full thickness cellular changes; includes those
Pelvic Inflammatory Disease (PID) changes previously referred to as severe dysplasia and
CDC 2010 carcinoma in situ.
Recommended Parenteral Regimen A CIN I
Cefotetan 2 g IV every 12 hours No penetration of Basement
OR membrane and do not extend
Cefoxitin 2 g IV every 6 hours more than half
PLUS
Doxycycline 100 mg orally or IV every 12 hours CIN II
Recommmended Parenteral Regimen B

Clindamycin 900 mg IV every 8 hours


PLUS
Gentamicin loading dose IV or IM (2 mg/kg of body weight), followed by a
maintenance dose (1.5 mg/kg) every 8 hours. Single daily dosing may be CIN III
substituted.
Alternative Parenteral Regimens

Ampicillin/Sulbactam 3 g IV every 6 hours


PLUS
Doxycycline 100 mg orally or IV every 12 hours
WITH OR WITHOUT
Metronidazole 500mg BID x 14 days NATURAL HISTORY OF CIN- (STUDY BY OSTOR)
Regress Persist Progress to Progress to
Tubo-Ovarian Abscess: more common in women with concurrent bacterial CIN III Cancer
vaginosis or HIV infection CIN 1 57% 32% 11% 1%
CIN 2 43% 35% 22% 5%
Management of Tubo- Ovarian Abscess (TOA) Guidelines: CIN 3 32% 56% ---- 12%
 Ruptured TOA: conservative management is inappropriate
 Unruptured TOA: 70% response rate to conservative medical Liquid-Based Pap Test
treatment
 Surgical tx: depends on the size
 No clinical Improvement within 48-72 hours- conservative
surgery
 Addition of Ampicillin: better results
PREMALIGNANT LESIONS OF THE CERVIX
SQUAMOCOLUMNAR JUNCTION Routine Pap Test
 Important landmark
 Where neoplastic
changes occurs
 Throughout the
reproductive life of the More accurate bec stacked up unlike diluted in a medium; evenly spread
woman, changes in
position WHEN TO DO PAP SMEARS
 Cytologic screening of the cervix should start 3 years after vaginal
intercourse and not later than 25 years old (SGOP practice
guidelines and DOH)
 Pap smear are used to screening tool for cervical cancer, to catch
it in its pre-malignant state!
When Do You Stop Screening?
 Women who have had a total hysterectomy (removal of the cervix
and uterus) for reasons other than cancer can stop being
TRANSFORMATION ZONE screened for cervical cancer unless they have a history of high-
 When exposed columnar grade CIN. (E.g from adenomyosis)
epithelium changes into  ACOG : women may be able to stop cervical cancer screening at
squamous epithelium age 65 or 70 if they’ve had three or more normal Pap results in a
 METAPLASTIC CHANGE row and no abnormal Pap in the previous ten years.
 May find abnormal or  Women at high-risk of cervical cancer may need to continue
neoplastic squamous screening beyond this age. (regardless of age)
epithelium can be found VIA : Visual Inspection with Acetic Acid
here  5% acetic acid (common table vinegar) is applied to the cervix
with a large cotton swab and left for 30-60 seconds, after which
the cervix is visually examined with the naked eye and a lamp.
Pre-cancerous lesions, with a higher ratio of intracellular proteins,
turn white when combined with acetic acid. Normal cervices  In the US, incidence is decreasing due to the widespread use of
without any precancerous lesions, do not change color cervical cancer screening tools…the Pap smear
 May be used in rural areas  In the Philippines, this has not yet been achieved
 Single and Basic approach, easy to do  HPV 16 AND 18 culprits for cervical cancer
 If there is a suspicious white lesion, the next step is, refer for
colposcopy- Common question in the board exam

Large Cell Keratinizing

 Acetic acid makes the specimen dark; while Lugol’s make it bright
COLPOSCOPY Large Cell Nonkeratinizing
 A colposcope is used to magnify abnormal cervical areas that
require biopsy
 Abnormal Pap smear results are usually referred for colposcopy/
any abnormal screening test.
 Solutions Used:
a. Normal Saline – remove cervical mucus and allows vascular and Small Cell Ca
surface features of lesion to be initially assessed
b. Acetic Acid – is 3-5% preparation serves as a mucolytic agent
that reversibly clumps nuclear chromatin causing various shade
of white depending on the degree of abnormal chromatin
density Adenocarcinoma
c. Lugols Iodine – stains mature epithelial cells mahogany in
estrogenized women due to high cellular glycogen content

Adenosquamous

(mosaicsism)
Clear cell CA
CRYOTHERAPY **signet ring appearance
 Freeze the lesion
 Has largely been supplanted by LEEP. If patients are carefully
selected, the success rate is approximately 95%.
 Larger CIN lesions have higher failure rates, most likely because CLINICAL PRESENTATION
the whole lesion is not covered by the cryoprobe. It is not EARLY SYMPTOMS
appropriate to use cryotherapy if the lesion extends into the 1. Vaginal bleeding - most important symptom
endocervix.  Induced by sexual intercourse or internal examination
 procedure is simple. After colposcopy and sampling has shown  Intermenstrual
that the lesion is confined to the exocervix, a probe is selected that 2. Vaginal discharge
will cover the entire lesion, in most systems, N2O is used as the LATE SYMPTOMS
refrigerant 1. Pelvic/flank pain
 Probe is applied to the cervix and the system is activated. The 2. Bone pain
cervix will freeze quickly, but the probe must remain in place until 3. Urinary disturbances: dysuria, hematuria
the ice ball that forms extends to at least 5 mm beyond the edge 4. Bowel disturbances: rectal bleeding
of the instrument. 5. Lower extremity edema
 Most cases, this takes 3 to 4 minutes 6. Signs/symptoms of uremia
 Refrigerant is then turned off, and the probe allowed to thaw and
separate from the cervix FIGO STAGING OF CERVICAL CANCER
 Because the tissue that was destroyed remains on the cervix, Stage 0 Carcinoma in situ (preinvasive carcinoma)
within a few hours to a day, the patient will begin to experience Stage 1 Carcinoma strictly confined to the cervix; extension to the
vaginal discharge uterine corpus should be disregarded.
 As the tissue sloughs, the amount of discharge increases, and Stage 1A Invasive cancer diagnosed only by microscopy.
malodor is common. It may take as long as 3 weeks for the All macroscopically visible lesions even with superficial
discharge to stop invasion are stage Ib cancers. Invasion is limited to
 The patient should be cautioned to place nothing in the vagina for measured stromal invasion with a maximum depth of 5
at least 3 weeks after the procedure to avoid causing dislodgment mm* and no wider than 7 mm.
of the eschar. Stage 1A1 Stromal invasion is no greater than 3 mm in depth and no
 First follow-up should occur in approximately 4 to 6 months and wider than 7 mm in horizontal spread.
include cytology and colposcopy. The cytology sample should Stage 1A2 Stromal invasion >3 mm but 5 mm in depth and with
include the endocervix
horizontal spread of 7 mm.
CERVICAL CANCER
 In the US is the 3rd most common malignancy of the lower female
genital tract after endometrial and ovarian cancers
 In the Philippines is the reverse, it is the #1
PHMS are derived from paternal and maternal chromosomes, resulting in
triploid genotype. Absence of the immunohistochemical nuclear stain p57 (a
maternally expressed gene) suggest paternal origin and can be used to
differentiate between CHM and PHM
PARTIAL COMPLETE
Karyotype 69XXX, 69XXY 46XX, 46XY
*with maternal
Pathology
Stage 1B Clinically visible lesions confined to the cervix or microscopic -embryo/fetus Often present Absent
lesions greater than stage IA2. -amnion/fetal rbc Often present Absent
Stage 1B1 Clinically visible lesions no greater than 4 cm in greatest -villous edema focal Diffuse
dimension. -tropho proliferation Variable, focal to slight to Variable, Slight to
Stage 1B2 Clinically visible lesions > 4 cm in greatest dimension. moderate severe
Clinical Presentation
-diagnosis Missed abortion Molar gestation
(1-3%)
-uterine size Small for dates 50% large for dates
-theca lutein cyst rare 25-50%
-medical complication rare frequent
-persistent trophoblastic 1-5% 15-20%
disease
Stage 2 Tumor extends beyond the cervix but has not extended
onto the pelvic wall. The carcinoma involves the vagina, but
Clinical Presentation: same for Partial and Complete
not as far as the lower third.
 Vaginal bleeding – most common
Stage 2A No obvious parametrial involvement. Involvement of up to
 Size greater than dates
the upper two-thirds of the vagina.
 Anemia
Stage 2B Obvious parametrial involvement, but not onto the pelvic
sidewall.
 *Due to B hCG:
o Preeclampsia
o Hyperemesis
o Hyperthyroidism
o Respiratory Distress
B-hCG
Stage 3 Tumor extends to the pelvic sidewall and/or involves the
lower third of the vagina and/or causes hydronephrosis or
nonfunctioning kidney. *the bigger the size the higher the value
On rectal examination, there is no cancer free space -releasing hormone
between the tumor and the pelvic sidewall.
Stage 3A No extension to the pelvic sidewall but involvement of the
lower third of the vagina.
Stage 3B Extension to the pelvic sidewall or hydronephrosis or THECA LUTEIN CYST
nonfunctioning kidney.  Regress spontaneously 8 to 12 weeks post evacuation
 Torsion rupture
CERVICAL CANCER IN PREGNANCY *do not remove, regress spontaneously
 The diagnosis of invasive carcinoma of the cervix during *remove if there is rupture/torsion/hemorrhage
pregnancy is managed in much the same fashion as the non- Diagnosis:
pregnant patient. In pregnancy, the treatment method depends  Ultrasound – Gold standard
on the patient’s wishes with respect to pregnancy continuation.
 If fetal viability has not been achieved and the lesion is Stage I or HUMAN CHORIONIC GONADOTROPHIN
IIA, treatment may be with radical hysterectomy and pelvic  Pregnancy hormone
lymphadenectomy with the fetus left within the uterus.  Glycoprotein with the highest carbon in human hormone
 If close to fetal maturity, if after discussion with the patient, the  2 subunits:
patient wishes to continue with the pregnancy, then cesarean  Alpha – LH, FSH, TSH
radical hysterectomy and bilateral pelvic lymphadenectomy is the  Before 5 weeks- both cytoT and syncytioT
treatment of choice for early lesions. More advanced disease is  Later gestation – only syncytioT
generally treated with radiotherapy.  7 to 9 days after LH surge – detectable in the plasma of pregnant
women
GESTATIONAL TROPHOBLASTIC DISEASE  hCG enters the maternal blood at the time of blastocyst
Complete Mole implantation
 Abnormality in chorionic villi  8 to 10 weeks- maximum level (doubles every 2 days)
 Trophoblastic proliferation  10 to 12 weeks – begins to decline
 Edema of the villous stroma  16 weeks- nadir
CHMS = completely derived from paternal origin, >90% is 46, XX genotype,
produced by fertilization of an empty (anuclear) ovum by a single haploid Diagnostic – *e.g. patient : 5 mos after NSD with bleeding, no contraceptive
(23, X) sperm, which then duplicates (w/o cell division) in the ovum use: initial dx: pregnant again, normal menstruation; diff dx: ectopic preg,
(androgenesis). A small percentage of CHMS have a 46,XY genotype, abortion
produced by dispermy 10%, in which a 23,X sperm and a 23,Y sperm fertilize Prognostication – *the higher the level, mas pangit
an empty ovum risk factor is 4 , high risk already
Treatment response – *chemotherapy, serial B hCG is done to see tx
response
Concentration in serum and urine : on
 HCG plasma level parallels urine level
 1 IU/ml by 6 weeks after LMP *normal B hCG for nonpreganant = 0-5
 100,000 m IU/ml : 60th – 80th days after LMP
 *100,000-200,000 B hCG – normal; If px has 300,000, most CHORIOCARCINOMA, GESTATIONAL
probably it’s molar pregnancy
o Rescue and maintenance of corpus luteum in early pregnancy (continued
progesterone production)
e syncytioT

*gross - necrotic, hemorrhagic

Treatment: Primary Gonadal Choriocarcinoma Nongestational


c appearance

1. Suction curettage

 *eto yung mga nasa male, testicular chorioCa; ovarian chorioCa w/o
 pregnancy; same histologic appearance; not responsive to chemoRx
 – Preop dilator
 Placental Site Trophoblastic Tumor
 – oxytocin

*how would you treat patient with Molar pregnancy? Evacuate by SUCTION
CURETTAGE AND REGULAR FOLLOW-UP
*no syncytioT which produces B hCG, so very low B hCG, dignosed by
immunostaining
2. Hysterectomy
 Completed family size
Classification and Staging FIGO STAGING SYSTEM
 Adjunctive therapy : decrease local persistence
STAGE I Disease confined in the uterus
*when do you do hysterectomy? High risk px, under medical complication,
STAGE II Disease extends outside the uterus but
thrombosed molar malignancy
confined to pelvic area
*42y/o px G6, 3 mos pregnant, uterine size is for 4 mos, suction or
hysterectomy? Preferred method is SUCTION CURETTAGE STAGE III Pulmonary metastasis
STAGE IV Metastasis to other sites

*Do you infuse Oxytocin prior to curettage? NO, but once evacuated that’s WHO PROGNOSTIC FACTORS
the time you put oxytocin 0 1 2 4
*when do you do hysterogram in molar px? After evacuation, because the Prognostic factors
uterus of Molar px is very soft, so do not do before or during. age <40 >40
*closed cervix is dilated by laminaria- toothpick /bamboo stick-like inserted Antecedent mole abortion Term
in the cervical canal, after 24hrs, it will dilate, absorbs water. pregnancy
*Do you do hysterotomy in molar preg? NO Pregnancy interval <4mos 4-7 7-12 >12
*when you do suction curettage, your left hand should be in the fundus, to B hCG <1000 1000- 10,000- >100,000
prevent perforation and at the same time you massage the uterus. 10,000 100,000
*benefit of hysterectomy: may lessen the local invasion but not the distal so
serial monitoring is still needed Largest tumor <3cms 3-4 >5
Site of metastasis lungs Spleen/kidney GIT Liver/brain
High Risk Patients: *(memorize)
# of metastasis 1-4 5-8 >8
Prior chemotherapy Single agent 2 or more

*once you’ve given prophylactic chemoRx, score would be 2 so as much as


possible inhibit from giving coz it would add to the risk
GTN III: 8 *meaning: stage III separated by colon (:) & a score of 8
*eg: 41 y/o px, with bleeding, hx of mole 5 mos ago, B hCG is 10,000; UTZ
– Preeclampsia, hyperthyroidism
reveals a 2cm tumor, negative Xray, no prophylactic chemoRx =
phic location - *pxs are not compliant to serial B hCG
monitoring which is badly needed
GESTATIONAL TROPHOBLASTIC NEOPLASIA
Surveillance following Molar Evacuation
pregnancy on the basis of B hCG criterion

