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100 Cards in this Set
- Front
- Back
gluagaon/insulin interaction
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insulin --| glucagon --| insulin (mutually inhibitory)
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neurophysins (what are they)
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carrier proteins for oxytocin and ADH produced within paraventricular and supraoptic nuclei, respectivelysubarachnoid hemorrhage vs sellar mass w/ suprasellar extension (pituitary tumor)
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pituitary apoplexy
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acute bleeding into preexisting pituatiry adenoma -- get acute sx (severe headaches, visual disturbances) on top of chronic mass-effect sx (chronic headaches, hormone deficiencies)
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suprasellar mass w/ 3 components (solid, cystic, and calcified)
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craniopharyngioma
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rule of 10s
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features of pheo: 10% hereditary (MEN@, VHL); 10% b/l, 10% extra-adrenal, 10% malignant
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three clinical presentations of glucagonoma
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1) DM; 2) necrolytic erythema; 3) anemia
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MEN I
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hyper parathyroidism (hypercalcemia); pancreatic tumor (gastrin --> zollinger elliso or insulin --> hypoglycemia or VIP --> diarrhea); ppituitary (prolactin, ACTH)
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what hormone to check if suspect hypothyroidism?
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TSH (rises below T4 levels drop -- T3 has exponential? feedback effect on TSH)... T3 declines even later
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branching paipllary structures with interspersed calcified bodies
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psammoma bodies
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which glucose transporter is responsive to insulin?
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glut-4
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which cells have insulin-depndent glucose transporters (and which glucose transporter is it?)
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glut 4: adipocytes, skeltal muscle cells
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distribution of glut-1
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red cells, CNS (basal glucose transport)
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distribution of glut-2
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hepatocytes, pancreatic beta-cells (relguation of insulin rlease)
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distribution of glut-3
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placenta, brain, kidney (placental glucose xport)
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distribution of glut-4
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muscle-cells, adipocytes (insulin-mediated)
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distribution of glut-5
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spermatocytes, GI tract (fructose transport)
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chvostek's sign
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facial muscle excitability due to hyPOcalcemia
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estrogen's effects on thyroid hormones
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estrogen increases TBG (thyroid binding globulin) levels --> increased total T4, but normal free T4 and T3 -- pts remain euthyroid, normal TSH
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hypertension with low plasma renin activity
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primary hyperaldosteronism --> hypokalemia, metabolic alkalosis
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replacment for aldosterone
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9-alpha fludrocortisone
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small, round, blue neuroblasts
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neuroblastoma: neuroendocrine tumor from neural crest; usu in kids
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drainage of L and R adrenal glands
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just like testes -- L to renal vein, R to IVC; (both via adrenal veins)
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source of melanotropin
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ant pit (aka MSH = melanocyte stimulating hormone --> production/relase of melanin)
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embryologic origin of pituitary
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anterior: oral ectoderm; posterior: neuroectoderm
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alpha subunit in pituitary gland
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common subunit for FSH, LH, TSH, and hCG (speicificity by unique beta subunit)
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site of prolactin secretion
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anterior pit
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hormonal regulation of prolactin secretion
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from hypothalamus: DA inhibits secretion, TRH promotes secretion
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prolactinoma: symptoms and tx
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sx: amenorrhea (women), galactorrhea (both?); tx: bromocriptine (DA agonist, inhibits prolactin secretion
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effects of PTH (4)
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1) inc bone resoroption --> Ca and Pi; 2) inc renal reabsorption of Ca; 3) dec renal reabsorption of Pi; 4) increased renal production of Vit D
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regulation of PTH
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decreased Ca --> inc PTH
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net PTH effects (w/o renal dz)
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inc serum Ca++, dec Pi, inc urine Pi, dec bone mass
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pth effects on osteoblasts/clasts
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directly stims osteoblasts --> indirectly stims osteoclasts
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regulation of Vit D3 formation
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positive: PTH; negative: Ca, Pi, Vit D3 (self-regulated)
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effects of calcitriol (vit D3)
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1) bone resoprtion --> inc Ca and Pi; 2) increases calcium and phosphate reabsorption from intestines
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renal insufficiency --> effects on Ca, Pi, Alk Phos, PTH
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renal insufficiency --> impaired Pi secretion --> inc Pi --| Vit D --> dec Ca reabsorption --> inc PTH; NET RESULT: dec Ca, inc Pi, inc PTH, n/c AlkPhos
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calcitonin: source, effects, regulation
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SOURCE: C-cells of thyroid (neural crest); EFFECT: inhibits bone resoprtion (opposed PTH); REGULATION: upregulated by Ca++
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what hormones act on intracellular receptors?
