Board Questions Renal

Pulmonary
How do you calculate the A-a

gradient?
Difference in partial pressure of Oxygen, PO2, between the alveolar

PO2 and arterial PO2 PAO2=FiO2(713) - arterial PCO2/0.8
What causes an A-a gradient

and how is it useful in
differentiating causes of
hypoxemia?
What are some causes of
ventilation defects?
perfusion defects?
diffusion defects?
shunting?
A-a gradient is caused by a mismatch between ventilation and

perfusion. Hypoxemia of pulmonary origin causes an increased A-a
gradient (>30). Hypoxemia of extrapulmonary origin has a normal
A-a gradient.
Impaired O2 delivery to the alveoli for gas exchange, e.g. from
airway collapse due to respiratory distress syndrome or atelectasis.
Decreased or absent blood flow to the alveoli, e.g. pulmonary
embolus
O2 cannot diffuse across alveolar-capillary interface, e.g.
pulmonary fibrosis or pulmonary edema. Causes decreased DLCO
A shunt is technically blood going from right to left because of
heart issues, e.g. right to left shunting from tetralogy of fallot.

hypoxemia with a normal A-a
gradient?
Depression of the respiratory center in the medulla (barbiturates,

brain injury); upper airway obstruction (epiglottitis, croup); Chest
bellows dysfunction (paralyzed diaphragm, ALS with degeneration
of anterior horn cells).
Define Functional Residual

Capacity, FRC (Refer to
Pulmonary
1).
Define
Totalattachment
Lung Capacity,
TLC
Define Residual Volume, RV
Define Tidal Volume, TV
Define Forced Vital Capacity,
FVC
Define Forced Expiratory
Volume, 1 second, FEV1
Total amount of air in the lungs at the end of normal expiration

Total amount
in ainfully
Volume
of air of
leftair
over
the expanded
lung after lung
maximal expiration: FRCERV
Volume of air that enters/exits the lungs during normal respiration
Total amount of air expelled after maximal inspiration
Amount of air expelled from the lungs in 1 second after maximal
inspiration
What is the normal

FEV1/FVC?
Define Expiratory Reserve
Volume, ERV
Describe spirometry in
restrictive lung disease
Describe spirometry in
obstructive lung disease
Define Dyspnea and list

some causes.
Where are cough receptors
located?
70-80%
Amount of air forcibly expelled at the end of normal expiration
TLC decreased, RV decreased, FEV1 decreased, FVC decreased,
FEV1/FVC normal to increased, PaO2 decreased, A-a gradient
increased (if disease of lungs, not just restriction of chest wall
TLC increased, RV increased, FEV1 decreased, FVC decreased,
FEV1/FVC decreased, PaO2 decreased, A-a gradient increased
Difficulty breathing. Can be due to stimulation of J receptors
causing decrease in full inspiration. Also decreased compliance,
e.g. interstitial fibrosis; increased airway resistance, e.g. chronic
bronchiti; chest bellows disease, e.g. obesity; kyphoscoliosis,
interstitial inflammation or fluid accumulation, e.g. left sided heart
failure.
They're at the bifurcation of airways, larynx and distal esophagus
What is the most common

cause of cough with a
normal CXR?
What causes nocturnal
cough?
What causes productive
cough?
Postnasal discharge
GERD from acid refluxing into the bronchial tree at night. Bronchial
asthma due to airway constriction
Chronic bronchitis, usually associated with smoking cigarettes.
Typical
bacterial pneumonia.
Bronchiectasis
ACE inhibitors-inhibit
degradation
of bradykinin which causes
What drugs cause cough?

Define hemoptysis and the
mechanisms.
hemoptysis?
mucosal swelling and irritation in the tracheobronchial tree.

Aspirin causes increases in Leukotriene C, D and E4 which are all
bronchoconstrictors
Coughing up blood-tinged sputum. Caused by parenchymal
necrosis bronchitis
and/or bronchial/pulmonary
vessel damage.
Chronic
(most common), pneumonia,
bronchogenic
carcinoma, tuberculosis, bronchiectasis, aspergilloma (fungus in a
cavitary lesion)
Define tachypnea and list the

causes.
Rapid, shallow breathing, more than 20 breaths/minute. Causes

are restrictive lung disease, pleuritic chest pain, pulmonary
embolus with infarction (tachypnea is the key finding)
Define tracheal shift and list

the mechanism.
What is vocal tactile
fremitus?
What causes decreased
tactile fremitus?
What causes increased
tactile fremitus?
What causes absent tactile
fremitus?
shift of trachea from large changes in pleural fluid volume. Causes

are pressure in contralateral lung, large tension pneumothorax,
large pleural effusion; decreased volume in ipsalateral lung, large
spontaneous pneumothorax, resorption atelectasis.
Palpable thrill (vibration) transmitted through the chest when the
patient says "99," or "E"
Emphysema or asthma with increased AP diameter from increased
total lung capacity.
Sound travels better through fluid/solid so any type of lung
consolidation, pneumonia, etc.
Atelectasis/collapse of airways, fluid/effusion, air in pleural space
(pneumothorax)
What causes dull and

hyperresonant percussion?
Dull percussion comes from pleural effusions, lung consolidations,

atelectasis. Hyperresonant percussion comes from pneumothorax,
asthma or emphysema
What is the origin and

mechanism of normal breath
sounds?
Where does laminar air flow
start?
Normal breath sounds come from the trachea and are caused by
air velocity and turbulence inducing vibrations in airway walls
Terminal bronchioles where the increased surface area converts
turbulent
laminar
flow
Sound liketoair
blowing
through a tube-this is normal over the
What are tubular breath

sounds?
trachea but is always abnormal over the bronchi. Causes a loud,

high pitched sound with a tubular or hollow quality. Expiration is
longer than inspiration. Means that there is consolidation or patent
but partially collapsed bronchi
What are crackles and how

are they caused?
Tracheal sounds that are modified in the alveoli. Inspiratory to

expiratory ratio is 3:1. Diminished in emphysema and asthma due
to increased AP diameter. Absent in pneumothorax, atelectasis or
effusion
Normal breath sounds over the main bronchi with an equal
inspiratory and expiratory ratio.
Extra sounds, usually inspiratory, that sound like (you guessed it),
crackles! Early and midinspiratory crackles are due to secretions in
proximal large to medium sized airways. These clear with
coughing. Late inspiratory crackles are due to reopening of distal
airways partially occluded by increased interstitial pressure (fluid,
transudate, pus). These do not clear with coughing and vary from
fine to course
What is wheezing and how is

it caused?
High pitched musical sound usually in expiration. Caused by

inflammation of segmental bronchi and small airways by asthma or
chronic bronchitis; pulmonary edema constricting airway (cardiac
asthma); pulmonary infarction (release of TXA from platelets in the
embolus causes bronchoconstriction
What are vesicular breath

sounds?
What are bronchovesicular
breath sounds?
What are Rhonchi and how

are they caused?
What is inspiratory stridor
and how is it caused?
What is a pleural friction rub

and how is it caused?
What does grunting in a
newborn mean?
Low pitched snoring sounds during inspiration or expiration. Due

to secretions in large airways (bronchus or trachea). Usually clear
with coughing,
common sound.
in chronic
bronchitis
High
pitched inspiratory
Indicates
upper airway
obstruction. Caused by epiglottitis (H. Influenzae), croup
(parainfluenza)
Two inflamed surfaces (pleural and parietal) rubbing against each
other. Usually happens at the end of inspiration and beginning of
expirations when things are changing direction. Caused by
pleuritis due to cancer, infarction, pneumonia, serositis (SLE).
Disappears with alrge effusion bc separates layers and stays with
holding breath.
Newborns should not grunt after 24 hours. It's a sign of respiratory
distress syndrome.
What is bronchophony and

egophony?
What is a flow volume loop?
Caused by alveolar consolidations. Spoken numbers, syllables are

heard more distinctly through stethoscope. Egophany is when the
patient
says E andand
youexpiratory
hear an A flow
through
the stethoscope.
Plot
of inspiratory
rate(L/sec)
versus lung
volume(L)
Where is maximal inspiration

on the diagram? (see
Pulmonary attachment 2 for
following)
Begins at point A, RV and goes to point B, TLC
Define Peak Expiratory Flow

(PEF)
What is the volume between
points B and
C?
Describe
the flow-volume
loop in obstructive lung
disease. the flow-volume
Describe
loop in restrictive lung
disease.
What is Choanal Atresia?
What is a Nasal Polyp?

Define Obstructive Sleep
Apnea
Begins at point B, TLC, and goes to point C, PEF. Occurs early in

expiratory phase of loop due to elastic recoil of the lungs with low
resistance and large caliber. Slope decreases to point A as
resistance increases and airways get smaller.
VitalisCapacity
TLC
increased and RV is increased. AKA left shifted curve.
Decreased PEF. Can have concavity at C from mucus plugs or
collapsed airways.
TLC is decreased, RV is decreased. AKA right shifted curve.
Unilateral or bilateral bony septum between the nose and pharynx.
Newborn urns cyanotic on breast feeding but crying causes them to
pink up again
Non-neoplastic tumefactions which develop as a response to
chronic inflammation. Allergic polyps are the most common and
are most often seen in asults with IgE mediated allergies. Also
associated with aspirin and other NSAIDs b/c Cyclooxegenase block
increases Leukotrienes whcih results in bronchoconstriction. Oten
associated with CF
Excessive snoring with intervals of breath cessation (apnea)
What causes obstructive

sleep apnea?
Most commonly a result of obesity causing the pharyngeal muscles

to collapse under the weight of the tissue. Can also result from
tonsilar hypertrophy or nasal septum deviation.
What is the pathogenesis

and clinical findings in sleep
apnea?
Airway obstruction causes CO2 retention resulting in hypoxemia.

Decreased PO2 and O2 saturation during apnea with increase in
PCO2. See excessive snoring with apneic periods and excessive
daytime somnolence. Can cause pulmonary arterial hypertension
leading to Right Ventricular Hypertrophy and polycythemia
secondary to hypoxemia.
Define Sinusitis and describe

its causes.
Inflammation of the sinuses, most often maxillary or ethmoid

sinuses. Caused by URI blocking drainage of sinuses into nasal
cavity. Can be caused by a deviated nasal septum, allergic rhinitis,
barotrauma, or cigarettes. Pathogens implicated are rhinovirus,
strep pneumoniae, anaerobes (chronic sinusitis), systemic fungi
(diabetics
due malignant
to Mucor species).
Most common
tumor of the nasopharynx, more common
What is a Nasopharyngeal
Carcinoma?
in males and increased incidence in the Chinese and African

populations. Closely related to EBV. Often causes squamous cell
carcinoma or undifferentiated cancers which can metastasize to
cervical lymph nodes.
Define Laryngeal Carcinoma.
Carcinoma most commonly located on the true vocal cords. Mostly

keratinizing squamous cell carcinomas, mostly in med. Related to
cigarette smoking, alcohol (synergistic with cigarettes), HPV 6 and
11 and squamous papillomas and papillomatosis. Persistent
hoarseness from cervical lymphadenopathy is common.
What is Atelectasis?
Loss of lung volume due to inadequate expansion of the airspaces

(collapse). Collapse happens because of lack of air and distal
resorption of air through pores of Kohn in the alveolar walls. May
see ipsilateral elevation of the diaphragm and tracheal deviation.
Treat with incentive spirometry, CPAP or PEEP.
What is resorption
atelectasis?
What is compression
atelectasis?
Airway obstruction in bronchiols, segmental bronchi or bronchi, by

thick secretions which prevents air from reaching the alveoli. Can
be caused by mucus or mucopruluent plug after surgery, aspiration
of foreign material or centrally located bronchogenic carcinoma.
Air or fluid in the pleural cavity under increased pressure collapses
small airways beneath the pleura.
What are complications of

respiratory distress
syndrome?
Synthesized by Type II pneumocytes starting in the 28th week of

gestation. Stored in lamellar bodies. Major component is
phosphatidylcholine (lecithin). Synthesis is increased by cortisol
and thyroxine but decreased by insulin. Surfactant reduces surface
tension so airways don't collapse. Without surfactant, airways can
collapse causing atelectasis.
Decreased surfactant in lungs results in atelectasis and respiratory
distress from massive intrapulmonary shunting. Collapsed alveoli
are lined by hyaline membranes (from protein leaking out of
damaged alveoli). Causes respiratory difficulty, grunting,
tachypnea, intercostal retractions and hypoxemia with respiratory
acidosis.
Superoxide radicals from O2 therapy can cause blindness
(retinopathy of prematurity) and damage to small airways
(bronchopulonary dysplasia). Can cause intraventricular
hemorrhage, patent ductus arteriosus from hypoxemia, necrotizing
enterocolitis from intestinal ischemia (allows entry of gut bacteria
into intestinal walls) and hypoglycemia leading to seizures and
neuronal
Collectiondamage.
of fluid. Can be due to Starling forces from left sided
What is Pulmonary Edema

and what are the causes?
heart failure, volume overload or mitral stenosis. This produces

transudate. Can be exudate from microvascular or alveolar injury
resulting from infection. Can be from aspiration, drugs, high
altitude or ARDS.
What is atelectasis due to

loss of surfactant?
What is Respiratory Distress

Syndrome?
What is Acute Respiratory

Distress Syndrome, ARDS?
Noncardiogenic pulmonary edema from acute alveolar-capillary

damage. Caused by direct injury to the lungs or systemic disease.
Risk factors are gram (-) sepsis, gastric aspiration, severe trauma
and shock, diffuse pulmonary infections (SARS, hantavirus),
Heroin, smoke inhalation, acute pancreatitis, cardiopulmonary
bypass, DIC, amniotic fluid or fat embolism.
What is the pathogenesis of

ARDS?
Acute damage to alveolar capillary walls and epithelial cells results

in alveolar macrophages releasing cytokines. Capillary damage
and chemotactic factors allow neutrophils and exudate to leak
producing hyaline membranes. Neutrophils damage Type I and II
pneumocytes, reducing surfactant and causing atelectasis.
What are clinical

signs/symptoms of ARDS?
What are the subtypes of
Pneumonia?
Dyspnea/tachypnea, late inspiratory crackles, severe hypoxemia

not responsive to 100% O2, increased pulmonary wedge pressure,
increased A-a gradient, bilateral infiltrates and consolidations.
Community acquired which can be typical or atypical and hospital
acquired, aka nosocomial.
Describe the pathogenesis of

typical pneumonia.
Most caused by bacterial pathogens, particularly Strep

Pneumoniae. Pathogenesis is via inhalation of aerosol from
infected person or aspiratin of nasopharyngeal flora while sleeping.
Describe the pathogenesis of

bronchopneumonia.
Describe clinical findings in

lobar pneumonia.
Begins as acute bronchitis and spreads locally into the lungs,

usually lower lobes or right middle lobes. Causes patchy
consolidations and may have microabscesses.
Complete or almost complete consolidation of a lobe of the lung.
Can be complicated by lung abscesses, empyema or sepsis. See
sudden onset of fever with productive cough, chest pain,
tachycardia, dullness to percussion, increased tactile fremitus, late
inspiratory crackles, bronchial breath sounds, bronchophany and
egophany.
Describe pneumonia from

Tuberculosis.
Usually caused by mycoplasma pneumoniae, also chlamydophilia

pneumoniae, RSV, influenzavirus, and adenovirus. Contracted by
inhalation of droplets. Causes patchy, mononuclear infiltrate but
the alveolar spaces are usually free of exudate. Insidious onset
with nonproductive cough, low grade fever, chest pain, flu like
symptoms including pharyngitis, laryngitis, myalgia and headache.
No consolidation.
Happens in patients with severe underlying disease,
immunosuppresion, or who are on antibiotic therapy. Respirators
are the most common source of infection. Usually gram (-)
bacteria, often pseudomonas, E coli, or gram (+) like staph aureus.
In immunocompromised, can be opportunistics like CMV,
Pneumocystis Jirovecis, Aspergillus-fumigatus.
From inhalation of Mycobacterium Tuberculosis. Infects
phagosomes of alveolar macrophages and produces a protein that
prevents fusion of the lysosome with the phagosome. Strict
aerobe, acid fast. Cord factor is major virulence factor. Drug
resistance by mutations in mycolic acid or catalase peroxidase
(activates Isoniazid).
Describe Primary TB
Infection.
Subpleural location, usually upper part of lower lobes or lower part

of upper lobes. Causes Ghon focus (caseous necrosis) in periphery
and Ghon complex in hilar lymph nodes. Produces a calcified
granuloma or area of scar tissue
Describe Secondary TB
Infection.
Due to reactivation of primary TB. Usually involves apices in upper

lobes b/c increased V/Q ratio. Causes cavitary lesions from release
of cytokines by T Cells. Causes fever, drenching night sweats,
weight loss. May cause miliary TB with invasion into bronchus,
lymphatics or extrapulmonary sites like the kidney. Spread to
vertebra is called Pott's disease.

atypical pneumonia.

nosocomial pneumonia.
Describe pneumonia from

Mycobacterium Avium
Intracellulare
cause of the common cold?
What does Coxsackievirus
cause?
Atypical mycobacterium causing atypical pneumonia in AIDS

patients. Happens when CD4+ T Cell count falls below 50
cells/mm3. Often disseminates and co-occurs with systemic fungal
infection. transmitted by hand to nose/eye contact. Less
Rhinovirus,
common are coronavirus, adenovirus, influenza C and
coxsackievirus
Acute chest syndrome: fever with pleuritis

viral cause of atypical
pneumonia and bronchiolitis
in children and otitis media
in older children?
Respiratory Syncitial Virus. Occurs in late fall and winter. Can give
Palivizumab to high risk kids (passive immunity)

viral cause of
laryngotracheobronchitis
(croup) in infants?
Parainfluenza. Causes inspiratory stridor from sunmucosal edema

obstructing the upper airway. Anterior CXR shows steeple sign in
anterior neck.

viral cause of pneumonia in
immunocompromised hosts?
Cytomegalovirus. Enlarged alveolar macrophages/pneumocytes

with basophilic inclusions surrounded by a halo.
What can happen with

aspirin ingestion when a
child has influenza?
Reye's Syndrome. Causes fatty liver, severe encephalopathy,

palmar rash, comiting, lethargy and stupor.
What are signs and

symptoms of Rubeola
infection?
What are signs and
symptoms of SARS
What is Hantavirus
pulmonary syndrome?
Measles. Fever, cough, conjunctivitis and excessive nasal mucous.

Koplik spots in the mouth precede rash. Warthin-Finkeldey
multinucleated giant cells are characteristic
Infects lower respiratory tract and then spreads systemically thus
severe respiratory infection and systemic symptoms.
Transmission is via inhalation of urine/feces from deer mice in SW
US. Causes ARDS, hemorrhage and renal failure.
What is the second most

common (bacterial) cause of
atypical pneumonia?
Chlamydophilia pneumoniae. Has a seroepidemiologic association

with coronary artery disease. Treat with doxycycline.
What is a common bacterial

cause of newborn
pneumonia?
Chlamydia trachomatis from passage through infected birth canal.

Afrebile with staccato cough, conjunctivitis and wheezing. Treat
with erythromycin.

baterial cause of atypical
pneumonia?
Mycoplasma Pneumoniae. Insidious onset with low grade fever. Can

cause bullous myringitis(inflamed Tympanic membrane), cold
autoimmune hemolytic anemia from anti-IgM antibodies.
Describe the signs and

symptoms of Coxiella
Burnetti infection
Atypical pneumonia, myocarditis, granulomatous hepatitis.

Associated with dairy farmers and vetrinarians.

cause of community acquired
lobar pneumonia?
What are signs/symptoms of
pneumonia from Staph
Aureus?
Strep pneumoniae. Rapid onset, productive cough and signs of

lobar
consolidation.
Can test
with urine
Commonly
superimposed
on measles
or screen.
influenza pneumonia or in
CF or IV drug users. Hemorrhagic pulmonary edema, yellow
sputum, abscess formation and tension pneumatocysts
(intrapleural blebs) which can rupture and produce tension
pneumothorax.
Causes toxin-induced pseudomembranous inflammation producing
Describe signs and

symptoms of infection with
Corynebacterium Diptheriae.
a shaggy gray membrane in the oropharynx and trachea. Can

cause toxic myocarditis from impaired B oxidation of fatty acids in
the heart.
What are signs and

Bacillus Anthracis?
Cutaneous anthrax initially looks like a scab but swells to form a

black scab (eschar) with an area of central necrosis. Pulmonary
anthrax causes necrotizing pneumonia, meningitis, splenomegaly
and systemic dissemination.
What are signs and

symptoms of Actinomyces
infection?
Normal flora in tonsils and adenoids. Can produce draining sinuses

in the jaw, chest cavity and abdomen. Pus contains yellow specks
(sulfur granules) which contain the bacteria.
What are signs and

symptoms of Nocardia
infection?
What are signs and

Bordatella Pertussis?
Granulomatous microabscesses in the lungs. Often disseminates

to CNS and kidneys.
Produces whooping cough-inspiratory whoop between coughing
fits. Catarrhal phase is 1-2 weeks and involves mild coughing,
rhinorrhea and conjunctivitis. Paroxysmal phase lasts 2-5 weeks
and involves coughing in succession followed by inspiratory whoop
and absolute lymphocytosis (20,000-50,000). Convalescent pahse
lasts 1-2 weeks or more and involves a slow decline in
lymphocytosis and coughing. Can cause hemorrhage into skin,
conjunctiva, bronchus, brain or rectal prolapse from coughing.
Also
otitiscause
mediaofand
meningoencephalitis.
Common
sinusitis,
otitis media, conjunctivitis, epiglottitis
What are signs and

H. Influenzae?
with inspiratory stridor. Swelling of epiglottis produces a

thumbprint sign on lateral xray of the neck. Can cause COPD
exacerbation.
What are signs and

symptoms of Moraxella
Catarrhalis infection?
Causes typical pneumonia, especially in the elderly. Causes acute

COPD exacerbation, chronic bronchitis, sinusitis and otitis media.
What are signs and

Pseudomonas Aeruginosa?
Green sputum (pyocyanin), nosocomial pneumonia and pneumonia

in CF patients. Often associated with infarction from vessel
invasion.
Most common gram negative that causes lobar pneumonia and
What are signs and

symptoms of Klebsiella
Pneumoniae infection?
typical pneumonia in nursing home patients and alcoholics.