Diagnosis:
ths  Consideration for the possibility – most important factor
 Only by B hCG determination
 No histopath diagnosis neede
*after 1 year, can get pregnant again  Quantitative B hCG
 Complete physical exam
Quiescent Gestational Trophoblastic Disease  CBC
-212 IU/L) of B hCG for 3 mos or longer with no  Renal function test
obvious decrease in level trend  Thyroid function test
 Utrasound, Doppler Low Risk GTD
 Chest Xray – for baseline purposes, for comparison if px is high
risk more cycles
 CT of the thorax – if negative for chest Xray, possible metastasis
 CT or UTZ of the abdomen
 MRI/CT of the brain – needed if postive for micrometatsasis in o Achieved by diligent follow-up and
lungs o Salvage therapy for failures

Clinical Features High Risk GTD


PSTT ETT ChorioCa of 7 or higher
Clinical monomorphic monomorphic Dimorphic
presentation o EMACO – etoposide, methotreaxate, actinomycin, cyclophosphamide,
Last known Variable, can be Varaiable, can be months vincristine
pregnancy remote remote *first-line
o EMA-EP – substitute etoposide and cisplatin for cyclophosphamide and
Hx of Mole 5-8% 14% 50%
vincristine
B hCG <2000 mIU/ml <2000 mIU/ml >10,000
*if with resistance
mIU/ml
o TE –TP – taxol, etoposide, cisplatin
behavior Self-limited, Self-limited, Aggressive if
o BEP – bleomycin, etoposide, cisplatin
persistent, persistent, untreated
o VIP – vinblastine, ifosfamide, cisplatin
aggressive aggressive
o ICE – ifosfamide, carboplatin, etoposide
ChemoRx variable variable good
Treatment surgery surgery ChemoRx Side Effects of EMCO
 Universal alopecia
 Stomatitis
Treatment
 Hematologic toxicities
Low Risk GTN
 Gastrointestinal toxicities
 Prognostic score of >6
 Risk for secondary malignancies
 Single agent of methotrexate or actinomycin D
 Debulking – decrease number of chemotherapy cycles
Granulocyte Colony Stimulating Factor
*can you have stage III patient that is low risk? Yes, E.g. 41y/o with mole,
lung mets, B hCG 50,000, what is the tx modality? chemoRx, basta low risk
*cannot give chemoRx to px with neutopenia
kaht anong stage, SINGLE AGENT OF METHOTREXATE/ ACTINOMYCIN D is
High Risk Sites of Metastasis (CNS, Pulmonary, Liver, Vagina)
given, based sa score not sa stage
*debulking – E.g. 42y/o G6, no blood, emergency, just do Suction Curettage,
o Recurrent drug resistant cases
px came back still bleeding w/ pulo mets
o Solitary metastasis
– hemostasis & shrinkage
Side Effects:
– control bleeding (tumor in vagina)
 Cutaneous side effects
 Mucositis
*in GTN, is surgery necessary? Depends, E.g. in recurrent resistant cases,
 GI toxicities advise px not to undergo hysterectomy if she has no kids yet.
 Alopecia *primary goal for tx in GTN = chemoRx
 Hematologic suppression
PSTT
 While on Chemotherapy: – primary tx
 Monitoring of B hCG
 Hematologic studies
 Metabolic studies Surveillance following GTN
 OCP  B hCG monitoring
 B hCG remission in 3 weekly cycles
Management of Low Risk GTN  Every 2 weeks for 3 weeks
-risk disease:  Monthly for 1 year
 Stage IV – monthly X 24 months
 I. Initiate single-agent methotrexate or dactinomycin; consider
hysterectomy, if infertility is not desired. Recurrence Rate:
 Monitor hematologic, renal, and hepatic indices before each cycle  Stage I = 3%
of chemotherapy.  Stage II = 4%
 Monitor B hCG levels while on treatment.  Stage III = 8%
 If severe toxicity or resistance develops, consider switching to the  Stage IV = 9%
alternative single agent
 If resistance to the alternative agent develops: Pregnancy following GTN

o II. Repeat the metastatic evaluation dysfunction, either transient or eventually premature ovarian failure,
o III. Consider hysterectomy if disease confined to uterus particularly those in their 30s or 40s.
o IV. Multiagent therapy with EMA-CO creased risk of molar pregnancy, from 1/1000 pregnancies to 1/100.

*primary drug is Methotrexate, if resistance or toxicity develop, change to


Actinomycin D Methotexate/Amethopterin
 Antimetabolite, anti-folate drug
 0.3 to 0.4 mg/kg/day every 12 to 14 days Indications for Hysteroscopy:
 All indications for myomectomy (persistent abnormal bleeding,
*in practice 10 days lang until normal pain or pressure, enlargement of an asymptomatic myoma more
 Toxicities : alopecia, mucositis, neutropenia, cutaneous toxicity, GI than 8 cm in a woman who has not completed child bearing
toxcicity,  Plus asymptomatic myomas when the uterus that has reached the
size 14-16 weeks gestation
*If liver profile 6x higher, STOP!
 Folinic Acid = rescue normal cell from dihydrofolate reductase MODULE 5
block
 Alternate dosing : MTX 1mg/kg & 0.1mg/kg BENIGN AND MALIGNANT DISEASES OF THE OVARY
Symptoms due to Size
Actinomycin  Lack of any specific symptoms, ovarian tumors are often large by
 Antibiotic that inhibit transcription the time the doctor is consulted.
 Interferes with DNA replication Complications of Ovarian Tumors
 9 to 13 ug/kg/d for 5 days every 14 days Torsion
 This is the most common
*Given IV so px is admitted in the hospital complication and may occur with any tumor
 Toxicities : alopecia, GI tox, transient bone marrow depression, except those with adhesions.
tissue necrosis (extravasation)  The thin-walled veins of the
pedicle are obstructed first while the
5-Fluorouracil
arterial supply continues.
 Antimetabolite irreversible inhibitor of thymidylate synthetase
 As a result there is hemorrhage
 28 to 30 mg/kg/d for 10 days every 24 to 31 days
into the tumor and into the peritoneum, and
 Toxicities : GI tox, hepatotoxicity, diarrhea, pseudomembranous
if not treated gangrene will occur.
colitis, hema tox
 Very rarely the pedicle atrophies and the tumor obtains a new
blood supply through its adhesions to surrounding viscera
Etoposide
(parasitic tumor).
 200mg/m2 for 5 days every 12 to 14 days Features suggestive of malignancy
 Toxicities : alopecia, myelosuppression, GI tox  Tumor markers, such as CA125, may be measured in the blood,
but a normal level does not exclude malignancy.
BENIGN LESIONS OF THE REPRODUCTIVE TRACT
Mucinous Tumors
I. Urethral Caruncle  consist of epithelial cells filled with mucin; most are benign
 Small fleshy outgrowths in the distal edge of the urethra  cells resemble cells of the endocervix or may mimic intestinal
 Mostly seen in menopausal women cells, which can pose a problem in the differential diagnosis of
 Due to chronic irritation of inflammation tumors that appear to originate from the ovary or intestine.
 Symptoms: Dysuria, frequency, urgency  Benign mucinous tumors are found primarily during the
 Dx: Biopsy reproductive years,and mucinous carcinomas (see Fig. 33-3 C )
 Treatment: Estrogen or excision usually occur among those in the
 30- to 60-year age range.
Clinical Features:  Mucinous Cystadenocarcinoma – usually in 30-60 years age range
 Many women are asymptomatic whereas others experience
dysuria, frequency, urgency MUCINOUS CYSTADENOMA

FIBROMA
 Most common benign solid tumor of the vulva
 Arises from deep connective tissue
 Treatment is excision- TOC

CERVICAL POLYPS
 Most common benign neoplastic growth of the cervix
 Common 40-50s age group
 Tx- polypectomy (forceps grasp the base of the polyp because the
pedicle is soft and friable then squeeze to remove the polyp

ENDOMETRIAL POLYP
 Localized growth of the endometrial glands and stroma beyond
the surface of the endometrium  A unilocular or multilocular cyst of ovary lined by tall columnar
 Peak incidence 40-49 yr epithelium resembling that of the cervix or large intestine
 Softer than myoma  It is usually large and may reach immense proportions, occupying the
 Sx bleeding, infertility whole peritoneal cavity and compressing other organs.
 It may occur at any age.
LEIOMYOMA  primary during reproductive years
 3 most common types  May become huge >300lbs
o Intramural  Rupture may occur and seeding of the epithelium on the
o Subserous peritoneal surface may cause pseudomyxoma peritonei.
o Submucous  Pseudomyxoma Peritonei
o transformation of peritoneal mesothelium to a mucin
secreting epithelium
o Continuous secretion of mucuc resulting in  Staging The Federation Internationale de Gynecologie
accumulation in peritoneal of gelatinous material et d'Obstetrique (FIGO) and the American Joint
o Evaluation at operation os followed by reaccumulation Committee on Cancer (AJCC) have designated staging.
 TX: repetitive surgical evacuation; long term nutritional support
Stage I ovarian cancer limited to the ovaries
SEROUS CYSTADENOMA Stage 1A tumor limited to 1 ovary,
 They are the most common benign epithelial tumors and form the capsule is intact,
20% of all ovarian neoplasm. no tumor on ovarian surface and no malignant
cells in ascites or peritoneal washings.
SEROUS CYSTADENOCARCINOMA Stage 1B tumor limited to both ovaries,
 This is by far the most common primary carcinoma, accounting for capsules intact,
60% of all cases, and in over half the cases it is bilateral. no tumor on ovarian surface and no malignant
cells in ascites or peritoneal washings
Endometrioid Carcinoma of the Ovary Stage 1C tumor is limited to 1 or both ovaries with any of
 It is now recognized that carcinoma of the ovary may be of the following:
endometrial type, sometimes arising in endometrioma. capsule ruptured,
 Attacks of pain, unusual with ovarian cancer, are common. tumor on ovarian surface,
 Sometimes there is uterine bleeding in post-menopausal cases. malignant cells in ascites or peritoneal washings.
 Usually the lesion is cystic and chocolate brown in color. Stage II ovarian cancer tumors involving 1 or both ovaries with pelvic
 If such a cyst ruptures spontaneously, malignancy should be extension and/or implants
suspected. Stage 2A extension and/or implants on the uterus and/or
Clear Cell Carcinoma fallopian tubes.
 It is doubtful if this exists as a distinct entity. No malignant cells in ascites or peritoneal
 Clear cells may be seen in almost any variety of ovarian washings.
carcinoma, but occasionally a carcinoma, usually solid, consists Stage 2B extension to and/or implants on other pelvic
almost entirely of polygonal cells with clear cytoplasm. tissues.
 It behaves in the same way as any other solid carcinoma and has No malignant cells in ascites or peritoneal
the same prognosis. washings
 Contain cells with abun-dant glycogen and so-called hobnail cells, Stage 2C Pelvic extension and/or implants (stage IIA or
in which the nuclei of the cells protrude into the glandular lumen.
stage IIB) with malignant cells in ascites or
 Tumors with identical histologic features are found in the peritoneal washings.
endometrium, cervix, and vagina, the latter two often associated
Stage III ovarian tumors involving 1 or both ovaries with
with intrauterine diethylstilbestrol exposure
cancer microscopically confirmed peritoneal implants
 They occur primarily in women 40 to 70 years of age and are
outside the pelvis.
highly aggressive.
Superficial liver metastasis equals stage III.
Dysgerminomas
Stage 3A microscopic peritoneal metastasis beyond pelvis
 Dysgerminomas are the most common type of malignant germ
(no macroscopic tumor).
cell tumors.
Stage 3B macroscopic peritoneal metastasis beyond pelvis
 The tumor can be discovered during pregnancy. Some arise in
less than 2 cm in greatest dimension
dysgenetic gonads
Stage 3C peritoneal metastasis beyond pelvis greater than 2
Granulosa-Theca Cell Tumors cm in greatest dimension and/or regional lymph
Incidence node metastasis
 consist primarily of granulosa cells and a varying proportion of Stage IV ovarian tumors involving 1 or both ovaries with distant
theca cells or fibroblasts or both cancer metastasis. Parenchymal liver metastasis equals
 One characteristic microscopic pattern is which demonstrates the stage IV
so-called Call Exner Bodies, eosino-philic bodies surrounded by
granulosa cells General Rule
 Functional granulosa cell tumors are primarily estrogenic  Benign ovarian over 10 cm in diameter must be removed, but
 For women who have completed childbearing, abdominal clinical and ultrasonically diagnosed cysts under 10 cm (the size of
hysterectomy and bilateral salpingo-oophorectomy are a lemon) in women under 35 years may be reviewed in a few
recommended. months if there is no suspicion of malignancy.
 A follicular or luteral cyst may resolve spontaneously.
Androblastoma
 tumors are very rare General Principle
 Sertoli (sex cord) and Leydig (stromal) cells are present in varying  Ovarian carcinoma is staged surgically, so laparotomy is an
amounts,and the tumor may consist almost entirely of either essential part of management for most patients.
Sertoli or Leydig cells
 These tumors tend to occur in young women of reproductive age GENERAL GUIDELINES:
and frequently are the cause of masculinization and hirsutism.  Standard treatment is surgery (staging and optimal debulking)
followed by adjuvant chemotherapy in most cases.
OVARIAN CANCER Stage I
Screening and Early Detection Tools  Generally a total abdominal hysterectomy, removal of both
 Periodic pelvic examination ovaries and fallopian tubes, omentectomy, biopsy of lymph nodes
 Sonography and other tissues in the pelvis and abdomen is done.
 Biomarkers (eg CA125)  Young women whose disease is confined to one ovary are often
 Conclusion: there is no evidence available yet that the treated by a unilateral salpingo-oophorectomy without a
current screening modalities can be used effectively hysterectomy and removal of the opposite ovary being performed
for widespread screening for ovarian cancer  Depending on the pathologist's interpretation of the tissue
removed, there may be no further treatment if the cancer is low
grade, or if the tumor is high grade the patient may receive  No primary malignancy uncovered – wide excision of the affected
combination chemotherapy. area
Stage II
 Treatment is almost always hysterectomy and bilateral salpingo- Carcinoma in Situ (VIN III)
oophorectomy as well as debulking of as much of the tumor as  Irritation and itching- common
possible and sampling of lymph nodes and other tissues in the  Full thickness - abnormal
pelvis and abdomen that are suspected of harboring cancer.
Prevention
 Diet: a high-fat diet may play a role in the etiology of ovarian
cancer.
 Oral contraceptives appear to reduce the risk of ovarian cancer
for up to 10 years following cessation of use.
 Patients who have used fertility drugs should be counselled as to
their possible increase in risk of ovarian cancer.
Full
CARCINOMA OF THE VULVA AND VAGINA Thickness
VULVAR CARCINOMA
 5% of malignancies of the lower genital tract
 Premalignant and malignant lesions grow on multifocal areas Colposcopy
 Biphasic age distribution
 Most in their 60-70s  magnification of the colposcope may be used to help follow
 Itchiness patients with VIN as well as to identify the discrete whitish or
 Drain: inguinal/pelvic nodes/femoral nodes pigmented areas that warrant biopsy
 2cm lateral to midline of vulva-ipsilateral spread!
Vulvectomy done in the past (but not in the present)
 Many lesions of intraepithelial neoplasia of the vulva tend to be
VULVAR ATYPIA posterior, predominantly in the perineal area
Lichen Sclerosus VULVAR CARCINOMA: FIGO 2008
 60-70s Stage I Tumor confined to the vulva
 Thinned out skin, smooth Stage 1A Lesions ≤2 cm in size,
 Chronic itching confined to the vulva or perineum and with
 markedly thinned with a loss or blunting of the rete ridges stromal invasion ≤1.0 mm⁎,
no nodal metastasis
Lichen Sclerosus Stage 1B Lesions N2 cm in size or with stromal invasion N1.0
mm⁎,
confined to the vulva or perineum,
with negative nodes
Stage II Tumor of any size with extension to adjacent
perineal structures (1/3 lower urethra, 1/3 lower
vagina, anus)
with negative nodes
Stage III of any size with or without extension to adjacent
Tumor perineal structures (1/3 lower urethra, 1/3 lower
vagina, anus) with positive inguino-femoral lymph
nodes
Paget’s Disease Stage 3A (i) With 1 lymph node metastasis (≥5 mm), or
(ii) 1–2 lymph node metastasis(es) (b5 mm)
Stage 3B (i) With 2 or more lymph node metastases (≥5 mm),
or
(ii) 3 or more lymph node metastases (b5 mm)
Stage 3C With positive nodes with extracapsular spread
Stage IV Tumor invades other regional (2/3 upper urethra,
2/3 uppervagina), or distant structures
Stage 4A Tumor invades any of the following:
(i) upper urethral and/or vaginal mucosa, bladder
mucosa rectal mucosa, or fixed to pelvic bone, or
(ii) fixed or ulcerated inguino-femoral lymph nodes

