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92 Cards in this Set

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Cushing's syndrome
increased cortisol due to a variety of causes
primary pituitary adenoma (Cushing's disease) (increased ACTH)
primary adrenal hyperplasia/neoplasia (decreased ACTH)
ectopic ACTH production (e.g., small call lung cancer) (increased ACTH)
iatrogenic (decreased ACTH)
Cushing's disease
primary pituitary adenoma (increased ACTH)
What are the clinical features of Cushing's syndrome?
HTN, wt. gain, moon facies, truncal ovesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning, striae), osteoperosis, amenorrhea, innume suppression
primary hyperaldosteronism
(Conn's syndrome)
aldosterone-secreting tumor -> HTN, hypokalemia, metabolic alkalosis, low plasma renin
secondary hyperaldosteronism
due to renal artery stenosis, chronic renal failure, CHF, nephrotic syndrome
What type of hyperaldosteronism is associated w/ high renin levels?
secondary
What type of hyperaldosteronism is associated w/ low renin levels?
primary (Conn's)
primary aldosterone and cortisol insufficiency
(Addison's disease)
adrenal atrophy -> deficiency of aldosterone and cortisol -> hypotension and skin hyperpigmentation
secondary aldosterone and cortisol insufficiency
similar to Addison's except w/o skin hyperpigmentation
What is the most common tumor of the adrenam medulla in adults?
pheochromocytoma
pheochromocytoma
neoplasm that secretes epinerphrine and NE intermittently -> episodes of increased BP accompanied w/ headache
(rules of 10; 10% malignant, 10% bilateral, 10% extraadrenal, 10% calcify, 10% occur in kids, 10% familial)
What is the most common tumor of the adrenal medulla in children?
neuroblastoma
What diseases is pheochromocytoma associated with?
neurofibromatosis, MEN types II & III
What is the treatment for pheochromocytoma?
alpha-antagonists (esp. phenoxybenzamine)
What are the hyperadernergic symptoms of pheochromocytoma?
(5 P's)
Pressure (elevated)
Pain (headache)
Perspiration
Palpitations
Pallor/diaphoresis
MEN type I
pancreas, parathyroid, pituitary tumors
presents w/ kidney stones and stomach ulcers
MEN type II
medullary carcinoma of the thyroid, pheochromocytoma, parathyroid tumor, or adenoma
MEN type III
(aka MEN IIb)
medullary carcinoma of the thyroid, pheochromocytoma, and oral and intestinal ganglioneuromatosis (mucosal neuromas)
MEN types are associated w/ the ret gene?
MEN types II and III
What MEN types include pheochromocytoma?
MEN types II and III
What MEN types present w/ kidney stones and stomach ulcers?
MEN type I
Which MEN types include pancreatic tumors?
MEN type I
Which MEN types include medullary carcinoma of the thyroid?
MEN types II and III
Which MEN types include parathyroid tumor?
MEN type I and II
Which MEN types include oral and intestinal ganglioneuromatosis (mucosal neuromas)?
MEN type III
MEN syndromes have what kind of inheritance?
autosomal dominant
hypothyroidism
high TSH, low total T4, low free T4, low T3 uptake
hyperthyroidism
low TSH (if primary), high total T4, high free T4, high T3 uptake
Grave's disease
autoimmune hyperthyroidism w/ thyroid stimulating/TSH antibodies
What is the clinical presentation of hypothyroidism?
cold intolerance , hypoactivity, wt. gain, fatigue, lethargy, decreased appetite, constipation, weakness, decreased reflexes, myxedema, dry, cool skin, coarse-brittle hair
What is the clinical presentation of hyperthyroidism?
heat intolerance, hyperactivity, wt. loss, hest pain/palpitations, arrhythmias, diarrhea, increased reflexes, warm-moist skin, fine hair
What is the clinical presentation of Grave's disease?
ophthalmopathy, pertibial myxedema, diffuse goiter
often presents during stress
What is the treatment for Grave's disease?
propylthiouracil - inhibits production of thyroid hormone as well as peripheral conversion of T4 to T3
Is Grave's disease hyper- or hypothyroid?
hyperthyroid
Is Riedel's thyroiditis hyper- or hypothyroid?
hypothyroid
Riedel's thyroiditis
thyroid replaced by fibrous tissue (hypothyroid)
Hashimoto's thyroiditis
autoimmune disorder resulting in hypothyroidism
60-80x risk of developing thyroid lymphoma compared to normal controls
Subacute thyroiditis
(de Quervain's)
Self-limited hypothyroidism often following a flulike illness
(may be hyperthyroid early in course)
Is Hashimoto's thyroiditis hyper- or hypothyroid?
hypothyroid
Is subacute thyroiditis hyper- or hypothyroid?
hypothyroid, however may be hyperthyroid early in course
What are the 4 types of thyroid cancer?
papillary
follicular
medullary
undifferentiates/anaplastic
Which type of thyroid cancer has excellent prognosis?
papillary
Which type of thyroid cancer has good prognosis?
follicular
Which is the most common type of thyroid cancer?
papillary
What is the origin of medullary thyroid cancer?
parafollicular "C cells"
Which type of thyroid cancer produces calcitonin?
medullary
Which type of thyroid cancer has horrible prognosis?
undifferentiated/anaplastic
Which type of thyroid cancer has psammoma bodies?