Associated with blood tinged, thick, mucoid sputum, lobar
consolidations and abscesses.
What are signs and

Legionella Pneumophila?
Pneumonia associated with high fever, dry cough, flu like

symptoms. May produce tubulointerstitial disease with destruction
of the JG apparatus leading to hyporeninemic hypoaldosteronism
(type IV renal tubular acidosis-hyponatremia, hyperkalemia,
metabolic acidosis). Urine antigen is an excellent screen.
What are signs and

Yersinia Pestis?
What are signs and
Cryptococcus Neoformans?
The plague!!! Macrophages cannot kill bacteria due to protection by

V and W antigens so you get really sick. Bubonic causes infected
lymph node which enlarge and mat together and drain to the
surface (buboes). Pneumonic and septicemic are just what they
sound like. Treat with gentamicin and doxycycline (pneumonic) or
gentamicin and streptomycin (bubonic)
What are signs and

Aspergillus Fumigatus?
Granulomatous inflammation with caseation. Acquired from pigeon

feces.
Aspergilloma-fungus ball that develops in a prior cavitary lesion
and cause massive hemoptysis. Allergic bronchopulmonary
aspergillosis-type I and III hypersensitivity. IgE increase,
eosinophilia, intense inflammation of airways and mucous plugs in
terminal bronchioles resulting in bronchiectasis and interstitial lung
disease. Vessel invasion with hemorrhagic infarctions and
necrotizing
Happens to bronchopneumonia.
diabetic and immunosuppressed patients. Vessel
What are signs and

Mucor species?
invasion producing hemorrhagic infarcts in the lungs. Invades the

frontal lobes when there is diabetic ketoacidosis (rhinocerebral
mucormycosis).
Contracted by inhaling arthrospores in dust in arid areas (increased
What are signs and

Coccidoides Immitis?
What are signs and

Histoplasma Capsulatum?
after earthquakes). Causes flu-like symptoms and erythema

nodosum and granulomatous inflammation of the lungs with
caseous necrosis.
Most common systemic fungal infection, endemic in Ohio and
Mississippi river valleys. Causes granulomatous inflammation with
caseous necrosis, simulating TB. Produces coin lesions,
consolidations, milary spread and cavitation. Causes marked
dystrophic calcification of granulomas and multiple calcifications in
the
Malespleen.
dominant disease, common in Great lakes, central and
What are signs and

Blastomyces Dermatitidis?
southern US. Causes skin disease that simulates squamous cell

carcinoma and lung disease with granulomatous inflammation and
caseous necrosis.
What are signs and

Pneumocystis Jiroveci?
Cysts and trophozoites attach to Type I pneumocytes. Most

common AIDS-defining infection, CD4+ count <200. Fever,
dyspnea and severe hypoxemia, diffuse intra-alveolar foamy
exudates with cup chaped cysts (under silver or Giemsa stain).
Diffuse alveolar and interstitial infiltrates.
What are the common

causesare
of the
lungmost
abscesses?
What
common
pathogens in lung
abscesses?
Aspiration of oropharyngeal material. Risk factors are alcoholism,

loss of consciousness and recent dental work. Can also be a
complication of pneumonia, a result of septic embolism or from an
obstructive lung neoplasia.
Aerobic and anaerobic streptococci, staph species, prevotella,
fusobacterium
What is the pathophysiology

of a pulmonary
thromboembolism?
Right side because the bronchi going to the right lobes are more
direct (straight) so it's easier to aspirate crap into there. Usually in
the upper portion of the right lower lobe, but it depends on the
position of the person when they aspirated.
Spiking fever with productive cough and foul smelling sputum.
CXR shows cavitation with an air/fluid level.
Venous clot, most commonly from the femoral vein. Risk factors
are Virchow's triad-stasis of blood flow, hypercoagulable states and
trauma to the vessel. Clot breaks off and goes to the lung-size of
the embolus determines what it will block. Large embolus blocks
major vessels (saddle embolus) while small emboli occlude
medium
small vessels.
Increase and
in pulmonary
artery pressure, decreased flow to
What are consequences of

pulmonary
thromboembolism?
pulmonary parenchyma which can cause hemorrhagic infarct, see a

red-blue, raised, wedge shaped area that extends to the pleural
surface. Fibrinous exudate on the pleural surface and hemorrhagic
pleural effusion.
What are clinical signs of

pulmonary
thromboembolism?
Sudden increase in PA pressure which can cause right ventricular

failure, sudden onset of dyspnea and tachypnea, fever, pleuritic
chest pain, plueral friction rub, pleural effusion, expiratory
wheezing from release of TXA2 from platelets.
Where are most lung

abscesses due to aspiration
located?
What are clinical findings in
a lung abscess?
What are lab findings of

pulmonary
thromboembolism?
What is Hampton's Hump?
Define Pulmonary
Hypertension
What causes primary
pulmonary hypertension?
What causes secondary

Respiratory alkalosis (PCO2<33mmHg), PaO2<80 mmHg,

increased A-a gradient, increased D-Dimer
Wedge shaped area of consolidation/infarction from PE
Mean pulmonary artery pressure >25 mmHg at rest or >30mmHg
with exercise.
Mutation associated with TGF-B resulting in vascular
hyperreactivity with proliferation of smooth muscle
Endothelial cell dysfunction, e.g. loss of vasodilation (NO), increase
in vasoconstriction (endothelin). Hypoxemia and respiratory
acidosis stimulate vasoconstriction of pulmonary arteries resulting
in smooth muscle hyperplasia and hypertrophy. Any sort of lung
disease that results in chronic hypoxemia or chronic respiratory
acidosis can do this, e.g. high altitude, chronic bronchitis, sleep
apnea, loss of pulmonary vasculature from emphysema or
recurrent PE, left to right shunting/volume overload, mitral stenosis
resulting in volume overload.
What are clinical findings of

How do you treat pulmonary
hypertension?
Exertional dyspnea (common), chest pain, tapering of arteries on

CXR, accentuated P2, left parasternal heave or other signs of right
ventricular hypertrophy.
Diuretics, O2, vasodilators-Ca channel blockers, prostanoids,
endothelin receptor antagonists, lung transplant
What is Goodpasture's
Syndrome?
Pulmonary hemorrhage with hemoptysis often preceding renal

failure. Autoantibodies to Type IV collagen in basement membrane
of lung and glomerulus.
What are common causes of

restrictive lung disease?
Chest wall disorders with normal lungs, e.g. kyphoscoliosis, pleural

disease like mesothelioma or obesity. Acute or chronic interstitial
lung diseases, e.g. ARDS, pneumoconiosis or other fibrosing
disorders, granulomatous diseases like amyloidosis or sarcoidosis.
Describe Coal Worker's

Pneumoconiosis.
Elveolitis-leukocytes release cytokines which stimulate fibrosis.

Causes functional loss of type I/II pneumocytes and capillaries
(decreased DLCO), and decreased expansion of lung parenchyma
during inspiration. Increased elasticity to recoil on expiration is
increased.
dry cough and exertional dyspnea, late inspiratory crackles in lower
lung fields, potential cor pulmonale, equal decreases on PFT's.
Inhalation of mineral dust into the lungs leading to interstitial
fibrosis. Can be silica, asbestos, beryllium or others.
"I think I've got the black lung pop" Coal dust, aka aanthracotic
pigment comes from coal mines, large cities, second hand smoke,
etc. Deposits in alveolar macrophages creating "dust cells."
Fibrotic opacities smaller than 1 cm in upper lobes and coal
deposits adjacent to respiratory bronchioles producing centriacinar
emphysema- simple CWP. Complicated CWP involves large fibrotic
opacities, crippling lung disease (black lung), may have cor
pulmonale or large cavitating rheumatoid nodules (Caplan
Syndrome).
No increase
in TB from
or primary
lung cancers.
Common occupational
disease
quartz/silicon
dioxide,
What is silicosis?
foundries, sandblasting and working in mines. Quartz is fibrogenic

and deposits in the upper lungs, activates and is cytolytic to
alveolar macrophages. Macrophages release cytokines resulting in
fibrosis.
Ground glass appearance on CXR or nodular opacities in more

silicosis.
advanced disease (concentric layers of collagen w/wo central

cavitation). Dystrophic calcification of lymph nodes. Can cause cor
pulmonale or Caplan syndrome and increased risk of lung cancer
and TB.
How do asbestos related

diseases occur?
Serpentine asbestos-interstitial fibrosis and lung cancer; amphilobe

asbestos-interstitial fibrosis, lung cancer and mesothelioma.
Deposits in respiratory bronchioles, alveolar ducts and alveoli.
Comes from insulating pipes, naval shipyards, roofing material,
ceiling tiles, old floor tiles and demolition of old buildings.

interstitial fibrosis?
restrictive lung disease?
What is a pneumoconiosis?

asbestos related disease?
Fibers are coated in iron and protein (ferruginous bodies) which are
then pahgocytosed, coated with ferritin and look golden and
beaded in sputum or distal small airways. Causes calcified pleural
plaques which don't predispose to mesothelioma, diffuse interstitial
fibrosis, primary bronchogenic carcinoma (esp if smoker),
malignant mesothelioma of the pleura arising from serosal cells of
the pleura. Can cause cor pulmonale or Caplan syndrome.
What is Sarcoidosis?
Beryllium exposure from nuclear and aerospace industry causes

diffuse interstitial fibrosis with noncaseating granulomas.
Increased risk for cor pulmonale and primary lung cancer.
Multisystem granulomatous disease of unknown origin. Common
in Black women and nonsmokers and causes 25% of chronic
interstitial lung disease. Granulomas in mediastinal/hilar lymph
nodes and interstitium. Granulomas contain multinucleated giant
cells, laminated calcium concretions (Schaumann bodies) and
stellate inclusions (asteroid bodies). Dyspnea is the most common
symptom.
What are other clinical signs

in Sarcoidosis?
Nodular lesions containing granulomas, violaceous rash on the

nose and cheeks (lupus pernio), erythema nodosum-painful
nodules on lower extremities, inflammation of subcutaneous fat.
Eye lesions produce uveitis, blurry vision, glaucoma and corneal
opacities. Can ahve granulomatous hepatitis, enlarged salivary
and lacrimal glands, diabetes insipidus, and granulomas in the
bone marrow and spleen. See increased ACE, hypercalcemia
(increased 1-alpha hydroxylase in granulomas), polyclonal
gammopathy, and cutaneous anergy of skin antigens like Candida
(due to consumption of CD4+ T cells in granulomas)
What is Berylliosis?
What is idiopathic pulmonary

fibrosis?
Idiopathic means the doctor is an idiot!!! Repeated cycles of

alveolitis, release of cytokines producing interstitial fibrosis,
alveolar fibrosis leading to proximal dilation of small airways giving
the lung a honeycomb appearance. See fever, dyspnea on
exertion, chronic, nonproductive cough, and late inspiratory
crackles.
Systemic Lupus causes interstitial disease in 50% of patients and
What collagen vascular

diseases cause lung disease?
What is hypersensitivity
pneumonitis?
pleuritis with effusion (serositis). Rheumatoid Arthritis can cause

rheumatoid nodules (if with a pneumoconiosis, Caplan's
syndrome).
Extrinsic allergic alveolitis associated with exposure to known
inhaled antigen. Does not involve IgE or have eosinophilia.
What is Farmer's Lung?

What is Silo Filler's Disease?
What is Byssinosis?
What drugs are associated
with interstitial fibrosis?
What is obstructive lung
disease?
What is Emphysema?
Exposure to thermophilic actinomyces (Saccharopolyspora

rectivirgula) in moldy hay causes precipitating IgG antibodies
which combine with inhaled antigens to form immune complexes.
Type III hypersensitivity. Immune complexes deposit in lung and
cause inflammation which chronically causes granulomatous
inflammation (type IV hypersensitivity).
Inhalation of gases (oxides of nitrogen) from plant material causes
an immediate hypersensitivity reaction associated with dyspnea.
Contact with cotton, linen and hemp in textile factories causes
exposure to gram negative endotoxin growing on the cotton.
Causes dyspnea on exposure to cotton, linen or hemp. Disease
occurs on returning to work-Monday Morning Blues (cyanosis)
Amiodarone, Bleomycin and Busulfan, Cyclophosphamide,
Methotrexate and methysergide, nitrosurea and nitrofurantoin.
Obstruction to airflow out of the lungs. Usually loss of elastic recoil
or obstruction of airways.
Permanent enlargement of all or part of the respiratory unitrespiratory bronchioles, alveolar ducts and alveoli.

Emphysema?
Smoking is the most common cause. Also can be from Alpha-1

Antitrypsin deficiency
Increased compliance and decreased elasticity (C=V/P). There can
be an imbalance between elastase and anti-elastases (A1AT), or an
imbalance between oxidants and antioxidants. Elastase and
oxidants all derive from macrophages so chronic inflammation
results in tissue destruction. Smoking produces a functional A1AT
deficiency.
Fibers attach to the outside of the walls of small airways and
What is the normal function

of elastic fibers in the lung?
provide radial traction to keep the lumen open. Destruction causes

loss of radial traction and small airway collapse, especially on
expiration.
During expiration, the distal terminal bronchioles collapse
What causes Emphysema?
Where is the site of

obstruction in emphysema?
What type of Emphysema is
most common in smokers?
What type of Emphysema is

most common in Alpha-1
Antitrypsin deficiency?
What are 2 non-obstructive

types of Emphysema?
What is Chronic Bronchitis?
preventing egress of air. Trapped air distends parts of the

respiratory unit that have no elastic tissue. Trapped air increases
TLC and RV
Centriacinar/Centrilobular.
Mostly apical segments of upper lobes,
distal terminal bronchioles and respiratory bronchioles lose elastic
tissue.
Panacinar emphysema. Autosomal dominant disorder. MM
phenotype is normal, Homozygous ZZ phenotype causes disease.
Primarily affects the lower lobes. Tissue destruction happens in
distal terminal bronchioles and all parts of the respiratory units.
See absent alpha-1 globulin peak in serum protein electrophoresis.
Dyspnea is sever and occurs early, causes pink puffers.
Frequently coexists with chronic bronchitis.
Paraseptal emphysema-localized to the subpleura and targets
alveolar ducts and alveoli. Increased incidence of spontaneous
pneumothorax from rupture of subpleural blebs. Irregular
Emphysema-localized disease associated with scar tissue.
Productive cough for at least 3 months. Most commonly from
smoking and Cystic Fibrosis.

chronic bronchitis?
Hypersecretion of mucous in bronchi, obstruction to airflow in the

terminal bronchioles, proximal to the obstruction seen in
emphysema. Causes irreversible fibrosis of terminal bronchioles.
What changes are seen in

the bronchi with chronic
bronchitis?
Hypersecretion of submucosal mucus-secreting glands in the

trachea and bronchi are responsible for sputum overproduction.
Acute inflammation with neutrophils are superimposed on chronic
inflammation. Causes loss of ciliated epithelium resulting in
squamous metaplasia. Mucus plugs can block the exodus of CO2.
GOblet cell metaplasia is seen with hypertrophy of mucus secreting
glands, fibrosis and narrowing of the airway.
What is Extrinsic Asthma?
Productive cough, dyspnea late in the disease, cyanosis of skin and

membranes, decreased SaO2 from hypoxemia. These patients are
called Blue Bloaters. Tend to be stocky or obese, have expiratory
wheezing and siliant rhonchi and often cor pulmonale. Also have
chronic respiratory acidosis with increased bicarb to compensate.
Episodic and reversible obstructive airway disease. Primarily
targets bronchi and terminal bronchioles.
Type I hypersensitivity reaction with exposure to extrinsic
allergens, typically in children with atopic family history. Initial
sensitization to inhaled allergens stimulates induction of Th2 cells
which release IL-4 and IL-5. IL-4 facilitates isotype switching to
IgE and IL-5 stimulates production and maturation of eosinophils.
Inflammatory mediators like histamine facilitate
bronchoconstriction, mucus production and influx of leukocytes.
Later Eotaxin is released which recruits eosinophils. Eosinophils
release major basic protein which damages epithelial cells and
produces airway constriction.
What are other chemical

mediators involved in
Extrinsic Asthma?
Leukotriene C, D, E4 cause prolonged bronchoconstriction.

Acetylcholine causes airway muscle contraction.
What are clinical findings of

chronic bronchitis?
What is Asthma?
What are some histologic

changes in Extrinsic Asthma?
Thickening of the basement membrane, edema and mixed

inflammatory infiltrate, hypertrophy of submucosal glands and
hypertrophy/hyperplasia of smooth muscle cells. Also see spiral
shaped mucus plugs which contain old epithelial cells-Curschmann
Spirals. This is a pathologic effect of major basic protein.
Crystalline granules in eosinophils coalesce to form Charcot-Leyden
crystals.
What is Bronchiectasis?
Episodic wheezing, nocturnal cough, increased AP diameter from

air trapping. Initially have respiratory alkalosis but may turn into
respiratory acidosis if bronchospasm is not relieved.
Nonimmune asthma caused by virus-induced respiratory infection,
or air pollutants.
Permanent dilation of bronchi and bronchioles due to destruction of
cartilage and elastic tissue by chronic necrotizing infections.

Bronchiectasis?
Cystic Fibrosis, Infection (TB, adenovirus, staph, HiB), bronchial

obstruction (bronchogenic carcinoma), Primary ciliary dyskinesia
(absent dynein arm in cilia aka Kartagener's Syndrome), Allergic
Bronchopulmonary Aspergillosis.
What are some clinical

findings in Bronchiectasis?
Cough productive of massive amounts of sputum, hemoptysis,

digital clubbing, cor pulmonale, crowded bronchial markings that
extend to lung periphery.
What is Cystic Fibrosis?
Autosomal Recessive disease. Three nucleotide deletion on

chromosome 7(should be phenylalanine) resulting in defective CF
transmembrane conductance regulator (CFTR) for chloride ions.
Defective protein is degraded in the Golgiso there is decreased
reabsorption of Na+ and Cl- from sweat glands, but decreased
secretion of Na and Cl into luminal secretions. This results in
dehydrated body secretions which are thick and easily infected.

Extrinsic Asthma?
What is Intrinsic Asthma?

CF?
Nasal polyps, heat exhaustion, respiratory infections/failure, cor

pulmonale, pneumothorax, malabsorption, type I diabetes from
pancreatic destruction, infertility in males (atresia of vas deferens),
meconium ileus, rectail prolapse from straining, gallstones from
thick bile and secondary biliary cirrhosis.
What are risk factors for lung

cancer?
Smoking, Radon gas (uranium mining), asbestos, metal exposurechromium, cadmium, beryllium, arsenic- secondhand smoke,
ionizing radiation, air pollution, prior TB
What are some features of

adenocarcinoma?
What are some features of
squamous cell carcinoma?
What are common sites for
metastasis?
Most common tumor, weakest smoking association, tends to be

peripherally located bc filters in cigarettes remove large
carcinogens leaving the small ones that can move peripherally.
2nd most common tumor, greatest smoking association. Tends to
be centrally located (mainstem bronchus)
Hilar lymph nodes (most common), adrenal glands, liver, brain,
bone
Which cancers are most

commonly responsible for
lung metastasis?
Where in the lung do tumors
commonly metastasize?
What are common findings
in primary lung cancer?
Primary breast cancer, colon cancer and renal cell carcinoma.

Parenchyma, pleura and pleural space (pleural effusions),
lymphatics (causes severe dyspnea)
Cough, weight loss, chest pain, hemoptysis, dyspnea, superior
vena cava syndrome
What
Pancoast tumor?
What is
area some
paraneoplastic changes
associated with lung
cancers?
Superior sulcus tumor. Usually a primary squamous cancer located

at the extreme apex of the lung. Causes desctruction of superior
cervical sympathetic ganglion producing Horner's syndrome.
Digital clubbing from reactive periosteal changes in underlying
bone. Muscle weakness (Eaton Lambert Syndrome). Ectopic
hormone secretion (ACTH)
What are the common

causes of mediastinal
masses?
Usually metastatic primary lung cancer in older patients, usually a

primary disease in younger patients. Neurogenic tumors (posterior
mediastinum)- neuroblastoma (malignant in children),
ganglioneuroma (benign in adults). Thymomas, pericardial cysts,
malignant lymphomas (anterior mediastinum, usually nodular
sclerosing Hodgkin's in a woman), teratomas-usually benign, in
anterior mediastinum.
What are some symptoms of

Thymoma?
Thymoma is usually benign (70%) neoplastic epithelial tissue.

Most patients have systemic symptoms of Myesthenia Gravis. Most
commonly have follicular B cell hyperplasia in the thymus (that's
where antiacetylcholine antibodies are synthesized). Also can have
hypogammaglobulinemia, RBC aplasia and increased incidence of
other autoimmune diseases.
Describe Pseudochylous fluid
Increased hydrostatic pressure in visceral pleura (CHF), decreased

oncotic pressure (nephrotic syndrome), obstruction of lymphatic
drainage from pleura (lung cancer), increased vessel permeability
of pleural capillaries (pulmonary infarction, pneumonia),
metastasis to the pleura (metastatic breast cancer).
Ultrafiltrate of plasma from disturbances in Starling pressures
(CHF, nephrotic syndrome)
Protein-rich
and cell-rich
fluidthoracic
from increased
vessel
permeability.
Indicates
interruption
of the
duct. Turbid,
milky
appearance. Can be from malignancy, trauma (iatrogenic) or too
many chylomicrons
Turbid, milky appearance from increased inflammation with
necrotic debris. Most often from rheumatoid lung disease.
How do you distinguish

between exudate and
transudate?
Ratio of pleural fluid protein and LDH to serum protein and LDH.
PF protein/serum protein <0.5 is transudate, >0.5 is exudate. PF
LDH/serum LDH <0.6 is transudate, >0.6 is exudate. PF LDH
<200 U/L is transudate, >200 U/L is exudate
What is the etiology of

pleural effusions?
Describe a transudate
Describe an exudate
Describe Chylous fluid
How does a spontaneous

pneumothorax happen?

a Tension Pneumothorax?
Commonly seen in tall, thin young men, 20-40 yrs old, increased
risk with smoking. Can be caused by rupture of apical subpleural
blebs (secondary to high negative intrapleural pressure), COPD,
Marfan syndrome, scuba diving, insertion of a subclavian catheter.
Loss of negative intrapleural pressure causes collapse of lung.
Sudden onset of dyspnea with pleuritic chest pain.
Penetrating trauma to the lungs, rupture of tension pneumocytes.
Flap like tear in pleura allows air into pleural cavity but prevents its
release resulting in increasing positive intrapleural pressure. This
results in compression atelectasis. Sudden onset of severe
dyspnea and plueritic chest pain, can cause trachea and
mediastinal structures to deviate to contralateral side. Can cause
compromised venous return to the heart.
Reproductive
What vein drains the ovaries/testes?
What is the lymphatic drainage of the
Ovaries/Testes?
Where does lymph from the
vagina/vulva/scrotum drain to?
What does the suspensory ligament of
the ovaries connect?
What does the Cardinal ligament
connect?
What does the Round ligament of the
uterus connect?
What is the round ligament of the
uterus derive from?
What does the Broad Ligament
connects?
What does the Ligament of the ovary
connect?
What does the Genital Tubercle
become?
What does the Urogenital Fold
become?
What does the labioscrotal swelling
become?
What is the pathway of sperm during
ejaculation?
What is the autonomic innervation
causing an erection?
causing Sperm Emission?
causing Ejaculation?
What are the different parts of the
sperm?
Where do the different parts of the
spermiscome
from? of
What
the function
spermatogonia?
What is the function of Sertoli Cells?
Left Gonadal vein to the left renal vein to the IVC. Right ovary/testis drains to right gonadal vein straight to
the IVC.
Ovary/Testis drains to the para-aortic lymph nodes.
Distal 1/3 of the vagina/vulva/scrotum drains to the superficial lymph nodes. Proximal 2/3 of vagina/uterus
drains to the obturator, external iliac and hypogastric lymph nodes
Connects ovaries to the lateral pelvic wall and contains the ovarian vessels.
Connects the cervix to the side wall of the pelvis and contains the uterine vessels.
Contains the Uterine fundus to the labia majora but carries no structures.
Derivative of the Gubernaculum. Travels through the round inguinal canal.
Connects the uterus, fallopian tubes, and ovaries to the pelvic side wall. Contains the ovaries, fallopian
tubes, and round ligaments of the uterus.
Connects the ovary to the uterus and does not contain any structures.
Becomes the Glans Penis or Clitoris
Becomes the shaft of the penis or the labia minora
Scrotum and Labia majora
(SEVEN UP) Seminiferous tubules to epididymis to vas deferens to ejaculatory ducts (nothing) to urethra to
the penis
Erection-Parasympathetic nervous system (pelvic nerve). Nitric oxide increases cGMP which causes smooth
muscle relaxation which causes vasodilation and is proerectile. Also Norepinephrine causes an increase in
Calcium which causes smooth muscle contraction which causes vasoconstriction and is antierectile.
Sympathetic nervous system via the hypogastric nerve
Visceral and somatic via the pudendal nerve
Acrosome, head, nucleus, neck, middle piece, tail
Acrosome-Golgi apparatus, Flagellum/Tail-Centrioles, Middle Piece-contains the mitochondria, Head and
nucleus come from the nucleus.
Maintaininhibin
the germ
pool
and produce
primary
spermatocytes
Secrete
which
inhibits
FSH. Secrete
Androgen
Binding Protein to maintain the level of testosterone.
Form tight junctions between adjacent Sertoli Cells to form the blood-testis barrier, isolating gametes from
immune attack. Support and nourish spermatozoa. Regulate spermatogenesis. Produce Anti-Mullerian
hormone.
What is the function of Leydig Cells?