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steroid/thyroid: Progesterone, Estrogen, Testosterone, Aldosterone, Cortisol, Thyroxine and T3 (all Adrenal cortex products + Thyroid hormones)
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effects of sex-hormone-binding globulin (SHBG)
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steroid hormones must travel in blood bound to SHBG b/c they are lipophilic (remember, intracellular receptor); changes in SHBG affects efficacy of hormones; eg inc SHBG --> dec free testosterone --> gynecomastia; dec SHBG --> inc free testosterone --> hirsutism
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T3 functions
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4 B's: 1) Brain maturation; 2) Bone growth (synergy with GH); 3) Beta adrenergic effects (on heart); 4) BMR increased (inc NaK pump activity)
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what causes fluctuation in TBG (thyroxine binding globulin)
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dec TBG in liver failure, inc TBG in pregnancy
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which organs depend on glucose for metabolism (normally)
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brain, RBCs (both use GLUT-1 transporter, insulin-independent
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whats the insulin-dependent GLUT and on which organs is it found?
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GLUT-4: skeletal muscle and adipocytes
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cortisol effects on skin
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thinning, striae (think cushing's)
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cortisol effects on bone
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osteoporosis
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cortisol effects on menstruation
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amenorrhea
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primary vs secondary hyperaldosteronism
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renin levels (high in secondary, low in primary)
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causes of secondary hyperaldosteronism
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renal artery stenosis, chronic renal failure, CHF, cirrhosis, nephrotic syndrome
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primary vs secondary adrenal insufficiency
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skin pigmentation: PRIMARY (addison's) --> inc ACTH --> inc MSH --> hyperpigmentation; SECONDARY: dec ACTH --> dec cortisol, no inc in MSH --> no skin hyperpigmentation
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adrenal medulla tumors: kids and adults
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adults: PHEOchromocytoma, chromaffin cells (neural crest), episodic HTN/hyperglycemia; kids: NEUROBLASTOMA, can occur anywhere along sympathetic chain, NON episodic, usually malignant
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what disorders is pheo a/w
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neurofibromatosis, MEN II, MEN III
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neurofibromatosis increases risk of which cancers
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pheochromocytoma, meningioma
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pheo rule of 10s
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10% extra-renal, 10% b/l, 10% malignant, 10% affect kids, 10% familial, 10% calcify
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periodicity of sx in pheo, neuroblastoma
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NEUROBLASTOMA: constant; PHEO: relapse/remit (need urine sample to integrate levels)
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tx for pheo
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phenoxybenzmine (irreversible nonselective alpha blocker), give before beta blocker (otherwise massively inc HTN)
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MEN I organs
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tumors of: Parathyroid, Pituitary, and Pancreas (Zollinger-ellison, insulinoma, glucagonoma, VIPoma)
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sx of MEN I
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kidney stones (parathryoid --> inc Ca), stomach ulcers (pancreatic --> Zollinger-ellison --> H++++)
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Riedel's thyroiditis
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thyroid replaced by fibrous tissue --> hypothyroidism; can extend into neighboring tissues like a malignancy
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thyroid hormone's effects on skin/hair
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hypothyroidism --> dry, thick, cool skin; coarse, brittle hair
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Subacute thyroiditis (de Quervain's)
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self-limited hypothyroidism following flu-like illness; elevated ESR, **jaw pain**, early inflammation, very tender thyroid gland; can be hypERthyroid at beginning (kinda like jarish-herxheimer rxn)
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which type of thyroid cancer has poor prognosis?
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undifferntiated / aplastic (OLDER patients)
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name the three types of thyroid cancers with good prognosis, + defining features
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1) PAPILLARY: most common, psammoma bodies, orphan annie (ground glass) nuclei 2) MEDULLARY: sheets of parafollicular C cells in amyloid stroma (MEN II and III) 3) FOLLICULAR: uniform follicles, more malignant (hematog. spread to lung/bones)
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cause and findings of cretinism
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CAUSE: iodine deficiency; FINDINGS: pot-bellied, pale, puff-faced child with protruding umbilicus and protuberant tongue, + MR (thyroid hormone needed for Brain maturation)
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relationship between cushings and sugar
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cushing's disease (excess cortisol) --> insulin resistance --> hyperglycemia; other diabeties like sx (weight gain, hypertension, truncal obesity)
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relationship between acromegaly and sugar
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acromegaly causes insulin resistance (like cushing's) --> hyperglycemia
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stimuli for GH release
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stress, exercise, hypoglycemia (same as cortisol)
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sx of hyperparathyroidism
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hypercalcemia --> "Stones, Bones, and Groans" (renal stones, bone pain, weakness/constipation)
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pseudohypoparathyroidism
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AR, kidney doesn’t respond to PTH --> hypocalcemia, shortened 4th/5th digits, short stature
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what hormones counter insulin's effects?
