Assessment and

Management of
Patients with
Endocrine Disorders
Glands of the Endocrine
System
 Hypothalamus
 Posterior Pituitary
 Anterior Pituitary
 Thyroid
 Parathyroids
 Adrenals
 Pancreatic islets
 Ovaries and testes
Hypothalamus

 Releasing and inhibiting hormones

 Corticotropin-releasing hormone
 Thyrotropin-releasing hormone
 Growth hormone-releasing hormone
 Gonadotropin-releasing hormone
 Somatostatin-=-inhibits GH and TSH
Anterior Pituitary

 Growth Hormone--
 Adrenocorticotropic hormone
 Thyroid stimulating hormone
 Follicle stimulating hormone—ovary in female, sperm in
males
 Luteinizing hormone—corpus luteum in females,
secretion of testosterone in males
 Prolactin—prepares female breasts for lactation
Anterior pituitary

 Anterior pituitary: connected to the

hypothalamus by hypothalmoanterior
pituitary portal vessels.
 The anterior pituitary produces six
peptide hormones:
 prolactin, growth hormone (GH),
 thyroid stimulating hormone (TSH),
 adrenocorticotropic hormone (ACTH),
 follicle-stimulating hormone (FSH),
 luteinizing hormone (LH).
 Anterior pituitary cells and hormones

Cell type Pituitary Product Target

population
Corticotroph 15-20% ACTH Adrenal gland
b-lipotropin Adipocytes
Melanocytes
Thyrotroph 3-5% TSH Thyroid gland
Gonadotroph 10-15% LH, FSH Gonads
Somatotroph 40-50% GH All tissues, liver
Lactotroph 10-15% PRL Breasts
gonads
Anterior pituitary hormones
 Posterior Pituitary

 Antidiuretic Hormone

 Oxytocin—contraction of uterus, milk ejection from

breasts
Adrenal Cortex

 Mineralocorticoid—aldosterone. Affects sodium

absorption, loss of potassium by kidney

 Glucocorticoids—cortisol. Affects metabolism, regulates

blood sugar levels, affects growth, anti-inflammatory
action, decreases effects of stress

 Adrenal androgens—dehydroepiandrosterone and

androstenedione. Converted to testosterone in the
periphery.
 Adrenal Medulla

 Epinephrine and norepinephrine

serve as neurotransmitters for sympathetic system
 Thyroid

 Follicular cells—excretion of triiodothyronine (T3) and

thyroxine (T4)—Increase BMR, increase bone and
calcium turnover, increase response to catecholamines,
need for fetal G&D
 Thyroid C cells—calcitonin. Lowers blood calcium and
phosphate levels
Parathyroid

 Parathyroid hormone—regulates serum calcium

 Pancreatic Islet cells

 Insulin

 Glucagon—stimulates glycogenolysis and

glyconeogenesis

 Somatostatin—decreases intestinal absorption of glucose

 Kidney

 1, 25 dihydroxyvitamin D—stimulates calcium absorption

from the intestine
 Renin—activates the RAAS
 Erythropoietin—Increases red blood cell production
 Ovaries

 Estrogen
 Progesterone—inportant in menstrual cycle,*maintains
pregnancy,
 Testes

 Androgens, testosterone—secondary sexual

characteristics, sperm production
 Thymus

 Releases thymosin and thymopoietin

 Affects maturation of T lymphocetes
 Pineal

 Melatonin
 Affects sleep, fertility and aging
 Prostaglandins

 Work locally
 Released by plasma cells
 Affect fertility, blood clotting, body temperature
 Assessment

 Health history—energy level, hand and foot size

changes, headaches, urinary changes, heat and cold
intolerance, changes in sexual characteristics,
personality changes, others
 Physical assessment—appearance including hair
distribution, fat distribution, quality of skin,
appearance of eyes, size of feet and hands, peripheral
edema, facial puffiness, vital signs
 Diagnostic Evaluation