What is the composition of Semen?
Describe the general process of
spermatogenesis
What is spermiogenesis?
Describe the process of
spermatogenesis.
Describe the hormonal regulation of

Spermatogenesis.
What are the common Androgens?
What are the functions of Testosterone
in development?
What is the function of
Dihydrotestosterone
in development?
How
is testosterone converted
to
DHT?
What are the sources of Estrogen in a
woman?
What is the function of Estrogen in
development?
What are the typical functions of

estrogen beyond development?
How much do estrogens increase in
pregnancy?
Describe the hormonal regulation of

estrogen.
What is the source of Progesterone?
What does elevation of progesterone
indicate?
Secrete testosterone
Seminal Vesicle Products(fructose, ascorbic acid, prostaglandins, phosphorylcholine, flavins), Prostate
Products (Zinc, citrate acid, phospholipids, acid phosphatase, fibrinolysin), Sperm
Spermatogenesis begins at puberty with spermatogonia. Full development takes 2 months. Occurs in
seminiferous
that undergo
spermiogenesis
to form
mature
spermatozoa
Maturation of tubules.
sperm asProduces
they losespermatids
their cytoplasmic
contents,
gain an acrosomal
cap
and become
mature
spermatozoa
Spermatogonium (diploid 2N) copies genome to make Primary spermatid (Diploid 4N). Primary spermatocyte
divides into 2 secondary spermatocytes (Haploid 2N). The Secondary spermatids divide again to produce 4
spermatids (Haploid, 1N). These undergo spermiogenesis to form mature spermatozoa
Hypothalamus releases GnRH which causes FSH and LH release from the anterior pituitary. LH stimulates
testosterone release from Leydig cells which release testosterone into the seminiferous tubules and the blood.
FSH stimulates Sertoli cells to produce Androgen Binding Protein and Inhibin. Testosterone from the Leydig
cells stimulates spermatogenesis and stimulates the Sertoli Cells to nurse the Spermatozoa. Inhibin from the
Sertoli cells feeds back and downregulates FSH release. Testosterone from Leydig cells feeds back and
downregulates LH production and GnRH release.
Testosterone (Testes), Dihydrotestosterone (Converted peripherally) and Androstendione (Adrenal)
Differentiation of the Epididymis, Vas deferens and seminal vesicles. Growth spurt of the penis, the seminal
vesicles, sperm, muscle, and red blood cell growth. Deepening of voice, closing of epiphyseal plates (via
estrogen converted from testosterone) and Libido.
In early differentiation it causes development of the penis, scrotum and prostate. In later/pubertal
development it causes prostate growth and sebaceous gland activity.
5 Alpha reductase converts Testosterone to DHT.
Ovary makes 17 Beta estradiol, Placenta makes estriol and blood/peripheral tissues can aromatize androgens
to estrogen.
Development of genitalia (external) and breast, and female fat distribution.
Growth of the follicle, endometrial proliferation, increased myometrial excitability. Upregulates LH, FSH and
estrogen receptors and thus upregulates itself. Feedback inhibition of LH and FSH and then the LH surge.
Stimulates prolactin secretion but blocks its action at the breast. Increases transport of proteins, Steroid
hormone binding globulin synthesis, increases HDL and decreases LDL.
50 fold increase in estradiol and estrone. 1000 fold increase in estriol indicates fetal well being.
Pulsatile GnRH from the Hypothalamus causes release of FSH and LH from the anterior pituitary. FSH
stimulates the granulosa cells of the ovaries to increase Aromatase which can then convert androstendione to
estrogen. LH acts on the Theca cells to upregulate Desmolase which convert cholesterol to androstendione.
The androstendione goes to the granulosa cells to be converted to estrogen.
Corpus Luteum, placenta, adrenal cortex and testes (in men obviously)
Ovulation!!!
What is the function of Progesterone?
What happens during the

proliferative/follicular phase of a
woman's cycle?
When is follicular growth fastest?
What stimulates endometrial
proliferation?
What maintains the endometrium?
What defines Oligomenorrhea?
What defines Polymenorrhea?
What defines Metorrhagia?
What defines Menometrorrhagia?
Stimulation of endometrial glandular secretions and spiral artery development. Maintains pregnancy.
Decreases myometrial excitability. Increases production of thick cervical mucous, which inhibits sperm entry
into the uterus. Increases body temperature (hence why you take your temp), inhibits gonadotropins (LH
and FSH), relaxes uterine smooth muscle (prevents contraction) and decreases estrogen receptor
expressivity.
Granulosa cells respond to FSH and stimulate growth of 10-20 follicles. LH responsive Theca cells stimulate
growth of the corpus luteum and produce androgens which are converted to estrogen by granulosa cells (to
stimulate the developing follicle). Estrogen encourages growth of the endometrium and provides positive
feedback to the anterior pituitary to stimulate release of more FSH/LH leading to the midcycle gonadotropin
surge. About 1 week before ovulation, one follicle becomes dominant meaning that it becomes more
responsive to FSH. The follicle secretes lots of inhibin which downregulates FSH and causes atresia of the
other follicles.
2nd week of the proliferative phase.
Describe the maturation of the Follicle

(see Reproductive Attachment 2).
Estrogen
Progesterone
Cycle greater than 35 days
Cycle less than 21 days
Frequent but irregular menstruation
Heavy, irregular menstruation
During the follicular phase, both estrogen and progesterone are low. FSH is fairly low as is LH initially. LH
spikes about halfway through the follicular phase which increases estrogen above its threshold. Estrogen
feeds back onto LH which causes it to spike along with an estrogen spike. FSH is also increased and has a
small spike along with the LH spike. This causes ovulation and begins the secretory/luteal phase. LH and
FSH then drop. Estrogen increases again but Progesterone increases a lot throughout the whole phase thus
maintaining the lining of the endometrium. Everything drops when entering the menstrual phase which
allows the endometrial llining to shed.
A primordial follicle consists of an oocyte surrounded by a single layer of squamuos granulosa cells. The
granulosa cells enlarge and become cuboidal turning the follicle into a primary follicle. The primary follicle
then enlarges and the granulosa cells form more than one layer. The Zona Pellucida then forms around the
oocyte. The structure becomes a secondary follicle when fluid filled vesicles develop among the granulosa
cells and a well developed capsule, Theca layer, becomes apparent around the granulosa cells. The Theca
has both internal and external layers. It becomes a mature follicle when the vesicles form a single antrum.
At full maturity, the oocyte is located in the cumulus mass.
What happens to the follicle during

ovulation?
What hormonal changes are seen
during ovulation?
What is Mittelschmerz?
During ovulation, the oocyte is released with some granulosa cells called the corona radiata. The remaining
granulosa cells divide rapidly and enlarge to form the corpus luteum which makes progesterone for the
remainder of the cycle or the beginning of pregnancy. The corpus luteum then degenerates to form the
corpus albicans and eventually becomes fibrotic.
Increased estrogen, increased GnRH and increased GnRH receptors on anterior pituitary, estrogen surge
precedes LH surge. Increased temperature from increased progesterone.
Blood from ruptured follicles which can cause peritoneal irritation that mimics appendicitis.
When does oogenesis begin and when

is it completed?
Primary oocytes begin Meiosis I during fetal life but don't complete Meiosis I until just before ovulation. Thus
Meiosis I is arrested in Prophase for years until ovulation. Meiosis II arrests in metaphase until fertilization.
If there is no fertilization, the secondary oocyte degenerates.
Describe the hormonal changes during

a woman's cycle (see Reproductive
Attachment 1).
What is the process of oogenesis?

Where does Fertilization most
commonly happen?
When does implantation into the wall
of the uterus typically occur?
How is lactation induces after labor?
How is milk production maintained
after birth?
What is the role of Prolactin in the
female?
What is the role of Oxytocin in the
female?
Where is hCG made?
What is the function of hCG?
How is pregnancy detected?
What changes in hCG are there in
pathologic states?
What hormonal changes are seen in
menopause?
What is the main source of Estrogen
after menopause?
What are some symptoms of
menopause?
What is Klinefelter's Syndrome?
How does Klinefelter's Syndrome
cause infertility?
What is Turner's Syndrome?
Describe
a double
Y malewould you
What hormonal
changes
see with a defective androgen
receptor?
What hormonal changes would you
see with a Testosterone-secreting
tumor, or exogenous steroids
Begins with a diploid Oogonium (2N) which replicates (interphase) to become a diploid primary oocyte (4N).
The Primary oocyte then arrests in Prophase I until ovulation. During ovulation it divides to become a
secondary haploid oocyte (2N) and a polar body which degenerates. It arrests in Metaphase II here until
fertilization. The secondary Oocyte divides again to become a Haploid Ovum (1N) and another polar body
that degenerates.
Most commonly happens in the upper end of the Fallopian tube (the ampulla). Typically within a day after
ovulation.
6 days after fertilization. The trophoblast secretes Beta-HCG which is detectable in the blood 1 week after
conception and in urine (home test) 2 weeks after conception.
The decrease in maternal steroids induces lactation.
Suckling increases nerve stimulation which increases oxytocin and prolactin production thus maintaining milk
production.
PRL induces and maintains lactation and decreases reproductive function.
Helps with milk letdown and may be involved with uterine contractions.
Syncytiotrophoblast of the placenta.
Maintains corpus luteum (thus progesterone) for the first trimester by acting LH. The Placenta synthesizes its
own estriol and progesterone during the 2nd and 3rd trimester and the corpus luteum degenerates.
hCG is used to detect pregnancy because it appears early in the urine.
hCG is elevated in Hydatidiform moles, Choriocarcinoma, Gestational trophoblastic tumors (and other tumors
IDecreased
think)
Estrogen production due to age linked decline in follicles. Significantly increased FSH, increased
LH, increased GnRH. Average age of onset is 51, earlier in smokers. Usually preceded by a few years of
irregular periods.
Estrone from peripheral conversion of androgens. Increased androgens can cause hirsutism (that's why your
grandma has a mustache)
HHAVOC-Hirsutism, Hot flashes, Atrophy of the Vagina, Osteoporosis, Coronary artery disease
47 (XXY). Causes testicular atrophy, eunuchoid body shape, tall, long extremities, gynecomastia, female hair
distribution. May cause developmental delay. Usually a Barr body is present (inactive X chromosome)
Dysgenesis of seminiferous tubules causes decreased inhibin which leads to increased FSH. Abnormal Leydig
cell
function
causes
decreased
and increased
and estrogen.
45 (XO).
Causes
short
stature,testosterone
ovarian dysgenesis
(streakLH
ovaries),
shield chest, bicuspid aortic valve,
webbing of the neck from cystic hygroma, preductal coarctation of the aorta, no Barr body and primary
amenorrhea.
47 (XYY). Phenotypically normal, very tall, severe acne, antisocial behavior in 1-2%, normal fertility.
Increased testosterone and increased LH (female phenotype I think)
Increased testosterone but decreased LH from negative feedback
What hormonal changes would you

see with
primarychanges
hypogonadism?
What
hormonal
would you
see with Hypogonadotropic
hypogonadism?
What is pseudohermaphroditism?
Decreased testosterone and increased LH from gonadal failure and lack of feedback.
Decreased testosterone and decreased LH from pituitary failure not stimulating the gonads.
Disagreement between the phenotypic (external genitalia) and gonadal (testes vs ovaries) sex.
What is a male pseudohermaphrodite?

What is a true hermaphrodite?
46 (XX). Ovaries are present but the external genitalia are virilized or ambiguous. It's due to excessive or
inappropriate androgen exposure during early gestation. Usually congenital adrenal hyperpasia or exogenous
androgen administration.
46 (XY). Testes are present but external genitalia are female or ambiguous. The most common reason is
androgen insensitivity syndrome aka testicular feminization.
(46, XX or 47, XXY). Both ovaries and testicular tissue present. Ambiguous genitalia. Very rare.
What is Androgen Insensitivity

Syndrome?
Defect in androgen receptors resulting in normal-appearing female. Female external genitalia with a
rudimentary vagina. Uterus, uterine tubes are generally absent. No sexual hair. Testes are often found in
the labia majora and must be surgically removed to prevent malignancy. Increased testosterone (although
no response), increased estrogen and LH
What is 5 alpha reductase deficiency?
Inability to convert testosterone to DHT. Ambiguous genitalia until puberty when the massive testosterone
increase causes masculinization and increased growth of the external genitalia. Testosterone/estrogen levels
are
normal;
LH of
is normal
or villi
increased.
Internal genitalia
are epithelium
normal. (trophoblast) that presents with
Cystic
Swelling
chorionic
and proliferation
of chorionic
What is a female
pseudohermaphrodite?
What is a Hyaditiform Mole?

What is a complete Hyaditiform Mole?
What characteristics are seen in a
complete mole?
What characteristics are seen in a
partial mole?
What are some common causes of
recurrent miscarriages?
What is pre-eclampsia?
What is eclampsia?
What are some risk factors for preeclampsia?
What is the pathogenesis of Preeclampsia?
What is HELLP Syndrome?
What are some clinical features of Preeclampsia?
How do you treat Pre-Eclampsia or
Eclampsia?
abnormal vaginal bleeding. Most common cause of Choriocarcinoma. See increased Beta-hCG, a
honeycombed uterus, looks like a cluster of grapes (if a cluster of grapes is totally disgusting looking). See
an
abnormally
uterus.
2 sperm
with aenlarged
completely
empty egg. Classically have a snowstorm appearance with no fetus during first
sonogram. Moles can lead to uterine rupture. Treat with dilitation and curettage and methotrexate. Monitor
Beta-hCG.
Karyotype is 46,XX or 46, XY. Massively increased hCG, increased uterine size, 2% convert to
adenocarcinoma, no fetal parts, 2 sperm +empty egg, 15-20% form malignant trophoblastic disease.
Karyotype is 69,XXY, slightly increased hCG, no change in uterine size, rare for it to convert to
choriocarcinoma, 2 sperm+1 egg, risk of malignancy is less than 5%
during the 1st weeks- low progesterone levels (no response to Beta-hCG, 1st trimester-chromosomal
abnormalities, 2nd trimester-bicornate uterus
Combination of hypertension, proteinuria and edema.
Pre-eclampsia + Seizures
Pre-existing hypertension, diabetes, chronic renal disease and autoimmune disorders.
Caused by placental ischemia due to impaired vasodilation or spiral arteries, resulting in increased vascular
tone. May be an issue with implantation.
Hemolysis, Elevated LFT's, Low Platelets from Pre-eclampsia
Headache, blurred vision, abdominal pain, edema of the face and extremities, altered mentation,
hyperreflexia. Lab findings include thrombocytopenia and hyperuricemia.
Delivery of the fetus as soon as it's viable. Otherwise bed rest, salt restriction, and monitoring/treatment of
hypertension. Treatment is IV magnesium sulfate and diazepam to prevent seizures of eclampsia.
What is Abruptio Placentae?
What is Placenta Acreta?

What is Placenta Increta?
What is Placenta Percreta?
What is Placenta Previa?
What is an Ectopic Pregnancy?
What is the problem with retained
placental tissue?
What are some risk factors associated
with ectopic pregnancy?
What is Polyhydramnios?
What is Oligohydramnios?
What is Potter's Syndrome?
Describe Dysplasia and Carcinoma in
Situ of the cervix.
What virus is associated with Cervical
dysplasia?
What risk factors are associated with
cervical dysplasia?
Describe invasice carcinoma of the
cervix
What is a Koilocyte?
What is Endometriosis?
How does Endometriosis manifest
clinically?
What are possible complications of
Endometriosis?
What is Adenomyosis?
Premature detachment of the the placenta from the implantation site. Fetal death and DIC may occur.
Increase in risk with smoking, hypertension and cocaine use.
Defective decidual layer allows the placenta to attach to the myometrium. No separation of the placenta after
birth. May cause massive bleeding after delivery. Associated with prior C-Section. Acreta does not penetrate
the entirety of the myometrium.
Just like Placenta Acreta but extends further into the myometrium.
The worst form of Placenta Acreta which involves the placenta extending all the way through the myometrium
to the serosa. The placenta may then attach to other organs like the bladder or rectum.
Attachment of the placenta to the lower uterine segment. May then occlude the internal os (so baby can't get
out). Associated with multiparity and prior C-Section.
Pregnancy that isn't in the uterus. Most often in the Fallopian tubes. Suspect with increased hCG and
sudden lower abdominal pain. Confirm with ultrasound. May be clinically mistaken for appendicitis.
May cause postpartum hemorrhage.
History of infertility, Salpingitis/PID, ruptured appendix (at any point), prior tubal surgery or any lower
abdominal surgery, endometriosis.
Greater than 1.5-2 Liters of amniotic fluid. Associated with esophageal and duodenal atresia, causing
inability to swallow amniotic fluid. Also associated with anencephaly.
Less than 0.5 Liters of amniotic fluid. Associated with placental insufficiency, bilateral renal agenesis or
posterior urethral valves (in men) and thus an inability to excrete urine. Can cause Potter's syndrome.
Atypical appearance of the fetus in the womb as a result of oligohydramnios. Causes clubbed feet,
pulmonary hypoplasia and cranial anomalies.
Disordered epithelial growth. Begins at the basal layer of the squamo-columnar junction and extends
outward. Classified as CIN I, CIN II or CIN III (Carcinoma in Situ), depending on the extent of the dysplasia.
HPV 16 and 18
Multiple
sexual
smoking,
early
sexual
intercourse,
HIV infection
Pretty
much
thepartners,
cervical cancer
gone
really
nasty.
Often squamous
cell carcinoma. Papsmear can catch
cervical dysplasia (koilocytes) before it becomes invasive carcinoma. Lateral invasion can block ureters
causinf renal failure.
Cervical cell infected with HPV that is undergoing dysplasia. See large nuclei and large ring of cytoplasm.
See Attachment 3 for some pics.
Non-neoplastic endometrial glands/stroma in an abnormal location outside the uterus. Characterized by
cyclic bleeding from the ectopic endometrial tissue resulting in blood filled "chocolate cysts." Does anyone
else want to puke right now? Often in the ovary or on the peritoneum.
Severe menstrual-related pain.
Often causes infertility, possibly due to retrograde mentrual flow or ascending infection.
Endometrium within the myometrium
What is Endometrial Hyperplasia?
Abnormal endometrial gland proliferaton usually caused by excess estrogen stimulation. Associated with
increased risk for endometrial carcinoma.
How does Endometrial Hyperplasia

manifest clinically and what are some
risk factors?
Postmenopausal vaginal bleeding. Risk factors are anovulatory cycles, hormone replacement therapy,
polycystic ovarian syndrome and granulosa cell tumors.
What is Endometrial Carcinoma?
Most common gynecologic malignancy, usually between 55 and 65 years of age. Usually a progression of
endometrial hyperplasia so presents with vaginal bleeding after menopause. Risk factors are prolonged
estrogen exposure without progesterone, obesity, diabetes, hypertension, nulliparity and late menopause.
The more it's invaded the myometrium, the worse the prognosis.
Describe a Leiomyoma?
Most common cause of all tumors in females. Essentially a Fibroid. Often causes multiple tumors with well
demarcated borders. This is a benign smooth muscle tumor and malignant transformation is very rare.
Mostly occurs between 20-40 years old and is often asymptomatic. may cause abnormal uterine bleeding or
result in miscarriage. If bleeding is severe it may cause Iron deficiency anemia. See a whorled pattern of
smooth muscle bundles (doesn't become Leiomyosarcoma). See attachment 4 for a picture.
What is a Leiomyosarcoma?
What is the epidemiology of
gynecologic tumors?
What is premature Ovarian failure?
what are the most common causes of
anovulation?
What is Polycystic Ovarian Syndrome?

