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5_2010 Endo


unexplained wgtloss in elderly need to check for hyperthyroid [esp wkness, +/- A fib]
what pattern of radioiodine scan uptake seen in Graves diffuse scan (all cells hyperfxn)
what's Plummers multinodular toxic goiter (hyperfxning nodular areas)
clinical features of hyperthyroid (CNS, mscl, GI, CVS) CNS=nervousness, insomnia, tremor, hyperactivity; mscl: sweating, heat intolerance, wkness; GI=wgt loss despite incrsd appetite, diarrhea; CVS: palpitations (+/- BP)
5 causes of hyperthyroid 1) Graves, 2) multinodular toxic goiter, 3) thyroid adenoma, 4) Hashimoto's thyroidits/subacute hypothyroidits, 5) post-partum hyperythyroid
new onset A fib, check for hyperthyroid
which thyroid dz more common in elderly? Radioiodide pattern uptake multinodular toxic goiter (hyperfxning nodular areas); patchy uptake
single hi uptake nodule on radioiodide scan, etiology? thyroid adenoma
when Graves diagnosed, what other diseases need to think about autoimmune dzs
which signs/symptoms hyperthyroidism are specific to Graves exophthalmos, pretibial myxedema, thyroid bruits
causes of incrsd TBG (4) 1) preg, 2) liver dz, 3) OCP, 4) ASA
when TBG is incrsd, what happens to T4? Active thyroid? total T4 incrses, but what care abt free T4
hormone levels in Graves? Other hyperthyroid dzs? TSH low, T3/T4 high
what are the 2 types of subacute thyroiditis, how are they difft? subacute viral (granulomatous), which is painful and usu viral prodrome few wks; subacute lymphocytic (painless, silent) non painful
radioiodide uptake of subacute thyroiditis low
Hashimoto's thyroiditis aka chronic lymphocytic
what other autoimmune diseases is Hashimoto's thyroiditis assoc w SLE, pernicious anemia [note: family hx is common]
when Hashimoto's thyroiditis is diagnosed, what also should you look for other autoimmune dzs, ie SLE, pernicious anemia [note: family hx is common]
what anti-thyroid Abs are seen in Hashimoto's anti-peroxidase (90%), microsomal Abs (50%)
tx of subacute thyroiditis? Hashimotos? subacute-pain tx (NSAIDs, steroids if nec), Hashimoto's-thyroid replacement so euthyroid
what must monitor when pt on methimazole and propylthiouracil leukocytes (WBC) for agranulocytosis
what Rx can be used for rapid lowering of thyroid hormones, when use? Na ipodate or iopanoic acid; for acute, severe hyperthyroidism unresponsive to other therapies
what use for acute management of palpitations, tremors, anxiety, etc propanolol (b-blocker)
what Rx use in hyperthyroid preg PTU
T/F: after 1-2 yrs on methimazole could the Rx be discont'd T, check for anti-thyroid Abs and potlly could discont
when can you not use radioactive iodine to tx hyperthyroidism during pregnancy or breast feeding (can cause cretism)
what 2 things look for after thyroid surgery for hyperthyroidism 1) hypothyroidism, 2) hypo Ca++ (parathyroid damaged)
what use to diagnose hyperthyroidism low TSH [although could also be 2 hypothyroid--and high TSH induced hyperthyroid is very uncommon]
features of thyroid storm very hi F, tachycardia, agitation/psych/confusion, N/V/diarrhea
tx of thyroid storm IV fluids, cooling blankets, glu, PTUq2, iodine (inihibits thyr H rel), b-blocker (HR), dexamethasone (inihibits T3-4, helps adrenal)
causes of primary hypothyroid (3) MC=Hashimotos, iatrogenic: tx of hyperthyroid, Lithium
describe subclinical hypothyroid thyroid fxn is inadequate, but incrsd TSH maintains T4 (so incrsd TSH, nml T4), mild hypothyr sympt and incrsd LDL
tx for subclinical hypothyr give thyroxine if TSH >20, or other sympt
what's a serious complication of hypothyroid myxedema coma: depressed consciousness, severe hypotherm, respir depression [often ppt by trauma, infxn, cold, narcotics]
tx myxedema coma maintain BP and respir, give thyroxine and hydrocortisone
causes of 2ry hypothyroid Hypothal (defic TRH), Pituit (defic TSH)
lab abnmlties in hypothyroid (other than thyroid hormones) hi LDL, low HDL, mild normocytic anemia + anti-microsomal Abs in Hashimotos