 Serum levels of hormones

 Detection of antibodies against certain hormones
 Urinary tests to measure by-products (norepinephrine,
metanephrines, dopamine)
 Stimulation tests—determine how an endocrine gland
responds to stimulating hormone. If the hormone
responds, then the problem lies w/hypothalmus or
pituitary
 Suppression tests—tests negative feedback systems that
control secretion of hormones from the hypothalamus or
pituitary.
 Disorders of the Pituitary

Pituitary Tumors
 Eosinophilic tumors may result in gigantism or in
acromegaly. May suffer from severe headaches, visual
disturbances, decalcification of the bone, endocrine
disturbances
 Basophilic tumors may cause Cushing’s syndrome
w/features of hyperadrenalism, truncal obesity,
amenorrhea, osteoporosis
 Chromophobic tumors—90% of pituitary tumors. Present
with lowered BMR, obesity, somnolence, scant hair, low
body temp, headaches, visual changes
 Growth hormone deficiency in childhood will result in
primary dwarfism.
Regulation of Growth
Hormone Secretion
 GH secretion controlled primarily by hypothalamic
GHRH stimulation and somatostatin inhibition
 Neurotransmitters involved in control of GH secretion–
via regulation of GHRH and somatostatin
Regulation of Growth
Hormone Secretion
 Neurotransmitter systems that stimulate GHRH and/or
inhibit somatostatin
 Catecholamines acting via a2-adrenergic receptors
 Dopamine acting via D1 or D2 receptors
 Excitatory amino acids acting via both NMDA and non-
NMDA receptors
Regulation of Growth
Hormone Secretion
 b-adrenergic receptors stimulate somatostatin release
and inhibit GH
 b-adrenergic receptors inhibit hypothalamic release of
GHRH
Regulation of Growth
Hormone Secretion
 Additional central mechanisms that control GH
secretion include an ultra-short feedback loop exerted
by both somatostatin and GHRH on their own secretion
Clinical assessment of GH

 Random serum samples not useful due to pulsatile

pattern of release
 Provocative tests necessary
 GH measurement after 90 min exercise
 GH measurement immediately after onset of sleep
 Definitive tests
 GH measurement after insulin-induced hypoglycemia
 Glucose suppresses GH levels 30-90 min after
administration– patients with GH excess do not suppress
 Measurement of IGF-1 to assess GH excess
Acromegaly and Gigantism

 Caused by eosinophilic adenomas of

somatotrophs
 Excess GH leads to development of gigantism if
hypersecretion is present during early life– a
rare condition
 Symmetrical enlargement of body resulting in true
giant with overgrowth of long bones, connective
tissue and visceral organs.
 Excess GH leads to acromegaly if hypersecretion
occurs after body growth has stopped.
 Elongation of long bones not possible so there is over
growth of cancellous bones– protruding jaw,
thickening of phalanges, and over growth of visceral
organs
 Acromegaly

Acromegaly
A) before presentation;
B) at admission
Harvey Cushing’s first
reported case
Gigantism

Identical twins, 22 years old, excess GH secretion

ACTH: adrenocorticotropic hormone:
synthesis and regulation of secretion

 Produced in corticotrophs
 ACTH is produced in the anterior
pituitary by proteolytic processing of
Prepro-opiomelanocortin (POMC).
 Other neuropeptide products include b
and g lipotropin, b-endorphin, and a-
melanocyte-stimulating hormone (a-
MSH).
 ACTH is a key regulator of the stress
response
ACTH

 ACTH is made up of 39 amino acids

 Regulates adrenal cortex and synthesis of
adrenocorticosteroids
 a-MSH resides in first 13 AA of ACTH
 a-MSH stimulates melanocytes and can darken skin
 Overproduction of ACTH may accompany increased
pigmentation due to a-MSH.
Pituitary Tumors—Assessment
and Diagnostic Findings
 H&P
 Vision tests
 CT, MRI
 Serum levels of pituitary hormones, others
 Diabetes Insipidus

