Endocrine Flashcards
cAMP
FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2 receptor), MSH, PTH, calcitonin, GHRH, glucagon
“FLAT CHAMP”
cGMP
ANP, NO “think vasodilators”
IP3
GnRH, Oxytocin, ADH (V1 receptor), TRH “GOAT”
Steroid receptor (cytosolic)
Vitamin D, Estrogen, Testosterone, Cortisol, Aldosterone, Progesterone
“VET CAP”
Steroid receptor (nuclear)
T3/T4
Intrinsic tyrosine kinase (MAP kinase pathway)
Insulin, IGF-1, FGF, PDGF (think growth factors)
Receptor-associated tyrosine kinase (JAK/STAT pathway)
GH, prolactin (also cytokine Il-2)
For the pituitary gland, what hormones is the alpha subunit common to?
TSH, LH, FSH, hCG
What are the four functions of T3?
4B’s: brain maturation, bone growth, increased basal metabolic rate, beta-adrenergic
Conn’s syndrome
primary hyperaldosteronism; caused by an aldosterone-secreting tumor –> hypertension, hypokalemia, metabolic alkalosis, and LOW plasma renin
What is secondary hyperaldosteronism?
Kidney perception of low intravascular volume –> overactive renin-angiotensin system (HIGH plasma renin); due to renal artery stenosis, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome
What is Waterhouse-Friderichsen syndrome?
acute primary adrenal insufficiency due to adrenal hemorrhage associated with N. meningitis septicemia, DIC, endotoxin shock
phenoxygbenzamine
nonselective, irreversible alpha-blocker; used for treatment of pheochromocytoma
What are the five episodic hyperadrenergic symptoms of pheochromocytoma?
5 P’s: pressure (elevated), pain (headache), perspiration, palpitations (tachycardia), pallor
What is the rule of 10’s for pheochromocytoma?
10%: malignant, bilateral, extra-adrenal, calcify, kids, familial
Neuroblastoma
most common tumor of the adrenal medulla in children; HVA (breakdown of dopamine) is elevated in urine; overexpression of N-myc associated with rapid tumor progression
What are the features of cretinism?
pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue (due to severe fetal hypothyroidism, lack of dietary iodine)
What is the action of insulin?
Binds insulin receptor (tyrosine kinase activity
Liver: increases glucose stored as glycogen
Muscle: increases glycogen and protein synthesis, K uptake
Fat: aids TG storage
What is the clinical use and toxicities of insulin?
Type 1 and 2 DM, gestational diabetes, life-threatening hyperkalemia, stress-induced hyperglycemia
Toxicities: hypoglycemia, hypersensitivity reaction (very rare)
What is the action of sulfonylureas?
Close K channel in the B-cell –> depolarizes –> triggering of insulin release via increased calcium influx
“Kicking the pancreas” to increase insulin output
What are the clinical use and toxicities of sulfonylureas?
Clinical use: stimulate release of endogenous insulin in type 2 DM; requires some islet fxn, so useless in DM type 1.
Toxicities; first generation: disulfiram-like effects, second generation: hypoglycemia
What is the action of biguanides (metformin)?
Decrease gluconeogenesis, increase glycolysis and increase peripheral insulin sensitivity
What are the clinical use and toxicities of biguanides?
Clinical use: oral, can be used with pts w/out islet fxn
Toxicities: most grave adverse effect is lactic acidosis (contraindicated for those with renal failure)
What is the action of glitazones/thiazolidinediones?
increase insulin sensitivity in peripheral tissue; binds to PPAR-gamma nuclear transcription regulator
