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100 Cards in this Set

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