What hormonal changes do you see in
PCOS?
What is a Follicular Cyst?
What is a Corpus Luteum cyst?
What is a Theca Lutein Cyst?
What is a Chocolate Cyst?
What age group most commonly gets
Ovarian Cell Tumors?
What is a Dysgerminoma?
What is a Choriocarcinoma?
Bulky, irregularly shaped tumor with areas of necrosis and hemorrhage. Nasty tumor. Typically arises de
novo, not from a Leiomyoma. Highly aggressive tumor with a tendency to recur. May protrude out of the
cervix and bleed (yuck!). More common in middle aged women and African American women.
Incidence- Endometrial>Ovarian>Cervical. Worst Prognosis- Ovarian>Cervical>Endometrial
Premature atresia of ovarian follicles in women of reproductive age. Presents with signs of menopause after
puberty
but
beforesyndrome,
age 40. See
decreased
estrogen
but increased
LH and HPO
FSH axis
b/c no
feedback. premature
Polycystic
ovarian
obesity,
Asherman's
Syndrome
(adhesions),
abnormalities,
ovarian failure, hyperprolactinemia, thyroid disorders, eating disorders, Cushing Syndrome and adrenal
insufficiency
Increased LH production leading to anovulation, hyperandrogenism due to deranged steroid synthesis by
theca cells. Enlarged bilateral cystic ovaries manifest clinically with amenorrhea, infertility, obesity and
hirsutism. Associated with insulin resistance, increased risk of endometrial cancer. Treatment is weight loss,
OCP, gonadotropin analogs, clomiphene or surgery.
Increased LH and FSH and increased Testosterone.
Distention of a ruptured Grafian Follicle. May be associated with hyperestrinism and endometrial hyperplasia.
Hemorrhage
into persistent
corpus
luteum.
regresses
spontaneously.
Commonly bilateral
or multiple
cysts.
Due toCommonly
gonadotropin
stimulation.
Associated with choriocarcinoma and
moles.
Blood-containing cyst from ovarian endometriosis. Varies with the menstrual cycle.
Most common
in adolescents
Malignant,
equivalent
to a male seminoma, but rarer (1% vs 30%). Sheets of uniform cells with hCG and
LDH.
Rare but malignant. Can develop during pregnancy in mother or the baby. Large, hyperchromatic
syncitiotrophoblastic cells. Increased frequency of theca-lutein cysts. Along with moles, comprise spectrum
of gestational trophoblastic neoplasia. hCG is the tumor marker.
What is a yolk sac (endodermal sinus)

tumor?
What is a teratoma?
What is a serous cystadenoma?
What is a serous cystadenocarcinoma?
What is a Mucinous Cystadenoma?
What is a Mucinous
Cystadenocarcinoma?
What is a Brenner tumor?
What is a Fibroma?
What is Meigs' Syndrome?
What is a Granulosa Cell Tumor?
What is a Krukenberg tumor?
What causes squamous cell carcinoma
of the vagina?
What predisposes to Clear Cell
Adenocarcinoma?
Who is affected by Sarcoma
Botryoides (variant of
Rhabdomyosarcoma)
How do Bartholin's gland cyst
present?
Aggressive malignancy in the ovaries (testes in boys) and sacrococcygeal area of young children. These are
yellow, friable, solid masses. 50% have Schiller Duval bodies that resemble glomeruli. Alpha fetoprotein is
the tumor marker.
90% of ovarian germ cell tumors. Contain cells from 2-3 germ layers. Mature teratomas/Dermoid cysts are
the most frequent benign ovarian tumors/teratomas. Immature teratomas are aggressively malignant.
Struma
Ovarii
contain
functional
thyroid tissue.
Can bilateral,
present as
hyperthyroidism.
Makes up
about
20% of
ovarian tumors.
Frequently
lined
with Fallopian tube-like epithelium.
Benign.
Makes up about 50% of ovarian tumors, malignant and frequently bilateral.
Multilobular cyst lined by mucus-secreting epithelium. Benign. Intestine-like tissue.
Malignant! Pseudomyxoma peritonei- intraperitoneal accumulation of mucinous material from ovarian or
appendiceal tumor.
Benign tumor that looks like the bladder.
Bundles of spindle
shaped fibroblasts.
Associated
with Fibromas.
Triad of ovarian fibroma, ascites and hydrothorax. Causes pulling sensation in the
groin.
Secretes estrogen-causes precocious puberty. Can cause endometrial hyperplasia or carcinoma in adults.
See Call-Exner bodies-small follicles filled with eosinophilic secretions. Abnormal uterine bleeding.
GI Malignancy that metastasizes to the ovaries, causing a mucin-secreting signet cell adenocarcinoma.
Secondary to squamous cell carcinoma of the cervix.
Affects women who had exposure to DES in utero.
What is a Phyllodes Tumor?
Affects girls < 4 years of age. Spindle shaped tumor cells that are desmin positive.
Rare. Present with pain in the labia majora. Can result from previous infection.
Small, mobile, firm mass with sharp edges. Most common tumor in those <25 years. See increasing siza
and tenderness with increasing estrogen such as during menstruation. Not a precursor to breast cancer.
Small tumor that grows in lactiferous ducts. Typically beneath areola. See serous or bloody nipple
discharge. Slight (1.5-2X) increased risk for breast carcinoma.
Large bulky mass of connective tissue and cysts with "Leaf like projections." Most common in the 6th
decade. Some may become malignant.
How do malignant breast tumors arise

and when/where are they most
common?
Common postmenopause. Arise from mammary duct epithelium or lobular glands. Overexpression of
estrogen/progesterone receptors on erb-B2 (HER-2 and EGF Receptor) is common. Affects therapy and
prognosis. Axillary lymph node involvement is the single most important prognostic factor.
What is a Fibroadenoma of the breast?

What is an Intraductal Papilloma?
What are some risk factors for

malignant breast tumors?
What is a Ductal Carcinom in Situ
(DCIS)?
What is invasive ductal carcinoma?
What is an invasive Lobular tumor?
Risk factors are increased estrogen exposure. Increased total number of menstrual cycles, older age at 1st
live birth, obesity (adipose tissue serves as a major source of estrogen in post-menopausal women by
converting androstenedione to estrone).
Malignant tumor of the breast that fills the ductal lumen. Arises from ductal hyperplasia. Early malignancy
without basement membrane penetration.
Worst and most invasive ductal carcinoma but also most common. Forms firm, fibrous, rock hard masses
with sharp margins and small, glandular duct like cells.
Malignant breast tumor, often multiple and often bilateral. See an orderly row of cells.
What is a medullary tumor of the

breast?
What is a comedocarcinoma of the
breast?
What is an inflammatory tumor of the
breast?
What is Paget's disease?
What is Fibrocystic disease?
What are the histologic subtypes of
Fibrocystic disease?
What is acute mastitis?
What is Fat Necrosis?
What is Gynecomastia?
What is the order of structures in the
breast starting at the nipple?
Malignant tumor with a good prognosis. See fleshy, cellular, lymphatic infiltrate.
Subtype of DCIS. See ductal caseous necrosis.
Nasty, malignant tumor with a 50% 5 year survival. See dermal lymphatic invasion by breast carcinoma.
See Peau d'orange-breast skin looks like orange peel.
Eczematous patches on nipples. Paget cells are large cells in the epidermis with clear halo around them.
May
be seen
on the
vulva.lumps
Suggests
underlying
carcinoma.
Mostalso
common
cause
of breast
after an
age
25. Presents
with premenstrual breast pain and multiple
lesions, often bilaterally. See a fluctuation in size of the mass. Usually does not indicate increased risk of
carcinomas.
Fibrosis-hyperplasia of breast stroma. Cystic-fluid filled, blue dome. Ductal dilation. Sclerosing adenosisincreases acini and intralobular fibrosis. Associated with calcifications. Epithelial hyperplasia-increase in
number of epithelial cell layers in terminal duct lobule. Increases risk of carcinoma with atypical cells.
Occurs in women >30 years of age.
Breast abscess. During breast feeding. Increases risk of bacterial infection through cracks in the nipple.
Staph
Aureus
is thelump.
most common
A
benign,
painless
Forms as pathogen.
a result of injury to breast tissue. Up to 50% of patients may not report
trauma.
Results from hyperestrogenism (cirrhosis, testicular tumor, puberty, old age), Klinefelter's syndrome or drugs
(estrogen, marijuana, heroin, psychoactive drugs, Spironolactone, Digitalis, Cimetidine, Alcohol,
Ketoconazole).
Nipple, Lactiferous sinus, major duct, terminal duct, lobules. All surrounded by stroma
What tumors occur at each of these

structures?
How does prostatitis present?
What are causes of acute prostatitis?
What are causes of chronic prostatitis?
Nipple-Paget's disease, breast abscesses. Lactiferous sinus-Intraductal papilloma, breast abscess, mastitis.
Major duct-Fibrocystic change, ductal cancer. Terminal ducts-Tubular carcinoma. Lobules-lobular carcinoma,
sclerosing adenitis. Stroma-Fibroadenoma, phyllodes tumor.
Dysuria, frequency, urgency, low back pain.
Usually bacterial, especially E. Coli
May be bacterial or abacterial.
What is Benign Prostatic Hyperplasia

(BPH)?
How do you treat BPH?
Hyperplasia (not hypertrophy) of the prostate gland. May be due to an age related increase in estradiol with
possible sensitization of the prostate to the growth-promoting effects of DHT. Characterized by a nodular
enlargement of the periurethral (lateral and middle) lobes, which compress the urethra into a vertical slit.
Often present with increased frequency of urination, nocturia, difficulaty starting and stopping the stream of
urine and dysuria. May lead to distention and hypertrophy of the bladder, hydronephrosis and UTI's. Not
considered premalignant. Do see increased free PSA but not rapidly increasing like in cancer.
Use
alphainantagonists
Terazosin,
tamulosin,
which
relaxation
smooth
muscle.
Common
men >50. like
Arises
most frequently
from
thecause
posterior
lobe of of
the
prostate(peripheral
zone) and is
What is Prostatic adenocarcinoma?

What is cryptorchidism?
How common are testicular germ cell
tumors?
most commonly diagnosed by digital rectal exam and prostate biopsy. Prostatic acid phosphatase and PSA
are the most useful tmor markers. See increased total PSA with decreased fraction of free PSA. Osteoblastic
metastases in bone may develop in later stages and appears as lower back pain and an increase in serum
alkaline phosphatase and PSA.
Undescended testis. Lack of spermatogenesis due to increased body temperature. Also associated with
increased risk of germ cell tumors. Prematurity increases the risk of cryptorchidism.
95% of all testicular tumors. May present as a mixed germ cell tumor.
What is a Seminoma?
What is an embryonal carcinoma?
What is a yolk sac (endodermal sinus)
tumor in a man?
What is a Choriocarcinoma in a man?
What is a teratoma in a man?
How common are testicular non-germ
cell tumors?
What
What
What
What
What
What
What
is
is
is
is
is
is
is
a Leydig Cell Tumor?

a Sertoli Cell Tumor?
testicular lymphoma?
a tunica vaginalis lesion?
a Variocele?
a Hydrocele?
a spermatocele?
What is Bowen's Disease?

Qhat is Erythroplasia of Queyrat?
What is Bowenoid papulosis?
What is Squamous Cell Carcinoma of
the penis?
What is Peyronie's Disease?
What changes are seen in
Decidualization?
When does Blastocyst hatching occur?
What is the Zona Pellucida?
What proteins characterize
preimplantation of the embryo?
What are the three stages of
implantation?
What is the Decidua Basalis?
What is the Decidua Capsularis?
What is the Decidua Paritalis?
What happens to RBC and Plasma
volume and mass in pregnancy?
Malignant, painless, homogenous testicular enlargement. Most common testicular tumor, mostly affecting
males age 15-35. See large cells in lobules with watery cytoplasm and a fried egg appearance. These are
radiosensitive, only metastasize late and have a great prognosis.
Malignant, painful tumor with a worse prognosis than a seminoma. Often glandular or papillary morphology.
Can differentiate and become other tumors and is associated with increased AFP and hCG.
Yellow, mucinous tumor analagous to an ovarian yolk sac tumor. See Schiller Duval bodies which resemble
primitive glomeruli.
Malignant, hCG secreting tumor. Has distinct syncytiotrophoblastic and cytotrophoblastic elements. Causes
hematogenous metastases.
Similar to females except that mature teratomas in men are usually malignant.
5% of all testicular tumors, most of which are benign.
Androgen producing tumor which causes gynecomastia in men, precocious puberty in boys. Contains Reinke
crystals and is golden brown in color.
Androblastoma from the sex cord stroma.
Most common testicular cancer in older men. It's pretty much lymphoma in the testicles.
A lesion in the serous covering of the testis. Presents as testicular masses that can be transilluminated.
Dilated vein in pampinoform plexus which can result in infertility. Looks like a bag of worms.
Increased fluid secondary to incomplete fusion of the processus vaginalis
Dilated epididymal duct
Gray, solitary, crusty plaque, usually on the shaft of the penis or on the scrotum. Peak incidence is in the 5th
decade of life. Progresses to invasive squamous cell carcinoma in <10% of cases.
Red, velvety plaques, usually involving the glans penis. Otherwise similar to Bowen's disease.
Multiple papular lesions. Affects younger men but isn't usually invasive
Essentially like any other SCC, just on the penis. Commonly associated with HPV and lack of circumcision.
More common in Asia, Africa and South America.
Bent penis due to acquired fibrous tissue formation.
Glycogen and lipid accumulation, extra-cellular matrix changes, prolactin and IGF binding proteins increased,
COX-2 increase which increases PGE2, and influx od dedidual NK cells.
When the blastocyst enters the endometrial cavity, about 5 days after fertilization.
Non-cellular, porous layer of glycoproteins around the oocyte.
Early pregnancy factor, Platelet activating factor, human Chorionic Gonadotropin, Matrix Metalloproteinases
and Inhibitors of Matrix Metalloproteinases, Heparin binding-EGF like growth factor receptors
Apposition, Adhesion and Invasion
Decidua that forms underneath the embryo
Capsule of decidua over the embryo
Other decidua lining the uterine cavity
Both are increased but plasma is increased more than RBC. This results in a dilutional effect in hematocrit.
What happens to GFR and Creatinine

Clearance during pregnancy?
Why does respiratory alkalosis happen
during pregnancy?
Why do women get dyspnea during
pregnancy?
Creatinine clearance is increased. GFR increases fairly significantly. Increased clearance of creatinine and
urea results in serum creatinine and urea that are really low. Thus normal creatinine and urea are
problematic.
Estrogen
and progesterone both stimulate the respiratory center. Greater tidal volume and increased
respiration rate also cause increased minute ventilation, thus more CO2 is blown off. Thus respiratory
alkalosis from decreased PaCO2
May be due to decreased CO2 stimulating the respiratory center and causing subjective shortness of breath.
Why are Thyroxin and Cortisol

increased in pregnancy?
What defines menopause?
What are the physiologic causes of
menopause?
What are non-physiologic causes of
menopause?
hCG simulates TSH since they share the same alpha subunit. Thus it stimulates T4 secretion during the first
10 weeks. Estrogen promotes growth of the pituitary and the thyroid and synthesis of thyroid binding
globulin. Thus T4 and cortisol are increased but free T4 and cortisol are the same.
No menses
one year
after age
40. from decreased ovarian function. Depletion of granulosa and thecal
Waxing
and for
waning
of estrogen
levels
cells. Lack of response to gonadotropins. Increased LH stimulates androgen production in stromal cells (thus
hirsutism)
Surgical removal or radiation of ovaries. Turner syndrome. Family history of early menopause and left
handedness (seriously???)
What is the average age of

menopause and how is age at
menopause determined?
Average age is 51. The age at which it's determined is genetically determined, but smokers reach
menopause early and peri-menopause is mid-to late 40's.
What are some clinical findings in

menopause?
What are some labroratory findings in
menopause?
What are some treatment options for
symptomatic menopause?
What are risks of long term hormone
replacement?
What is Hirsutism?
What is virilization?
What are male secondary sex
characteristics?
Secondary amenorrhea, hot flushes, night sweats, atrophic vaginitis with pruritis, burning, bleeding and
dyspareunia. Also see mood swings, anxiety, depression, insomnia, decreased libido, urinary incontinence,
headaches, tiredness, lethargy, and osteoporosis with increased risk of Colle's and vertebral fractures.
Increase in LH and FSH from a drop in estrogen (LH) and progesterone (FSH)
Estrogen replacement, progestins added if the uterus is still present to prevent endometrial adenocarcinoma.
Thromboembolism, Coronary heart disease, stroke, slightly increased risk for breast cancer, increased risk for
dementia in women over 65.
Excess hair in normal hair-bearing areas.
Hirsutism plus male secondary sex characteristics
What causes virilization or hirsutism?
Increased muscle mass, acne, enlarged clitoris

Both caused by increased androgens of either ovarian or adrenal origin. In the ovaries, the androgen is
testosterone, in the adrenals it's DHEA-S
What are some causes of virilization

and hirsutism?
Polycystic ovary syndrome, idiopathic causes, adrenogenital syndrome, insuline resistance, drugs like
androgenic progestins, phenytoin, cyclosporin, minoxidil. Can also be from ovarian tumors like a leydig or
sertoli-leydig cell tumor, adrenal tumors producing Cushing syndrome, decreased steroid hormone binding
globulin from obesity and hypothyroidism.
What is Polycystic Ovarian Syndrome?

What are clinical findings in polycystic
ovarian syndrome?
What are some lab findings in PCOS?
What is the treatment in PCOS?

What is Menorrhagia?
What is Dysmenorrhea?
What is the treatment for Primary
Dysmenorrhea?
What is the treatment for secondart
Dysmenorrhea?
What is dysfunctional uterine
bleeding?
What are some types of dysfunctional
uterine bleeding?
What is most common cause of
irregular bleeding?
What causes anovulatory
dysfunctional uterine bleeding?
What causes ovulatory dysfunctional
uterine bleeding?
How do you treat ovulatory
dysfunctional uterine bleeding?
What is Primary Amenorrhea?
What is Secondary Amenorrhea?
amenorrhea?
What are causes of abnormal vaginal
bleeding in a pre-pubertal girl?
What are some causes of abnormal
vaginal bleeding between menarche
and 20 years?
Syndrome that occurs around menarche. See increased synthesis of LH and decreased synthesis of FSH.
Increased LH increases androgen synthesis resulting most often in hirsutism. Androgens are then aromatized
to estrogen in adipose cells increasing the risk of endometrial carcinoma. The increased estrogen feeds back
positively on LH and negatively on FSH. Suppression of FSH causes follicle degeneration resulting in fluid
accumulating and producing subcortical cysts that then enlarge the ovaries.
Menstrual irregularities, mostly oligomenorrhea and often hirsutism, infertility or obesity.
LH:FSH ratio >2. Increased serum testosterone and androstendione. Increased serum estrogen.
Weight reduction in obese women. Low dose OCP's or medroxyprogesterone to suppress steroidogenesis and
LH. Can use Spironolactone if OCP's are unacceptable to block androgen receptors on the hair follicle. LHreleasing hormone analogs inhibit ovarian androgen production.
Loss of blood >80 mL per period. It's likely if sheets are stained despite heavy protection. Excessive
passage of clots indicates that plasmin does not have enough time to dissolve clot.
Painful menses, occuring in approximately 50% of women. Primary type occurs in ovulatory cycles due to
increased prostaglandin PGF-2alpha. See increased uterine contractions from increased prostaglandins. The
secondary type is from endometriosis, adenomyosis, leiomyomas, or cervical stenosis.
NSAID's, OCP, nifedipine, magnesium sulfate
Essentially deal with the underlying disease.
Abnormal uterine bleeding that is unrelated to an anatomic cause. Note that this is a diagnosis of exclusion.
Menorrhagia, Hypomenorrhea, Metrorrhagia, Menometrorrhagia, Oligomenorrhea, Polymenorrhea
Anovulatory cycle in 90% of cases but less than 10% due to anovulation during reproductive years.
Excessive estrogen stimulation relative to progesterone resulting in an absent secretory phase. It produces
excessive endometrial
hyperplasia
and
excessivematuration
bleeding. of the corpus luteum. This causes inadequate
Inadequate
luteal phase
resulting in
inadequate
synthesis of progesterone and delay in the development of the secretory phase. May see decreased 17-OH
progesterone .
If the follicle size is normal, supplement progesterone. If the follicle size is inadequate, give clomiphene
sulfate.
Absence of menses by age 16. Most cases are due to constitutional delay with a family history of delayed
menses.
Absence of menses for 3 months, most commonly due t pregnancy.
Hypothalamic or pituitary dysfunction resulting in decreased LH and FSH which results in decreased estrogen
and progesterone. Ovarian disorders cause problems in synthesis of estrogen or progesterone.
Vulvovaginitis, poor hygeine, infection, gonrrhea, sexual abuse, foreign bodies, embryonal
rhabdomyosarcoma
Anovulatory dysfunctional uterine bleeding, Von Willebrand's disease

vaginal bleeding between ages 20-40?
vaginal bleeding after age 40?
What part of the placenta covers the
fetal surface?
What covers the chorion?
What covers the maternal surface of
the placenta?
Wheredoes
do the
villispace
project?
What
thechorionic
intervillous
contain?
What lines the chorionic villi?
What forms the outside layer of the
trophoblast?
What does the Syncytiotrophoblast
do?
What forms the inside layer of the
trophoblast?
How many vessels are contained in
the umbillical cord?
What risks are related to a single
umbillical
artery?
What
causes
most placental
infections?
How should you treat a placental
infection even if culture is negative?
What is Funisitis?
What is Placentitis?
What is chorioamnionitis?
What complications might arise from
chorioamnionitis?
What is Placenta Previa?
How does Placenta Previa present?
How do you diagnose Placenta Previa?
What is Abruptio Placentae?
What are risks for abruptio placentae?
What are the clinical signs of abruptio
placentae?
Pregnancy and related complications, ovulatory dysfunctional uterine bleeding, PID, hypothyroidism,
submucosal leiomyomas, adenomyosis, endometrial polyp, endometriosis
Anovulatory dysfunctional uterine bleeding, endometrial hyperplasia, cancer.
Entirely covered by the chorionic plate. The chorionic villi vessels converge with the umbillical cord.
Chorion is covered with amnion
Contains cotyledons covered by decidua basalis.
Into the intervillous
space oxygen and nutrients and spiral arteries from the uterus that empty into the
Maternal
blood that delivers
space
Trophoblastic tissue
Syncytiotrophoblast.
Synthesizes hCG, and HPL which directly correlates with placental mass and has anti-insulin activity.
Cytotrophoblastic tissue
One umbillical vein and two umbillical arteries. The vein carries the oxygenated blood in this case
Increased incidence of congenital anomalies, defects including cardiovascular defects, trisomy 18 and
esophageal atresia.
Ascending infections, often from premature rupture of membranes
Treat prophylactically with IV Ampicillin+Erythromycin followed by PO amoxicillin and erythromycin. If
culture positive you can give IV penicillin or ampicillin
Infection of the umbillical cord
Infection of the placenta
Infection of the fetal membranes
Neonatal sepsis and meningitis. Treat with Cefoxitin or Ticaricillin-Clavulanate
Implantation over cervical os. Previous C Section is major risk factor
Painless vaginal bleeding, usually second or third trimester. The uterus is soft and non-tender and fetal
distress is usually not present.
Do not do a pelvic exam. Transabdominal ultrasound localizes the placenta and transvaginal ultrasound
confirms placenta previa.
Premature separation of the placenta due to formation of a retroplacental clot. This separates the placenta
from the implantation site. This is most common cause of late pregnancy bleeding
Hypertension, smoking, cocaine, advanced maternal age, trauma, chorioamnionitis, premature membrane
rupture, previous abruptio placentae.
Painful uterine bleeding, forceful uterine contractions or signs of preterm labor, usually see evidence of fetal
distress
What is Placenta Acreta?
What is Velamentous insertion?