describe clinical features of thyroid assoc ophthalmo, how it's related to thyroid fxn, and tx lid retraction, eyelid edema, diplopia, etc; thyroid dysfxn not related to ophthal; usu self-limited but steroids can help
clinical features of hypothyroid (skin, mscl, joints, CNS, CVS) skin: cold intolerance, dry skin, coarse hair, edema from GAGs in tissues, lateral part of eyebrows gone; mscl: wknss, fatigue; jts: arthralgias, carpal tunnel; CNS: lethargy, sl wgt gain, depression; CVS: bradycardia
what suggests that a thyroid nodule is malignant fixed nodule, not moving w swallowing; unusually firm or irregular; single nodule w rapid develop; radiation (risk papill cancer); cervical lymphadenopathy, vocal cord paralysis, incrsd calcitonin (medullary cancer)
dx of thyroid nodule FNA, if indeterminant then do thyroid scan (hot=not malignant, cold could be (20%) so resect); follicular always resect
risks for thyroid cancer head and neck radiation (risk for papill cancer); Gardner's and Cowden, (papillary); MENIII (medullary)
order of prognosis for thyroid cancers 1) papillary, 2) follicular, 3) medullary, 4) anaplastic
most common thyroid cancers (2) MC: papillary,
tx of papillary thyroid cancer lobectomy w isthmusectomy, but total thyroidectomy if >3cm, bilat or mets; adjuvant: TSH suppression, radioiodine if large
describe iodine uptake and spread of 1) papillary, 2) follicular cancer 1) papillary: positive iodine uptake, spreads via lymphatics, 2) follicular: avidly absorbs iodine, hemorrh spread
tx of follicular thyroid cancer total thyroidectomy w post op iodine ablation
is radioiodine therapy used in medullary thyroid cancer no, usu unsuccessful, so just total thyroidectomy
sporadic, familial, syndrome contribution to medullary thyroid cancer 1/3 sporadic, 1/3 familial, 1/3 MEN
if medullary thyroid cancer, think also abt another endocrine dz MENIII, look for pheo
what lab value look for in medullary thyroid cancer incrsd calcitonin
describe demographics, progression and tx of anaplastic thyroid cancer usu seen in elderly, very malignant w local invasion, tx: chemo and radiation may lead to modest improvement
list hypothal hormones and actions TRH (+TSH, prolactin), dopamine (-prolactin), GHRH (+GH), somatostatin (-GH, TSH), GnRH/LHRH (+FSH, LH), CRH (+ACTH), oxytocin, ADH
malignancy of pituitary adenomas? almost all benign
clinical features of pit adenomas usu clinical due to hypersxn of hormones (prolactin, GH, ACTH, TSH) + mass effects (headache&bitemporal hemianopsia); rarely hypopit if stalk compression causing defic GH and hypogonad
dx and tx of pit adenomas dx: MRI + screen of hormones, tx: transsphenoidal resxn + radiation therapy and medication therapy adjunct [**exc prolactinoma can try Rx first]
causes of hyperprolactinemia MC=prolactinoma; Rx=psych, H2 blockers, metoclopramide, verapamil, estrogen; preg, hypothyroid, RF
how does prolactin affect estrogen & testosterone prolactin decrses GnRH, decrses LH/FSH, decrses estrogen and testosterone
clinical features of hyperprolactinemia men: hypogonad, infertility, visual field, headaches (parasellar mass effect); female: menstrual, parasellar signs less common
dx and tx of hyperprolastinemia dx: check TSH and preg; tx: if symptomatic use bromocriptine or cabergoline (dopa agonists) for 2 yrs
features of acromegaly (joints, CVS, CNS) coarsened facial features, abnmlly large hands&feet, arthralgias; CVS: cardiomyopathy, HTN; CNS: headache, sleep apnea, bitemporal hemianopsia
acromegaly lab values glu intolerance (+/- incrsd glu, TG, P, prolactin)
dx of acromegaly (2) IGF1 incrsd; if IGF is equivocal give glu doesn't decrs GH [note: random testing of GH is not helpful]
tx of acromegaly transsphenoidal rsxn + radiation if IGF1 remains elevated; octreotide suppresses GH
features of craniopharyngioma visual field, headache, papilledema; may cause incrsd prolactin, DI, or panhypopituit
tx of craniopharyng rsxn +/- radiation
what hormones are most freq altered in hypopituitar LH, FSH, GH (as opposed to TSH, ACTH)