Stage 4B Any distant metastasis including pelvic lymph

Deep pelvic nodes: external radiation


 Because the deep pelvic nodes are virtually never involved unless the
inguinal nodes are also involved, only the inguinal-femoral nodes are
removed at the time of the primary operation and the deep pelvic
nodes subsequently treated with external radiation if the superficial
 Rare nodes are involved with tumor
 Histologically resembles that of the breast
 Large pale cells VAIN/Vaginal Intraepithelial Neoplasia
 Cells occur in nests and infiltrate upward through the epithelium  Clear cell carcinoma – associated with intrauterine exposure to
 Itching is a common problem diethylstilbesterol
 Most squamous cell carcinoma occur in the upper third of the proteins and 2 late open reading frame proteins (i.e., L1, L2),
vagina which make up the viral capsid
 The major difference between the low risk and high risk types is
Treatment Option: that after infection, the low – risk HPVs are maintained as
Excisional biopsy for small lesions extrachromosomal DNA episomes, while the high – risk HPV
genome is found integrated intothe host cellular DNA
 The recombination event often leaves E6 and E7 directly coupled
to the viralpromoter and enhancer sequences,, allowing their
continued expression after integration
 Because E7 binds and inactivates the Rb protein while E6 binds
p53 and directs its degradation, the functional loss of both TP53
and the RB genes leads to resistance to apoptosis, causing
uncensored cell growthafter DNA damage
 This ultimately results in progression to malignancy
 E6 and p53 – increase cancer cell growth and continued
proliferation of cells

Conventional Pap test Liquid Based (thin Prep)


Require special care to avoid rying of Sampling and cell transfer to a liquid
cells medium
Fixation is carried out mmediately by
spray or immersion
Can be obscured by blood, mucus Preserves the cells and minimizes cell
Radiation therapy is the preferred treatment for most carcinomas of the
andinflammation overlap, blood, mucus and
vagina!!! inflammation.
It creates a mono layer, a layer one
Sarcoma Botryoides(Embryonal Rhabdomyosarcoma) cellthick, with no overlapping cells
The conventional Pap Smear is made The ThinPrep Pap Test makes Pap
by hand Smear slides by an automated slide
*the physician smears the sampling preparation unit
device across a microscope slide to *the ThinPrep 2000 Processor that
spread a layer of cells produces uniform thin layer slides, a
*each physician may do it 1 thick monolayer, vitually free of
differently,leading to some slides obscuring artifacts such as blood,
with clear areas of no cells mucus and inflammation
Up to 90%of those False Negatives Return of visits and repeat Pap
Treatment: pelvic exenteration are due to limitations of sampling or smears is
slide preparation diminished
Pathogenesis of Carcinoma in situ Discarded after a single conventional Residual LBC can undergo testing for
smear is done HPV, herpes simplex virus, N
 It used to have several hypothesis gonorrhea,C. trachomati
o Sexually transmitted via gonorrhea
o Oral contraceptive pills
 Presently, CIN (cervical intraepithelial neoplasia) is caused by HPV Updated ACOG Guidelines for Cervical Ca screening
in 99% of the time  Cervical cancer screening should begin at the age of 21.
 HPV – condyloma acuminata  Most women under the age of 30 should be screened every two
 >100 types identified2 years.
 ~30–40 anogenital2,3  Women age 30 and older who have had three consecutive normal
 Double stranded DNA Pap tests can be screened every three years.
o ~15–20 oncogenic*,2,3  Women with certain risk factors may need to be screened more
 HPV 16 and HPV 18 types account for the frequently. These risk factors include HIV positivity;
majority of worldwide cervical cancers.4 immunosuppression; DES exposure in utero; or history of
o Nononcogenic** types treatment for cervical intraepithelial neoplasia (CIN) 2, CIN 3, or
 HPV 6 and 11 are most often associated cervical cancer.
with external anogenital warts.
How does HPV Cause Carcinoma? CRYOTHERAPY
 The transformation zone is in its most active state of cellular  Freeze the lesion
transformation during birth, adolescence and first pregnancy  Has largely been supplanted by LEEP. If patients are carefully
 The zone is the area of the cervix and vagina initially covered by selected, the success rate is approximately 95%.
columnar epithelium  Larger CIN lesions have higher failure rates, most likely because
 Through metaplasia, there is replacement by squamous the whole lesion is not covered by the cryoprobe. It is not
epithelium appropriate to use cryotherapy if the lesion extends into the
 Exposure of this cervical zone to carcinogenic factors/events endocervix.
during these active periods may increase the risk of development  procedure is simple. After colposcopy and sampling has shown
of carcinoma in the new squamocolumnar junction (starts with a that the lesion is confined to the exocervix, a probe is selected that
break in the epithelium) will cover the entire lesion, in most systems, N2O is used as the
 A cancer associated HPV Types cause neoplastic cellular changes refrigerant
when its DNA becomes integrated into the host cell genome  Probe is applied to the cervix and the system is activated. The
 The HPV viral genome encodes 6 early open reading frame cervix will freeze quickly, but the probe must remain in place until
proteins (i.e., E1, E2, E3, E4, E6, E7), which function as regulatory the ice ball that forms extends to at least 5 mm beyond the edge
of the instrument.
 Most cases, this takes 3 to 4 minutes Stage 3 Tumor extends to the pelvic sidewall and/or involves the
 Refrigerant is then turned off, and the probe allowed to thaw and lower third of the vagina and/or causes hydronephrosis or
separate from the cervix nonfunctioning kidney.
 Because the tissue that was destroyed remains on the cervix, On rectal examination, there is no cancer free space
within a few hours to a day, the patient will begin to experience between the tumor and the pelvic sidewall.
vaginal discharge Stage 3A No extension to the pelvic sidewall but involvement of the
 As the tissue sloughs, the amount of discharge increases, and lower third of the vagina.
malodor is common. It may take as long as 3 weeks for the Stage 3B Extension to the pelvic sidewall or hydronephrosis or
discharge to stop nonfunctioning kidney.
 The patient should be cautioned to place nothing in the vagina for
at least 3 weeks after the procedure to avoid causing dislodgment
of the eschar.
 First follow-up should occur in approximately 4 to 6 months and
include cytology and colposcopy. The cytology sample should
include the endocervix
Stage 4 Stage IV is carcinoma that has extended beyond the true
pelvis or has clinically involved the mucosa of the bladder
FIGO STAGING OF CANCER and/or rectum.
Stage 0 Carcinoma in situ (preinvasive carcinoma) Stage 4A Spread of the tumor onto adjacent pelvic organs. Tumor
Stage 1 Carcinoma strictly confined to the cervix; extension to the invades mucosa of bladder or rectum and/or extends
uterine corpus should be disregarded. beyond true pelvis
Stage 1A Invasive cancer diagnosed only by microscopy. Stage 4B Spread to the distant organs
All macroscopically visible lesions even with superficial
invasion are stage Ib cancers. Invasion is limited to
measured stromal invasion with a maximum depth of 5
mm* and no wider than 7 mm.
Stage 1A1 Stromal invasion is no greater than 3 mm in depth and no TREATMENT OF CERVICAL CANCER
wider than 7 mm in horizontal spread. 1. Radical Hysterectomy with Bilateral Pelvic Lymph Node Dissection
Stage 1A2 Stromal invasion >3 mm but 5 mm in depth and with  Surgical procedure done for early stage cervical cancers
horizontal spread of 7 mm. (stage IA2 and selected cases of stages IB and IIA)
 Procedure which includes the removal of the:
a) uterus and its ligaments, ligated as close to the pelvic
sidewalls as possible (round, infundibulopelvic,
uterosacral, cardinal ligaments);
b) the parametria and paracervical tissues;
c) upper half of the vagina or as much as 3 cm of the
vagina;
d) all pelvic lymph nodes (external and internal iliacs,
obturator nodes).
Stage 1B Clinically visible lesions confined to the cervix or microscopic
lesions greater than stage IA2.
 *Removal of the ovary is not mandatory in the procedure and is
Stage 1B1 Clinically visible lesions no greater than 4 cm in greatest
done on case-to-case basis
dimension.
Stage 1B2 Clinically visible lesions > 4 cm in greatest dimension. 2. RADIATION THERAPY WITH CHEMOTHERAPY
 “concurrent chemoradiation”
 mainstay of treatment because it can be done to all stages
a) External Beam Radiotherapy (EBRT)/Teletherapy:
 Cobalt or LINAC (linear accelerator).
 Initial external beam fields encompass a clinical
target volume that includes the primary tumor and
adjacent areas at risk for direct occult invasion or
regional lymph node metastases

Stage 2 Tumor extends beyond the cervix but has not b) Internal Radiotherapy/Brachytherapy
extended onto the pelvic wall. The carcinoma  Brachytherapy involves the temporary placement of
involves the vagina, but not as far as the lower intrauterine tandem and intravaginal ovoid that are
third. afterloaded with radioactive material.
Stage 2A No obvious parametrial involvement.  is associated with the most severe and difficult to
Involvement of up to the upper two-thirds of manage complications, notably pelvic fistulas.
the vagina.
Stage 2B Obvious parametrial involvement, but not onto CERVICAL CANCER IN PREGNANCY
the pelvic sidewall.  The diagnosis of invasive carcinoma of the cervix during
pregnancy is managed in much the same fashion as the non-
pregnant patient. In pregnancy, the treatment method depends
on the patient’s wishes with respect to pregnancy continuation.
 If fetal viability has not been achieved and the lesion is Stage I or
IIA, treatment may be with radical hysterectomy and pelvic
lymphadenectomy with the fetus left within the uterus.
 If close to fetal maturity, if after discussion with the patient, the
patient wishes to continue with the pregnancy, then cesarean
radical hysterectomy and bilateral pelvic lymphadenectomy is the
treatment of choice for early lesions. More advanced disease is  Lead to pseudomyxoma peritonei
generally treated with radiotherapy. o Adenofibroma
 epithelial component may be serous, mucinous,
clear-cell, or endometrioid
Neoplastic diseases of the ovary  have fibrous component
o Brenner tumor
A. EPITHELIAL STROMAL TUMORS  rare and often incidental findings
o 2/3 of ovarian neoplasms  occur in women in their 40s and 50s
o Serous tumors: MC ovarian epithelian tumor  almost always benign
o Mucinous tumors: epithelial cells filled with mucin  oophorectomy
o Endometrioid tumors: epithelial cells resembling the
endometrium b. Intermediate
o Clear cell tumors: cells with abundant glycogen and hobnail o Occur in women 30-50
cells o BRCA1 highly expressed in ovarian borderline carcinoma
o Brenner tumors: resemble transitional epithelium of the o Excellent prognosis
bladder and walthard nests if the ovary o do not invade the stroma of the ovary
o UTZ o occur in young women during the reproductive years
 define criteria to allow conservative follow-up and the o Mucinous Borderline: excellent prognosis
risk of malignancy of some adnexal masses  widespread growth of mucin-producing cells in the
 addition of a CA 125 serum assay to their ultrasound peritoneum (pseudomyxoma peritonei).
criteria in postmenopausal women increased the o Treatment:
accuracy of preoperative evaluation  Unilateral oophorectomy, if:
 malignancy rates were 8% for multilocular cysts, 65%  tumor is confirmed to be at stage IA
for multilocular solid tumors, and 39% for solid ovarian  histologic sampling of the tumor confirms it to be a
masses borderline tumor
 unilocular cysts smaller than 10 cm in diameter are  contralateral ovary appears normal
rarely malignant  biopsy specimens of areas of omental or peritoneal
nodularity are negative
o Socring systems for malignancy  of peritoneal cytologic tests are negative for tumor
 Is the finding a simple (unilocular) or complex cells
(multicystic/multilocular with solid components) cyst?  Radiation and chemotherapy
 Are there papillary projections?
 Are the cystic walls and/or septa regular and smooth? c. Malignant
 What is the echogenicity (tissue characterization)? o Women older than 40
o Ovarian carcinomas are usually diagnosed by detection of
o Transvaginal color Doppler an adnexal mass on pelvic or abdominal examination
 resistance index: measures resistance to flow in the o serous carcinomas:
vessels, low in malignant tumors  MC invasive epithelial CA
o Borderline and Stage I: larger, contained more papillary  worst prognosis
projections, and more often were multilocular without o transitional cell carcinoma: rare but chemosensitive
solid components but were less often purely solid and less o Endometrioid: endometrial CA
likely to be associated with ascites o diagnosis is made from radiographic survey executed for
evaluation of nonspecific gastrointestinal symptoms
o Ovarian Cancer Screening o infiltrate the peritoneal surfaces of both the parietal and
 Physical exam: least sensitive intestinal areas
 Biomarkers
o CA 125
 UTZ DYSGERMINOMA
o most common type of malignant germ cell tumors
a. Benign o consist of primitive germ cells with stroma infiltrated by
o Occur mostly in the reproductive years lymphocytes
o Age and menstrual status should be considered in o analogous to seminoma in the male testis
evaluating an ovarian mass o occur primarily in women younger than the age of 30
o Those taking OCP’s should be monitored carefully o can be discovered during pregnancy
o Unilocular 5-8 cm cysts are likely to be functional o Some arise in dysgenetic gonads
o Multilocular or partly solid more likely neoplastic o bilateral in approximately 10% of cases
o CA 125: expressed by approximately 80% of ovarian o 15% of dysgerminomas produce human chorionic
epithelial carcinomas gonadotropin
o Increased in endometrial and tubal carcinoma (>35
U/ml) SEX CORD STROMAL TUMORS
o increased in 22% of cases of benign masses o Derived fromsex cords of the ovary and the specialized stroma
o Benign conditions where CA 125 is elevated of the developing gonad
 Endometriosis o elements can have a male or female differentiation
 Peritoneal inflammation, PID o can be hormonally active
 Leiomyoma o sex cord component is the granulosa cell, and the stromal
 Preagnancy component is the theca cell or fibroblast (female)
 Hemorrhagic ovarian cyst o Sertoli cell and the Leydig cell (male)
 Liver disease
o Most are asymptomatic a. Granulosa Theca Cell Tumor
o Mucinous tumors: >30 cm o consist primarily of granulosa cells and a varying proportion
 Can perforate and rupture of theca cells or fibroblasts or both
o Call Exner bodies o poorly differentiated: poor prognosis, metastasis
 eosino-philic bodies surrounded by granulosa cells o Treatment
o Functional granulosa cell tumors are primarily estrogenic  Surgery: excision
o 5% occur before puberty  Adjuvant chemotherapy
 Can cause precocious puberty  symptoms of virilization usually regress after tumor
o Iproduce increased levels of blood estrogens, uterine removal, but temporal hair recession and a deeper voice
bleeding, and occasionally endometrial carcinomas in tend to remain.
postmenopausal women
o functional granulosa cell tumor can produce abnormal
menstrual patterns, menorrhagia, and even amenorrhea. Most patients with malignant ovarian germ cell tumors can be treated
o can become large and may present as a ruptured mass, successfully with fertility-sparing surgery followed by BEP chemotherapy.
leading to laparotomy for an acute abdomen with
Patients who clearly do not require postoperative chemotherapy include
hemoperitoneum
o 90 % present as stage I those with stage IA dysgerminoma and stage IA grade 1 immature teratoma.
o Advance clinical tage present with tumor rupture, a large However, there is a trend toward the study of surveillance rather than
primary tumor (>15 cm), and a high mitotic rate chemotherapy for patients with stage I tumors of any histologic subtype
o granulosa cell tumors can be confused histologically with
poorly differentiated adenocarcinomas MODULE 6
o Juvenile granulose cell tumor (found in females younger
than 20) PRE-MALIGNANT AND MALIGNANT DISEASES OF THE ENDOMETRIUM
o Treatment
 Surgical removal
ENDOMETRIAL HYPERPLASIA
 unilateral adnexectomy or salphingo-oophorectomy
Classification Sample Image
 Unilateral salphingo-oophorectomy have high
Simple Hyperplasia
reccurence rate—close follow-up
 For women who have completed childbearing,
abdominal hysterectomy and bilateral salpingo-
oophorectomy are recommended
 Radiotherapy
 VAC regimen
 Combination of ciplastin, doxorubicin and
syclophosphamide for metastatic tumors
 Patients with stage II-IV and those with recurrent Complex Hyperplasia
tumors should undergo post op therapy
 Hormone Therapy for metastatic tumors
 medroxyprogesterone acetate
 gonadotropin-releasing hormone antagonists