What risks do accessory lobes of the
placenta pose?
What can cause an enlarged placenta?
What type of placentas do
Monozygotic twins have?
What risks are associated with
monochorionic, diamnionic placentas?
What is Preeclampsia?
What are risk factors for
Preeclampsia?
What is the pathogenesis of Preeclampsia?
What are pathologic findings in PreEclampsia?
What are clinical findings in PreEclampsia?
What are some other symptoms in
Pre-Eclampsia?
What is a Hyaditiform Mole?
What is a complete Hyaditiform Mole?

Which type of Mole has an increased
risk of Choriocarcinoma?
What is a partial Hyaditiform Mole?
What is a Choriocarcinoma?
Where does Choriocarcinoma
metastasize?
What is the composition of amniotic
fluid?
Direct implantation into muscle without intervening decidua. Causes great risk for hemorrhage during
delivery, commonly requiring surgery to control bleeding. Often requires hysterectomy.
Umbilical cord inserts away from the placental edge-the vessels pass to the placenta through the membranes
between the amnion and chorion. Causes increased risk for hemorrhage if the vessels are torn. Deliver by C
Section to avoid vessel tear.
Increased risk of hemorrhage if they are detached.
Diabetes mellitus, Rh hemolytic disease of the newborn, congenital syphilis
Monochorionic and monoamniotic although they can have dichorionic placentas
Twin Twin Transfusion syndrome.
Toxemia of pregnancy
First pregnancy, more common in women <20 years and >35 years, history of previous preeclampsia,
positive family history, multiple gestations, african american, thrombocytosis, obesity
Abnormal placentation causing mechanical or functional obstruction of the spiral arteries. The abnormal
trophoblastic tissue invades the spiral arteries. Imbalance favors vasoconstriction over vasodilation
(decreased PGE2 and NO, increased TXA2, Ang II and increased sensitivity to Ang II)
Premature
aging
of the placenta,
multiple
placental
infarctions,
spiral arteries
show atherosclerosis
Hypertension,
proteinuria
from leaky
capillaries
(increased
inflammation),
dependent
pitting edema from loss
of albumin, weight gain, seizures in eclampsia, swollen endothelial cells in glomerular capillaries producing
oliguria.
Right upper quadrant pain and hepatomegaly, periportal necrosis with increased transaminases, HELLP
syndrome
Benign tumor of the chorionic villus from an empty egg and 2 sperm or an egg and 2 sperm.
The entire placenta is neoplastic. Dilated swollen villi without fetal blood vessels. No embryo is present.
Ovum 46, XX, lacking maternal chromosomes. The chromosomesare derived from the father, either 2 sperm
or duplicated 23X sperm in the ovum
Complete mole. Presents with painless vaginal bleeding in fourth, fifth month of pregnancy. Causes severe
vomiting, pre-eclampsia, uterus that is too large for gestational age, increased hCG for gestational age, and
snowstorm
appearance
onorultrasound.
Not all villi are
neoplastic
dilated? Embryo is present but this is triploid. Egg with 23X is fertilized by 23X
and 23Y sperm. (Not that if the embryo is doubled, it's not considered a mole). This has a low risk of
choriocarcinoma.
malignant tumor composed of syncytiotrophoblast and cytotrophoblast without chorionic villi. Risks are
complete mole, spontaneous abortion and normal pregnancy
Lungs and vagina-hemorrhagic lesions
Predominantly fetal urine, initially plasma ultra-filtrate from mom. High salt content causes ferning when
dried on a slide-good sign of premature rupture of amniotic sac.
What is the quantity of amniotic flud

maintained?
What is Polyhydramnios?
What is Oligohydramnios?
What can Alpha Fetoprotein indicate in
pregnancy?
What does the Lecithin to
Sphingomyelin ratio indicate?
What can increase surfactant
production in the fetus?
Where is estriol made in pregnancy?
What part of estriol synthesis does the
fetal adrenal cortex control?
What does the fetal liver do in estriol
synthesis?
What does the maternal placenta do in
estriol synthesis?
What does the maternal liver do to
estriol?
What does decreased estriol indicate?
What is the triad of markers in Down
syndrome?
What is the most high density location
of breast
tissue?
What
effects
do sex hormones have
on the breast during the menstrual
cycle?
What hormones affect lactation?
Where do outer quadrant breast
cancers drain?
Where do inner quadrant breast
cancers
What
aredrain?
normal causes of
Galactorrhea?
What are pathologic causes of
Galactorrhea?
Bloody nipple
discharge?
What causes prululent
nipple
discharge?
Swallowed and recycled by the fetus.

Excessive amniotic fluid. Causes are tracheoesophageal fistula, duodenal atresia, maternal diabetesmaternal hyperglycemia causes fetal hyperglycemia resulting in fetal polyuria.
Decreased amount of amniotic fluid. Caused by juvenile polycystic kidney disease, fetal genitourinary
obstruction, uteroplacental insufficiency and premature rupture of membranes.
Increased maternal AFP indicates open neural tube defects (often related to Folate deficiency). Decreased
maternal AFP can indicate Down syndrome.
Lecithin is synthesized by type II Pneumocytes which decreases alveolar tension to prevent atelectasis. L:S
ratio >2 indicates adequate surfactant.
Cortisol and thryroxine increase surfactant synthesis. Maternal administration of glucocorticoids can increase
surfactant if the baby must be delivered before term. Insulin inhibits surfactant synthesis.
Derived from fetal adrenal gland (DHEA-S) which is aromatized by the placenta.
Fetal adrenal cortex converts pregnenolone from the placenta to DHEA-S.
Hydroxylates DHEA-S to 16-OH-DHEA-S
Initially converts LDL to pregnenolone for fetal processing. Placental sulfatase then cleaves off the sulfate
from 16-OH-DHEA-S and converts it to free unbound estriol via aromatase.
Conjugates it to estriol sulfate and estriol glucosiduronate which is then excreted in the maternal urine and
bile.
Sign of fetal-maternal-placental dysfunction
Decreased urine estriol, decreased AFP, increased serum Beta-hCG
Upper outer quadrant-thus cancer is most commonly located in this location. Also underneath the nipple.
Estrogen stimulates ductal and alveolar growth. Progesterone stimulates alveolar differentiation.
Prolactin-stimulates and maintains lactogenesis. Oxytocin-released by the suckling reflex which causes
expulsion of milk into the ducts.
Axillary lymph nodes
Internal mammary lymph nodes.
Mechanical stimulation of the nipple from prolonged suckling or sexual intercourse.
Prolactinoma, primary hypothyroidism (decreased T4 causes increased TRH which stimulates PRL), drugs like
OCP's, phenothiazines, methyldopa, H2-Receptor blockers and angiolytics.
Intraductal papilloma, ductal cancer
Acute mastitis due to Staph A., usually related to breast feeding
What causes Green-Brown nipple

discharge?
What is the most common cause of
Breast Pain?
What is Mondor's disease?
Mammary duct ectasia (plasma cell mastitis)

Fibrocystic change
Superficial thromboplebitis of veins overlying the breast, presenting as a palpable, painful cord.
What is Ductal Hyperplasia?

What is Mammary duct
ectasia/plasma cell mastitis?
Most common painful breast mass in women <50 years old. Causes distortion of normal cyclic breast
changes. Some cysts have hemorrhage into the cyst fluid-called blue-domed cysts. Vary in size with the
menstrual cycle but have no malignant potential
Proliferation of small ductules/acini in the lobule-pattern is often confused with infiltrating ductal cancer.
Often contains microcalcifications.
Ducts are estrogen sensitive. See papillary proliferation called papillomatosis, apocrine metaplasia (change
to sweat producing glands), and atypical ductal hyperplasia (increased risk for carcinoma)
Main ducts fill up with debris causing dilation, rupture and inflammation. Results in greenish-brown nipple
discharge. May result in skin and nipple retraction stiulating cancer but no increased risk for breast cancer.
What is traumatic fat necrosis?
Trauma to breast tissue. Microscopic findings are lipid-laden macrophages with foreign body giant cells,
fibrosis and dystrophic calcification. See a painless indurated mass which is painful in the acute stage and
may
retraction
stimulating
cancer.
Most produce
commonskin
breast
tumor in
women <35
years. Discrete movable, painless or painful mass. It's a benign
What is Fibrocystic change?

What is sclerosing adenosis?
What is a Fibroadenoma of the breast?

What is a Phyllodes tumor?
What is an Intraductal Papilloma?
What are risk factors for breast
cancer?
What are some genetic markers for
breastdecreases
cancer? risk for breast
What
cancer?
What are clinical findings in breast
cancer?
What is the primary screening test for
breast cancer?
Where do microcalcifications most
commonly
occur?and progesterone
How
is estrogen
receptor expression related to
prognosis?
What is a Ductal Carcinom in Situ
(DCIS)?
tumor derived from the stroma which proliferates and compresses the ducts. The duct epithelium is not
neoplastic. Estrogen sensitive so increases in size during pregnancy. May spontaneously involute during
menopause.
Bulky tumor derived from stromal cells. Most commonly benign but can be malignant in some cases-see
hypercellular stroma with signs of mitoses in malignancy. Lobulated tumor with cystic spaces containing leaflike extensions.
Most common cause of bloody nipple discharge in women <50. Develops in the lactiferous ducts or sinuses.
No increased risk for cancer.
Prolonged estrogen stimulation, genetic susceptibility, especially if first generation relatives. Prolonged
estrogen stimulation from either early menarche or late menopause or nulliparity.
BRCA 1 and BRCA 2, Li-Fraumeni, RAS oncogene, ERBB2, RB suppressor gene
Breast feeding, moderate or vigorous physical training, healthy body weight.
Painless mass in the breast, usually the upper outer quadrant. Skin or nipple retraction, painless axillary
lymphadenopathy, hepatomegaly and bone pain if there are metastases.
Mammography-detects 80-90% of non-palpable breast masses. Does not distinguish benign from malignant
lesions. Can identify microcalcifications and spiculated masses with or without microcalcification.
Ductal carcinoma in situ, and sclerosing adenosis. Five or more microcalcifications that are punctate,
microlinear or branching all suggest malignancy
ER/PR expression generally confers a good prognosis whereas ERB2/NEU has a poor prognosis if amplified.
Nonpalpable mass. Forms a cribiform pattern (seive like) or comodo like pattern (necrotic center).
Commonly contains microcalcifications which allow it to be detected on mammogram.
What is a Lobular Carcinoma in Situ

(LCIS)?
What is Infiltrating Ductal Carcinoma?

What is Paget's disease?
What is Medullary Carcinoma of the
breast?
What is inflammatory carcinoma of
the breast?
What is Invasive Lobular Carcinoma?
Tubular
What is a
ColloidCarcinoma?
(Mucinous)
Carcinoma?
What is Gynecomastia?
What causes pathologic

gynecomastia?
What is the most common cause of
Bartholin gland abscesses?
What is Lichen Sclerosis?
What is Lichen Simplex Chronicus?
What is a Papillary Hidradenoma?
What is Vulvar Intraepithelial
Neoplasia?
What are risk factors for squamous
cell carcinoma of the vulva?
What is extramammary Paget's
disease?
What is Malignant melanoma of the
vulva?
What type of lesion results from
infection with Calymmatobacterium
Granulomatis?
Nonpalpable mass. Virtually always an incidental finding on breast biopsy for something else. Not
identifiable on mammography. Lobules are distended with bland neoplastic cells. Usually ER/PR positive.
Increased incidence of cancer in the opposite breast, that isn't LCIS.
Malignant, invasive breast tumor. Has a stellate morphology. Indurated, gray-white tumor. 1/3 have ERB2
amplification conferring poor prognosis. These look gritty on cut section and have reactive desmoplasia
causing induration.
Extension of DCIS into the lactiferrous ducts and skin of the nipple producing a rash with or without nipple
retraction. Palpable mass often present, see Paget's cells as well.
Invasive tumor associated with BRCA1 mutations. Bluky, soft tumor with large cells and a lymphoid infiltrate.
Most are ER/PR negative.
Invasive tumor that presents with erythematous breast with dimpling of the skin like an orange peel from
fixed opening of the sweat glands. Plugs of tumor block the lumen of dermal lymphatics causing localized
lymphedema. Has a very poor prognosis.
Invasive mass of neoplastic cells arranged in a linear fashion or in concentric circles.
Invasive mass that develops in terminal ductules. Increased incidence of cancer in the opposite breast.
Invasiveglandular
mass that
usually occurs
in male
older breast
women.
cells
surrounded
extracellular
mucin.
Benign
proliferation
in the
dueNeoplastic
to estrogen
from
increasedby
enstrogens,
decreased
androgens or a defect in androgen receptors. Most often unilateral. Normal in newborns, puberty or the
elderly.
Cirrhosis causes an inability to metabolize estrogen or to metabolize 17-ketosteroids which are then
aromatized to estrone. Genetic diseases like Klinefelter's and testicular feminization cuase gynecomastia.
Drugs that displace estrogen from SHBG, such as spironolactone or ketoconazole or drugs with estrogen
activity like DES or digoxin, or androgen blocking drugs like spironolactone or flutamide or that decrease
androgen production like leuprolide. These all increase estrogen.
Infection with Neisseria Gonorrhea
Thinning of the epidermis with parchment appearing skin. Most commonly in post-menopausal women.
White plaque like skin lesion (leukoplakia) due to squamous cell hyperplasia. Small risk for developing
Squamous Cell Carcinoma.
Benign tumor of the apocrine sweat gland. Causes painful nodule on the labia majora.
Dysplasia of the vulva, ranging from mild to carcinoma in situ. Strong association with HPV 16 and high risk
of developing squamous cell carcinoma
HPV 16, smoking, immunodeficiency.
Red, crusted vulvar lesion. Intraepithelial adenocarcinoma derived from primitive epithelial progenitor cells.
Malignant Paget cells contain mucin which is Periodic Acid Schiff positive. Spreads along the epithelium but
rarely invades the dermis.
Melanoma cells, histologically similar to Paget cells except these are PAS negative.
Gram negative coccobacilli that causes granuloma inguinale. It's phagocytosed by macrophages forming
Donovan bodies and results in creeping, raised sores that heal by scarring. Treat with bactrim or doxy.
What types of lesions result from

infection with Candida Albicans?
Yeast and pseudohyphae which should be part of the normal vaginal flora. Causes vaginitis, pruritic vaginitis
with
a white discharge
and fiery
red mucosa.
Risk factors
and OCP's
STD-commonly
coinfecting
with Neisseria
Gonorrhea.
See are
red diabetes,
inclusionsantibiotics,
(reticulate pregnancy
bodies) in squamous
What type of lesion results form

infection with Chlamydia Trachomatis?
cells which then divide and form elementary bodies which can reinfect other cells. Causes sterile pyuria,
epididdmitis, proctitis (in males obviously) and urethritis, cervicitis, PID, perihepatitis (Fitz-Hugh Curtis),
proctitis and bartholin gland abscesses (in females obviously). Can also cause conjunctivitis and pneumonia
in a newborn.

infection with Chlamydia Trachomatis
subspecies?
What types of lesions are seen with
infection by Gardnerella Vaginalis?
infection with Hemophilus Ducreyi?
infection with HSV-2?
Lymphogranuloma venerum, papules with no ulceration, inguinal lymphadenitis with granulomatous

microabscesses and draining sinuses. Lymphedema of the scrotum or vulva and possibly rectal strictures in
women
Gram negative rod that causes bacterial vaginosis. Most common vaginitis which presents with malodorous
discharge. Organisms adhere to the squamous epithelium forming clue cells.
Gram negative rod that causes Chancroid. Male dominant disease, often correlated with HIV. Causes painful
genital warts and perianal ulcers with suppurative inguinal nodes which main have draining sinuses.
STD with the virus remaining latent in the sensory ganglia. Causes recurrent vesicles that ulcerate on the
vulva, penis, cervix and perianal area. See multinucleated squamous cells on Tzanck prep

infection with HPV?
How do you treat HPV?
Types 6 and 11 associated with Condyloma Acuminata (warts)-fernlike or flat lesions in the genital area.
Types 16 and 18 associated with dysplasia and squamous cell carcinoma. See koilocytes in squamous
epithelium. Cells have wrinkled, pyknotic nuclei surrounded by a clear halo.
Vaccine! Topical podophyllin, alpha-IFN injections and imiquimod cream

infection with Neisseria Gonorrhoeae?
What are signs of disseminated
Gonococcemia?

infection with Treponema Pallidum?
What are the non-specific screening
tests for Syphillis?
What are the confirmatory tests for
Syphillis?
What is the Jarisch-Herxheimer
reaction?
what types of lesion results from
infection with Trichamonas Vaginalis?
What is Rokitansky-Kuster Hauser
Syndrome?
What is a Gartner's Duct cyst?
What is a Rhabdomyoma?
Gram negative diplococcus that infects glandular transitional epithelium in sites similar to Chalmydia. Causes
prululent lesions and urethritis. Can cause ectopic pregnancy, male sterility, disseminated gonococcemia,
septic arthritis, and Fitz Hugh Curtis.
Septic arthritis in the knee, tenosynovitis of the hands and feet, pustules on the hands and feet
Gram negative spirochete that causes syphillis. Primary syphillis presents with a solitary, painless, indurated
chancre on the penis, labia or mouth. Secondary presents with a maculopapular rash on the trunk, palms
and soles along with generalized lymphadenopathy, condylomata lata (flat lesions) and alopecia. Tertiary
syphillis presents with neurosyphillis, aortitis and gummas.
RPR or VDRL. Titers should decrease after treatment.
FTA-ABS which is positive with or without treatment
Intensification of rash in primary or secondary syphillis after proteins are released from the dead organisms
following penicillin treatment
Flagellated protozoan with jerky motility which produces vaginitis, cervicitis and urethritis. Causes a
strawberry colored cervix and fiery red vaginal mucosa with greenish, frothy discahrge.
Absence of the upper vagina and uterus resulting in primary amenorrhea
Remnant of the Wolffian/mesonephric duct which presents as a cyst on the lateral wall of the vagina.
Benign tumor of skeletal muscle in the vagina (can also be on the tongue or heart)
What is an Embryonal
Rhabdomyosarcoma?
What is clear cell adenocarcinoma of
the vagina?
What is Vaginal Adenosis?
What are some other DES related
abnormalities?
What is vaginal squamous cell
carcinoma?
What
does the cervix actually consist
of?
What lines the exocervix?
What lines endocervical glands?
How does the endocervical epithelium
transform into the exocervical
epithelium?
What is the pathogenesis of a
Nabothian cyst?
What is acute cervicitis?
What are clinical findings in acute
cervicitis?
What causes chronic cervicitis?
What is follicular cervicitis?
What is the purpose of a Cervical Pap
test?
What do superficial squamous cells
indicate on Pap?
What do intermediate squamous cells
on
Papdoindicate?
What
parabasal cells on Pap
indicate?
What types of cells are seen on Pap
from a non-pregnant and pregnant
woman?
What is a Cervical Polyp?
Describe Cervical Intraepithelial
Neoplasia, CIN
What is CIN I?
What is CIN II?
What is CIN III?
Necrotic, grape like mass protruding from the vagina, most often in girls <5 years
Adenocarcinoma of the vaginal wall (pretty self explanatory). Occurs in women with DES exposure since DES
inhibits mullerian
differentiation-tubes,
uterus, Produces
cervix andred,
upper
third of ulcerations
the vagina in the upper portion of
Precursor
lesion for
squamous cell carcinoma.
superficial
the vagina
Abnormally shaped uterus that thwarts implantation (T shape). Cervical incompetence which can cause
recurrent miscarriage.
It's what it sounds like. That said, primary SCC is associated with HPV 16. Most of these are actually
extensions of cervical SCC into the vagina.
Endocervix and exocervix. The exocervix begins at the cervical os
squamous epithelium
Mucus secreting columnar cells
Endocervical epithelium migrates down to the exocervix where exposure to the acid pH of the vagina causes
squamous metaplasia. This area is called the transformation zone and is the most likely location for
squamous dysplasia and cancer.
Metaplastic squamous cells block endocervical gland orifices resulting in obstruction to outflow of mucus.
This is a normal finding however.
Acute inflammation is often present in the transformation zone, however pathologic acute inflammation may
be due to infection-Chlamydia, Neisseria, Trichomonas, Candida, HSV, HPV.
Vaginal discharge, pelvic pain, dyspareunia, pain on palpation (chandelier sign), easy bleeding and
erythematous or exudative cervical os.
Essentially persistence of acute cervicitis
Pronounced lymphoid infiltrate with germinal centers caused by Chlamydia Trachomatis.
Screening test for squamous dysplasia and cancer. Evaluate the hormone status of the patient.
Adequate estrogen
Adequate progesterone
Lack of estrogen and progesterone.
Non-pregnant: 70% superficial, 30% intermediate squamous cells. Pregnant: 100% intermediate squamous
cells from progesterone effect.
Non-neoplastic polyp that protrudes from the cervical os. Arises from the endocervix, most commonly in
perimenopausal or multigravida women.
Most cases associated with HPV which produces koilocytes in squamous cells. Associated with early age of
sexual intercourse, multipe high-risk partners, high risk HPV types, smoking, OCP's and immunodeficiency.
Mild dysplasia involving the lower third of the epithelium
Moderate dysplasia involving the lower 2/3 of the epithelium
Severe dysplasia to carcinoma in situ involving the full thickness of the epithelium
What is the epidemiology of cervical

cancer?
What are clinical findings in cervical
cancer?
What are some characteristics of
cervical cancer?
What is the sequence to menarche?
When does ovulation occur?
What mediates the secretory phase of
the cycle?
Least common GYN cancer with higher incidence in developing countries. Most are squamous cell carcinomas
with the same risk factors as CIN
Abnormal vaginal bleeding, often post coital, malodorous discharge
Cancer often extends down into the vagna and out into the lateral wall of the cervix and vagina. May
infiltrate the bladder wall and obstruct the uterus causing postrenal azotemia and possibly death. May
metastasize distantly, e.g. to the lungs.
Breast budding (Thelarche), growth spurt, pubic hair, axillary hair, menarche (mean age is 12.8 years).
Between days 14 and 16
Progesterone
What are the functions of FSH?
Fertilization usually occurs in the ampullary portion of the Fallopian tube. The fertilized egg spends 3 days
there, 2 days in the uterine cavity and then implants in the endometrial mucosa on day 21. There is an
exaggerated secretory phase in pregnancy called the Arias-Stella phenomenon.
Drop-off in serum estrogen and progesterone signalling endometrial cells to undergo apoptosis.
Prepares the follicle of the month, increases aromatase synthesis in the granulosa cells, increased synthesis
of LH receptors.
What are the functions of LH?

What hormonal changes are seen in
pregnancy?
Increases synthesis of 17-ketosteroids in the theca interna (DHEA and androstenedione). Convert DHEA to
androstenedione and androstenedione to testosterone. Increase aromatization of testosterone. (Obviously
LH isn't doing these things directly but it uprgulates necessary enzymes)
Human chorionic gonadotropin-synthesized in the syncytiotrophoblast lining the chorionic villus. hCG acts as
an LH analog and maintains the corpus luteum to produce progesterone.
What changes occur after fertilization?

