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Assessment and Management of
Patients with Endocrine Disorders
Ian Van V. Sumagaysay, RN, MAN
St. Anthony’s College
Nursing Department
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:
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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
population
Target
Corticotroph
15-20%
Thyrotroph
3-5%
Adrenal gland
ACTH
b-lipotropin Adipocytes
Melanocytes
TSH
Thyroid gland
Gonadotroph
10-15%
LH, FSH
Gonads
Somatotroph
40-50%
GH
Lactotroph
10-15%
PRL
All tissues, liver
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, antiinflammatory 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-melanocytestimulating 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
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result in adaptive decline in utilization called the WolfChaikoff 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
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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
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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,
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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
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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
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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
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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
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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,
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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
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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
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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
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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
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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
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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
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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?