causes of hypopituit MC=hypothal or pituit tumor; Sheehans, infiltrate (sarcoid, hemochromo)
what clinical features of decrsd GH, prolactin, FH/LSH, ADH GH=decrsd mscl mass; prolactin=fail lactate; LH/FSH=infertility, amenoerrhea, loss of 2ry sex charact; ADH (if hypothal)=DI
dx and tx of hypopituit dx=hormone levels and MRI; tx=hormone replacement
differential for polyuria, polydipsia DI, diuretic, DM, primary polydipsia
2 types of DI, which more common central (MC) and nephrogenic
pathophysiol and causes of central DI low ADH from P pituit, 50% idiopathic, but can incl desctructive processes (ie tumors, sarcoid, TB, syph, neoplasm)
causes of nephrogenic DI metabolic: decrsd K, incrsd Ca; Rx: lithium, demeclocycline, methoxyfurane; pyelonephritis
how make dx when polyuria and polydypsia water deprivation: in primary polydipsia U_osm>280, doesn't repons more ADH; central DI U_osm not grtr than 280 and does respond further to ADH (decrsd urine output, incrsd U_osm); nephrogenic U_osm not grtr than 280 and doesn't respond to ADH
plasma osmol for DI v primary polydipsia DI: 280-310; primary polydipsia: 255-280
tx central DI, nephrogenic DI central DI: DDAVP, chlorpropamide incrses ADH sxn and enhances its effect; neph DI: thiazide + Na restriction and water restriction
causes of SIADH neoplasms, CNS, post-op, pulmonary dz (sarcoid, PNA), Rx: anti-psych, anti-depress
physiology of SiADH, lab values retaining water and excreting concentrated urine (U_osm >100), all electrolytes decrsd, incl uric acid, BUN, Cr, decrsd Na, Serum osmol decrsd (<270); but no edema, not hypervol (and some say euvolemic),
what need to check for siADH no thyroid, adrenal, cardiac, renal, liver dz
what Rx can be used to inihibit ADH effect on kidney demeclocycline, Li carbonate
tx of siADH water restriction, if sympt also give NS; if actively sz or Na<110 cautiously give hypertonic very carefully
key lab findings of hypoparathyroid serum decrsd Ca++, incrsdP, decrsd urine cAMP, decrsd PTH
how are lab findings difft for pseudohypoparathyroid v hypoparathyroid both have serum decrsd Ca++, incrsdP; but incrsd PTH
causes of hypoparathyroid head and neck surgery
clinical features of hypoparathyroid rickets and osteomalacia, neuromuscl decrsd Ca++: numbness/tingling (circumoral, fingers, toes), tetany (incrsd DTR, Chvostek, Trousseau), szs; incrsd QT
tx hypoparathyroid oral Ca++ or IV Ca gluconate + vitD (calcitriol); watch for stones
causes of primary hyperparathyroid MC=adenoma (80%, usu 1 gland); hyperplasia (all glands); cancer (<1%)
clinical features of hyperparathyroid stones, bones (incl osteitis fibrosa cystica brown tumors), abd groans (mscl pain/wknss, pancreatitis, PUD, gout, constipation), Psyh; +polydipsia, polyuria, HTN, decrsd QT
dx of hyperparathyroid hi Ca++, hi PTH relative to Ca++ (ie PTH should be decrsd), low P, incrsd cAMP and Ca++, **Cl/P>33
tx hyperparathyroid surgery (but not nec is asympt >50), encourage fluids and furosemide if incrsd Ca++ is high
relative indications for surgery incrsd Ca++, Urine Ca++ >400mg/d, stones, renal insuffic, decrsd bone mass, <50yo
how treat acute Ca++ fluids, furosemide, biphosphamide, calcitonin
pheo is assoc w VHL, MEN, NF
clinical findings suggesting pheo HTN w paroxysmal severe HTN, pounding HA, sweating, incrsd glu, lipid and decrsd K
what Rx used for pheo tx phenoxybenzamine (b-blocker)
how dx pheo urine: metanephrine or VMA; MIBG (metaiodobenzylguanidine) scan can help localize it
what Rx need in addition to b blocker for pheo First Aid says to give a-adrenergic blocker first otherwise b-blocker will give reflex HTN
what hormones control prolactin rel dopamine (-) and TRH (+)
what hormones does somatostatin regul inhibits GH and TSH release; also inhibits rel of GI and pancreatic hormones
what 2 hypothal hormones regul TSH TRH (+) and somatostatin (-)
what 2 hypothal hormones regul GH GHRH (+) and somatostatin(-)
general effects of cortisol protein catabolism, anti-insulin, impaired immunity, incrsd catecholamines (HTN)
what's the diff bw Cushing syndrome and disease syndrome=any cause of incrsd steroids, disease=pituitary adenoma that secretes ACTH