b. Thecomas and Fibromas

Thecoma
o benign tumors that consist entirely of stroma (theca) cells Atypical Hyperplasia
o occur in women in the perimenopausal and menopausal
years
o can be associated with estrogen production
o Treatment
 Removal of the tumor for women in the reproductive
years
 total abdominal hysterectomy and bilateral salpingo-
oophorectomy for older women
WHO Classifications of Endometrial Hyperplasia
Fibroma 1. Simple Hyperplasia
o most common benign solid ovarian tumor  defines an endometrium with dilated glands that may
o can occur at any age but is more common in older contain some outpouching and abundant endometrial
women stroma
o does not secrete hormones  Glands cystically dilated and focal crowding
o contain spindle cells and can grow to a large size  Lined by psuedostratified tall columnar epithelium
o excision is adequate treatment  Glands separated by abundant cellular stroma
o associated with ascites in approximately 40% of cases if  term cystic hyperplasia has been used to describe
the tumor exceeds 10 cm dilation of the endometrial glands, which often occurs
o Meigs’ Syndrome: hydrothorax and benign ascites which in a hyperplastic endometrium in a menopausal or
regresses following tumor removal postmenopausal woman (cystic atrophy). It is
considered to be weakly premalignant.
c. Sertoli-Leydig Cell Tumors (Androblastoma) 2. Complex Hyperplasia (without atypia)
o Rare  this condition, glands are crowded with very little
o consist almost entirely of either Sertoli or Leydig cells endo-metrial stroma and a very complex gland pattern
o occur in young women of reproductive age and outpouching formations
o frequently cause masculinization and hirsutism  This is a variant of adenomatous hyperplasia with
o also to have estrogenic activity moderate to severe degrees of architectural atypia but
o behave as low-grade malignancies with no cytologic atypia.
o well differentiated: benign 3. Atypical Complex Hyperplasia
 refers to hyperplasias that contain glands with
cytologic atypia and are considered premalignant
 an increase in the nuclear/cytoplasmic ratio with
irregularity in the size and shape of the nuclei
 Cytologic atypia occurs primarily with complex
hyperplasia, and simple hyperplasia with atypia is
rarely seen.
 Has the greatest malignant potential.
 Crowding of glands with disparity in their size and
irregularity in their shape.
 Budding with fingerlike outpouching in the adjacent
endometrial stroma
4. Atypical Simple Hyperplasia

**wulei sa trans/ppt to
Simple hyperplasia - 1% rate of progression to cancer
Complex hyperplasia without atypia - 3% rate of progression to cancer
Complex atypical hyperplasia had a 29% rate of progression to cancer.
c
Schematic Diagram of Endometrial Management for Reproductive Patients

c c
c FIGO STAGING
Stage I: The tumor is confined to the body of the uterus.
 Stage IA: The tumor is limited to the endometrium
 Stage IB: The tumor invades less than ½ of the myometrium
 Stage IC: The tumor invades more than 1/2 of the myometrium

Stage II: The tumor extends to the cervix (the lower part of the uterus).
 Stage IIA: Cervical extension is limited to the endocervical glands
 Stage IIB: Tumor invades the cervical stroma
Stage III: There is regional tumor spread.
 IIIA:The tumor invades the uterine serosa or adnexa or both, or
(+) peritoneal cytology , or both
 IIIB:Vaginal metastases
c  IIIC:Metastases to pelvic or para-aortic lymph nodes , or both
Stage IV: There is bulky pelvic disease or distant spread.
 IVA: Tumor has spread to the bladder or bowel mucosa , or both.
 IVB:Distant metastases are present.

Histologic Grade DOES NOT change the Stage (from book and ppt)
c  Grade 1 : Well differentiated: <6% solid components
 Grade 2 : Moderately differentiated: 6-50% solid components
 Grade 3 : Poorly differentiated: >50% solid components

Pathologic Features
 75% of Endometrial Ca are pure ADENOCARCINOMAS
 Less often types but carries a worse prognosis : CLEAR CELL ,
SQUAMOUS , SEROUS CA
Adenocarcinoma

ENDOMETRIAL CARCINOMA
Risk Factors:
• Diminishes the Risk
 Ovulation
 Progestin therapy Clear Cell Carcinoma
 Combination oral contraceptives
 Menopause prior to 49 years
 Normal weight
 Multiparity

Ultrasound Criteria for Endometrial Thickness


Squamous Cell Carcinoma
Serous Carcinoma

Pattern of Spread
 Most common : Direct extension of tumor to the adjacent
structures
 Exfoliated cells may pass through the FT and implant on the • Fleshy outgrowth, soft, smooth, friable, red
ovaries , visceral or parietal peritoneum or the omentum • Postmenopausal
 Lymphatic spread : common in pxs with deep myometrial
• Caused by: Chronic irritation or infection
involvement

 Pelvic lymph nodes
 Para-aortic lymph nodes • URETHRAL CARCINOMA: SCC
o Elderly
 Hematogenous route : uncommon; may result in parenchymal
metastases (lungs , liver, or both) • Biopsy: if benign, oral/topical estrogen
• Surgical management: cryoTx, laser tx, excision
Clear Cell Carcinoma NOTES:
 Resemble clear cell adenocarcinoma of the ovary, cervix and vagina -when you see this mass, differentiate benign from malignant
 Tend to develop in postmenopausal women - oral and topical applied twice a day-> regress
 Prognosis much worse than typical endometrial adenocarcinoma
FIBROMA
 Survival rates of 39% - 55% have been reported, much less the 65% or
better usually recorded for endometrial carcinoma

Prognostic Factors
I. Clinical determinants:
 patient age at diagnosis: older > young
 race: white > black
 clinical tumor stage

II. Pathologic determinants


 tumor grade • Most common benign solid tumor of the vulva
 histologic type • All age groups
 uterine size • LOCATION: Labia majora
 depth of myometrial invasion • Slow growing
 microscopic involvement of vascular spaces in the uterus by • Smooth, distinct contour
tumor • Gray-white cut surface
 spread of tumor outside the uterus to the retroperitoneal lymph • Low-grade potential for Malignancy
nodes, perito-neal cavity, or uterine adnexa. NOTES:
- SOLID TUMOR
III. Histologic Grade - Excise and biopsy
 major determinant of prognosis
HEMATOMAS
IV. Histologic Type • Blunt trauma
• Best Prognosis:
• Spontaneous: varicose veins
 Typical Adenocarcinoma
• Observation
 Secretory carcinoma o >10 cm
• Poor Prognosis
• Compression, application of ice pack, NSAIDS
 Papillary serous carcinoma
• Surgical: drainage and Debridement
 Clear cell carcinoma
NOTES:
 Poorly differentiated carcinoma
- Complain of PAIN, difficulty of ambulating, inability to void
- Most common cause of vulvar hematoma: STRADDLE INJURY
Leiomyosarcoma
- Other cause: rape, bite on vulva, vaginal delivery
- Histologic Features: comparable with a 12-week pregnancy or
o Hematoma is (sometimes) seen on the contralateral
larger
side of the area of episiotomy due to spontaneous
- Risk of sarcoma increased with age,
ruptures during labor or
- Determination of malignancy is made in part by ascertaining the
- What to do: give pain reliever, catheter, if too big, incise and
number of mitoses in 10 hpf as well as the presence of cytologic
drain.
atypia, abnormal mitotic figures, and nuclear pleomorphism
- Incision will depend on the size of hematoma
- finding of more than five mitoses per 10 hpf with cytologic atypia
- Incision is done if hematoma is >10 cm or symptomatic
leads to a diagnosis of leiomyosarcoma; when there are four or
- Ice pack further expansion of hematoma
fewer mitoses per 10 hpf, the tumors usually have a more benign
- Pedia: limit to conservative management if possible
clinical course
DERMATOLOGIC DISEASES
BENIGN GYNECOLOGIC LESIONS CONTACT DERMATITIS:
VULVA
URETHRAL CARUNCLE
• Fleshy, reddish, Smooth, soft, fragile
• Pathophysiology:
o Inflammation,
o abnormal focal responsiveness to hormonal
stimulation
• Intermenstrual bleeding
• Malignancy?
NOTES:
- If it is usually in the cervical canal: it has a stalk
- If in the cervix: sessile (broad based)
• Usually caused by an irritant - Non tender polyp
• Distinguish between immunologic and non immunologic cause - Complaint: post coital spotting, actual bleeding,
o Immunologic: may occur after 1 day before symptoms - Polyp: low malignant potential
appear o 40’s- 50’s patient presenting with polyp: do
o Non immunologic: may occur after 3 encounters with polypectomy
irritant, and effects are seen - Polypectomy:
• Rashes is resolved if irritant is removed o Office procedure
o Ovum forceps grasp the mass and twist
• Red, edematous, inflamed eczematoid or weeping vesicle
• If px has itch scratch: there may be excoriation or secondary
ENDOCERVICAL POLYPS
infection
 polyps are most common in multiparous women in their 40s and
• Complaint: tenderness, burning and pruritus
50s
• Not consult may result into lichen simplex chronicus  may be single or multiple and are a few millimeters to 4 cm in
o Rough, thick and leathery (elephant-skin) diameter
• What to do: burrow’s solution, keep hydrated and mositurized  are more common than are cervical polyps
(petroleum jelly)  usually have a narrow, long pedicle and occur during the
• Intense pruritus: may give HYDROCORTISONE, PREDNISONE reproductive years
• Antihistamine is only given if px cannot sleep or do work due to  usually secondary to inflammation or abnormal focal
itchiness responsiveness to hormonal stimulation
• Initial treatment for mild disease is 1% hydrocortisone cream  cherry red in color
 classic symptom is intermenstrual bleeding, especially following
VAGINA contact such as coitus or a pelvic examination
LOCAL TRAUMA  managed in the office by grasping the base of the polyp with an
• most frequent cause is coitus appropriately sized clamp, twisting motion
• 80% of vaginal lacerations occur secondary to sexual intercourse.
• predisposing factors believed to be related to coital injury include CERVICAL MYOMAS
virginity
• state of the postpartum and postmenopausal
• vaginal epithelium, pregnancy, intercourse after a prolonged
period of abstinence, hysterectomy, and inebriation
• most common injury is a transverse tear of the posterior fornix.
• often occur in the right or left vaginal fornices
• location of the coital injury is believed to be related to the poor
support of the upper vagina, which is supported only by a thin
layer of connective tissue - Firm masses that are similar to myomas of the fundus
- Solitary growth in contrast to uterine myomas
• most prominent symptom of a coital vaginal laceration is profuse
- Relative paucity of smooth muscle fibers in the cervical stroma, the majority
or prolonged vaginal bleeding
of myomas that appear to be cervical actually arise from the isthmus of the
• The most troublesome but extremely rare complication of vaginal
uterus
laceration is vaginal evisceration
- Small and asymptomatic
• Management of coital lacerations involves prompt suturing - When symptoms do occur, they are dependent on the direction in which
• Secondary injury to the urinary and gastrointestinal tracts should the enlarging myoma expands
be ruled out. - Cervical myoma may become pedunculated and protrude through the
external os of the cervix. These prolapsed myomas are often ulcerated and
CERVIX infected
POLYPS - may produce distortion of the cervical canal
- Rarely, a cervical myoma causes dystocia during Childbirth
- The occurrence and persistence of symptoms from a cervical myoma are an
indication for medical therapy with gonadotropin-releasing hormone (GnRH)
agonists or myomectomy or hysterectomy

UTERUS
ENDOMETRIAL POLYPS (etiology: Unopposed estrogen)

• Most common benign neoplasm (cervix)