papillary
Which type of thyroid cancer has "ground-glass" nuclei?
papillay
Which type of thyroiod cancer has uniform follicles?
follicular
endemic cretinism
lack of dietary iodine
sporadic cretinism
caused by defect in T4 formation or developmental failure in thyroid formation
What are the clinical findings of cretinism?
mentally retarded, pot-bellied, pale, puffy-faced child w/ protuding umbilicus and protuberant tongue
acromegaly
excess GH in adults
What are the clinical findings of acromegaly?
large tongue w/ deep furrows, deep voice, large hands and feet, coarse facial features
gigantism
excess GH in children
What are the acute manifestations of diabetes mellitus?
polydipsia, polyuria, polyphagia, wt. loss, DKA (type 1), hyperosmolar coma (type 2), unopposed secretion of GH and epinephrine (exacerbating hyperglycemia)
What are the chronic manifestations of diabetes mellitus?
1) small vessel disease -> retinopathy, glaucoma, nephropathy
2) large vessel atherosclersis, CAD, peripheral vascular occlusive disease and gangrene, cerebrovascular diseaes
3) neuropathy
4) cataracts (sorbitol accumulation)
What are the tests used to diagnose diabetes mellitus?
fasting serum glucose
glucose tolerance test
HbA1c (measures long-term diabetic control)
diabetic ketoacidosis
usually due to an increase in insulin requirements from an increase in stress (e.g., infection)
excess fat breakdown and the increase in free fatty acids, which are then made into ketone bodies
What are the signs/symptoms of diabetic ketoacidosis?
Kussmaul respirations (rapid/deep breathing)
hyperthermia
nausea/vomiting
abdominal pain
psychosis/dementia
dehydration
fruity breath odor
What are the lab values in diabetic ketoacidosis?
hyperglycemia
increased H
decreased HCO3
increased blood ketone levels
leukocytosis
hyperkalemia (but depleted intracellular K)
What are the complications of diabetic ketoacidosis?
life-threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythmias, heart failure
What is the treatment for diabetic ketoacidosis?
fluids, insulin, potassium
glucose to prevent hypoglycemia
central diabetes insipidus
lack of ADH
(pituitary tumor, trauma, surgery, histocytosis X)
nephrogenic diabetes insipidus
lack of renal response to ADH
(hereditary or secondary to hypercalcemia, lithium demeclocycline)
What are the lab findings for diabetes insipidus?
urine spec. gravity < 1.006
serum osmolality > 290 mOsm/L
What is the treatment for central diabetes insipidus?
intranasal desmopressin (ADH analog)
What is the treatment for nephrogenic diabetes insipidus?
hydrochlorothiazide (diauretic - paradoxical effect)
indomethacin
amiloride
SIADH
excessive ADH secretion caused by
1) ectopic ADH (small cell lung cancer)
2) CNS disorders/head trauma
3) pulmonary disease
4) drugs (e.g., cyclophosphamide)
What are the symptoms of SIADH?
excessive water retention
hyponatremia
urine osmolarity > serum osmolarity
What are the causes of hypercalcemia?
(CHIMPANZEES)
Calcium ingestion
Hyperparathyroid
Hyperthyroid
Iatrogenic (thiazides)
Multiple myeloma
Paget's disease
Addison's disease
Excess vit. D
Excess vit. A
Sarcoidosis
hyperparathyroidism
excessive PTH
What are the causes of primary hyperparathyroidism?
usually an adenoma
What are the lab findings of primary hyperparathyroidism?
increased PTH
hypercalcemia
hypercalciuria
hypophosphatemia
increased cAMP in urine
What are the lab findings of secondary hyperparathyroidism?
increased PTH
hypocalcemia
hyperphosphatemia
osteitis fibrosa cystica
(aka von Recklinghausen's syndrome)
cyctic bone spaces filled w/ brown fibrous tissue
renal osteodystrophy
bone lesions due to secondary hyperparathyroidism due in turn to renal disease
hypoparathyroidism
low PTH -> hypocalcemia, tetany
due to accidental surgical excision or DiGeorge syndrome
pseudohypoparathyroidism
kidney unresponsive to PTH -> hypocalcemia, shortened 4th/5th digits, short stature
autosomal recessive
carcinoid syndrome
recurrent diarrhea, cutaneous flushing, asthmatic wheezing, right-sided valvular disease
Why is carcinoid syndrome not seen if carcinoid tumor is limited to the GI tract?
b/c serotonin undergoes 1st pass metabolism in the liver
What is the most common tumor of the appendix?
carcinoid tumor
What is the cause of carcinoid syndrome?
carcinoid tumors (neuroendocrine cells) which secrete high levels of serotinin
What is the treatment for carcinoid syndrome?
octreotide
What fraction of carcinoid tumors metasitasize?
1/3
Zollinger-Ellison syndrome
gastrin-secreting tumor of pancreas -> recurrent ulcers
may be assoc. w/ MEN type I
osteoperosis
reduction of bone mass in spite of normal mineralization
type I osteoperosis
postmenopausal
increased bone resorption due to decreased estrogen levels
type II osteoperosis
senile osteoporosis
affects men and women > 70 years old
Osteoperosis affects what population the most?
whites > blacks > Asians
What is the cause of type I osteoperosis?
decreased estrogen levels -> increased bone resorption
postmenopausal