What initiates menses?
What is in Oral Contraceptive Pills and

how do they work?
Where does Estradiol come from?
Where does Estrone come from?
Where does Estriol come from?
Where does androstendione come
from in a woman?
Where does DHEA come from in a
woman?
Where does testosterone come from
in a woman?
What is Sex Hormone Binding
Globulin?
What does SHBG have a greater
affinity for?
Mixture of estrogens and progestins which then prevent the midcycle LH surge and ovulation. Progestin
arrests the proliferative phase and cause gland atrophy and also inhibit LH directly. OCP's also render the
cervical mucus hostile to sperm and alter Fallopian tube motility.
Aromatized testosterone in granulosa cells. Primary estrogen in non-pregnant women.
Weak estrogen produced during menopause from adipose cell aromatization of androstendione
End product of estradiol metabolism. Primary estrogen of pregnancy derived from fetal adrenal, placenta and
maternal liver.
Equal derivation from ovaries and adrenal cortex
Almost exclusively from the adrenal cortex
derived from conversion of androstenedione to testosterone in the ovaries and adrenal glands. Can be
converted to DHT peripherally.
Binding protein for both estrogen and testosterone, mostly synthesized in the liver. Androgens, obesity and
hypothyroidism all decrease SHBG
SHBG preferentially binds testosterone over estrogen thus lack of SHBG can cause hirsutism in women.
What is acute endometritis?

What are clinical findings in acute
endometritis?
What causes chronic endometritis?
What is the key histologic finding in
chronic endometritis?
What is Adenomyosis?
adenomyosis?
What is Endometriosis?
Endometriosis?
What is an endometrial polyp?
What are clinical findings of an
endometrial polyp?
What is a Hyatid Cyst of Morgagni?
What is pelvic inflammatory disease?

What are some risk factors for PID?
What is Salpingitis Isthmica Nodosa
(SIN)?
What is ectopic pregnancy?
What are risk factors for ectopic
pregnancy?
Where in the tubes do ectopic
pregnancies most commonly implant?
ectopic pregnancy?
How do you diagnose ectopic
pregnancy?
What is Oophoritis?
Acute inflammation of the endometrium, most commonly as a result of bacterial infection following delivery
or miscarriage. Group B strep, staph a, bacteroides, C. trachomatis, N. Gonorrhoeae, E Coli.
Fever, uterine tenderness, prululent or foul vaginal discharge and abdominal pain.
Retained placenta, gonorrhea, IUD (with infection)
Like all chronic inflammatory conditions, you see plasma cells
Invagination of the stratum basalis into the myometrium. See glands and stroma thickening in the
myometrium and general enlargement of the uterus.
Menorrhagia,
dysmenorrhea
or pelvic
pain located outside the uterus causing cyclic bleeding of gland and
Functioning endometrial
glands
and stroma
stromal implants. Essentially reverse menses through the Fallopian tube allows inplantation of viable
endometrial cells. Can also be from vascular spread. Most common sites are ovaries, rectal pouch, Fallopian
tubes and intestines.
Dysmenorrhea, abnormal bleeding, painful stooling during menses, intestinal obstruction and bleeding during
menses, increased risk for ectopic pregnancy and enlargement of the ovaries with blood filled cysts
Benign polyp on the endometrium that enlarges with estrogen stimulation. Does not progress to endometrial
carcinoma but it can protrude through the cervix into the vagina.
Common cause of menorrhagia, spotting in between periods or after menopause
Cystic mullerian remnant most often in the fibriated end of the tube. May undergo torsion causing pain.
Inflammation in the pelvis, often due to N. Gonorrhoeae or C. Trachomatis. See Fallopian tubes that are filled
with pus or see hydrosalpinx (clear fluid in Fallopian tube). Causes fever, lower abdominal pain, cervical
motion tenderness, abnormal uterine bleeding, vaginal discharge, mucopurulent discharge in the cervical os,
and right upper quadrant pain (FHC Syndrome)
Multiple sex partners, vaginal douching, prior PID, unprotected sex
Invagination of the mucosa of the tube into muscle (tubal diverticulosis). Produces nodules in the tube that
narrow the lumen. Most likely a result of infection and can result in infertility and ectopic pregnancy.
Pregnancy that isn't in the uterus. Most often in the Fallopian tubes. Suspect with increased hCG and
sudden lower abdominal pain. Confirm with ultrasound. May be clinically mistaken for appendicitis.
Scarring from previous PID, Endometriosis, Altered tubal motility (SIN), progestin only pill, previous tubal
ligation, prior abdominal surgery.
Most occur in the broad ampullary region below the fimbriae.
Sudden onset of lower abdominal pain and tenderness, usually about 6 weeks after LMP, adnexal tenderness,
peritoneal signs, abnormal uterine bleeding, hypovolemic shock as a result of intraperitoneal hemorrhage.
Beta hCG is a good screening test but a positive hCG doesn't mean that there is an ectopic pregnancy.
Vaginal ultrasound showing an amniotic sac is confirmatory.
Inflammation of the ovary, possible as a result of mumps or PID.
What is stromal hyperthecosis?
Bilateral ovarian enlargement from hypercellular ovarian stroma. Stroma have vacuolated (leutenized)
stromal hilar cells which synthesize excess androgens. May cause hirsutism or virilization. Associated with
obesity, acanthosis nigracans, insulin resistance, and hypertension.
What are risk factors for Ovarian

cancer?
Nulliparity-increased number of ovulatory cycles increases risk, also causes increased risk for surface-derived
ovarian tumors. Genetic factors are BRCA1 and BRCA2 suppressor gene mutations, Lynch syndrome, Turner
syndrome (dysgerminoma), Peutz-Jeghers syndrome (sex cord tumors with annular tubules), history of
breast cancer, postmenopausal estrogen replacement, obesity
How can ovarian tumors be classified?
cancers are similar to those seen in the testicle, not many are malignant. Sex cord stromal tumors-derive
from stromal cells, may be hormone producing, most are benign. Metastases-most commonly from breast,
and stomach (Krukenberg tumors)

Ovarian tumors?
What is a common tumor marker of
malignant ovarian tumors?
What is a Serous Ovarian tumor?

What is a Mucinous tumor of the
ovary?
What is an endometroid tumor?
What is a Brenner tumor?
What
What
What
What
is
is
is
is
a
a
a
a
cystic teratoma?
Thecoma-Fibroma?
Granulosa-Theca cell tumor?
Sertoli-Leydig cell tumor?
What is a Gonadoblastoma?
What is a Krukenberg tumor?
Abdominal enlargement from fluid. Malignant ascites may cause induration in the rectal pouch on digital
rectal exam and intestinal obstruction with colicky pain. Palpable ovarian mass in postmenopausal woman,
malignant pleural effusion, torsion and infarction (cystic teratomas), signs of hyperestrinism in estrogen
secreting tumors or virilization in androgen secreting tumors.
Increased CA-125- only in surface derived tumors
Most common group of primary benign and malignant tumors, many are bilateral. Cysts are lined by ciliated
cells (like Fallopian tubes). A Serous Cystadenoma is benign. A Serous Cystadenocarcinoma is malignant
and has psammoma bodies and dystrophic calcification.
Cysts lined by mucus-secreting cells (like endocervical cells). Cause large multi-nucleated tumors. Seeding
of tumor produces pseudomyxoma peritonei. A mucinous cystadenoma is benign and may be associated with
Brenner tumors. A mucinous cystadenocarcinoma is malignant.
Malignant tumor associated with endometrial carcinoma. Commonly bilateral
Usually
a benign
tumor
thatcell
contains
rests (traditional-like
epithelium)
Most
common
benign
germ
tumor.Walthard's
See ectodermal
differentiation (hair,
sebaceous glands, teeth) mostly
found in a nipple like structure called Rokitansky Tubercle. A Struma Ovarii subtype has functioning thyroid
tissue
Benign tumor associated with Meigs' syndrome (ascited, right sided pleural effusions). Commonly calcify.
Low grade malignant tumor which produces estrogen and contains Call-Exner bodies
Benign tumor that produces androgens. Pure leydig cell tumors contain cells with crystals of Reinke.
Malignant tumor with a mixture of germ cells (dysgerminoma) and sex-cord stromal cells. Associated with
abnormal sexual development. May calcify
Metastasis to the ovary. Contains signet ring cells from hematogenous spread of gastric cancer.
Renal
What does the urinary system
derive from?
How many sets of kidneys are
there?
What is the pronephros?
Intermediate mesoderm of the posterior wall of the abdominal

cavity.
Three sets of kidneys-pronephros, mesonephros and
metanephros
First kidney. Nonfunctional and disappears by week 4
What is the mesonephros?

What is the metanephros?
What is the excretory system
of the kidneys derived from?
Forms after the pronephros and forms the mesonephric/Wolffian

duct. That eventually connects the mesonephros to the cloaca
and forms adult genital structures.
Forms
definitive
Primarythe
ureteric
bud.kidney
Becomes the glomerulus, Bowman's
capsule, Loop of Henle, Distal Collecting tubule and collecting
system
What are the collecting ducts

of the kidney derived from?
Outgrowth of the Mesonephric duct which joins the

metanephros to form the ureteric bud. Forms the major and
minor calyces, renal pelvis and ureters.
What is Potter's Sequence?

What are the limb deformities
in Potter's Syndrome?
Allantois goes to Urachus and becomes the Median umbilical

ligament. Don't confuse this with the medial umbilical ligament
which is a remnant of the umbilical artery.
Malformation of the Ureteric Bud which results in bilateral renal
agenesis. Results in oligohydramnios/Potter's syndrome
Clubfoot, flipper hands, hyperextensible joints, and compressed
thorax
What are the facial deformities

in Potter's Syndrome?
Sloping forehead, flattened nose, recessed chin, low floppy

ears. Results from compression of the fetus against the wall of
the the amniotic sac.
What adult structure does the

Allantois become?
Why does Pulmonary

Hypoplasia result from Potter's
Syndrome?
What can occur if the allantois
fails to obliterate?
Fetal lungs mature through swallowing of amnion which allows

the lungs to expand. Thus decreased amnion causes decreased
expansion of the lungs.
Patent Urachus results in Urachal fistula at birth
What does the urogenital

sinus become?
Urinary bladder and urethra
Wat causes a pelvic kidney?

How do pelvic kidneys
present?
During development, the embryologic kidneys must ascend and

pass under the umbilical arteries. If a kidney can't pass, it
remains in the pelvis
Obstructive hydronephrosis and vesicoureteric reflux. May have
pain or infection.
What is a Horseshoe kidney?
Kidneys are pushed close together while ascending under the

umbilical arteries. Causes the lower poles to fuse which causes
it to look like a horseshoe and get trapped underneath the
inferior mesenteric artery. Associated with Turner's

presentation of horseshoe
kidney?
What
is required for definitive
diagnosis of Horseshoe
kidney?
Most are asymptomatic but can present with UTI followed by

obstructive hematuria or abdominal pain. Predisposes to
nephrolithiasis
IV pyelogram shows rotated calyces but doesn't show the
isthmus. Need a Dimercaptosuccinic Acid Scan (DMSA)

insertion, innervation, blood
supply and action of the Psoas
major muscle?
Origin-vertebral column (T12-L5), insertion-lesser trochanter of

the femur. Innervation-Ventral rami of L1-3. Blood supplymucular branches of the medial femoral and circumflex artery.
Actions-flex thigh and trunk and laterally rotate the hip.

supply and action of the Psoas
minor muscle?
Origin-Vertebral column (T12-L1), insertion-pectinate line.

Innervation-Anterior rami of lumbar nerves L1-2. Actions-with
the Psoas major, flexes the trunk at the hip and stabilizes the
thigh

supply and action of the
Iliacus muscle?
Origin-Iliac fossa, insertion-lesser trochanter of the femur.

Innervation-femoral nerve L3-4. Blood supply-Muscular
branches of the medial femoral circumflex artery. Actionspowerful hip flexor and lateral rotator

supply and action of the
Quadratus Lumborum muscle?
Origin-Transverse process of L3-5, insertion-lower border of the

12th rib. Innervation-Ventral branches of T12 and L1-4.
Action-extends and laterally flexes vertebral column.
Which structures are

retroperitoneal?
Where are the kidneys
located?
Pancreas (except tail), Duodenum (second, third and fourth

parts), ascending and descending colon, aorta, IVC, rectum,
adrenal glands, and since this is the renal section-the kidneys!!!
Located at T12-L3 on the left and slightly lower on the right,
embedded in Gerota's Fascia.
Where do the ureters pass in

relation to the uterine artery
or vas deferens?
What is the arterial supply to
the kidneys?
What is the venous return
from the kidneys?
What is unique about the Left
Renal Vein?
Water goes under the bridge. Pass across the bifurcation of the
common iliac and pass under the uterine arteries or vas
deferens and then join the bladder on the posteroinferior side.
What are the structures of the

Renal filtration system in the
order in which filtrate would
pass through?
What
is the direction of
urinary drainage out of the
kidneys?
What types of epithelium line
the Urethra?
convoluted tubule the the straight portion of the proximal

tubule, then thick descending, the Loop of Henle, then thick
ascending limb, then the distal collecting tubule followed by the
collecting duct.
Renal pyramids to the renal papillae to the minor calyces to the
major calyces
Transitional
epithelium as it exits the bladder, then stratified
columnar epithelium followed by stratified squamous
epithelium.
What are the anatomic

divisions of the male urethra?
Prostatic, Membranous (surrounded by striated muscle forming

the voluntary external urethral sphincter), Bulbous then
Pendulous (surrounded by Littre's glands. Does that mean it
swings like a pendulum? Just wondering
Renal arteries which branch off the abdominal aorta

Renal veins drain into the IVC
It also drains blood from the left gonad and is longer than the
right
renal vein
since it must
cross thecapsule
IVC
Glomerulus
surrounded
by Bowman's
then proximal
What are the anatomic

divisions of the female
urethra?
What comprises a Renal
Corpuscle?
Much shorter so not really divided. Lined by stratified

squamous and pseudostratified columnar epithelium. At the
mid-portion it's surrounded by the striated muscle of the
voluntary external urethral sphincter. Also surrounded by
Littre's glands
Primary filtering component, comprised of the glomerulus and
Bowman's capsule
What is the glomerulus?
Collection of dilated capillaries with a fenestrated endothelium,

which emerge from the afferent arteriole and drain into the
efferent
arteriole
Double-walled
epithelial capsule enclosing the glomerulus.
What is Bowman's capsule?
Consists of visceral and parietal layers with urinary space in

between. Visceral layer filters the blood while the parietal layer
covers the outside and is continuous with the proximal
convoluted tubules.
What is special about the

visceral layer of Bowman's
capsule?
Specialized filtration lining that is made of Podocytes resting on

a
basement
membrane,
primary
processes
foot processes.
Yes!
It's a fused
basement
membrane
full ofand
heparan
sulfate
Is the basement membrane of

the Glomerulus charged?
Describe the histology of the
Proximal Convoluted Tubule
which gives it a negative charge and makes it more

impenetrable to things like albumin that are also negatively
charged.
Lined by simple cuboidal epithelium with a microvilli brush
border. Interdigitations between the cells prevent loss of fluid
and solutes system for absorption and secretion of electrolytes.
Specialized
Describe the histology of

Loop of Henle
Distal Convoluted Tubule
collecting tubule
Collecting Ducts
the
Consists of the thick descending, thin descending, thin

ascending and thick ascending loops (see more about transport
later)
the
the
Lined by simple cuboidal epithelium without a brush border

Lined by simple cuboidal epithelium. Transports urine from the
functional nephron to the hilum
the
Lined by columnar epithelium
What doe Juxtamedullary

nephrons do?
Exceptionally long Loops of Henle allow them to set up a

hypertonic gradient in the kidney, regulating the production of
concentrated urine
What is the Juxtaglomerular

Apparatus?
Consists of macula densa cells in the proximal portion of the

distal tubule and juxtaglomerular cells in the afferent and
efferent arterioles. Controls GFR in response to BP in the
afferent arterioles. JG cells secrete Renin leading to increased
angiotensin II and aldosterone in response to decreased renal
blood pressure, decreases sodium delivery to the distal tubule
and
increases
sympathetic
tone
(Beta
1).
Group
of epithelial
cells in the
distal
tubules
that contact the
What is the Macula Densa?
afferent and efferent arterioles (JGA). Cells are sensitive to

sodium concentration and rates of flow through the Distal
Convoluted Tubule. Regulates GFR through locally active
hormones.
What are Juxtaglomerular

cells?
What are extraglomerular
mesangial cells?
Specialized myoepithelial cells located on the afferent arterioles

which act as baroreceptors. Monitor BP and maintain GFR
through Renin release
Contractile cells with receptors for angiotensin II and natriuretic
factor allowing them to regulate glomerular flow.
What types of cells line the

bladder?
Transitional epithelium-can stretch and thin as it's distended.

Smooth muscle in 3 layers arranged in multiple dimensions
which evevntually become three distinct layers at the bladder's
neck. Innermost is the involuntary sphincter.
Walk through a Darrow-Yannet

Diagram (see following
questions as well)
What are clinical implications
of Water deprivation?
What are the clinical
implications of Diarrhea?
Diagram shows volume of ICF and ECF in the body. Osmolarity

should be equal between ICF and ECF. Normovolemia is 42
liters total with 28L in the ICF. See Attachment 1 and walk
through
the diagram.
ICF decreased,
ECF increased, osm increased. Technically
volume contraction and hypotonic but water more contracted
that solute.
No change in ICF, ECF decreased, no change in osm.
Essenitally volume and solute contraction but equal contraction.

implications of Adrenal
Insufficiency?
implications of Infusion of
isotonic
What
areNaCl?
the clinical
implications of high NaCl
intake?
implications of SIADH?
ICF increased, ECF decreased, Osm decreased. Volume and

solute contracted because not holding onto water and salt
ICF unchanged, ECF increased, osm unchanged. Giving
increasing amounts of fluid and solute so volume expansion.
ICF decreased, ECF increased, osm increased. Volume
expansion but solute pulls water into ECF
ICF increased, ECF increased, osm decreased. Holding onto
water and salt but water in excess of salt.
is Renal
Clearance?
What does
is mean
if
Cx<GFR?
What does it mean if Cx>GFR?
What does it mean if Cx=GFR?
How is Inulin used to calculate
GFR?
Cx=UxV/Px Volume of plasma from which the substance is

completely cleared per unit of time. C-clearance of X, U-urine
concentration of X, V-urine flow rate, P-plasma concentration of
X. (mL/minute)
Net tubular reabsorption of X
Net tubular secretion of X.
Neither secretion or reabsorption of X
Inulin can be used because it is freely filtered and neither
reabsorbed nor secreted. GFR=Uinulin *V/Pinulin = Cinulin
How are Creatinine Clearance

and GFR related?
Creatinine Clearance is an approximate measure of GFR.

Slightly overestimates GFR because there is moderate secretion
of creatinine by the renal tubules.
What is the Clearance ratio

(with Inulin)?
Clearance Ratio=Cx/Cinulin. 1 if equal to inulin. <1 means

that clearance is less than inulin so either not filtered or filtered
and reabsorbed. >1 means that clearance is more than inulin
so
filtered and
excreted/activelly
pumped.
Fenestrated
capillary
endothelium.
Glomerular basement
What forms the Glomerular

Filtration Barrier?
membrane-composed of type IV and V collagen, laminin,

heparan sulfate. Three layers-Lamina rara interna, lamina
densa and lamina rara externa. Epithelial layer consists of
podocytes which help form a barrier.
How can you estimate

Effective Renal Plasma Flow
(ERPF)?
Estimate using PAH clearance because it's filtered and actively

secreted in the proximal tubule-thus all PAH is excreted.
ERPF=UPAH *V/PPAH = CPAH
How do you estimate Renal

Blood Flow?
RBF=RPF/(1-Hct). Note that ERPF underestimates RPF by

about
10%dilates
so RBFthe
is overestimated.
Dopamine
vessels and suppresses sodium
What is Dopamine's effect on

the nephron?
reabsorption in the proximal tubule by inhibiting the action of

the basolateral Na/K ATPase. Released directly by the proximal
tubule in response to an increase in BP resulting in decreased
RBF and GFR.
How does Afferent arteiole

constriction affect RPF, GFR
and Filtration Fraction?
Decreased RPF, Decreased GFR, No change in filtration fraction
How does Efferent arteiole

constriction affect RPF, GFR
and Filtration Fraction?
Decreased RPF, Increased GFR, increased filtration fraction
How does increased Plasma

protein affect RPF, GFR and
Filtration Fraction?
No change in RPF, decreased GFR and filtration fraction
How does decreased plasma

protein affect RPF, GFR and
No change in RPF, increased GFR and increased filtration

fraction
How does constriction of the

ureter affect RPF, GFR and
Describe autoregulation of
blood flow in the kidneys
What is Filtration Fraction?
What is Filtered Load?
No change in RPF, decreased GFR, decreased filtration fraction

Two autoregulatory mechanisms-stretch/myogenic and
tubuloglomerular feedback. Stretch-when BP increases,
arterioles are stretched leading to vasoconstriction in the
afferent arteriole thus maintaining constant RBF.
Tubuloglomerular feedback- increased arterial pressure leads to
increased RBF and increased flow to the distal tubule which is
sensed by the macula densa. This results in constriction of the
afferent arteriole, attenuating RBF.
Fraction of plasma filtered across the membrane of the
glomerular capillaries. FF=GFR/RPF. Normal FF is about 20%
GFR * Plasma concentration.
What is Free Water Clearance?

Where does free water
clearance occur?
How does ADH affect Ch2o?
How can you calculate
Excretion rate?
Reabsorption?
Secretion?
How is glucose reabsorbed

and how does it go wrong?
How are amino acids cleared?
What is Hartnup's Disease?
Define
Nephron.
How
dothe
tubules
of the nephron
maintain low intracellular Na
and the Na gradient across the
tube?
Ability to dilute urine. Free water (Ch2o)= V-Cosm

(Cosm=Uosm*V/Posm)
Thick ascending limb and early distal tubule. NaCl is
reabsorbed
reabsorption/permeability
H2O.
ADH
causes without
retention
of free water so Ch2o<0.to Concentrated
urine
Excretion rate= V*Ux
Reabsorption=Filtered-Excreted
Secretion=Excreted-Filtered
Should be completely reabsorbed in the proximal tubule by
Na/Glucose cotransport. At a plasma glucose >160-200 mg/dL
you start to see glucosuria because the transport is being
overwhelmed. At 350 mg/dL, all transporters are fully
saturated be
so clinical
develops
Shouldn't
cleared.glucosuria
Na dependent
transporters in the
proximal tubules reabsorb amino acids with multiple carrier
systems.
Deficiency of neutral amino acid (tryptophan) transporter.
Causes
Pellagra.of the glomerulus, through which fluid is filtered,
Unit composed
and the tubular system where filtered fluid is modified through
the reabsorption and secretion of various solutes to produce
urine.
Na/K ATPase on the basolateral membrane maintains the Na
gradient from the lumen to the cell.
Describe transport across the

luminal and basolateral side of
the Proximal Tubule (see
attachment 2).
The proximal tubule is the major site of reabsorption, based on

the transmembrane Na gradient. Reabsorbs all filtered glucose
and amino acids via cotransport with Na. Reabsorbs most
bicarb, sodium, chloride and water. Isotonic absorption.
Generates and secretes ammonia which buffers secreted H. Na
and H are exchanged, Cl is absorbed in exchange for bicarb.
How is bicarb
regulated/excreted in the
Proximal tubule?
CO2 and H2O cross the membrane and are made into bicarb by
carbonic anhydrase. That is excreted and then made into CO2
and H2O again.
How do Angiotensin II and

Atrial Natriuretic Peptide act
on the
Proximal
tubule?
How
does
Parathyroid
hormone affect
excretion/absorption?
Ang II stimulates Na reabsorption which ANP blocks Na

reabsorption.
PTH inhibits Na/Phosphate cotransport resulting in phosphate
excretion.