• Endocervical, cervical
• Stalk, sessile
• Usually Seen in: Multiparous, 40-50’s
o Maybe confused with myoma uteri
o If it has pseudocapsule and able to remove from
surrounding tissue: (+) myoma uteri
- Diffuse: entire myometrium is involved
o Symptomatic
o Severe and cyclic pelvic pain
o Menorrhagia
- Palpation:
o Adenomyosis: Symmetrically enlraged globular, tender
esp. in menstruation
• localized overgrowths of endometrial glands and stroma that project o Myoma uteri: asymmetric, enlarged uterus
beyond the surface of the endometrium. - Histologic finding: hyperplasia and hypertrophy of myocyte
• Polypoid hyperplasia - Hysterectomy: both ovaries are removed to ensure that
o benign condition in which numerous small polyps are malignancy will not developed
discovered throughout the endometrial cavity
• Endometrial polyps may have a broad base(sessile) or be attached by FALLOPIAN TUBES
a slender pedicle (pedunculated). TORSION
• Peak incidence between the ages of 40 and 49 • Ovarian mass, paratubal cyst
• Endometrial polyps are noted in approximately 10% of women when • Sxs: acute lower abdominal and pelvic pain
the uterus is examined at autopsy. o Nausea and vomiting
• Menorrhagia, premenstrual and postmenstrual staining, and scanty • Mx: exploratory laparotomy
postmenstrual spotting are the most common o Untwist the tube
• Succulent and velvety, with a large central vascular core. o Sutured to a secure position
• Color is usually gray or tan but may occasionally be red or brown o Excision
• Endometrial polyp has three components: NOTES:
• endometrial glands - usual complaint is sudden severe pain
• endometrial stroma - Size matters
• central vascular channels - Emergency case: management: explore lap
• Immature endometrium differs from surrounding endometrium and - Delay may cause necrosis
often appears as a “Swiss cheese” cystic hyperplasia during all phases **part II
of the menstrual cycle UTERUS
• Tip of a prolapsed polyp often undergoes squamous metaplasia, LEIOMYOMA
infection, or ulceration. • Benign tumors of muscle cells origin
• One in four reproductive-age women with abnormal bleeding will • Also known as fibroids or fibromyomas, fiboruterines
have endometrial polyps discovered in her uterine cavity. • most frequent pelvic tumor and the most common tumor in
• Overall the incidence of malignancy is 3% to 4%. women> 30 years and above, but can occur in any age group
• Most endometrial polyps are asymptomatic • highest prevalence at the 5th decade of woman’s life
• -Unusual polyps have been described in association with chronic - found in 30-50% of perimenopausal women
administration of the nonsteroidal antiestrogen tamoxifen • Symptomatic leiomyomas are the primary indication for
• Optimal management of endometrial polyps is removal by approximately 30% of all hysterectomies
hysteroscopy with D&C • In general 1/3 of myomas will be symptomatic
• Postcurettage hysteroscopic studies • Myomas are prone to grow and become symptomatic in
• have demonstrated that routine use of a long, narrow polyp forceps at nulliparous women
the time of curettage at best results in discovery and removal of only • Risk factors:
approximately one in four endometrial polyps - Increasing age
- Low parity
• Unusual polyps have been described in association with
- Obesity- hyperestrogen state
• Chronic administration of the nonsteroidal antiestrogen tamoxifen.
- Early menarche
- Tamoxifen use
ADENOMYOSIS
- High fat diet(some studies)
• Ectopic endometrial glands and stroma - Smoking has been found to be associated with a decreased incidence
o Aberrant glands of the basalis layer of EM  do not of myomata
undergo hormonal changes - familial tendency
o Direct extension from EM lining • In the Pelvis, majority are found in the corpus of the uterus,
• Risk factors: inc parity, uterine manipulation occasionally in the fallopian tube, round ligament, 5% are found in the
• Focal VS diffuse cervix, rare- retroperinoneum produce symptoms of “mass effect”
• Globular uterus • Myomas may be single or most often multiple, mmay be micronodular
o Hyperplasia and hypertrophy of myocytes or macronodular.
• 50% asymptomatic • Most myomas develop initially develop as intramural myomas- growth-
• Severity  inc involvement of myometrium myometrium at edge of the tumor is compressed- pseudocapsule
• Sxs: secondary dysmenorrhea, AUB
• Dx: globular uterus (14-weeks), tender, histologic findings 3 most common types:
o UTZ, MRI • Intramural
• Mx: medical, TAH/TAHBSO - Large intramural can also cause bleeding
• subserous
NOTES: - beneath the serosa
- Not responsive to hormonal stimulation - knobby contour during pelvic examination
- Uterine manipulation: tissues may implant or seeding - may lead to a pedunculated myoma into the peritoneal cavity
- Focal: adenomyoma • submucous
- just below the endometrium
- 5-10%
- most troublesome clinically (Cigarrete Shaped nuclei, markedly elongated smooth muscle cells,
- may be associated with abnormal vaginal bleeding, distortion of eosinophilic cytoplasm)
the uterine cavity that may produce infertility or abortion Types of Degeneration: because of severity of discrepancy between the
- rarely enlarges and becomes pedunculated myoma’s growth and its blood supply, determines the extent of
- uterus may try to expel, prolapsed myoma may protrude through degeneration
the external cervical os • Hyaline- mildest form of degeneration
- may become a parasitic myoma obtaining blood supply from • Calcific
another organ • Fatty
- lateral growth may result in a broad ligament myoma- difficult to • RED OR CARNEOUS
differentiate from an ovarian tumor/ ovarian new growth (UTZ),  most common, most acute form of degeneration
may produce a hydroureter  acute muscular infarction causes severe pain and localized
• Other types: intraligamentary and parasitic myomas perineal irritation
• Some may have both submucous and intramural components  best treated with NSAIDS for 72 hours as long as the woman is
less than 32 weeks of gestation
 occurs during pregnancy (cannot cope) , operative removal is not
done
 UTZ- mixed echodense and echolucent areas
 Not a contraindication to myomectomy, in non pregnant
• myxomatous
• cystic
• necrosis
Malignant Transformation is 0.3 to 0.7% usually into a Sarcoma

