Assessment and Management of

Patients with Endocrine Disorders

By Linda Self
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
 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.
 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?