 Deficiency of ADH
 Excessive thirst, large volumes of dilute urine
 Can occur secondary to brain tumors, head trauma,
infections of the CNS, and surgical ablation or
radiation
 Nephrogenic DI—relates to failure of the renal tubules
to respond to ADH. Can be related to hypokalemia,
hypercalcemia and to medications (lithium
demeocycline)
 Manifestations

 Excessive thirst
 Urinary sp. gr. of 1.001.1.005
Assessment and Diagnostic
Findings
 Fluid deprivation test—withhold fluids for 8-12 hours.
Weigh patient frequently. Inability to slow down the
urinary output and fail to concentrate urine are
diagnostic. Stop test if patient is tachycardic or
hypotensive
 Trial of desmopressin and IV hypertonic saline
 Monitor serum and urine osmolality and ADH levels
Pharmacologic Tx and Nursing
Management
 DDAVP—intranasal bid
 Can be given IM if necessary. Every 24-96h. Can cause
lipodystrophy.
 Can also use Diabenese and thiazide diuretics in mild
disease as they potentiate the action of ADH
 If renal in origin—thiazide diuretics, NSAIDs
(prostaglandin inhibition) and salt depletion may help
 Educate patient about actions of medications, how to
administer meds, wear medic alert bracelet
 SIADH

 Excessive ADH secretion

 Retain fluids and develop a dilutional hyponatremia
 Often non-endocrine in origin—such as bronchogenic
carcinoma
 Causes: Disorders of the CNS like head injury, brain
surgery, tumors, infections or medications like
vincristine, phenothiazines, TCAs or thiazide diuretics
 Meds can either affect the pituitary or increase
sensitivity to renal tubules to ADH
 Management: eliminate cause, give diuretics (Lasix),
fluid restriction, I&O, daily wt., lab chemistries
 SIADH

 Restoration of electrolytes must be gradual

 May use 3% NaCl in conjunction with Lasix
 Thyroid

 T3 and T4
 Need iodine for synthesis of hormones—excess will
result in adaptive decline in utilization called the Wolf-
Chaikoff mechanism
 Thyroid is controlled by TSH
 Cellular metabolism, brain development, normal
growth, affect every organ in the body
 T3 is five times as potent as T4
 Calcitonin—secreted in response to high levels of serum
calcium, increases deposition in the bone
 Thyroid

 Inspect gland
 Observe for goiter
 Check TSH, serum T3 and T4
 T3 resin uptake test useful in evaluating thyroid
hormone levels in patients who have received diagnostic
or therapeutic dose of iodine. Estrogens, Dilantin,
Tagamet, Heparin, amiodarone, PTU,steroids and
Lithium can cloud the accuracy
 T3 more accurate indicator of hyperthyroidism
according to text
 Thyroid

 Antibodies seen in Hashimoto’s, Grave’s and other auto-

immune problems.
 Radioactive iodine uptake test measures rate of iodine
uptake. Patients with hyperthyroidism exhibit a high
uptake, hypothyroidism will have low uptake
 Thyroid scan—helps determine the location, size, shape
and size of gland. “Hot” areas (increased function) and
“cold” areas (decreased function) can assist in
diagnosis.
 Nursing Implications

 Be aware of meds patient is taking (see list in text) that

can affect accuracy of testing
 Also be aware if patient is taking multivitamins and food
supplements
 Hypothyroidism

 Most common cause is Hashimoto’s thyroiditis

 Common in those previously treated for hyperthyroidism
 Atrophy of gland with aging
 Medications like lithium, iodine compounds, antithyroid
meds can cause
 Radiation treatments to head and neck
 Infiltrative diseases like amyloidosis, scleroderma
 Iodine deficiency and excess
 Hypothalamic or pituitary abnormality
 More common in women, especially over age 50
 Manifestations