Clinical Manifestation:
Most common symptoms:
• pressure from an enlarging mass
• pain including dysmenorrheal
• acquired dysmenorrheal is one of the most frequent complaints
• Origin:
• abnormal bleeding-
o each tumor develops from a single muscle cell a progenitor
o 30% of patients with myomas
myocyte- may undergo somatic mutation
o Most common is menorrhagia
o Cytogenetic analysis demonstrated that myomas have
o Intermenstrual spotting and disruption of normal
multiple chromosomal
pattern-frequent complaints
o abnormalities affecting regulation of growth inducing
o Exact cause is poorly understood
proteins and cytokines
• severity of symptoms depend on the number, location, and size of
• Current theory:
the myoma
- neoplastic transformation from normal myometrium to
• 2/3 are asymptomatic
leiomyomata is the result of a somatic mutation in the single
• Pelvic pain
progenitor cell affecting cytokines that affect cell growth. The
• Pelvic discomfort- described as pelvic heaviness or a dull, aching
growth may be influenced by estrogen and progesterone levels
sensation, that may be secondary to an edematous swelling in the
- Guidelines- can be treated with OCP (estrogen and progesterone
myoma
can decrease size), but do not give Progesterone only pill/
• Abdominal girth increasing without appreciable change in weight
injectables
• Anterior myoma pressing on the bladder- urinary frequency and
Clinical Characteristics:
urgency
• rare before menarche, diminish in size after menopause with the
• rapid growth after menopause -consider leiomyosarcoma- classic
reduction of a significant amount of circulating estrogen
symptom
• enlarges during pregnancy and occasionally during OCP use
o very uncommon
• Medically induced hypoestrogenic states decreases myoma size
o like term pregnancy
• Women who smoke cigarettes- relatively estrogen deficient- lower
o must have total abdominal hysterectomy
incidence of myomas
Diagnosis:
Gross Appearance
• lighter in color than the normal myometrium • PE – internal examination, palpation of an enlarged, firm, irregular
• cut surface: glistening, pearl white with smooth muscle arranged in uterus, asymmetrically enlarged
trabeculated or whorl configuration -other differentials:
Histologic Appearance:  pregnancy
- with proliferation of mature smooth muscle cells  adenomyosis
- nonstriated muscle fibers are arranged in interlacing bundles with  ovarian neoplasm
variable amount of fibrous connective tissue in between - mobility of the pelvic mass and whether the mass moves
- amount of fibrous tissue proportional to extent of atrophy and independently or as part of the uterus may be helpful
degeneration diagnostically
• Utrasound- diagnostic, whorled
• Hysteroscopy
• CT Scan or MRI- MRI is helpful in differentiating adenomyosis or
an adenomyoma from a single, solitary myoma, especially in a
woman desiring preservation of her fertility
Management:
• Observation – for small, may be multiple but still asymptomatic,
 tumor first discovered
o appropriate to perform a pelvic examination, serial UTZ at 6-
12 month intervals to determine the rate of growth
 Majority of women will not need an operation, especially  Vaginally
perimenopausal- condition improves with diminishing estrogen levels. - Hysterectomy
 Cases of abnormal uterine bleeding and leiomyomas should be o >90% patient satisfaction
investigated thoroughly for concurrent problems such as endometrial o Higher rate of Urinary tract injuries (abdominal
hyperplasia, if symptoms do not improve with conservative hysterectomy)
management, operative management may be considered o E.g Late 50’s
• Medical o Indications:
- Causing symptoms  Same as myomectomy
- medical treatment majority of the reduction in size occurs  Asymptomatic myomas that has reached
within the first 3 months the size of a 14 to 16 week gestation
- GnRH agonist – danazol  Rapid growth
o Block production of estrogen - Prolapse of a myoma through the cervixs is optimally treated with
o Hypoestrogenic state vaginal removal and ligation of the base of the myoma
o May reduce blood loss at the time of hysterectomy and - choice between myomectomy and hysterectomy depends on the
myomectomy patient’s age, parity, and MOST IMPORTANT, future reproductive
- Medroxyprogesterone acetate – RU 486 plans
o Significant reduction in soze, bleeding and
improvement of quality of life Uterine Artery Embolization
Advantages and Disadvantages of Preoperative GnRH Agonist • Gelatin sponge (gelfoam) silicon spheres (multiple embolic materials)
Treatment (read daw) • Polyvinyl alcohol (PVA) particles
Advantages: • Metal coils
May allow vaginal hysterectomy • Gelatin microspheres
May decrease intraoperative blood loss
May allow Pfannenstiel incision *Complication of Uterine Artery Embolization
May facilitate endoscopic myomectomy • Post embolization fever
Advantages gained by induction of Amenorrhea: • Sepsis from infarction of the necrotic myometrium
May correct hypermenorrhea–menorrhagia-associated anemia • Ovarian failure
May improve ability to donate blood • Abdominal pain- postprocedural, common, in the first 24 hours up
May decrease need for nonautologous blood transfusion to 2 weeks
May atrophy endometrium, facilitating hysteroscopic resection of •
submucosal tumors Associated Rare Disease:
Disadvantages: • Intravenous Leiomyomatosis
Delay to final tissue diagnosis o benign smooth muscle fibers invade and slowly grow
Degeneration of some leiomyomas, necessitating piecemeal into the venous channels of the pelvis
enucleation at o grossly appears like a “spaghetti” tumor
myomectomy • Leiomyomatosis peritonealis dessiminata (LPD)
Hypoestrogenic side effects (e.g., trabecular bone loss, vasomotor o benign multiple small nodules over the surface of the
flushes) pelvis and abdominal peritoneum
Cost o usually associated with recent pregnancy
Need to self-administer or receive injections in many cases o management: progestational therapy
Vaginal hemorrhage in approximately 2% of patients
GnRH, gonadotropin-releasing hormone. ADENOMYOSIS
fdiJrrsFFeeoooagnnAUmm:ldhiitrrrseeooooaagnnnpm- • Often been referred to as endometriosis interna
• Operative: • Term is misleading because endometriosis and
-failed medical management, too large myomas • adeno-myosis arediscovered in the same patient in less than 20%
- Myomectomy of women.
o Longer hospital stays • only common feature is the presence of ectopic endometrial
o Reproductive years glands and stroma in the endometrium
o More pelvic adhesions • Adenomyosis is derived from:
o 80% resolution of symptoms -aberrant glands of the basalis layer of the endometrium
o CS is recommended for all degrees of myomectomy -glands do not usually undergo the traditional proliferative and
other than removal of pedunculated leiomyomata, or secretory changes that are associated with cyclic ovarian hormone
small hyteroscopic resection production. (not responsive to hormonal stimulation)
o Indications for myomectomy: • The symptoms of menorrhagia and dysmenorrhea form a
 Persistent abnormal bleeding, pain or spectrum and are subjective, thus delineating an incidence of
pressure associated symptomatology with adenomyosis is problematic.
 Enlargement of asymptomatic myoma to • Diagnosed incidentally by the pathologist examining histologic
more than 8 cm in a woman who has not sections of surgical specimens
completed childbearing
• a common incidental finding during autopsy
o Contraindications:
Disease is associated with:
 Pregnancy
• increased parity
 Advanced adnexal disease
• particularly uterine surgeries and traumas
 Malignancy
• higher rates of induced abortion with presumed curettage with
 Situation in which enucleation of the
adenomyosis
myoma would severely reduce the
• Pathogenesis of adenomyosis is unknown but is theorized to be associated
endometrial surfaceso that the uterus
with disruption of the barrier between the endometrium and myometrium as
would not be functional
an initiating step
o Myomectomy maybe performed through:
Pathology:
 Laparosopy
• Two distinct Pathologic presentations:
 Hysteroscopy
o Focal area or adenomyoma- do not confuse with myoma
 Laparotomy
uteri.
 Results in asymmetrical uterus • acquired dysmenorrhea becomes increasingly more severe as the
 No pseudocapsule- cannot remove mass disease progresses.
o Most common is a diffuse involvement of both anterior and • Occasionally the patient complains of dyspareunia, which is
posterior walls, posterior wall is usually involved more than midline in location and deep in the pelvis.
the anterior wall. Pelvic examination:
 Usually show symptoms such as severe and • Uterus is diffusely enlarged, usually two to three times normal
progressing pelvic pain during menses and size.
menorrhagia(AUB) • It is most unusual for the uterine enlargement associated with
 Palpate the uterus- globular, symmetric adenomyosis to be greater than a 14-week-size gestation unless
enlargement and tender the patient also has uterine myomas.
 Found in 2/3 of cases • The uterus is globular and tender immediately before and during
 Diffuse type of adenomyosis the uterus is menstruation
uniformly enlarged, usually two to three times Diagnosis
normal size. • adenomyosis is usually confirmed following histologic examination
 often difficult to distinguish on physical of the hysterectomy specimen.
examination from uterine leiomyomas. • Traditionally the patient will have endometrial sampling to rule
Gross: out other organic causes of abnormal bleeding.
• Adenomyosis may coexist with both endometrial hyperplasia and
endometrial carcinoma
• Approximately2/3 women with adenomyosis have coexistent
pelvic pathology, most commonly myomas but also
endometriosis, endometrial hyperplasia and salpingitis nodosa.
• When the myometrium is transected by a knife, the cut surface • Ultrasound and MRI are useful to help differentiate between
protrudes convexly and has a spongy appearance adenomyosis and uterine myomas in a young woman desiring
• cut surface of a uterus with adenomyosis is darker than the white future childbearing.
surface of a myoma • T2-weighted images are superior in making the diagnosis and
• Sometimes there are discrete areas of adenomyosis that are not documenting widened junctional zones.
densely encapsulated and contain small, dark cystic spaces. o Poorly defined junctional zones markings in the
• There is not a distinct cleavage plane around focal adenomyomas as endometrial-myometrial interface help confirm the
there is with uterine myomas diagnosus
o These bands most likely represent the glands and
Histologic examination: hypertrophied muscle of adenomyosis.
• MRI is used fro those who may choose uterine artery
embolization for treatment of myomata.
Management:
• There is no satisfactory proven medical treatment for
adenomyosis
• patients with adenomyosis are treated with GnRH agonists,
progestogens, progesterone containing IUD, cyclic hormones, or
• benign endometrial glands, and stroma are within the prostaglandin synthetase inhibitors for their abnormal bleeding
myometrium. and pain.
• glands rarely undergo the same cyclic changes as the normal • Hysterectomy is the definitive treatment if this therapy is
uterine endometrium. appropriate for the woman's age, parity, and plans for future
• standard criterion used in diagnosis of adenomyosis is the finding reproduction.
of endometrial glands and stroma more than one low-powered • Size of the uterus, degree of prolapse, and presence of associated
field (2.5 mm)n from the basalis layer of the endometrium. pelvic pathology determine the choice of surgical approach.
• small areas of adenomyosis have the same general appearance as • Women in their late 40’s- ovaries, menopausal are often removed
the basalis layers of the endometrium general there is a lack of as a risk reducing measure against ovarian carcinoma
inflammatory cells surrounding the fossae of adenomyosis. • Increased risk for complications for those who are pregnant with
• Some fossae of adenomyosis undergo decidual changes either adenomyosis
during pregnancy or during estrogen–progestin therapy for o Increased premature labor and dlivery
endometriosis. o Low BW
• The reaction of the myometrium to the ectopic endometrium: o Preterm PROM
o Hyperplasia
o hypertrophy of individual muscle fibers PARATUBAL CYST
• Surrounding most foci of glands and stroma are localized areas of • Frequently incidental
hyperplasia of the smooth muscle of the uterus. • Often multiple, vary from 0.5 to >20 cm in diameter
• change in the myometrium produces the globular enlargement of • Most cysts are small, asymptomatic, and slow growing, discovered
the uterus on the 3rd-4th decade of life
Clinical Diagnosis: • May rupture, on examination or vigorous coitus
• Over 50% of women with adenomyosis are asymptomatic or have • Pedunculated Paratubal cysts- near the fimbrial end, they are
minor symptoms called Hydatid cysts of Morgagni
• attribute the increase in dysmenorrhea or menstrual bleeding to • Cysts near the oviduct may be of mesonephric, mesothelial, or
the aging process and tolerate the symptoms. paramesonephric in origin.
• Symptomatic adenomyosis usually presents in women between • Cysts are translucent, and contain clear or pale yellow fluid
the ages of 35 and 50.
• severity of pelvic symptoms increases proportionally to the depth
of penetration and the total volume of disease in the myometrium.
• classic symptoms of adenomyosis:
o secondary dysmenorrhea
o menorrhagia.
o associated with nausea and vomiting in two thirds of
the cases.
o pelvic pain, secondary to hypoxia, is so intense-
difficult to perform an adequate pelvic exam.
• histogenesis of the majority of paratubal cysts had been believed • Twisted mass or paratubal cyst
to be from the mesonephric duct, with the cysts arising from the • SIZE matters- bigger- torsion
main duct or accessory tubules. • Unless there is associated torsion of the ovary, a specific mass is
o These latter cysts often develop between the leaves of usually not palpable on pelvic examination.
the broad ligament in the mesosalpinx, with the ovary • number of cases diagnosed preoperatively
being separate. • has increased dramatically with the use of vaginal
• Occasionally there is a papillomatous proliferation on the internal ultrasonography
wall • Because of the severity of the pain, a wide differential diagnosis of
• Low grade malignant cysts- were in women of reproductive age abdominal and pelvic pathology must be considered.
who had cysts greater than 5 cm in diameter with internal • The differential diagnosis includes :
papillary projections o acute appendicitis
• Inflammatory cysts of the peritoneum may be found anywhere in o ectopic pregnancy
the pelvis. o pelvic inflammatory disease
• majority of paratubal cysts are asymptomatic and are usually o rupture or torsion of an ovarian cyst.
discovered incidentally during ultrasound or during gynecologic • Exploratory operation determines the extent of hypoxia and the
operations. choice ofoperative techniques.
• symptomatic paratubal cysts- generally produce a dull pain. • EMERGENCY case
• During a pelvic examination it is difficult to distinguish a paratubal • tubal torsion- usually the tubes are gangrenous (eg. In delayed
cyst from an ovarian mass. management) and must be excised.
• Do not assume that it benign,(paratubal cysts) specially in the • The twisted tube is usually filled with a bloody or serous fluid
elderly, as much as possible do not aspirate- spilling of cancer cells • may be possible to restore normal circulation to the tube by
• practice of aspirating cysts via the laparoscope should be limited manually untwisting it.
to cysts that are completely simple and associated with normal • The tube is usually sutured into a secure position to prevent
cancer antigen-125 (CA-125) levels recurrence
• Paratubal cysts may grow rapidly during pregnancy, and most of
the cases of torsion of these cysts have been reported during Ovary
pregnancy or the puerperium. FOLLICULAR CORPUS LUTEUM THECA LUTEIN CYSTS
• Menopausal-hysterectomy CYSTS CYSTS
• Treatment is simple excision. Most frequent Most clinically Least common
relevant
TORSION Dependent on >3cm Bilateral, moderate
• Acute torsion of the oviduct is a rare event; however, it has been gonadotropins for to massive
reported with both normal and pathologic fallopian tubes. growth enlargement
• Pregnancy Predisposes to this problem. Prolonged
• Tubal torsion usually accompanies torsion of the ovary- they have exposure/inc
a common vascular pedicle. sensitivity to
• Torsion of the fallopian tube is secondary to an ovarian mass in gonadotropins
approximately 50% to 60% of patients. Reproductive age Mature Graafian Pregnancy, ovarian
• right tube is involved more frequently than is the left follicles hyperstimulation
• degree of tubal torsion varies from less than one turn to four Asymptomatic Dull, unilateral, Pressure sxs, ascites,
complete rotations. LAb pain abdl enlargement
• Torsion is usually seen in women of reproductive age. May delay menses
• it occurs also in preadolescent children, especially when part of Intraperitoneal
the tube is enclosed in the sac of a femoral or inguinal hernia. bleeding
• Tubal torsion may be divided into intrinsic and extrinsic causes: Transparent, thin- Small, purplish- Thin-walled,
o Intrinsic: walled red/brown hemorrhagic
 Congenital abnormalities- such as increased “Follicular Halban’s classic Hyperreactio
tortuosity caused by excessive length of the hematomas” triad luteinalis
tube Ovarian cortex Secretes Luteoma of
 Pathologic process- hydrosalpinx, progesterone pregnancy
hematosalpinx, tubal neoplasma, previous
Observation Pregnancy test UTZ
operation- specially tubal ligation (usually at
OCPs x 4-6 weeks UTZ Regresses
the distal end)
Cystectomy Cystectomy spontaneously
o Extrinsic
**Corpus Luteum Cyst:
 Ovarian, peritubal tumors
Differentials include: Ectopic pregnancy, Ruptured Endometrium, Adnexal
 Adhesions
Torsion
 Trauma
 pregnancy
FOLLICULAR CYSTS
• The most important symptom of tubal torsion is acute lower
• By far the most frequent cystic structures in normal ovaries.
abdominal and pelvic pain.
• May be young as early as 20 weeks gestation in female fetuses and
• Pain
throughout a woman’s reproductive life
o Severe hypogastric pain
• Frequently multiple and may vary from a few millimeters to as large as
o May be gradual or sudden
15 cm in diameter.
o Located in the iliac fossa with radiation to the thigh
• A normal follicle may develop into a physiologic cyst.
and flank
• A minimum diameter to be considered as a cyst is between 2.5 and 3
o duration of pain is generally less than 48 hours
cm.
• Follicular cysts are not neoplastic and are believed to be dependent on • The majority of follicular cysts disappear spontaneously by either
gonadotropins for growth. reabsorption of the cyst fluid or silent rupture within 4 to 8 weeks of
• Clinically they may present with the signs and symptoms of ovarian initial diagnosis
enlargement -must be differentiated from a true ovarian neoplasm. • ,a persistent ovarian mass necessitates operative intervention to
• Functional cysts may be solitary or multiple. These cysts are found most differentiate a physiologic cyst from a true neoplasm of the ovary.
commonly in young, menstruating women. • Endovaginal ultrasound examination is helpful in differentiating simple
• Solitary cysts may occur during the fetal and neonatal periods and from complex cysts and is also helpful during conservative management
rarely during by providing dimensions to determine if the cyst is increasing in size.
• childhood, but there is an increase in frequency during the • When the diameter of the cyst remains stable for greater than 10
perimenarcheal period weeks or enlarges- neoplasia should be ruled out.
• CA-125 may be used to evaluate large cysts in pregnancy, values for CA- • Oral contraceptives may be prescribed for 4 to 6 weeks for young
125 should be within the normal range past 12 weeks' gestation women with adnexal masses
• Multiple follicular cysts in which the lining is luteinized are associated - This therapy removes any influence that pituitary gonadotropins
with either intrinsic or extrinsic elevated levels of gonadotropins. may have on the persistence of the ovarian cyst
• Reproductive-age women with cystic fibrosis appear to have an • Evaluation of an asymptomatic cyst, found incidentally, is based on the
increased propensity for developing individual follicular cysts. principle that the cyst should be removed if there is any suspicion of
• Follicular cysts are translucent, thin-walled, and are filled with a watery, malignancy.
clear to straw-colored fluid. • Suspicion may develop because of history, including family history,
• If a small opening in the capsule of the cyst suddenly develops-cyst fluid patient age, and other nongynecologic signs and symptoms.
under pressure will squirt out. • The size and physical characteristics of the cyst are as important as are
• These cysts are situated in the ovarian cortex- sometimes they appear other laboratory parameters.
as translucent domes on the surface of the ovary. • CA-125 is helpful in evaluating the adenexal mass in postmenopausal
• Histologically the lining of the cyst is usually composed of a closely women.
packedlayer of round, plump granulosa cells, with the spindle-shaped - In general, complex cyst or persistent simple cysts larger than 10
cells of the cm should be evaluated
• Theca interna deeper in the stroma. • Cyst in a perimenopausal or postmenopausal woman should be
• Temporary disturbance in follicular function that produces the clinical removed if the CA-125 is abnormal (>35), or if the cyst is persistent or
picture of a follicular cyst is poorly understood. large (>10 cm).
• Follicular cysts may result from: • A small simple cyst in a perimenopausal or postmenopausal woman (<5
o either the dominant mature follicle's failing to rupture cm) with a normal CA-125 may be observed with regular reevaluation
(persistent follicle) including ultrasound
o immature follicle's failing to undergo the normal process of • Management of cysts between 5 and 10 cm that are otherwise not
atresia. suggestive should be individualized.
o Incompletely developed follicle fails to reabsorb follicular • premenopausal women, operative management of nonmalignant cysts
fluid is cystectomy, not oophorectomy
• Some follicular cysts lose their ability to produce estrogen, and in • Many clinicians will manage simple cysts with the laparoscope- Since
others the granulosa cells remain productive, with prolonged secretion this procedure has an accompanying risk of spilling malignant cells into
of the peritoneal cavity if the cyst is an early carcinoma, strict
• Estrogens preoperative criteria should be fulfilled before laparoscopy is
• Follicular Hematomas- blood from the vascular theca zone fills the attempted.
cavity of the cyst • Criteria: include the woman's age; size of the mass; and ultrasound
characteristics, such as nonadherent, smooth, and thin-walled cysts,
Diagnosis: without papillae or internal echoes. (simple).
• majority of follicular cysts are asymptomatic and are discovered during
ultrasound imaging of the pelvis or a routine pelvic examination
• Ultrasound cannot distinguish between benign or malignant BENIGN NEOPLASMS OF THE OVARY
• May correlate with malignancy:
o Septations **Benign Cystic Teratoma –Doughy consistency upon palpation;
o Internal papillations Histologically composed of mature cells, usually from all three germ layers;
o Loculations Treatment of a dermoid in pregnancy, as is nonpregnant state, is
o Solid lesions/ cystic lesions with solid components cystectiomy.
o Smaller cyst adjacent to or part of a larger cyst-daughter cyst
• Because of their thin walls, these cysts may rupture during ENDOMETRIOMAS
examination. • 2/3 of women with endometriosis have ovarian involvement
• The patient may experience tenesmus, a transient pelvic tenderness, • One of the most common cause of enlargement of the ovary
deep dyspareunia, or no pain whatsoever • Varies from small, superficial, blue black implants 1-5mm in diameter to
• Rarely- significant intraperitoneal bleeding associated with the rupture large, multiloculated, hemorrhagic cysts 5-10 in diameter
of a follicular cyst. • Surface is often irregular, puckered and scarred
• women who are chronically anticoagulated or • Areas of ovarian endometriosis that become cystic are termed
• those with von Willebrand's disease may bleed endometriomas
• menstrual irregularities and abnormal uterine bleeding -associated with • Rare- large chocolate cyst 15-20 cm
follicular cysts- produce elevated blood estrogen levels. • Common symptoms
• consists of a regular cycle with a prolonged intermenstrual interval, o Asymptomatic-most common
followed by episodes ofmenorrhagia. o pelvic pain
• Some women with larger follicular cysts notice a vague, dull sensation o dyspareunia
or heaviness in the pelvis. o infertility
Diagnosis:
Management: • pelvic exam findings: ovaries are tender and immobile due to adhesions
• initial management of a suspected follicular cyst is conservative to surrounding structures
observation up tp 3-6 cycles- does not regress- ocp’s- still does not
regress- oopherectomy
• Ultrasonography: thick walled cyst with homogenous echogenic pattern • Histologically: connective tissue, stromal cells, and varying amount of
collagen, spindle shaped, mature fibroblast, imperfect pattern, must be
distinguished from stromal hyperplasia fibrosarcomas, and Brenner
tumors
Management:
• Straightforward, any woman with a solid ovarian neoplasm should have
an exploratory operation soon after the tumor is discovered
• surgery (TAH-BSO), oopherectomy