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CORTISOL (--| response to insulin), EPINEPHRINE (inc glycogenlolysis and lipolysis), GROWTH HORMONE (inhibits cellular uptake of gluc, stims lipolysis), THYROID HORMONE (permits epi's efficts and reqd for GH production), GLUCAGON (inhibits insulin response, promotes catabolism)
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HLA association of DM type I
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HLA-DR3 and -DR4
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kussmaul's respiration
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rapid deep breathing seen in DKA to blow off excess acid
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signs of DKA
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kussmaul respirations, hyperthermia, psychosis/dementia, dehydration, FRUITY BREATH (acetone)
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labs in DKA
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inc ketones --> dec HCO3- (anion gap metabolic acidosis); inc H+ --> inc K+ (pulled from inside cells as excess H+ goes into cells); hyper glycemia, leukocytosis
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complications of DKA
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MUCORMYCOSIS (Mucor or Rhizospus infection, also seen in leukemic patients, tx mucor with capsofungin); CEREBRAL EDEMA, cardiac ARRYTHMIAS, HEART FAILURE
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mucor vs aspergillus morphology
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both MOLDs with hyphae, MUCOR has WIDE angle branching, ASPERGILLUS has ACUTE angle (<45') branching
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causes of central DI
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pit tumor, trauma, surgery, histiocytosis X
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causes of nephrogenic DI
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hypercalcemia, Lithium, Demeclocycline (a Tetracycline) --> used as tx for SIADH
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tx for NDI
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HCTZ, indomethasin, amiloride (K+ sparing diuretic)
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tx for central DI
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ADH analog (desmopressin = DDAVP)
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what drugs can cause SIADH
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cyclophosphamide
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carcinoid tumor, rule of thirds
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1/3 metastasize, 1/3 present with 2nd malignancy, 1/3 multiple
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tx for carcinoid syndrome
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octreotide (somatostatin analog, neutralizes 5-HT)
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side effects of first-generation sulfonylureas
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disulfiram like reaction
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role of sertoli cells
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produce MIF, inhibin (--| FSH), ABP, and promote spermatogenesis
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concentrically calcified structures found in thyroid tumors
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psammoma bodies -- papillary thyroid cancer
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marfinoid habitus
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tall, slender, disporoportionately long arms -- a/w MEN III (MEN IIb)
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mediators of islet cell destruction in DM type I
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T- cells (Abs are believed to be generated in response to cell destruction)
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consequences of celiac disease
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fat malabsorption --> dec nutrients, minerals, ADEK
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where is ADH synthesized?
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in the hypothalamus (paraventricular or supraoptic nuclei, along with oxytocin)
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damage to post pit vs hypothalamus
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damage to post pit causes only transient DI-like sx (polydipsia, polyuria), because ADH from hypothalamus eventually enters circulation directly from pituitary stalk; hypothalamic damage, however, is permanent
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how does excess of sex hormones produce short stature?
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sex hormones promote growth (initially early growth spurt), but also close epiphyseal plates (eventually these kids are short)
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histo appearnce of medullary carcinoma of the thyroid
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uniform polygonal / spindle-shaped cells w/ extracellular amyloid deposits; secreted calcitonin forms AMYLOID
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types of amyloid
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AL: primary (mult myeloma, waldenstroms); AA: secondary (chronic inflam disease like TB, RA, osteomyelitis, syphilis); A-BETA (alzheimers); CALCITONIN (medullary carcinoma of thyroid); AMYLIN (DM type II)
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histo appearance of anaplastic thyroid cancer
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pleomorphic giant cell nests w/ occasional multinucleated cells
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histo appearance of papillary thyroid cancer
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well differentiated, branching structures with interspersed calcified bodies
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role of hCG in infertility
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can stimulate LH surge
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causes of polyuria and polydipsia
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DM, DI, primary (psychogenic) polydipsia
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use of indomethacin in NDI
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inhibits prostaglandins which inhibit ADH
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what in overweight individuals causes insulin resistance?
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elevated FFA and serum triglycerides
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hCG and TSH -- similarities and implications
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both share beta unit, so some homology between the two. Excessively high hCG levels (eg germ cell testicular/ovarian tumors) can cause hyperthyroidism
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consequences of untreated prolactinoma
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prolactin --| GnRH (remember no menstruation while prolactin is high -- sex during first 6 months) ==> amenorrhea, anovulation, hypogonadism; direct effect at breast ==> galactorrhea; can see normal sequelae of hypoestrogen (osteoporosis, hot flashes, etc)
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