 From mild symptoms to myxedema

 Myxedema –accumulation of mucopolysaccharides in sc
and interstitial tissues. Is the extreme form of
hypothyroidism. Can progress to shock.
 S/S—fatigue, hair loss, dry skin, brittle nails, numbness
and tingling of the fingers, amenorrhea, weight gain,
decreased heart rate and temperature, lassitude,
cognitive changes, elevated cholesterol levels,
constipation, hypotension
 Pharmacologic Management
of hypothyroidism
 Levothyroxine is preferred agent
 Dosage is based on TSH
 Desiccated thyroid used infrequently due to inconsistent
dosing
 Angina can occur when thyroid replacement is initiated
as it enhances effects of cardiovascular catecholamines
(in pt. w/pre-existent CAD). Start at low dose.
 Hypnotics and sedatives may have profound effects on
sensorium
 Management in Myxedema

 Cautious fluid replacement

 Glucose to restore to normal glycemic levels
 Avoid rapid overheating due to increased oxygen
demands but keep warm
 May give levothyroxine intravenously
With recovery,
 Modify activity
 High fiber foods
 Home health for follow-up
 Hyperthyroidism

 Extreme form is Grave’s disease

 Caused by thyroiditis, excessive amount thyroid
hormone, abnormal output by immunoglobulins
 Is more common in women
Manifestations of
hyperthyroidism
 Thyrotoxicosis—nervousness, irritable, apprehensive,
palpitations, heat intolerance, skin flushing, tremors,
possibly exophthalmos
 Have an increased sensitivity to catecholamines
 Can occur after irradiation or presence of a tumor
 Assessment and Diagnosis

 Thyroid thrill and or bruit may be present

 Thyroid may be enlarged
 Decreased TSH, increased free T4 and an increased
radioactive iodine uptake
 Management

 Reduce thyroid hyperactivity—usually use radioactive

iodine, antithyroid meds or surgery)
 Beta blockers
 Can be relapse with antithyroid meds
 Pharmacologic Therapy

 Irradiation with administration of radioisotope iodine

131—initially may cause an acute release of thyroid
hormones. Should monitor for thyroid storm
 S/S of thyroid storm—high fever. Tachycardia, delirium,
chest pain, dyspnea, palpitations, weight loss, diarrhea,
abdominal pain
 Management of thyroid storm—oxygen, IV fluids with
dextrose, hypothermic measures, steroids to treat shock
or adrenal deficiency, iodine to decrease output of T4,
beta blockers, PTU or Tapazole impedes formation of
thyroid hormone and blocks conversion of T4 to T3
 Antithyroid Medications

 PTU—propylthiouracil—blocks synthesis of hormones

 Tapazole (methimazole)—blocks synthesis of hormones.
More toxic than PTU.
 Sodium Iodide-suppresses release of thyroid hormone
 SSKI (saturated solution of potassium chloride)–
suppresses release of hormones and decreases
vascularity of thyroid. Can stain teeth
 Dexamethazone—suppresses release of thyroid
hormones
 Surgical Management

 Reserved for special circumstances, e.g. large goiters,

those who cannot take antithyroid meds, or who need
rapid normalization
 Subtotal thyroidectomy
 Before surgery, give PTU until s/s of hyperthyroidism
have disappeared
 Iodine may be used to decrease vascularity
 Nursing Management

 Reassurance r/t the emotional reactions experienced

 May need eye care if has exophthalmos
 Maintain normal body temperature
 Adequate caloric intake
 Managing potential complications such as dysrhythmias
and tachycardias
 Educate about potential s/s of hypothyroidism following
any antithyroid tx.
 Parathyroid Glands

 Parathormone maintains sufficient serum calcium levels

 Excess calcium can bind with phosphate and precipitate
in various organs, can cause pancreatitis
 Hyperparathyroidism will cause bone decalcification and
development of renal calculi
 More common in women
 Secondary hyperparathyroidism occurs in those with
chronic renal failure and renal rickets secondary to
excess phosphorus retention (and increased
parathormone secretion)
 Manifestations of
Hyperparathyroidism
 May be asymptomatic
 Apathy, fatigue, muscle weakness, nausea, vomiting,
constipation, hypertension and cardiac dysrhythmias
 Excess calcium in the brain can lead to psychoses
 Renal lithiasis can lead to renal damage and even
failure
 Demineralization of bones with back and joint pain,
pain on weight bearing, pathologic fractures
 Peptic ulcers and pancreatitis can also occur
 Assessment and Diagnostic
Findings
 Persistent elevated calcium levels
 Elevated serum parathormone level
 Bone studies will reveal decreased density
 Double antibody parathyroid hormone test is used to
distinguish between primary hyperparathyroidism and
malignancy
 Ultrasound, MRI, thallium scan, fine needle biopsy also
can be used to localize cysts, adenomas, or hyperplasia
 Management

