Endo/Repro Flashcards
Mech of glucose as insulin stimulator
- Glucose into cell, metabolized –> ATP
- ATP => close K+ channels -> depolarize
- open volt-gated Ca2+ channels –> Ca2+ influx => insulin secretion
Glucose Receptor types:
GLUT-1
GLUT-2
GLUT-4
1: insulin INdependent (RBCs, brain)
2: BIdirectional (B islet cells, liver, kidney, small intestine)
4: insulin DEpendent (fat, skeletal muscle)
Effects of insulin (on ALL parts of body!) “anabolic”
- skel. m/fat: increase glucose uptake, increase protein synthesis
- liver: increase glycogen synthesis, and TG synthesis/storage
- kidneys: increase Na+ retention
- increase cell uptake of K+ & AAs
- decrease glucagon release
Effect of adrenergic signalers on insulin secretion
B2 antagonists: increase insulin
Alpha2 agonists: decrease insulin
3 types of pancreatic cells
- alpha –> glucagon
- beta –> insulin
- delta –> somatostatin *inhibits glucagon and insulin secretion
regulation of growth hormone (“somatotropin”)
secretion = in pulses, increases during exercise and sleep
Inhibitors: glucose, somatostatin
Case:
Child with hypertension, hypokalemia and ambiguous genitalia/lack of secondary sex characteristics
congenital bilateral adrenal hyperplasia (CAH), w/ 17a hydroxylase def.
=> high mineralcorticoids, low cortisol and sex hormones
Male: undescended testes, ambig. genitalia (insuff. DHT)
Female: normal int. & external sex genitalia, no secondary sex features
Case:
young female with hypotension, hyperkalemia, increased renin activity & volume depletion, and pseudohermaphroditism
CAH (congenital adrenal hyperplasia) w/ 21-hydroxylase def.
*most common form of CAH
low mineralcorticoids & cortisol, high sex hormone levels
–> masculinization bc shunting of products towards testosterone
Case:
Young adult female with hypertension and masculinization
CAH (congenital adrenal hyperplasia) w/ 11B-hydroxylase def.
=> low aldosterone! but high 11-deoxycorticosterone, low cortisol, HIGH sex hormone levels
Masculinization bc shunt products toward testosterone
major functions of cortisol (4)
- maintain BP (upregulate a1 Rs in arterioles)
- inhibit Bone formation & fibroblasts
- Immune-suppression/anti-inflam. (–l leukotrienes, prostaglandins, histamine, eosinophils, IL-2, and leuk adhesion)
- Increase Gluconeogenesis and insulin resistance
function of PTH (parathyroid hormone)
Goal: increase serum Ca2+
- increase bone reabsorption
- increase renal reabsorption of Ca2+ & decrease renal PO4- reabs.
- increase 1,25-D3 production (stimulate renal 1a-hydroxylase)
* opposed by calcitonin*
effect of 1,25D3 on gut absorption
active Vit D (1,25D3 aka calcitriol) acts on gut to increase Ca2+ AND PO4- absorption!
(vs PTH acts on kidney, increases Ca reabs. & decreases PO4- reabs.)
Function of T3 (thyroid hormone)
“4 B’s”
- Brain maturation
- Bone growth
- B1 adrenergic (increase CO, HR, SV, contractility)
- increase Basal metabolic rate (via Na+/K+ ATPase –> incr. O2 consumption, RR, body temp; also incr. glycogenolysis/gluconeogen.)
Wolff-Chaikoff effect
excess iodine in system –> temporarily inhibits thyroid peroxidase
=> less iodine processing = less T3 & T4 production
Distinguishing between types of abnormal ACTH secretion
Cushing’s syndrome
use dexamethasone suppression test (low and high dose)…
normal: cortisol suppressed by low OR high dose.
Pituitary adenoma: high ACTH, low - elevated, high - suppressed.
Ectopic tumor: high ACTH, low - elevated, high - still elevated.
Cortisol tumor (adrenal): less ACTH, low - elevated, high - elevated.
symptoms of Cushing’s disease/syndrome
HTN, weight gain, truncal obesity and buffalo hump, hyperglycemia, stria/thin skin, osteoporosis, amenorrhea, immune suppression
Conn’s syndrome
aldosterone-secreting adrenal adenoma (primary hyperaldosteronism)
=> HTN, hypOK+, metabolic alkalosis, low plasma renin
Tx: spironolactone and/or surgical resection
primary vs. secondary hyperaldosteronism
Primary: too much aldosterone (adrenal hyperplasia or ectopic)
=> LOW plasma renin
Secondary: overactive RAAS bc kidneys percieve low volume
=> HIGH plasma renin level (ie: renal a stenosis, CHF, cirrhosis, etc)
Primary vs. Secondary adrenal insufficiency
Primary (Addison’s disease): adrenal destruction bc disease process
=> hypotension, hyperK+, acidosis, skin hyperpigmentation (bc MSH)
Secondary: NO skin hyperpigmentation or hyperK+
Case:
Child with swollen belly & diarrhea, also generalized fatigue, etc. Testing shows increased HVA (Homovanillic acid) in urine.
= Neuroblastoma (of adrenal medulla/sympathetic chain)
- over-expression of n-myc => risk rapid tumor progression
- similar to pheochromocytoma but HTN less likely
Types of hypOthyroidism
1: Hashimoto’s: autoimmune, w/ HLA-DR5 & anti-thyroiglobulin Abs
- congenital (Cretinism): hypotonic, poor feeding, umbilical hernia
- Subacute/DeQuervain’s: post-flu, self limited w/ granulomatous inflamm. Very tender thyroid.
- Riedel’s: replace thyroid w/ fibrous tissue, “rock hard” & immobile.
types of hypERthyroidism
- Toxic/Multinodular goiter: focal “hot nodules” bc TSH R mutation
- Grave’s disease: IgG Ab to TSH R (“thyroid-stimulating globulins”), w/ diffuse goiter.
* complication:
Thyroid storm…catecholamine surge -> arrhythmia -> death *high AlkP
Common presentations for pituitary adenoma
1: prolactinoma –> amenorrhea, galactorrhea, bitemporal hemianopia. Tx = bromocriptine (dopamine agonist)
- Acromegaly (excess GH)
* Dx: GH doesn’t suppress w/ oral glucose tolerance test
Diabetes Insipidus: nephrogenic vs. central
=> LOW urine specific gravity (can’t [ ] urine), polydipsia/polyuria.
Nephrogenic DI: no rxn to ADH => does NOT correct w/ desmopressin
Central DI: lack ADH => DOES correct w/ desmopressin
