Exam 2 Flashcards
Primary hyperparathyroidism
Painful bones (osteoporosis) Renal stones (neprolithiasis) Abdominal groans (constipation, gallstones) Psychic moans (depression, lethargy, siezures)
Causes: adenoma (85-95%)
hyperplasia
carcinoma
Osteitis fibrosis cystica
symptom of primary hyperparathyroidism
aka brown tumor, can look like metastatic cancer
osteoclast driven bone destruction, small fractures and hemorrhage
Parathyroid adenoma
Most common cause of primary hyperparathyroidism
Affects only 1 parathyroid gland
normal rim of parathyroid tissue
Parathyroid hyperplasia
Indicates primary or secondary hyperparathyroidism
affects all 4 glands
no normal rim of parathyroid tissue
Parathyroid carcinoma
Causes Primary hyperparathyroidism
metastasis
local invasion
elevated PTH that does not go down after surgery
Hypercalcemia, symptomatic vs asymptomatic
asymptomatic → primary hyperparathyroidism
symptomatic → malignancy
Hypercalcemia of malignancy
caused from PTHrP, analogue of PTH, released from lung and breast cancers
or lymphomas releasing vitamin D
or just osteolysis from breast/lung cancer
Secondary hyperparathyroidism
Renal failure causes ↓Ca++ which triggers ↑ PTH
all 4 glands will undergo hyperplasia
renal osteodystrophy (rugby jersey)
Calciphylaxis → patients may die from sepsis from gangrene
Tertiary hyperparthyroidism
prolonged hypocalcemia causes parathyroids to lose regulation and just always release a bunch of PTH
Hypocalcemia
Trosseau sign (BP cuff wrist flexion) Chvostek sign (CNVII twitching) prolonged QT interval Muscle cramps, spasms, tetany Convuslsions Numbness and parathesia Behavioral disturbances
DiGeorge syndrome’s effects on parathyroids
parathyroid hypoplasia/aplasia
hypocalcemia
DiGeorge syn: facial abnormalities, cyanosis, infection, tetany
Familial hypocalciuric hypercalcemia
LOF mutation of CaSR
↑ PTH
↑ Ca++
↓ renal excretion (hypocalciURIA)
Autosomal dominant hypoPTH
GOF mutation of CaSR
↓ PTH
↓ Ca++
↑ renal excretion of Ca++
Pseudohypoparathyroidism
hypocalcemia despite ↑↑PTH
Albrights heriditary osteodystrophy
short stature
shortened fingers and toes
obesity
Mass effect of pituitary enlargement
headache confusion shallow breathing nausea papilledema HTN bradycardia
Lactotroph adenoma
Most common secretory pituitary adenoma
Psammoma bodies, pituitary stone
Women → menstrual irregularities, galactorrhea, diminished libido, infertility, mass effect
Men → decreased libido, decreased sperm count, mass effect
Treatment is dopamine agonists (bromocriptiine and cabergoline) or surgery
Somatotroph adenoma
gigantism, acromegaly
↑IGF-1
Glucose tolerance test to confirm
glucose should cause ↓ GH, if it doesn’t then they have adenoma
Cushing syndrome
centripetal obesity moon face abdominal thick stria thin skin hirsutism usually caused iatrogenically, glucocorticoid administration
corticotroph adenoma
aka cushing's disease ↑ cortisol ↑ ACTH cortisol decreases in response to high dose dexamethasone suppression test USP8 mutations possible
Ectopic ACTH producing tumor
paraneoplastic syndrome of small cell carcinoma of the lung, or pancreatic carcinoma
↑ cortisol
↑ ACTH
Cortisol levels do not respond to high dose dexamethasone suppression test
Nelson syndrome
A syndrome caused by adrenal removal in the case of corticotroph adenoma.
ACTH has no adrenals to act on, but nothing is suppressing ACTH secretion
Hyperpigmentation remains, because ACTH → MSH
Tumor keeps on growing so mass effect may occur
Gonadotroph adenoma
asymptomatic until tumor is large enough to cause mass effect
GNAS mutations
Gs loses GTPase activity making GTP always active, and cascade always turned on
Craniopharyngioma
Causes hypopituitarism
kids → adamantinomatous, growth retardation
adults → papillary, intracranial pressure
derived from rathke’s pouch remnants
Things that cause hypopituitarism
pituitary gets squashed, has ischemia, or hemorrhaged
Empty sella syndrome
CSF leaks and squished pituitary
Pituitary expands, infarcts, and then necrotizes, leaving empty sella
Sheehan syndrome
postpartum necrosis of ant pituitary from ischemia or infarction
Diabetes insipidus
Central vs nephrogenis
↓ ADH (AVP) ↑ water excretion hyperosmolarity hypernatremia polyuria which is dilute ↑ thirst
Central: DDAVP adminstration fixes it
Nephrogenic: DDAVP administration does nothing