Loop of Henle.
Thin descending loop absorbs about 20% of filtered water but

no solute via medullary hypertonicity. Thin ascending limb is
impermeable to water and has no significant reabsorption.
Thick ascending limb is the diluting segment of the tubular
system. Actively absorbs Na, K and Cl (NK2Cl). This induces
the paracellular absorption of Mg and Ca because K leaks back
into the lumen creating a positive charge in the lumen. It's
impermeable to H2O so it dilutes urine.

distal convoluted tubule.
Impermeable to water and urea. Early distal tubule actively

reabsorbs Na and Cl making urine hypotonic. PTH increases
Ca/Na exchange thus increasing Ca absorption.

late distal tubule and
collecting ducts.
How does Aldosterone affect
the collecting ducts?
Principle cells reabsorb Na and H2O and secrete K via the Na/K
ATPase. Intercalated cells secrete H and reabsorb K and HCO3.
Inserts more Na channels on the luminal side increasing Na
reabsorption.
How does ADH affect the

collecting tubules?
Acts at V2 receptors and inserts aquaporins H2O channels into

the
luminal
side.
U shaped
capillaries
which are freely permeable to H2O and
What is the Vasa Recta?

What does it mean if Tubular
Fluid (TF)/Plasma (P) >1?
What does it mean if TF/P=1
What does it mean if TF/P<1
solutes except protein. Situated close to the Loop of Henle.

Enables the cortico-medullary osmolar concentration gradient.
Preserves hyperosmolarity of renal medulla to maintain
absorption.
Solute is being reabsorbed more slowly than water or there is
net secretion of solute.
Solute and water are reabsorbed at equal rates
Solute
reabsorbed more
quickly
water. which would
Affects is
baroreceptors,
limits
reflex than
bradycardia

Angiotensin II?
normally accompany pressors. Constricts efferent arteriolesincreased FF to maintain GFR in low volume states. Increases
proximal tubule Na/H activity and can stimulate thirst in the
hypothalamus.
What is the function of ANP?
Released from the atria in response to low volume. Relaxes

vascular smooth muscle via cGMP resulting in increased GFR
and decreased renin.
What is the function of ADH?
Regulates osmolarity and responds to low blood volume which

takes precedence over osmolarity. Increases H2O channel
insertion
principle
cells
resulting
in H2O
reabsorption.
IncreasesinNa
channel,
increases
Na/K
pump
insertion in

Aldosterone?
principle cells, enhances K and H excretion creating a favorable

Na gradient for Na and H2O reabsorption. Primarily regulates
blood
volume.hormone that stimulates RBC production in
Glycoprotein
What is Erythropoietin?
response to hypoxia. Released from endothelial cells of

peritubular capillaries. Epo receptors are on proerythroblasts
which mature in response.
What is 1, 25-(OH)2 Vitamin

D?
Active Vitamin D. Proximal tubule cells convert 25-OH-Vitamin

D to the dihydroxy form. This increases intestinal reabsorption
of both calcium and phosphate.
How does Parathyroid

Hormone affect the kidney's
endocrine function?
PTH directly acts on the kidney to increase renal calcium

reabsorption and decrease renal phosphate excretion. Also
stimulates proximal tubule cells to make 1, 25
dihydroxycholicalciferol.
What do prostaglandins do in
the kidney?
Secreted by JG cells in response to increased renal arterial

pressure and increased renal sympathetic discharge (Beta 1
effect).
Angiotensin
ParacrineStimulates
secretion of
PGE2 vasodilates the afferent arterioles to
increase GFR. NSAIDs can cause acute renal failure by
inhibiting PGE thus preventing the arterioles to vasodilate to
maintain GFR.
Where do each of the above

hormones act on the kidney?
(this rehashes all the functions
as well)
ANP is secreted in response to increased atrial pressure.

Causes increased GFR and increased Na filtration. Acts right at
the beginning of proximal convoluted tubule. PTH is secreted in
response to decreased plasma Ca, increased plasma PO4 or
decreased plasma vitamin D. Causes increased Ca reabsorption
in the distal convoluted tubule, decreased PO4 reabsorption at
the proximal convoluted tubule, increased Vitamin D production
and increased Ca and PO4 absorption from gut. Renin is
released from the JGA and acts on the distal convoluted tubule.
Ang II is synthesized in response to decreased BP and causes
the efferent arteriole constriction thus increasing GFR and FF
but with compensatory Na reabsorption. ADH is secreted in
response to increased plasma osmolarity and decreased blood
volume. Binds receptors on principal cells causing increased
aquaporins. Acts on collecting ducts. Aldosterone is secreted
in response to decreased blood volume and increased plasma K,
resulting in increased Na reabsorption and increased Kand H
secretion. Acts on collecting duct.
What causes K shift out of

cells?
Insulin deficiency (decreased Na/K ATPase), Beta Adrenergic

antagonists (decreased Na/K ATPase), Acidosis or severe
exercise (K/H exchange), Hyperosmolarity, Digitalis (blocks
Na/K ATPase), Cell lysis
What is Renin?
What
What
What
What
causes K shift into cells?

is normal pH of blood?
is metabolic acidosis?
is metabolic alkalosis?
Whatmuch
is Winter's
How
shouldFormula?
PCO2
increase when bicarb
increases?
What is respiratory acidosis?
What is respiratory alkalosis?
Respiratory Acidosis?
Anion Gap Metabolic Acidosis?
What are some causes of nonAnion Gap Metabolic Acidosis?
Respiratory Alkalosis?
Metabolic Alkalosis?
What is Type 1 (Distal) Renal
Tubular Acidosis?
What is Type 2 (proximal)
Renal Tubular Acidosis?
What is Type 4 (hyperkalemic)

Renal Tubular Acidosis?
Insulin (increased Na/K ATPase), Beta Adrenergic agonists

(increased Na/K ATPase), Alkalosis (K/H exchanger), Hypoosmolarity.
About 7.4
Decreased Bicarb. Compensation by hyperventilation
Increased bicarb. Compensation by hypoventilation.
Respiratory compensation in response to metabolic acidosis.
PCO2=1.5 (HCO3) +8 (+/-2)
PCO2
increases
mmHg for every
mEq/L HCO3
Increased
PCO2.0.7
Compensation
with1increased
bicarb
absorption
Decreased PCO2. Compensate with less bicarb reabsorption.
Hypoventilation-Airway obstruction, acute lung disease, chronic
lung disease, opiods/narcotics, weak respiratory muscles.
MUDPILES-Methanol, Uremia, Diabetic Ketoacidosis,
Paraldehyde or Phenformin, Iron tablets or INH, Lactic Acidosis,
Ethylene glycol, Salicylates
Diarrhea, Glue sniffing, Renal Tubular Acidosis, Hyperchloremia
Hyperventilation-(early) high altitude exposure, Aspirin
ingestion (early)
Diuretic use, vomiting, antacid use, hyperaldosteronism.
Defect in the collecting tubule's ability to excrete H. Associated
with hypokalemia and risk for Ca containing kidney stones.
Defect in proximal tubule HCO3 reabsorption. Associated with
hypokalemia and hypophosphatemic rickets.
Hyperaldosteronism or lack of collecting tubule response to
aldosterone causes hyperkalemia- inhibition of ammonia
excretion in proximal tubule. Leads to decreased urine pH due
to decreased buffering capacity.
How does Aldosterone act on

the Late Distal Tubule?
How do you calculate the
anion gap?
Stimulated Mineralocorticoid receptors on Principal Cells. This

increases their permeability to sodium and potassium by adding
Na channels and increases enzymes of the citric acid cycle thus
increasing ATP to pump Na/K out the basolateral side. Also
stimulated alpha-intercalated cells to secrete more H, thus
regulating plasma HCO3 and acid-base balance.
Na- (HCO3 + Cl) normal =10-12
What is a delta delta?

How do you calculate a delta
delta?
Secondary to a loss of bicarb or an excess of acid. Essentially

there's a lot of something in the blood that's neither Na, HCO3
or
Cl that isn't
accounted
for so
in the math.
Comparison
of being
change
in anion gap
to there's
changeaingap
bicarbonate.
Can tell you what there is in excess if there is a mixed acid base
disorder.
Change in anion gap = AG-12. Change in Bicarb = 24measured HCO3. Delta delta is ratio of the two
How do you interpret a delta

delta?
How much should CO2 rise in
response to increased bicarb?
AG>HCO3 - Metabolic alkalosis + metabolic acidosis.

AG<HCO3 -Wide AG + non AG metabolic acidosis. Equal-wide
anion gap metabolic acidosis.
For every 10 mmol/L rise in HCO3, PCO2 should increase
6mmHg
Excretes harmful waste (urea, creatinine, uric acid, etc.),
What are the general functions

of the Kidneys?
Maintains acid-base homeostasis, Reabsorbs essential

substances, Regulates water and sodium metabolism, Maintains
vascular tone, Produces erythropoeitin, Maintains calcium
homeostasis.
What is hematuria and what

are some common causes?
What is Proteinuria?
Blood in the urine. Causes fro, the upper urinary tract- renal
stone, glomerulonephritis (dysmorphic RBC's), Renal cell
carcinoma. Causes from the lower urinary tract- Infection,
transitional cell carcinoma, benign prostatic hyperplasia. Drug
related causes-anticoagulants, cyclophosphamide (hemorrhagic
cystitis and risk for transitional cell carcinoma)
Protein >150 mg/24 hours or >30 mg/dL via dipstick.
Why does an anion gap occur?
What are diagnostic tests for

proteinuria?
What is Functional Proteinuria?
Dipstick-detects albumin only. Sulfosalicylic acid-detects

albumin and globulins.
Protein <2g/24 hour, not associated with renal disease. Causes
are fever, exercise, CHF.
What is Overflow proteinuria?
Postural-only occurs when standing. First void in the morning

has no protein but subsequent during the day does have
protein. No association with renal disease.
Variable protein loss with LMW proteins. Essentially the amount
filtered is greater than the tubular reabsorption. Causes are
multiple myeloma with Bence Jones proteinuria, Hemoglobinuria
from intravascular hemolysis, myoglobinuria from crush
injuries, McArdle's glycogenosis and increases in serum creatine
kinase.
What is Serum BUN?

What does serum BUN depend
on?
BUN is a normal end product of amino acid and pyrimidine

metabolism that is produced by the liver in the urea cycle. It is
filtered in the kidneys and partially reabsorbed in the proximal
tubule (amount reabsorbed is flow dependent).
GFR, protein content of the diet, proximal tubule reabsorption
and the functional status of the urea cycle.

increased BUN?
Decreased cardiac output (decreased GFR), increased protein

intake/breakdown, increased tissue catabolism (burns, surgery,
etc), acute glomerulonephritis, acute or chronic renal failure,
postrenal disease.

decreased BUN?
Increased plasma volume (pregnancy, SIADH, etc), decreased

urea synthesis (cirrhosis, Reye syndrome, fulminant liver
failure), decreased protein intake (Kwashiorkor, starvation
gluconeogenesis in kideys)
What is Serum Creatinine?

What is Azotemia?
Metabolic end product of creatine in muscle. Filtered in the

kidneys and not reabsorbed or secreted. Serum concentration
varies with age and muscle mass.
Increased serum BUN and creatinine
What is Orthostatic
Proteinuria?
What is a normal Serum BUN:

Creatinine ratio?
15. Urea is filtered and partly reabsorbed whereas Creatinine is

filtered entirely. BUN:Cr ratio depends on changes-can be
prerenal, renal or postrenal
What is Prerenal Azotemia and

what are some causes?
Increased BUN and creatinine caused by something before the

kidneys. Most common cause is decreased cardiac
output/hypoperfusion of the kidneys decreasing GFR. BUN:Cr
>15 because proportionately more Urea is reabsorbed from the
low flow rate.
What is Renal Azotemia and

what are some causes?
Increased BUN and Cr from parenchymal damage to the

kidneys. Some causes are Acute Tubular Necrosis and Chronic
Renal Failure. BUN:Cr <15. Both are filtered, there is
extrarenal loss of urea and urea may not be reabsorbed as well.
What is Postrenal Azotemia

and what
some
What
is a are
normal
Crcauses?
Clearance?
Increased BUN and Cr from urinary obstruction below the

kidneys. Prostate hyperplasia, blockage or ureters by stones or
cancer. Serum BUN:Cr ratio >15. Obstruction to flow
decreases GFR resulting in back diffusion of urea (not Cr) into
blood and a disproportionate increase in BUN.
97-137 mL/minute. Less than 100 mL/minute is abnormal.

increased Cr Clearance?
Normal pregnancy (Increased plasma volume means increased

GFR), early diabetic glomerulopathy (constricted efferent
arteriole from hyaline sclerosis causing increased GFR)

decreased CR Clearance?
What does dark yellow color
indicate in Urinalysis?
What does Red or Pink color
indicate in Urinalysis?
What does smoky-colored
urine indicate?
Elderly people (decreasing GFR with age), Acute and Chronic

Renal disease (ARF from tubular sclerosis, CRF from diabetic
glomerulopathy)
Concentrated urine, Bilirubinemia, Increased UBG, Vitamins
Hematuria, hemoglobinuria, myoglobinurua, drugs
(phenazopyridine), porphyria
Acid pH converts Hb to hematin. Common in nephritic
glomerulonephritis
What does black urine after

exposure to light indicate?
Alkaptonuria. Deficiency of homogentisate oxidase resulting in

buildup of homogentisic acid
What does clarity of the urine

indicate?
Cloudy urine with alkaline pH is normal, probably from

phosphates. Cloudy urine with acid pH is normal probably from
uric acid. Otherwise, bacteria, WBC's, Hb, myoglobin
What does the specific gravity

of the urine indicate?
Urine concentration and dilution. SG>1.023 indicates urine

concentration and excludes intrinsic renal disease. Hypotonic
<1.015. Fixed SG (1.008-1.010) may indicate a lack of
concentration
possibly
renal of
failure.
Determined byand
dietdilution
and acid
base status
person. Vegan
What does the pH of the urine

indicate?
often have alkaline pH, meat eaters have acidic pH. An alkaline
pH plus strong ammonia smell indicates a urease producing
pathogen.
What does glucose indicate in

the urine?
What does microalbuminuria
indicate?
What do ketones in the urine
indicate?
What does bilirubin in the
urine indicate?
What does Urobilinogen

indicate?
What does blood in the urine
indicate?
What do nitrites in the urine
indicate?
Increased serum glucose means glucosuria and DM. Normal

serum glucose and glucosuria can happen in normal pregnancy,
benign glucosuria
First sign of diabetic nephropathy
Acetone and acetoacetic acid. Ketonuria from DKA, starvation,
ketogenic diets, pregnancy and isopropyl alcohol poisoning
Bilirubinuria may indicate hepatitis or obstructive jaundice
Trace amounts are normal. No UBG with increased urine
bilirubin may be obstructive jaundice. Increased UBG with
absent urine bilirubin means extravascular hemolytic anemia.
Increased UBG with increased urine bilirubin means hepatitis
Hematuria from renal stone, hemoglobinuria from intravascular
hemolytic anemia, myoglobinuria from increased serum creatine
kinase and crush injuries.
Nitrites produced by nitrate reducing uropathogens.
What does Leukocyte Esterase

in the urine indicate?
Esterase in neutrophiles (pyuria). Infections from urethritis,

cystitis, pyelonephritis. Sterile pyuria-Chalmydia trachomatis
urethritis, TB, drug induced interstitial nephritis
What do cells in the urine

indicate?
Bacteria-UTI, RBC's-hematuria from renal stones, cancer,

glomerulonephritis. Dysmorphic RBC's-hematuria of glomerular
origin. Neutrophils-pyuria from UTI or sterile pyuria. Oval fat
bodies-renal
tubular
cells with
lipids in
(nephrotic
syndrome)
Casts are formed
in tubular
lumens
the kidney
and are
What types of crystals can be

seen in the urine and what do
they indicate?
composed of a protein matrix with entrapped cells, debris or

protein leaking through the glomeruli. Proves renal origin of
the disease.
Acellular, ghost like cast containing protein. Only significant if
there is accompanying
proteinuria resulting in a cast made of
Nepritic
type of glomerulonephritis
RBC's
Cast of WBC's indicating acute pyelonephritis, acute
tubulointerstitial
nephritis
Cast
of a sloughed
off renal tubule. Indicates acute tubular
necrosis
Cast of cells with lots of lipid. Indicates nephrotic syndrome
Refractile, acellular cast seen in chronic renal failure.
Calcium oxalate crystals-pure vegan diet, ethylene glycol
poisoning, calcium oxalate stone. Uric acid crystalshyperuricemia from gout or massive cell destruction after
chemotherapy. Triple phosphate crystals-sign of UTI from
urease producing pathogens like Proteus. Cystine crystalshexagonal crystals seen in Cystinuria
Describe the blood supply to

the kidney.
What is minimal change
disease?
Renal cortex receives 90% of the blood supply. Medulla is

relatively ischemic from reduced blood supply. Renal vessels
are all end arteries with no collateral circulation so occlusion of
any branch produces infarction. Afferent blood flow is
controlled by renal-derived PGE2 and renin. Efferent blood flow
is controlled by ATH (vasoconstrictor)
Loss of charge of the glomerular basement membrane which
produces selective proteinuria.
What do casts indicate in the

urine?
What is a hyaline cast?
What is a RBC Cast?
What
What
What
What
is
is
is
is
a
a
a
a
WBC cast?
renal tubular cast?
fatty cast?
Waxy/Broad cast?
What protein produces the

charge on the glomerular
basement membrane?
Heparan Sulfate
What are some causes of GBM

thickening?
Deposition of immunocomplexes such as in membranous

glomerulopathy. Increased synthesis of Type IV Collagen such
as in DM.
What do Visceral Epithelial

Cells do in the glomerulus?
Production of the GBM. Contain podocytes and slit pores

between podocytes which serve as a distal barrier to prevent
protein loss in the urine. Podocytes fuse in nephrotic
syndrome, no matter what the cause.
What do Mesangial Cells do in

the glomerulus?
What do parietal epithelial
cells do in the glomerulus?
Support the glomerular capillary. Can release inflammatory

mediators and proliferate-IgA glomerulopathy has mesangial
immune complex deposits.
Lining cells of Bowman's capsule. Proliferation causes crescents
that encroach upon and destroy the glomerulus.
What is Renal Dysplasia?

What is Juvenile Polycystic
Kidney Disease?
Most common cystic disease in children. See abnormal

development of one or both kidneys with abnormal structures
persisting in the kidneys (cartilage, immature collecting
ductules). Present as enlarged, cystic, unilateral or bilateral
flank
mass. May
leadcystic
to chronic
renal
failure.
AR
disease.
Bilateral
disease
with
cysts involving all
parts of the nephron in the cortex and medulla. Bilaterally
palpable kidneys.
What other types of conditions

are seen in Juvenile Polycystic
Kidney Disease?
Cysts present in liver. Associated with congenital hepatic

fibrosis which leads to portal hypertension. Also associated
with oligohydramnios and Potter's Syndrome.
What is Adult Polycystic

Kidney Disease?
AD disease with defect on chr 16. Bilateral cystic disease with

the cysts involving all parts of the cortex and medulla. Develop
chronic renal failure a lot of the time.
What other conditions are

associated with Adult PKD?
Cysts may be present in the liver, pancreas and spleen. Also

have intracerebral Berry aneurysms. May cause hemorrhage if
hypertension results in rupture, intracerebral hemorrhage and
lacunar infarcts. Other associations are sigmoid diverticulosis,
hematuria, mitral valve prolapse, and risk for developing renal
cell
carcinoma.
Multiple
cysts in the collecting ducts present in the medulla.
What is Medullary Sponge

Disease?
See striations in the papillary ducts of the medulla (swiss

cheese appearance). Recurrent UTI's, hematuria and renal
stones.
What is Acquired Polycystic

Kidney Disease?
Most commonly caused by renal dialysis. Tubules become

obstructed by interstitial fibrosis or oxalate crystals. Small risk
for renal cell carcinoma.
What are simple retention

cysts?
What is Focal
Glomerulonephritis?
What is Diffuse
Glomerulonephritis?
What is Proliferative
Glomerulonephritis?
What is Membranous
Glomerulonephropathy?
What is Membranoproliferative
Glomerulonephritis?
What is Focal Segmental
Glomerulosclerosis?
What is Crescentic
Glomerulonephritis?
What is Primary Glomerular
Disease?
Most common adult renal cyst. Derived from tubular

obstruction. May cause hematuria and may resemble renal cell
carcinoma. Needle aspiration will distinguish it from RCC
Only a few glomeruli are abnormal
All glomeruli are abnormal
>100 nuclei in affected glomeruli
Thick GBM, no proliferative change
Thick GBM, hypercellular glomeruli
Fibrosis involving only a segment of the involved glomerulus
Proliferation of the parietal cells around the glomerulus (in
Bowman's Space, thus forming a crescent)
Involves only glomeruli and no other target organs. Essentially
something like minimal change disease.
What is Secondary Glomerular

Disease?
Look at Golijan page 400 and
go through all the histology
Involves glomeruli and other organs, e.g. SLE

Ya, definitely do that :-)
What does a Linear pattern

indicate on
Immunofluorescence?
What
does a Granular or
Antibodies line upagainst evenly distributed antigens in the

GBM. Think Goodpasture's Syndrome
Lumpy Bumpy appearance

indicate on
Immunofluorescence?
Think immunocomplex deposits in the glomerulus forming

lumps
of dense
Ig. Not
attached
Electron
giving
themto
a the
darkGBM.
color. Subendothelial are
What do immune complexes

look like on Electron
Microscopy?
trapped between the endothelial cell and GBM. Subepithelial

has passed through the GBM but is stuck in the podocytes.
Intramembranous is within the GBM and Mesangial is within the
mesangium.
How does Type III Immune

complex disease cause
glomerular disease?
Circulate and deposit in glomeruli or develop in situ. Immune

complexes then activate complement, procude C5a which is
chemotactic to neutrophils which attack the GBM.
How does something like

Goodpasture's Disease cause
glomerular damage?
How does T Cell production of
cytokines
damage the GBM?
What
are clinical
manifestations of glomerular
disease?
Describe the pathophysiology

of Nephritic Syndrome?
Anti GBM antibodies attack the glomerular basement membrane

Cytokines cause the GBM to lose its negative charge. Cytokines
also damage podocytes causing them to fuse.
Nephritic syndrome, nephrotic syndrome and chronic
glomerulonephritis
Glomerular injury primarily occurs due to neutrophils which
damage See hypertension from salt retention, periorbital
puffiness from salt retention, oliguria (decreased GFR from
inflamed glomeruli) and Hematuria. The hematuria features
dysmorphic RBC with irregular membranes from inflamed
glomeruli with IC deposition. Often see neutrophils in the
sediment, especially if immune complex. RBC casts are a key
finding, and occasionally there are WBC casts.
What are some lab findings in

Nephritic syndrome?
What is IgA Nephropathy

(Berger's Disease)?
What does Berger's disease
often immitate?
What happens after a URI in
Berger's disease?
Proteinuria>150mg/day but less than 3.5 g/day. Azotemia with

BUN:Cr ratio >15 because tubular function is intact in acute
glomerulonephritis
Most common nephropathy, mostly nephritic. Increased
mucosal synthesis and decreased clearance of IgA with
increased serum IgA. Produces Focal Proliferative
Glomerulopathy. Also see Mesangial IgA immune complex
deposits with granular immunofluorescence. IC's activate the
alternative complement pathway.
Henoch Schonlein Purpura
Episodic hematuria and hypertension following URI because of
increased IgA deposits.
What is Post-Streptococcal
Glomerulonephritis?
Most common type of post-infectious glomerulonephritis,

usually after group A strep infection of skin (scarlet fever) or
pharunx. Subepithelial immune complex deposits with granular
immunofluorescence. IC's activate the alternative complement
pathway. See a diffuse proliferative pattern with neutrophilic
infiltrate.
How does Post-Streptococcal

Glomerulonephritis present?
Hematuria, 1-3 weeks following group A strep infection by a

nephritogenic strain (never produces rheumatic fever). Causes
periorbital edema from sodium retention not hypoalbuminemia,
transient, sometimes severe hypertension.
What lab tests are indicative

of Post-Strep
Glomerulonephritis?
Increased DNAase B titers. ASO is degraded by oil in the skin

and is thus not increased. Streptozyme test is positive (antiDNAase B, ASO, anti-AH and anti-NAD antibodies).
What is Diffuse Proliferative

Glomerulonephritis?
Most common type of glomerular disease in SLE.

