Endocrine Flashcards
MEN 1: Werner
3 P’s: pituitary (often prolactinoma), parathyroid (adenoma or hyperplasia), pancreas
MEN 2A: Sipple
2 P’s: parathyroid hyperplasia, pheochromocytoma, medullary thyroid cancer
MEN 2B: Gorlin
1 P: pheochromocytoma, medullary thyroid cancer, mucosal neuromas
Signs of hyperPTH
increased Ca, decreased PO4 osteoporosis kidney stones polydipsia, polyuria constipation bone and muscle pain
Signs of hypoPTH
low Ca, increased phosphate
tingling, numbness
Trousseau: BP cuff on triceps occluding brachial artery –> carpal spasm
Chvostek: tapping the cheek causes contrxn of facial muscles
Muscle spasms
Seizures
CAH (3 types)
all p/w decreased cortisol
- 17a-hydroxylase deficiency: HTN d/t increased mineralocorticoids; all pts phenotypically F
- 21-hydroxylase deficiency: virilized F d/t high androgens; increased renin activity but reduced mineralocorticoids. most common. presents in infancy (salt wasting) or childhood (precocious puberty)
- 11b-hydroxylase deficiency: HTN d/t 11-deoxycorticosterone (even though mineralocorts & renin activity decreased); virilized F d/t increased androgens
starts w/ a 1: HTN; ends w/ a 1: virilized F
Cushing & dexamethasone suppression test
- high ACTH (ACTH-dependent Cushing)
- low ACTH (ACTH-independent Cushing)
- high ACTH: do HIGH dose dexamethasone test. If suppressed w/ high dose: pit adenoma (Cushing disease). If not suppressed w/ high dose, ectopic ACTH secretion (e.g. PNPS of small-cell lung cancer)
- low ACTH: this is d/t exogenous glucocorticoids, or an adrenal tumor
Histology of medullary thyroid cancer
From parafollicular C cells; produces Calcitonin. Sheets of polygonal or spindle cells in amyloid stroma (derived from calcitonin; stains w/ Congo red)
Histology of anaplastic thyroid cancer
Pleiomorphism; irregular giant cells, biphasic spindle cells. Older pts (60+); invades local structures, poor prog
Histology of papillary thyroid cancer
Empty “orphan annie” nuclei, psammoma bodies, nuclear grooves. Tall cell variant will have follicular hyperplasia lined by tall epith cells (seen in older pts, worse prognosis)
Renal osteodystrophy
HyperPTH secondary to renal disease: will have high PTH causing increased bone resorption/osteomalacia; decreased vit D (can’t make in kidney) –> reduced PO4 excretion so PO4 increases in serum and binds Ca2+ (hypocalcemia)
Familial hypocalciuric hypercalcemia
Defective GPCR Ca2+ sensing ability –> takes more than normal Ca2+ levels to suppress PTH. Will have hypercalcemia, low urine Ca2+, and normal to high PTH
Think of an old, blind “grandpa” GPCR who has a hard time seeing Ca2+
Distinguishing primary and secondary hyperPTH
Primary: d/t parathyroid hyperplasia, adenoma or carcinoma. PTH overproduction leads to hypercalcemia
Secondary: d/t vit D deficiency, reduced Ca2+ intake, or CKD. Ca2+ will be low, causing compensatory increase in PTH. If d/t CKD: PO4 will be high (can’t excrete), Epo will be low (anemia) and vit D will be low (can’t activate in kidney)
Distinguishing primary and secondary hypoPTH
Primary: low PTH d/t surgical resection or AI cause, resulting in low Ca2+
Secondary: PTH-independent hypercalcemia. D/t increased Ca2+ intake, cancer, or increased vit D - causes compensatory decrease in PTH and increased PO4
Side effects of glucocorticoids
- hyperglycemia/DM: increase gluconeogenesis/glycolysis in liver, and block insulin
- osteoporosis & avascular necrosis (femoral head)
- amenorrhea & hypogonadism
- adrenocortical atrophy; adrenal insufficiency if stopped abruptly after chronic use
- peptic ulcers
- psychosis
- cataracts
- skeletal muscle atrophy
- skin thinning, striae, impaired wound healing
- artificial leukocytosis (demarginates WBCs)