TRANSITIONAL CELL TUMORS-BRENNER TUMORS**


• rare, small, smooth, solid, fibroepithelial ovarian tumors that are
• Histologically: endometrial glands, endometrial stroma, large generally asymptomatic
phagocytic cells containing hemosiderin • The benign, proliferative (low malignant potential), and malignant
• Management: medical or surgical forms together comprise approximately 2% of ovarian tumors.
• Factors • Usually occur in women ages 40 to 60 years.
- patient’s age • small, solid tumors in association with a concurrent serous cystic
- future reproductive plans neoplasia, such as serous or mucinous cystadenomas of the ipsilateral
- severity of symptoms ovary.
• Medical therapy rarely successful if disease has produced ovarian • Some are microscopic, with the entire tumor contained in a single low-
enlargement powered microscopic field, and others may reach a diameter of 20 cm;
• Common surgical procedure: Cystectomy, TAHBSO- surgical menopause the majority are less than 5 cm in diameter.
o Complicated by formation of de novo and recurrent • Unilateral 85-95% of the time
adhesions • Theory- these tumors result from metaplasia of the coelomic
• On histopathology: distinguish between adenofibromas- true epithelium into uroepithelium
neoplasm, has a malignant counterpart Clinical Manifestations:
• Infertility is a problem • Approx. 90% are aymptomatic, although large tumors may produce
unilateral pelvic discomfort.
FIBROMA • Postmenopausal bleeding is sometimes associated with Brenner tumors
• Most common benign solid neoplasm of the ovary • It is postulated that luteinization of the stroma produces estrogen with
• Arise from the undifferentiated fibrous stroma of the ovary resulting hyperplasia
• Extremely slow growing- predominant character • The extensive fibrous content of these tumors results in lower signal
• Vary in size from small nodules to huge pelvic tumors weighing 50 intensity T2-weighted images
pounds • During CT scanning, Brenner tumors characteristically demonstrate a
• Average diameter- 6 cm finding of extensive amorphous calcification within the solid
o Size is important components of the ovarian mass.
o Incidence of associated ascites is directly proportional • Grossly, Brenner tumors are smooth, firm, gray-white, solid tumors that
to the size of the tumor grossly resemble fibromas, gray, yellowish tinge with small cystic spaces
• Average age of affected women: 48 yrs (usually postmenopausal) • Similar to fibromas, transitional cell tumors areslow growing.
• Bilateral ovarian fibromas are commonly found in women with the rare • Histologically, Brenner tumors have two principal components:
genetic transmitted basal cell nevus syndrome o Solid masses or nests of epithelial cells
• Symptoms o surrounding fibrous stroma.
- pressure on adjacent structures • The epithelial cells are uniform and do not appear anaplastic
- abdominal enlargement • The histology and ultrastructure of the epithelial cells of a Brenner
- may be secondary to size and acites tumor are similar to transitional epithelium of the urinary bladder.
- smaller tumors- asymptomatic • The pale epithelial cells have a “coffee bean”-appearing nucleus, which
- do not elaborate hormones- no change in menstrual flow is also described as a longitudinal groove in the cell's nucleus.
- may be pedunculated- easily palpable during one examination,
but difficult on the next
• Meig’s Syndrome: association of ovarian fibroma, ascites and
hydrothorax
o Both ascites and hyrdrothorax resolve after removal of
the ovarian tumor
o Ascites is caused by the transudation of fluid from the
ovarian fibroma
o Hyrdrothorax-secondary to flow of ascetic fluid into the
pleural space via the lymphatics of the diaphragm
• Grossly
• Electron microscopy has demonstrated that the longitudinal groove
during routine microscopy is produced by prominent indentation of the
nuclear membrane.
• An addition ovarian neoplasm is frequently found associated with
Brenner tumor- serous and mucinous cystadenoma

Management:
• operative simple excision being the procedure of choice
• as with ovarian fibromas, the patient's age often is the principal factor
in deciding the extent of the operation.
- heavy, solid, well encapsulated and grayish white
- Cut surface: homogenous white or yellowish solid tissue with
trabeculated or whorled appearance
- 50% grossly edematous
Torsion
• Torsion of the ovary may occur separately from torsion of the fallopian
tube, but most commonly the two adnexal structures are affected
together.
• An important cause of acute lower abdominal and pelvic pain
• most commonly during the reproductive years, with the average
patient being in her mid-20s.
• Adnexal torsion is also a complication of benign ovarian tumors in the
postmenopausal woman.
• Pregnancy appears to predispose women to adnexal torsion
• Most susceptible are ovaries that are enlarged secondary to ovulation
induction during early pregnancy. MATURE FIBROMA TRANSITIONAL ENDOMETRIOMA
• The most common cause of adnexal torsion is ovarian enlargement by CYSTIC CELL TUMORS
an 8- to 12-cm benign mass of the ovary. However, smaller ovaries may TERATOMA
also undergo torsion Dermoid cyst Malignant Brenner tumor Common
• Ovarian tumors are discovered in 50% to 60% of women with adnexal potential low
torsion.
• Torsion of a normal ovary or adnexum is also possible and occurs more All 3 germ cell Variable size Small Variable size
frequently in children. layers
• The right ovary has a greater tendency to twist (3 to 2) than does the Most common Slow growing Rare, unilateral Uni/bilateral
left ovary.
• Patients with adnexal torsion present with acute, severe, unilateral,
lower abdominal and pelvic pain Slow-growing Most common Low malignant Replace a portion of
• Often the patient relates the onset of the severe Uni/bilateral benign solid potential normal ovarian
pain to an abrupt change of position. tumor of ovary tissue
• These associated gastrointestinal symptoms sometimes lead to a Doughy Easily palpable Smooth, solid, Endometrial glands +
preoperative diagnosis of acute appendicitis or small intestinal consistency Pedunculated fibroepithelial stroma,
obstruction Unilocular Solid hemosiderin-laden
• Many patients have noted intermittent previous episodes of similar Sebaceous masses/nest of phagocytes
pain for several days to several weeks fluid, hair, epithelial cells
• Fever is more common in women who have developed necrosis of the teeth, cartilage + stroma
adnexa. Solid + cystic Heavy, solid, “coffee bean” UTZ: thick-walled,
• Most patients with adnexal torsion present with symptoms and signs Tubercle of well- nucleus echogenic,
severe enough to demand operative intervention Rokitansky encapsulate, echolucent
• Abnormal color Doppler flow is highly predictive of torsion of the ovary white
• The most common differential gynecologic conditions are a ruptured Thyrotoxicosis, Basal cell Endometrial Pelvic pain,
corpus luteum or an adnexal abscess. carcinoid nevus hyperplasia dyspareunia,
• Because the majority of cases of adnexal torsion occur in young women, syndrome, syndrome infertility
a conservative operation is ideal autoimmune Meig’s Densely adherent
• Conservative surgery either through the laparoscope or via laparotomy hemolytic syndrome
entails gentle untwisting of the pedicle, possibly cystectomy, and anemia
stabilization of the ovary with sutures Torsion, abdl Pressure, Asymptomatic Malignancy?
• With severe vascular compromise, the appropriate operation is pain enlargement
unilateral salpingo-oophorectomy. The vascular pedicle should be Cystectomy Oophorectomy Oophorectomy Cystectomy/TAHBSO
clamped with care so as not to injure the ureter, which may be tented
up by the torsion.
FROM COMPRE-GYNE:
MENOPAUSE:
THE MENOPAUSE • Permanent cessation of menstruation caused by failure of ovarian
follicular development and estradiol production in the presence of
elevated gonadotropin levels
• Defined by the last menstrual period
• Because cessation of menses is variable and many of the symptoms
thought to be related to menopause may occur prior to cessation of
menses, there is seldom a precise timing of this event
• AGE OF MENOPAUSE
1. General health status: (Western Countries) between 51 and 52
years
2. Socioeconomic status: associated with an earlier age of
menopause Higher parity: associated with a later menopause
3. Smoking: associated with menopause onset taking place 1 to 2
years earlier
4. Body mass: greater body mass index [BMI] with later
menopause
5. Ethnic differences: Black and Hispanic women have been found
to have menopause approximately 2 years earlier than white
women
6. Geographic Location: age of menopause appears to be
somewhat earlier outside the United States
• Malay women: age 45
• Thai women: age 49.5
• Filipina women: ages 47 and 48
• Countries at higher altitude (Himalayas or Andes): menopause 1 to
1.5 years earlier
• Average age of menopause in the United States is 51 to 53 years

CLIMACTERIC
o Refers to the time after the cessation of reproductive function
o Time after the cessation of reproductive function

*0: signifies menopause


Perimenopause: average duration is 4 yrs; skip menses

Aging Ovary
• No more follicles
• No inhibin b or estradiol production
• FSH rises
• Later LH will rise
• Fewer follicles less production of inhibin b
• Pituitary is released from its supression
• FSH rises earlier and follicular development is advanced
PREMATURE OVARIAN FAILURE:
• Measure Day 3 FSH and estradiol will be high compared to
• Defined as hypergonadotropic ovarian failure occurring prior to
younger women
age 40
• Occurred in 5% to 10% of women who are evaluated for
Perimenopause
amenorrhea
• Follows period of declining fertility
• Ongoing rate of atresia of oocytes, this process is accelerated
with various forms of gonadal dysgenesis due to defective X
• Precedes menopause
chromosomes, one possible cause of POF is an increased rate • Characterized by
of atresia that has yet to be explained • Cycle irregularity (shortening then lengthening)
• A decreased germ cell endowment or an increased rate of • Increasing symptoms (*hot flushes)
germ cell destruction can also explain POF • Duration 2 to 8 years (average 4 years)
• Causes: *if the ave age of menopause is 51, the average age of start of
o Genetic perimenopause in 47
o Enzymatic
o Immune Diagnosing Perimenopause
o Gonadotropin defects • Clinical diagnosis based on menstrual cycle pattern.
o Ovarian Insults • Early follicular phase FSH and symptoms may help solidify
o idiopathic diagnosis
Management of Premature Ovarian Failure Symptoms: Highly Variable
• Evaluation of POF in women younger than 30 should include: •
o screening for autoimmune disorders and a karyotype • - physically warm bec you perspire; NOT the brain
o vaginal ultrasound may be useful for assessing the size of telling you that you are warm
the ovaries and the degree of follicular development •
• Treatment: •
o Estrogen replacement •
o If fertility is a concern: the most efficacious treatment is - Fatigue, palpitations, headache, increased migraine, breast pain
oocyte donation. and enlargement.
• Oligo-
• Heavier or irregular cycles.
Oocytes and Follicles *pagwalang corpus luteum, endometrium gets thicker, so by the time you
• menstruate, it’s heavy.
• - 6 - 7 million follicles.
• - 1.5-2 million follicles MENOPAUSE
• - 300,000- 400,000 follicles “The ovaries, after long years of service, have not the ability of retiring in
• graceful old age, but become irritated, transmit their irritation to the
• ted (<1000), menopause abdominal ganglia, which in turn transmit the irritation to the brain,
occurs. producing disturbances in the cerebral tissue exhibiting themselves in
*in a woman’s life, in the utero, that’s the time where in the woman has the extreme nervousness or in an outburst of actual insanity.”
most oocyte ((1.5-2M), paglumbas oonti na lng (hundred thousands na lng). • Marks the end of reproductive life
As the px ages the oocytes decline until the age of 37. Eggs progressive • Cessation of menses for 12 months
decline at 37 until you reach menopause, you don’t have estrogen anymore • Clinical diagnosis (not labs)
(non-functioning eggs) • Result of egg depletion and estrogen production by the ovary due
to Natural aging or surgery
*if you removed the bilateral ovaries, will you remove the uterus? The usual
practice is to remove both ovaries and uterus to avoid development of *a lot of organ system is affected but the most concern is the cardiovascular
cancer disease
*using HRT- some concern will be Breast Cancer. However, some studies
Menopause Facts have shown that women with Breast Ca using HRT had already cancer cells
• Average age at menopause: 51 years before using HRT. Its 5-10 years to develop.
o (1% at age 40, 5% after age 55) *most women think that #1 cause of death in menopausal women with
• Factors impacting age at menopause regards to cancer is Breast Ca but the fact is, its Lung Ca, and the most
o Maternal age at menopause common cause of death is heart-related problem like MI, stroke
o Tobacco use *menopause is a risk factor for MI
o Alcohol use
o Body Mass Index OSTEOPOROSIS (trabecular bone is more affected)
• Decreased bone mass and microarchitectural deterioration of bone tissue
o OCP use leading to enhanced bone fragility and an increase in fractures
o Parity Consequences of Osteoporosis
o Race •
o Height o Back pain
o Loss of height and mobility
Physical Changes o Postural deformities
• Vasomotor instability- *affects primarily the brain •
• Metabolic Changes •
• Coronary Artery Disease •
• Accelerated bone loss- *prone to fractures
• Skin changes- *dry skin *what will you advice women who are approaching menopause? Advice to
take Ca supplements and exercise.
• Urogenital atrophy- *uterine prolapse, cystocele
*50% of women over 65 have spinal compression fractures
• Cognition (?)
The average untreated potmenopausal white women can expect to shrink
• Libido (?) 2.5 inches
*all organ system is affected 25% of patients over the age of 50 with hip fracture die due to the fracture or
Hot Flushes- pathognomonic sign of Menopause
its complications within one year.
• “Sudden onset of reddening of the skin over the head, neck, and Survivors are frequently serrely disaabled
chest accompanied by a feeling of intense body heat and 1.3M osteoperotic fractures in the US annuallly
sometimes concluded by profuse perspiration”
• Number 1 complaint to physicians Premature Menopause
• Few seconds to several minutes Definitions:
• Most severe at night and during times of stress  Early: age 40-44
• 25% will last for more than 5 years  Premature: <40
Causes
Managing Hot Flushes/Flashes  Surgical removal of uterus**
• Set realistic goals!  Surgical removal of ovaries
• Lower the ambient temperature  Premature ovarian failure
• Estrogen (80-95% reduction)
• Alternative therapies Premature Ovarian Failure
o High dose progestins
o Tibolone
o SERM (selective estrogen receptor modulators)
• Complementary Approaches
• May be effective
o Black Cohosh Evaluation of Premature Ovarian Failure
o Soy/Phytoestrogens
• Vitamin E (1 hot flash per day less) Assessment for Fragile X premutation (number of CGG repeats)

The Menopausal Metabolic Syndrome insufficiency)


Lipid Triad
– Hypertriglyceridemia Premature Ovarian Failure is Different from Menopause
– LDL Cholesterol -20% of women with POF with normal karyotypes will ovulate again
– HDL Cholesterol