Subendothelial IC deposits with granular immunofluorescence.
DNA-anti-DNA IC's activate the classical complement pathway.
See "wire looping of capillaries" as well as neutrophil infiltration
with hyaline thrombi in capillary lumens.
What does the serum ANA test

look like in Diffuse Proliferative
Glomerulonephritis?
How
do you treat Diffuse
Proliferative
Glomerulonephritis?
What is Rapidly progressive

Crescentic Glomerulonephritis?
Which diseases are associated
with Rapidly Progressive
Crescentic Glomerulonephritis?
What HLA type is common in
Goodpasture's syndrome?
How do you treat
Goodpasture's syndrome?
Serum ANA has a rim pattern, corresponding to the presence of

anti-ds DNA antibodies
Corticosteroids and Cyclophosphamide
Clinical syndrome that may be either primary or secondary
disease. See a rapid loss of renal function that progresses to
acute renal failure within weeks. May or may not be associated
with crescent formation.
Goodpasture's syndrome, microscopic polyarteritis (p-ANCA),
Wegener's granulomatosis (c-ANCA)
80% are HLA-BR2 positive
Plasma exchange to remove antibodies, immunosuppressive
therapy with steroids and cyclophosphamide or renal transplant
What is Nephrotic Syndrome?
Glomerular injury due to cytokines not neutrophils. Cytokines

released from T Cells destroy the negative charge of the
membrane thus allowing protein leak. They also cause the
podocytes to fuse together.
What are the key findings in

nephrotic syndrome?
Proteinuria >3.5 g/24 hr, pitting edema and ascited due to

hypoalbuminemia. Increased risk for spontaneous peritonitis
from strep pneumoniae. Sometiems there is hypertension from
salt retention. Hypercoagulability due to loss of Antithrombin
III causing potential for renal vein thrombosis.
Hypercholesterolemia from increased synthesis (after albumin
loss). Hypogammaglobulinemia from protein loss. Fatty casts
with
maltese
crosseswith
and Nodular
oval fat bodies.
Nephrotic
syndrome
Glomerulosclerosis
What type f kidney disease

does Diabetic Glomerulopathy
cause?
(Kimmelstiel-Wilson disease). Risk factors are poor glycemic

control, hypertension and high correlation with coexisting
diabetic retinopathy.

Diabetic Glomerulopathy?
What is Diabetic
Microangiopathy?
What microscopic changes are
seen in Diabetic
Glomerulopathy?
What lab values are significant
in Diabetic Glomerulopathy?
Are there any other diseases
of the kidney associated with
Diabetic Glomerulopathy?
Nonenzymatic glycosylation of the GBM, also affecting the

tubule basement membranes. Results in increased vessel and
tubular permeability to proteins. NEG of the afferent and
efferent arterioles also results in hyaline arteriolosclerosis
(efferent first). There is also osmotic damage to the glomerular
capillary endothelium because glucose is converted to sorbitol
by aldolase reductase resulting in an osmotic gradient. Selective
hyaline arteriolosclerosis of the efferent arterioles results in
increased GFR and causes hyperfiltration damage to the
mesangium.
Increased Type IV collagen deposition in the GBM, tubular
basement membrane and mesangium results in a
microangiopathic state.
Fusion of podocytes, afferent and efferent hyaline
arteriolosclerosis, nodular masses of type IV collagen and
trapped proteins in the mesangium
Microalbuminuria
What is renal amyloidosis?
Renal papillary necrosis and acute or chronic pyelonephritis

Amyloid deposits in the kidney secondary to primary or
secondary amyloidosis
What is Alport's Syndrome?
X-Linked recessive (sometimes AR or AD) mutations in A chains

of type IV collagen in the GBM. Lipid accumulates in VEC's
producing foam cells. Also see sensorineural hearing loss and
ocular abnormalities
What is Thin Basement

Membrane Disease?
Benign familial hematuria. AD disorder with extremely thin

basement membranes in the setting of normal renal functin.
See mild proteinuria and persistent microscopic hematuria
What are the common causes

of Chronic Glomerulonephritis?
Rapidly progressive glomerulonephritis, focal segmental

glomerulosclerosis, type I membranoproliferative
glomerulonephritis, membranous glomerulopathy, type IV
diffuse proliferative glomerulonephritis in SLE, IgA nephropathy.
What are gross and

microscopic findings in chronic
glomerulonephritis?
Shrunken kidenys with glomerular sclerosis and tubular atrophy
What is ischemic Acute

Tubular Necrosis?
Most often caused by prerenal azotemia due to hypovolemia.

Ischemia damages endothelial cells decreasing vasodilators and
increasing vasoconstrictors, thus worsening the situation and
further decreasing GFR. Ischemia also damages tubular cells
which then detach into the lumen, cause obstruction and
produce pigmented renal tubular cell casts. The casts further
obstruct the lumen increasing tubular pressure, decreasing GFR
and
pushing
fluid into
the
interstitium
resulting
oliguria.
Straight
segment
of the
Proximal
tubule
(part ofinthe
degree
What segments of the nephron

are damaged in ischemic ATN?
most susceptible to hypoxia), Medullary segment of the thick

ascending limb (location of the NK2C transporter), and the
Tubular basement membrane (interferes with renal tubular cell
regeneration)
What is Nephrotoxic Acute

Tubular Necrosis?
What is the epidemiology of
Acute Tubular Necrosis?
What is Acute Renal Failure?
ATN from nephrotoxic substances. Aminoglycosides are most

common, radiocontrast agents and heavy metal poisoning are
also causes. Most commonly see oliguria, occasionally polyuria.
This primarily damages proximal tubule while the tubular
basement membrane is intact. Also see pigmented renal
tubular cell casts, hyperkalemia and anion gap metabolic
acidosis, increased BUN and Cr with ratio of BUN:Cr <15. Often
have issues with hypokalemia in the diuresis phase.
10% of ICU patients, 40% iatrogenic, 20% of patients with
sepsis suppression
and >50% of
with septic
shock in 24 hours,
Acute
ofpatients
renal function
developing
accompanied by oliguria or anuria. Most commonly caused by
ATN.

Acute Renal Failure?
What is RPGN?
Postrenal obstruction, vascular disease (malignant htn), RPGN,

drugs, DIC, urate nephropathy.
Rapidly progressive glomerular nephritis
How do you treat Acute Renal

Failure?
Treat prerenal azotemia-volume expansion if hypovolemic to

increase renal blood flow. Low dose dopamine. Fenoldopam
(dopamine Alpha-1-receptor agonist), Dialysis
What is Tubulointerstitial
Nephritis?
Acute or chronic inflammation of tubules and interstitium. May

be caused by acute pyelonephritis, drugs, infections
(legionaire's, leptospirosis), SLE, lead poisoning, Urate
nephropathy and multiple myeloma.

acute pyelonephritis?
E Coli is most common followed by Enterococcus. Risk factors

are indwelling catheter, obstruction, medullary sponge kidney,
DM, pregnancy and sickle cell
How does vesicoureteral reflux

cause pyelonephritis?
What is Oliguria?
Oliguria?
What does decreased Urine
Osm indicate?
How do you calculate a FENa?
What does a FENa less than
1% indicate?
What does a FENa greater
than 2% indicate?
What can UNa tell you about
tubular function?
How do you distinguish
postrenal azotemia from ATN?
Intravesical portion of the ureter is not compressed during

micturition so urine refluxes up. Causes ascending infection
into the renal pelvis and parenchyma.
Urine output <400 mL/day or less than 20 mL/hr.
Prerenal azotemia, acute glomerulonephritis, acute tubular
necrosis/renal azotemia, and postural azotemia.
Urine osm <350 mOsm/kg indicates poor concentrating ability
and thus tubular dysfunction
FENa = (Una * PCr)/(PNa * Ucr) *100
Sodium filtration closely mimics creatinine filtration. FENa less
than 1% means good tubular function
Tubular dysfunction. Good predictor of ATN
UNa<20 mEq/L indicates good tubular function aka you're not
dumping salt like crazy. UNa >40 mEq/L indicates poor tubular
function aka you're not reabsorbing salt.
ATN usually presents with pigmented tubular casts. In
postrenal azotemia, the sediment is usually normal.
What should you suspect if

there is staph a. cultured in
the
urine?
What
are gross and
microscopic findings in
pyelonephritis?
What are the clinical and lab
findings in pyelonephritis?
Acute Pyelonephritis?
What are pathological findings
in Chroninc Pyelonephritis?
Hematogenous
spread
of the infection
to the
kidneys.
Grayish white areas
of abscess
formation
in the
cortex and
medulla. Microabscesses form in the tubular lumens and
interstitium.
Clinical-spiking fever, flank pain, frequency and dysuria. LabWBC casts, pyuria, bacteruria, hematuria
Chronic Pyelonephritis, Perinephric Abscess, Renal Papillary
necrosis, septicemia with endotoxic shock
U shaped cortical scars overlying a blunt calyx, visible on IV
pyelogram.
What pathological findings are

seen in obstructive Chronic
Pyelonephritis?
Uniform dilation of the calyces and diffuse thinning of cortical

tissue.
What are microscopic findings

of Chronic Pyelonephritis?
What can reflux nephropathy
cause in children?
What drugs are associated
with acute drug induced ATN?
Chromic inflammation with scarring of the glomeruli. Tubular

atrophy-tubules contain eosinophilic material resembling thyroid
tissue (thyroidization)

Drug induced ATN?
Hypertension
Penicillin esp. methicillin. Rifampin, sulfonamides, NSAIDs,
diuretics
Combination of Type I and IV hypersensitivity. Abrupt onset of
fever, oliguria and rash that resolves with withdrawal of the
drug. Causes tubular disease with a BUN:Cr <15, eosinophilia
and eosinophiluria
What is Analgesic Nephritis?
Chronic drug induced Tubulointerstitial nephritis. Chronic use of

Acetominophen with Aspirin because Acetominophen causes
free radical damage while aspirin inhibits renal synthesis of
PGE2 leaving AT II unopposed.

Analgesic Nephritis?
Renal papillary necrosis-sloughing of renal papillae producing

gross hematuria, proteinuria and colicky flank pain. Ring defect
where papillae used to reside. Hypertension, CRF and Renal
pelvic and bladder transitional cell carcinomas.
What is Urate Nephropathy?

How does lead poisoning
cause Urate Nephropathy?
What is seen microscopically
in Urate Nephropathy resulting
from lead poisoning?
How does Multiple Myeloma

cause renal disease?
Deposition of Urate crystals in the tubules and interstitium.

May be caused by massive release of purines (often after
chemo), lead poisoning or gout.
Decreased excretion of uric acid from the lead. Also direct toxic
effects cause TIN
Nuclear acid-fast inclusions in the proximal tubule

Bence Jones light proteins are toxic to the tubular epithelium
and result in tubular casts. Casts obstruct the lumen and incite
a foreign body giant cel reaction of the tubules and interstitium,
leading to renal failure. Nephrocalcinosis from bone
breakdown/hypercalcemia also causes metastatic calcification of
the basement membrane collecting tubules. Finally, BJ proteins
may be converted to amyloid and cause primary amyloidosis
resulting in nephrotic syndrome.
What is Renal
Osteodystrophy?
Normocytic anemia with low corrected reticulocyte count. Due

to decreased Erythropoietin production. Also see qualitative
platelet defects.
Chronic kidney disease-mineral bone disorder. Osteitis fibrosia
cystica due to hypovitaminosis D. Causes hypocalcemia which
then stimulates the production of PTH-secondary
hyperparathyroidism. Hyperparathyroidism causes bone
resorption causing cystic lesions in the bone. Hemorrhage into
cysts caused brown discoloration.
What are some complications

of Renal
What
areOsteodystrophy?
some cardiovascular
findings in Chronic Renal
Failure?
Osteomalacia from decreased mineralization of the osteoid.

Osteoporosis from loss of organic bone mass and minerals
(often due to chronic metabolic acidosis because excess H is
buffered by bone minerals).
Hypertension from salt retention, hemorrhagic fibrinous
pericarditis, CHF and accelerated atherosclerosis.
What are hematologic findings

in Chronic Renal Failure?
What are some other clinical

consequences of Chronic Renal
Failure?
Hemorrhagic gastritis and uremic frost (urea crystals deposit on

the skin). Also hyperkalemia and anion-gap metabolic acidosis.
Why does renal failure cause

hypocalcemia?
Hypovitaminosis D from decreased 1-Alpha Hydroxylase and

thus decreased reabsorption of calcium from the small
intestines. Also hyperphosphatemia from decreased renal
excretion drives calcium into bone and soft tissue.
Why is there increased Serum

Cystatin C?
What is seen on urinalysis in
Chronic Kidney Failure?
Why do you give ACE
inhibitors in kidney disease?
Cystatin in a Cysteine protease inhibitor produces by the

nucleus of all cells. It should be filtered by the glomerulus but
not secreted so it's a good marker of renal function.
Fixed specific gravity because no concentrating ability, free
water clearance is 0, waxy/broad casts are present.
What is benign
nephrosclerosis?
Reduce
proteinuria
and in
treat
hypertension.
Common
renal disease
essential
hypertension caused by
hyaline arteriolosclerosis of arterioles in the renal cortex.
Results in tubular atrophy, interstitial fibrosis and glomerular
sclerosis. See small kidneys with a finely granular cortical
surface.
Sudden onset of accelerated hypertension with end organ
What is Malignany
Hypertension?
damage. Risk factors are pre-existing BNS, Hemolytic Uremic

syndrome, thrombotic thrombocytopenic purpura and systemic
sclerosis
Fibrinoid necrosis and necrotizing arteriolotis and glomerulitis
What microscopic changes are

seen in Malignant
Hypertension?
with pinpoint hemorrhages on the cortical surface. Also

hyperplastic arteriolosclerosis (onion skin lesions) with smooth
muscle hyperplasia and reduplication of the basement
membrane.

Malignant Hypertension?
What causes Renal infarction?
Hypertensive encephalopathy-cerebral edema, papilledema,

retinopathy with flame hemorhages and potential for an
intracerebral bleed.
Embolization from thrombi in the left heart, atheroembolic renal
disease, vasculitis especially polyarteritis nodosa.
What is the gross and

microscopic appearance of a
renal infarction?
What is Diffuse cortical

necrosis?
Hydronephrosis?
What are some clinical
findings of hydronephrosis?
Irregular wedge-shaped pale infarct in the renal cortex. Old

infarct have a V shape from scar tissue.
Complication of obstetric emergencies. Due to DIC in the renal
cortex which results in fibrin clots in arterioles and glomerular
capillaries and bilateral, diffuse, pale infarcts of the renal
cortex. See anuria in a pregnant woman followed by ARF.
Renal stones, retroperitoneal fibrosis, cervical cancer and BPH
Compression atrophy of the renal medulla and cortex and
dilated ureters and renal pelvis
What is a calcium stone?

What is a Magnesium
Ammonium Phosphate stone?
Hypercalcuria in the absence of hypercalcemia (absorptive

hypercalcuria), decreased urine volume, reduced urine citrate
(citrate chelates calcium), primary hyperparathyroidism, diet
high in dairy (contains phosphates or oxalate), and urinary
infectionsoxalate
due tostone-from
urease producers
Calcium
vegans(proteus)
or people with Crohn's.
Calcium Phosphate stone-dairy products and distal renal tubular
acidosis.
Struvite stone causing a Staghorn calculus. Associated with
urease producing bugs. Urine is alkaline and smells like
ammonia.
How do you treat a calcium

stone?
How do you treat a Uric Acid
stone?
How do you treat a struvite
stone?
Most pass. Can give hydrochlorothiazide which increases renal

tubule reabsorption of calcium. Cellulose phosphate binds
calcium
in the
intestine.
Allopurinol,
increase
urinary pH to make the stone soluble.
Cotreat chemo patients with allopurinol to prevent urate
nephropathy.
Surgical removal because of size. Antibiotic to eliminate urease
producer.
What is an Angiomyolipoma?
Hamartoma composed of blood vessels, smooth muscle and

adipose cells. Associated with tuberous sclerosis causing
mental retardation and multisystem hamartomas.
What causes Urolithiasis?
What are risks for Renal Cell

Carcinoma?
Smoking, Von Hippel-Lindau, Adult PKD, obesity, asbestos and

lead exposure, and gasoline or petroleum product exposure.
What is Von Hippel Lindau

disease?
AD disease with defect on chr 3. Increased VEGF causes

hemangiobalstomas of the cerebellum and retina and bilateral
renal cell carcinomas.
What are some gross and

microscopic findings in Clear
Cell renal carcinoma?
Upper pole mass with cysts and hemorrhage composed of clear

cells that contain lipids and glycogen. Tendency for renal vein
invasion and invasion into the IVC and right heart.
What are clinical signs of clear

cell renal carcinoma?
Hematuria, abdominal mass, flank pain, hypertension, triad of

hematuria, abdominal mass and flank pain. Constitutional
symptoms. Left sided variocele from blocking of left renal vein.
What hormonal changes are

seen in renal clear cell
carcinoma?
What is Renal Pelvic Cancer?
EPO is elevated causing secondary polycythemia. PTH-related

protein
produces
hypercalcemia.
Transitional
cell carcinoma.
Risk factors are smoking,
Phenacetin abuse, aromatic amines (aniline dyes),
cyclophosphamide.
AD tumor with the defect on chromosome 11. WAGR
What is a Wilm's Tumor?
Syndrome-wilms tumor, aniridia (absent iris), genital

abnormalities, retardation. Beckwith-Wiedmann syndromewilms tumor with enlarged body organs, hemihypertrophy of
extremities.
Where do Wilm's tumors come

from?
How does a Wilm's tumor
present?
Large necrotic gray tumors derived from mesonephric

mesoderm, containing abortive glomeruli and tubules with
primitive blastemal cells and rhabdomyoblasts.
Unilateral palpable mass in a child with hypertension (renin
secretion). Metastasis to the lungs.

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Pulmonary

How do you calculate the A-a

Difference in partial pressure of Oxygen, PO2, between the alveolar

What causes an A-a gradient

A-a gradient is caused by a mismatch between ventilation and

What are some causes of

Depression of the respiratory center in the medulla (barbiturates,

Define Functional Residual

Total amount of air in the lungs at the end of normal expiration

What is the normal

Define Dyspnea and list

What is the most common

What drugs cause cough?

mucosal swelling and irritation in the tracheobronchial tree.

Define tachypnea and list the

Rapid, shallow breathing, more than 20 breaths/minute. Causes

Define tracheal shift and list

shift of trachea from large changes in pleural fluid volume. Causes

What causes dull and

Dull percussion comes from pleural effusions, lung consolidations,

What is the origin and

What are tubular breath

trachea but is always abnormal over the bronchi. Causes a loud,

What are crackles and how

Tracheal sounds that are modified in the alveoli. Inspiratory to

What is wheezing and how is

High pitched musical sound usually in expiration. Caused by

What are vesicular breath

What are Rhonchi and how

What is a pleural friction rub

Low pitched snoring sounds during inspiration or expiration. Due

What is bronchophony and

Caused by alveolar consolidations. Spoken numbers, syllables are

Where is maximal inspiration

Begins at point A, RV and goes to point B, TLC

Define Peak Expiratory Flow

What is Choanal Atresia?

What is a Nasal Polyp?

Begins at point B, TLC, and goes to point C, PEF. Occurs early in

What causes obstructive

Most commonly a result of obesity causing the pharyngeal muscles

What is the pathogenesis

Airway obstruction causes CO2 retention resulting in hypoxemia.

Define Sinusitis and describe

Inflammation of the sinuses, most often maxillary or ethmoid

in males and increased incidence in the Chinese and African

Define Laryngeal Carcinoma.

Carcinoma most commonly located on the true vocal cords. Mostly

Loss of lung volume due to inadequate expansion of the airspaces

Airway obstruction in bronchiols, segmental bronchi or bronchi, by

What are complications of

Synthesized by Type II pneumocytes starting in the 28th week of

What is Pulmonary Edema

heart failure, volume overload or mitral stenosis. This produces

What is atelectasis due to

What is Respiratory Distress

What is Acute Respiratory

Noncardiogenic pulmonary edema from acute alveolar-capillary

What is the pathogenesis of

Acute damage to alveolar capillary walls and epithelial cells results

What are clinical

Dyspnea/tachypnea, late inspiratory crackles, severe hypoxemia

Describe the pathogenesis of

Most caused by bacterial pathogens, particularly Strep