 Recommended treatment for hyperparathyroidism is

surgical removal
 Hydration therapy necessary to prevent renal calculi
 Avoid thiazide diuretics as they decrease renal excretion
of calcium
 Increase mobility to promote bone retention of calcium
 Avoid restricted or excess calcium in the diet
 Fluids, prune juice and stool softeners to prevent
constipation
 Watch for s/s of tetany postsurgically (numbness,
tingling, carpopedal spasms) as well as cardiac
dysrhythmias and hypotension
 Hypercalcemic crisis

 Seen with levels greater than 15mg/dL

 Can result in life-threatening neurologic, cardiovascular
and renal symptoms
 Treatments include: hydration, loop diuretics to
promote excretion of calcium, phosphate therapy to
promote calcium deposition in bone and reducing GI
absorption of calcium
 Give calcitonin or mithramycin to decrease serum
calcium levels quickly
 Hypoparathyroidism

 Seen most often following removal of thyroid gland,

parathyroid glands or following radical neck surgery
 Deficiency of parathormone results in increased bone
phosphate and decreased blood calcium levels
 In absence of parathormone, there is decreased
intestinal absorption of dietary calcium and decreased
resorption of calcium from bone and through kidney
tubules
 Clinical Manifestations of
Hypoparathyroidism
 Irritability of neuromuscular system
 Tetany—hypertonic muscle contractions , numbnes,
tingling, cramps in extremities, laryngeal spasm,
bronchospasm, carpopedal spasm ( flexion of the elbows
and wrists, dorsiflexion of the feet), seizures
 Assessment and Diagnostic
Findings
 Trousseau’s sign—can check with a BP cuff
 Chvostek’s sign—tapping over facial nerve causes spasm
of the mouth, nose and eye
 Lab studies may reveal calcium levels of 5-6 mg/dL or
lower
 Serum phosphate levels will be decreased
 Management of
Hypoparathyroidism
 Restore calcium level to 9-10 mg/dL
 May need to give IV calcium gluconate for immediate
treatment
 Use of parathormone IV reserved for extreme situations
due to the probability of allergic reactions
 Monitor calcium levels
 May need bronchodilators and even ventilator assistance
 Diet high in calcium and low in phosphorus; thus, avoid
milk products, egg yolk and spinach.
Management of
Hypoparathyroidism
 Keep calcium gluconate at bedside
 Ensure has IV access
 Cardiac monitoring
 Care of postoperative patients who have undergone
thyroid surgery, parathyroidectomy or radical neck
surgery. Be watchful for signs of tetany, seizures, and
respiratory difficulties
Adrenals--Pheochromocytoma

 Usually benign tumor

 Originates from the chromaffin cells of the adrenal
medulla
 Any age but usu. Between 40-50 years old
 Can be familial
 10% are malignant
 May be associated with thyroid carcinoma or
parathyroid hyperplasia or tumor
 Clinical Manifestations

 Headache, diaphoresis, palpitations, hypertension

 May have hyperglycemia related to excess epinephrine
secretion
 Tremors, flushing and anxiety as well
 Blurring of vision
 Feeling of impending doom
 BPs exceeding 250/150 have occurred
Assessment and Diagnostic
Findings
 Associated with the 5 H’s—hypertension, headache,
hyperhidrosis, hypermetabolism and hyperglycemia
 Urinary catecholamines and metanephrine are direct and
conclusive tests
 Serum epinephrine and norepinephrine levels will be
elevated
 Urinary vanillymandelic acid also diagnostic
 Must avoid coffee, tea, bananas, chocolate, vanilla and ASA,
nicotine, amphetamines, decongestants before 24h urine
testing
 Clonidine suppression test—in normal individual, would
block catecholamine release
 Imaging studies
 Management