Abnormalities in Insulin
– Insulin resistance Treatment of Premature Menopause
– Insulin elimination
– Insulin secretion
– Hyperinsulinemia
– HT reduces onset of DM and improves insulin resistance From Ice Soria’s notes:
HORMONAL CHANGES WITH ESTABLISHED MENOPAUSE
Other Factors COLLAGEN – nearly 30% of skin collagen is lost within 1st 5yrs after
– Endothelial dysfunction menopause, and collagen decreases approximately 2% per year for the 1st 10
– Visceral fat years after menopause.
– Uric acid
– Blood pressure BONE LOSS
• Role of Estrogen:
o Cortical Bone: With estrogen deficiency, bone density  Although cardiovascular disease becomes more prevalent only in
decreases more slowly in cortical bone the later years following a natural menopause, premature
o Cancellous or Trabecullar Bone: With estrogen cessation of ovarian function (before the average age of
deficiency, osteoporosis develops more rapidly in menopause) constitutes a significant risk
trabecular than in cortical bone. o Premature menopause, occurring before
o Loss of trabecular bone (spine) is greater with estrogen age 35, has been shown to increase the risk
deficiency than is loss of cortical bone. of myocardial infarction two- to threefold,
and oophorectomy before age 35 increases
BONE MASS CAN BE DETECTED BY A VARIETY OF WAYS: the risk sevenfold
1. Dual-energy X-ray absorptiometry (DEXA) scans have become the WHY THERES INCREASE RISK?
standard of care for detection of osteopenia and osteoporosis 1. Accelerated rise in total cholesterol in postmenopausal women is the most
 T score: reflect the number of standard deviations of bone loss prevalent finding. This increase in total cholesterol is explained by :
from the peak bone mass of a young adult. The T score is  increases in levels of low-density lipoprotein cholesterol (LDL-C)
expressed as the difference in standard deviations of the  oxidation of LDL-C is also enhanced
measured bone density from the mean value of young adults.  decrease levels of very low density lipoproteins and lipoprotein
 decrease HDL-C levels
OSTEOPENIA: 2. The changes of weight, blood pressure, and blood glucose with aging,
 Decreased quantity of bone mass of lesser amount although important, are not thought to be as important as the rate of rise in
than osteoporosis. An early state of osteoporosis with bone total cholesterol, which is substantially different in women versus
density T score between -1 to -2.5 standard deviations men.
3. Blood flow in all vascular beds decreases after menopause
OSTEOPOROSIS: 4. Prostacyclin production decreases
 A systemic skeletal disease characterized by low 5. Endothelin levels increase
bone mass and microarchitectural deterioration of bone tissue 6. Reduced nitric oxide synthetase activity
with a bone mineral density T score less than -2.5 standard
deviations Risk–Benefit Assessment
 The WHI was conceived in an attempt to determine the overall
2. Biochemical assays are also available to assess bone resorption and risks and benefits of ET/HT in a prospective randomized trial
formation in both blood and urine  Endpoints: ET (CEE 0.625 mg with MPA 2.5 mg)
 At present, serum markers appear to be most useful for o reduces cardiovascular disease
assessing changes with antiresorptive therapy o may increase the risk of breast cancer (primary endpoints)
o secondary endpoints were also assessed: venous
Osteoporosis thromboembolism, stroke, osteoporotic fracture, colon
 Estrogen deficiency cancer, and mortality
 Peak bone mass at 30-35 years old BENEFITS:
 Bone loss at a rate of 0.5-1% per year afterward  HT ARM: protection of osteoporotic fracture and colon cancer
 Bone loss at a rate of 2-3% per year for 10 years after menopause  ET ARM: protection of osteoporotic CHD, breast cancer
 Osteoporosis is associated with fracture ( femoral neck, vertebral RISK:
body and distal radius)  A tally of the various endpoints pointed to overall risks rather
than benefit
Risk factors of osteoporosis  “ATTRIBUTABLE” risk:
1. Family history o This is the risk per year for 10,000 women exposed
2. Ethnicity o Thus, an attributable risk of 8/10,000 women/year from
3. Early menopause cancer with HT is a very small risk and according to WHO
4. Hypoestrogenism (excessive exercise, anorexia, bulimia) terminology has been described as “rare.”
5. Hyperthyroidism, excessive thyroxine therapy o This concept has been lost by the media and others who have
6. Cigarette smoking misinterpreted both relative risk and attributable risk.
7. Caffeine Recently there has been a trend to reduce potential risks and adverse effects
8. High alcohol intake by using lower doses of ET/HT, which have been shown to be beneficial.

Cardiovascular disease Possible mechanism of cardioprotection by HRT


 Rapid increase in mortality and morbidity from cardiovascular  Favorable lipid profile:
disease after menopause o Inc HDL,
 Epidemiological evidence suggests that HRT is associated with o Dec LDL,
50% reduction in cardiovascular risk in menopausal women o Dec Lipoprotein (a)
 There is no prospective randomized data to show that HRT is  Other effects:
effective in the primary prevention of cardiovascular disease. o Inc insulin sensitivity,
o Vascular dilatation,
o Inc coagulation factors
Cardiovascular Effects
 After menopause, the risk of cardiovascular disease in women is HRT regimens
increased. Data from the Framingham study:  Women who have had a hysterectomy only need to take estrogen
 Incidence is three times lower in women before menopause than  Women with an intact uterus must take progestogen for
in men (3.1 per 1000 per year in women ages 45 to 49) endometrial protection to prevent endometrial cancer or
 The incidence is approximately equal in men and women hyperplasia
ages 75 to 79 (53 and 50.4 per 1000 per year, respectively)  Regular surveillance of endometrium is required for women
 This trend also pertains to gender differences in mortality (extreme intolerance of progestogen) on unopposed estrogen
due to cardiovascular disease
 Coronary artery disease is the leading cause of death in women, Sequential preparation:
and the lifetime risk of death is 31% in postmenopausal women  progestogen added for 12-14 days each month.
versus a 3% risk of dying of breast cancer
 Some women will not bleed on sequential preparations and this is result of either a gonadal disorder or a CNS
not a cause for concern provided that the progestogen is taken hypothalamic-pituitary abnormality
correctly.
The Genital Outflow Tract
Continuous combined HRT: Secondary Sexual Characteristic Present
 give estrogen and progestogen daily. 1. Mullerian anomalies/ paramesonephric duct
 These preparation induces endometrial atrophy.  paired ducts of the embryo that run down the lateral sides of the
 Intermittent bleeding and spotting are common in the first few urogenital ridge and terminate at the Müllerian eminence in the
month of use. primitive urogenital sinus.
 More suitable for women who are at least one year since their  In the female, they will develop to form the Fallopian tubes,
last spontaneous period. uterus, cervix, and the upper two-thirds of the vagina;
 in the male, they are lost. These ducts are made of tissue of
Progestogen mesodermal origin.
 Can prevent bone loss  development of the Müllerian ducts is controlled by the presence
 Whether the addition of progestogens by stimulating bone or absence of "AMH", or Anti-Müllerian hormone (also known as
formation increases bone mass beyond that produced by estrogen "MIF" for "Müllerian-inhibiting factor", or "MIH" for "Müllerian-
alone is unclear inhibiting hormone")
 The androgenic activity of certain progestogens such as a) Imperforate hymen
norethindrone acetate (NET) also has been suggested to play a  hymenal opening nonexistent
role b) Transverse vaginal septum
 Transverse septum can form during
1. Oral or transdermal form embryogenesis when the mullerian ducts
2. Levo-norgestrel releasing intra-uterine system fuse improperly to the urogenital sinus.
 A complete transverse will block menstrual
Oral progestogens flow and is a cause of primary amenorrhea.
 C21 progesterone derivatives : The accumulation of menstrual debris
 dydrogesterone or medroxyprogesterone acetate behind the septum is
 C19 nor-testosterone derivatives: termed cryptomenorrhea
 norethisterone acetate or levonorgestrel c) Mayer-rokitansky-kuster-hauser syndrome (MRK
syndrome)
Side effects of HRT  Uterine agenesis/uetrovaginal
1. Nausea agenesis/congenital absence of uterus
2. breast pain  Second most frequent cause of primary
3. heavy or painful withdrawal period amenorrhea
4. premenstrual syndrome type of side effects  With normal oavries with regular cyclic
5. weight gain ovulation and normal endocrine function
 With normal breast and pubic and axillary
Risk of HRT hair but shortened or basent vagina
1. Breast cancer  May have renal, skeletal, cardiac anomalies
2. Thrombo-embolism 2. Androgen Insensitivity
 Androgen resistance/ testicular feminization
RALOXIFENE  Genetically transmitted disease in which androgen
 Selective estrogen receptor modulators (SERMs) receptor synthesis or action does not occur
 Agonist and antagonist properties  Due to the absence of an x-chromosomal gene
 Bone protective and reduce cholesterol responsible for the cytoplasmic or nuclear
 No effect on the endometrium testosterone receptor function
 Evidence to suggest that it is protective against breast cancer 3. True Hermaphrodites
 Does not help menopausal symptoms and may worsen them  an intersex condition in which an individual is born
 Raloxifene has been shown to decrease vertebral fractures in a with ovarian and testicular tissue
large prospective trial. 4. Absent endometrium
 SERMs have not been shown to prevent hip fractures 5. Asherman’s Syndrome
 "uterine synechiae" or intrauterine adhesions (IUA),
AMENORRHEA presents a condition characterized by the presence of
AMENORRHEA adhesions and/or fibrosis within the uterine cavity due
 Absence of menses during the reproductive years to scars
 Either physiologic (pregnancy) and postpartum (when nursing) or  Initial diagnostic test : placement of a uterine sound
pathologic (endocrine and anatomic abnormalities) into the uterine cavity followed by a hysterohraphy or
 Women with cryptomenorrhea caused anatomic disorders hysteroscopy
interfering with outflow of menses, such as imperforate hymen or
transverse vaginal septum have a symptom of amenorrhea a) Secondary to prior uterine or cervical surgery
Primary Amenorrhea o Curettage, esp postpartum  most frequent
 No menses by age 14 in the absence of growth or pubertal antecedent
changes o Cone biopsy
 No menses by 16 regardless of the presence of growth or pubertal o Loop electroexcision procedure
changes b) Secondary to infection
 Grouped base on whether secondary sexual characteristics  Pelvic inflammatory disease/PID
(breasts) and female internal genitalia (uterus are present)  IUD-related
 Tuberculosis
Breast Absent and Uterus Present  Schistosomiasis
 all individuals with no breast development and uterus
present have no ovarian estrogen production as a Chronic anovulation : HYPERPROLACTINEMIA
 Prolactin : normal values: <15-20 ng/ml
 Values are affected by sleep, exercise, breast stimulation, meals
 Cause: hypothyroidism, pituitary tumors or adenomas
 Drugs: amphetamines, antidepressants, phenothiazines,
reserpines,
 Surgery: chest wall, cervical spine, herpes zoster(affecting breast
dermatome)

Pathophysiology
 Increase in Prolactin inhibits the GnRH pulsatility
 Decrease in FSH
 Oligomenorrhea to amenorrhea
 >100 ng/ml: hypogonadism  MRI

Ovarian Failure/ Gonadal Failure


 Low estrogen
 Accelerated atresia of follicles
 High FSH
 2D echocardiography  determine cardiac abnormality
 MC cause of primary amenorrhea
 Renal UTS --> renal abnormality
 Most frequently due to a chromosomal disorder or deletion of all
 FT 4 TSH  hypothyroidism
part of an X chromosome
 CBC, lipid profile, BUN, crea
 May be due to a genetic defect and rarely 17-a hydroxylase
 audiometry
deficiencies
 If gonadal development is absent in the presence of a 46XX or
HYPOTHALAMIC AMENORRHEA
46XY karyotype (called pure gonadal dysgenesis), a gene disorder
 Low or normal FSH
may be present
 Low estrogen
 Deletion of the entire X chromosome (as in Turner’s syndrome) or
 Diagnosis of exclusion
of the short arm (p) of the X chromosome results in short stature
 Eating Disorders
 When ovarian follicles are absent, synthesis of ovarian steroids
Anorexia nervosa
and inhibin does not occur
Bulimia nervosa
 Breast development does not occur because of the vry low
circulating E2 levels
o bec negative hypothalamic-pituitary action of estrogen
STRESS
and inhibin is not present, gonadotrophon levels are
markedly elevated, with FSH levels higher than LH
 Since estrogen is not necessarily for mullerian duct development
or wolffian duct regression, the internal and external genitalia are
INCREASE CRH
phenotypically normal female
 Individuals with 17a-hydroxylase deficiency do not have
primordial follicles but can not synthesize sex steroids Increase Increase
endorphins ACTH

OVARIAN FAILURE
 < 30 years old woman: do karyotyping
 Fragile X: MC of inherited cause of mental retardation and autism DECREASE GnRH
Increase
Cortisol
due to an unstable trinucleotide (CGG)
 FMR1 gene on long arm of chromosome X

 Previous ovarian surgery  Stress can lead to inhibition of the GnRH axis
 Radiation  Mechanism: inc secretion of CRH  releasing ACTH and cortisol
 CRH known to inhibit GnRH
GONADAL DYSGENESIS
 Incomplete or defective formation of the gonads resulting from POLYCYSTIC OVARIAN SYNDROME /PCOS
the disturbance in germ cell migration or organization caused by  Heterogenous disorder and may present with prolonged periods of
chromosomal abnormlities or mutations amenorrhea; typical menstrual pattern is of irregularity or
 Gonads appear streaks oligomenorrhea
o Deletion of the long arm (q) usually do not affect  1935 Stein & Leventhal
height; in place of the ovary a band of fibrous tissue  Symptom complex associated with anovulation
called gonadal streak is present  7 obese patients with amenorrhea , hirsutism, enlarged polycystic
o Streaks also present in individuals without gonads ovaries
(pure gonadal dysgenesis)  Wedge resection
 MC form: Turner’s syndrome  Follicles could not escape the thick capsule
 Chronic anovulation
Gonadal dysgenesis: Turner’s Syndrome  Genetic variant
Karyotype: 45X  Environmental factors
 Increased daily androgen and estrogen production
 Elevated serum testosterone, DHEAS,DHEA, 17-
hydroxyprogesterone

diagnostic criterion
 FSH is low
 Increased LH:FSH ratio
At least 2 of the 3 major criteria
1. Oligo/anovulation
2. Clinical or biochemical hyperandrogenism
3. PCO on ultrasound

PCOS : Ferriman Gallwey Hirsutism Scoring ≥ 8


 simply a representation of hair growth in a male pattern on a
woman shown in four different degrees of severity in 11 different
body parts; namely the
o upper lip,
o chin,
o chest,
o upper back,
o lower back,
o upper abdomen,
o lower abdomen,
o arm,
o forearm,
o thigh,
o and lower leg
 used to score the degree of excess male pattern body hair by
doctors Module 1- Tin
 scorecard of every body location under survey begins from 0 (no Module 2- Gara
excessive terminal hair growth) to 4 (extensive terminal hair Module 3- Steph Esguerra
Module 4- CoCat & Nina
growth) and the numbers are added up to a maximum count of Module 5- Zarah & Binggoy
36. Module 6- Tere
While most experts refer to a modified score of 8 or more to diagnose
hirsutism, some suggest a final tally of 6 or more is enough to indicate
hirsutism
Sources: Trans made by OB Transcom, Ice Soria, & Ate Zen’s highlighted trans ;)

PCOS : Complications
 Menstrual dysfunction
 Infertility
 Increased risk of having endometrial hyperplasia/neoplasia
 Increased risk of developing DM type 2
 Increased risk of developing CVD
 Metabolic syndrome ***
o combination of medical disorders that, when occurring
together, increase the risk of developingcardiovascular
disease and diabetes

Treatment of women with PCOS


Complaint Treatment Option
Infertility Metformin
Clomiphene
Gonadotrophins
Ovarian cautery
Skin Manifestation OCP +antiandrigen (spironolactone,
flutamide, finestride)
GnRH agonists
Dysfunctional Bleeding Cyclic progesterone
OCP
Weight/Metabolic Concerns Diet/lifestyle management
Metformin

END
“The more solid your Batch is, the BETTER you will be.”

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