 Bedrest
 Elevated HOB
 ICU
 Nipride
 Calcium channel blockers and Beta blockers
 Surgical management (manipulation of the tumor can
cause excessive release of catecholamines)
 Steroid therapy if adrenalectomy performed
 Hypotension and hypoglycemia can occur post-op
 Addison’s Disease

 Adrenocortical insufficiency
 Autoimmune or idiopathic atrophy
 Can be caused by inadequate ACTH from pituitary
 Therapeutic use of steroids
 Manifestations

 Muscle weakness
 Anorexia
 Dark pigmentation
 Hypotension
 Hypoglycemia
 Low sodium levels
 High potassium levels
 Can result in Addisonian crisis
 Addisonian crisis

 Circulatory shock
 Pallor, apprehension, weak&rapid pulse, rapid
respirations and low blood pressure
 Headache, nausea, abdominal pain and diarrhea
 Can be brought on by overexertion, exposure to cold,
acute infection, decrease in salt intake
 Assessment and Diagnostic
Findings
 Early morning serum cortisol and plasma ACTH are
performed. Will distinguish between primary and
secondary adrenal insufficiency. In primary, will have
elevated ACTH levels and below normal cortisol levels.
 If the adrenal cortex is not stimulated by the pituitary,
a normal response to doses of exogenous ACTH (see
text)
 Blood sugar levels and electrolyte values
 Management

 Restore circulatory status—fluids, steroids

 May need antibiotics if infection precipitated crisis
 May need lifelong steroid therapy and mineralocorticoid
therapy
 May need additional salt intake
 Check orthostatics
 Daily weights
 Aware that stressors can precipitate crises
 Medic alert bracelet or similar identification of history
 Cushing’s Syndrome

 Results from excessive adrenocortical activity

 May be related to excessive use of corticosteroid
medications or due to hyperplasia of the adrenal cortex
 Oversecretion of corticosteroids can also be caused by
pituitary tumor
 Can be caused by bronchogenic carcinoma or other
malignancy
 Manifestations of Cushing’s
syndrome
 Cataracts, glaucoma
 Hypertension, heart failure
 Truncal obesity, moon face, buffalo hump, sodium
retention, hypokalemia, hyperglycemia, negative
nitrogen balance, altered calcium metabolism
 Decreased inflammatory responses, impaired wound
healing, increased susceptibility to infections
 Osteoporosis, compression fractures
 Peptic ulcers, pancreatitis
 Thinning of skin, striae, acne
 Mood alterations
 Assessment and Diagnostic
Findings
 Overnight dexamethasone suppression test frequently
used for diagnosis
 Administered at 11pm and cortisol level checked at 8am
 Suppression of cortisol to less than 5mg/dL indicates
normal functioning
 Measurement of plasma ACTH (radioimmunoassay) in
conjunction with dexamethasone suppression test helps
distinguish pituitary vs. ectopic sites of ACTH.
 MRI, CT and CT also help detect tumors of adrenal or
pituitary
 Medical Management

 If pituitary source, may warrant transphenoidal

hypophysectomy
 Radiation of pituitary also appropriate
 Adrenalectomy may be needed in case of adrenal
hypertrophy
 Temporary replacement therapy with hydrocortisone or
Florinef
 Adrenal enzyme reducers may be indicated if source if
ectopic and inoperable. Examples include: ketoconazole,
mitotane and metyrapone.
 If cause is r/t excessive steroid therapy, tapering slowly
to a minimum dosage may be appropriate.
 Primary Aldosteronism or
Conn’s Syndrome
 Excessive aldosterone secondary to adrenal tumor
 retain sodium and excrete potassium
 Results in alkalosis
 Hypertension—universal sign of hyperaldosteronism
 Inability of kidneys to concentrate the urine
 Serum becomes concentrated
 Excessive thirst
 Hypokalemia interferes with insulin secretion thus will
have glucose intolerance as well
 Assessment and Diagnostic
Findings
 High sodium
 Low potassium level
 High serum aldosterone level
 Low renin level
 Aldosterone excretion rate after salt loading is
diagnostic for primary aldosteronism
 Renin-aldosterone stimulation test
 Management

 Surgical removal of tumor

 Correct hypokalemia
 Usual postoperative care with abdominal surgery
 Administer steroids
 Fluids
 Monitoring of blood sugar
 Control of hypertension with spironolactone
 Corticosteroid Therapy

 Hydrocortisone--Cortisol
 Cortisone--Cortate
 Prednisone--Deltasone
 Prednisolone-Prelone
 Triamcinolone--Kenalog
 Betamethasone--Celestone
 Fludrocortisone (contains both mineralocorticoid and
glucocorticoid) Florinef
 Indications

 RA
 Asthma
 MS
 COPD exacerbations
 Lupus
 Other autoimmune disorders
 Dermatologic disorders
 Dosing

 Lowest dose
 Limited duration
 Best time to give dose is in early morning between 7-8
am
 Need to taper off med to allow normal return of renal
function
 Side Effects of Steroids

 Hypertension, thrombophlebitis, accelerated

atherosclerosis
 Increased risk of infection
 Glaucoma and corneal lesions
 Muscle wasting, poor wound healing, osteoporosis,
pathologic fractures
 Hyperglycemia, steroid withdrawal syndrome
 Moon face, weight gain, acne
 Case Study 1

 35 year old male presents with BP of 188/112 at a yearly

physical exam. Previous exams noted blood pressures of
160/94 and 158/92. On questioning, patient admits to
twice a month episodes of apprehension, severe
headache, perspiration, rapid heartbeat, and facial
pallor. These episodes had an abrupt onset and lasted
10-15 minutes.
 Routine hematology and chemistry studies are wnl and
chest xray and ECG are normal.
 What is your impression?
 What labs would you draw?
 Case Study 2

 50 year old woman presents with enlargement of left

anterior neck. She has noted increased appetite over
the past month with no weight gain, and more frequent
bowel movements over the same period. Patient feels
jittery at times, experiences palpitations and feels
“hot” a lot recently.
 She is 5’8” tall and weighs 150#. Heart rate is 110 and
blood pressure is 110/76.
 What might be this patient’s problem?
 What lab tests might you draw?
 Case study 3

 48 year old woman with a past history of mental illness

presents with a new onset of bizarre psychotic behavior.
She had been well over the past two years.
 She is 5’5” tall and weighs 138#. Her heart rate is 65,
irreg and BP is 130/75. Exam is normal except that she is
confused to place, time and year. Patient c/o joints
aching and of feeling fatigued.
 Lab tests reveal serum calcium level of 13.8mg/dL
(reference range is 8.4-10.1)
 Phosphorus is 2.4 (reference range is 2.5-4.5)
 What is your diagnosis?
 Case Study 4

 40 year old deeply tanned woman presents with a 6

month history of increasing fatigue. For the past three
months she has suffered from recurrent URIs, poor
appetite, abdominal cramps, fatigue and diarrhea. She
has lost 25#. She has noted joint pains, muscle
weakness, and has not menstruated for the past 3
months.
 Labs reveal blood glucose of 59, Na+ 130, K+ 6.0.
 What disorder do you expect?
 Case Study #5

 27 year old woman presents with depression, insomnia,

increased facial fullness and recent increase in acne.
She had an episode of depression and acute psychosis
following uncomplicated delivery of normal baby boy 9
months previously. Her menses have been irregular since
their resumption after the birth (she is not breast
feeding). Patient relates has had several vaginal yeast
infections recently.
 Heart rate is 90bpm, BP is 146/100. Her face is puffy and
has acne vulgaris. Thin extremities and with truncal
obesity.
 What are your suspicions?
 What labs will you draw?