causes of Cushing syndrome MC=iatrogenic (which means no androgen excess), Cushing dz, adrenal adenoma+cancer, ectopic ACTH (small cell lung cancer)
signs more specific to Cushing disease (as opposed to syndrome) virilizing signs (although also small cell cancer ACTH), bruising, stria, myopathy, may have hyperpigment
how use CRH stimulation test to differentiate bw causes of Cushings syndrome CRH stimulation will cause incrs in ACTH/cortisol in Cushing's disease, but no incrs in ectopic ACTH sxn or adrenal tumor
how use dexamethasone test to differentiate causes of Cushings syndrome adrenal adenomas and cancer and ectopic ACTH will not respond to low or high dexamethasone; Cushing dz will show incrsd cortisol with low dose dex and decrsd with high dose
clinical features of Cushings syndrome (skin, muscle/bones, sexual, ID, CNS, CVS) skin=purple stria, hirsuitism, bruising, acne; central obesity/buffalo hump; muscle/bone=prox mscle wasting, wkness, osteoporosis; sex=hypogonad, menstrual irreg; iD=infxns; CNS=depression, mania; CVS=HTN
what acute bone complication can occur w exogenous steroid use aseptic necrosis of femoral head
what metabolic abnormalities are seen w Cushings syndrome incrsd lipid, deecrsd K and incrsd glu
progression of diagnosis of Cushings syndrome 1)low dose dex, >5=Cushing;2)ACTH lvl:hi=Cushing or ACTH tumor, low=adrenal tumor or exo steroids;3)hi dose dex: Cushing's dz causes decrs 50%, ACTH tumor no change;4)CRH stim test: ACTH/cortisol incrsd=Cushing dz, no change=ectopic ACTH or adrenal tumor
tx of Cushings syndrome surgical
Key lab findings of primary hyperaldosteronism incrsd aldosterone, decrsd renin
when suspect 1ry hyperaldosteronism HTN and low K if NOT on diuretic
causes of 1ry hyperaldosteronism MC=Conn's adrenal adenoma, adrenal hyperplasia, cancer (<1%)
features of 1ry hyperaldost HTN, no edema, decrsd K, incrsd Na, metabolic alkalosis, polydypsia, polyuria
how differentiate be adenoma and hyperplasia (3); why is it impt to differentiate? 1) test ea adrenal vein (hi on 1 side=adenoma), 2) CT/MRI; 3) iodochol; impt to differentiate bc adenoma requires sx and hyperplasia is treated w spironolactone
dx of 1ry hyperaldosteron (2) aldosteron:renin >30; definitive dx saline infusion should decrs aldost <8.5
tx of 1ry hyperaldosteron hyperplasia=spironolactone; adenoma=surgery
MC cause of incrsd aldosteron; what are accompanying lab values 2ry hyperaldosteron (due to low perfusion kidneys (CHF, nephrotic, cirrhosis, renal artery stenosis)); renin is high, K can be nml or even hi
symptoms and tx of adrenal crisis *note: can present like acute abd; severe hypotension, abd pain, ARF; tx=IV fluids, cortisone
causes of adrenal insuffic MC=stopping steroids, for 1ry (Addisons): MC worldwide=TB, MC industrial world=autoimmune
Addisons? Conns? Addisons=1ry adrenal insuffic; Conn's=1ry hyperaldost from adrenal adenoma
clinical features of adrenal insuffic CVS=hypotension (esp orthostatic), CNS=lethargy, confusion, GI=anorexia, N/V, vague abd pain; hypogly
what features are part of 1ry adrenal insuffic but not 2ry adrenal insuffic *hyperpigment, aldosterone defic [since depends on adrenals not ACTH] which causes decrsd Na, decrsd volume, and incrsd K
dx of adrenal insuffic imaging + decrsd cortisol, decrsd ACTH (2ry adrenal insuffic--check other pit); to confirm 1ry adrenal insuffic: infuse ACTH and measure cortisol (if 2ry they won't respond the 1st time but will after reptd 4-5d--adrenals aren't used to being stimulated
tx of 2 types of adrenal insuffic 1ry: glucocorticoid (hydrocortisone or prednisone), mineralcorticoid (fludcortisone); 2ry: just glucocorticoid
causes of congenital adrenal hyperplasia AR, 90% due to 21-hydroxylase defic (next MC is 11-hydroxylase which also has HTN)
pathophysiol of congenital adrenal hyperplasia decrsd cortisol and aldosterone, so precursors for these are shunted to androgens causing virilization
features of congenital adrenal hyperplasia in females, males females: ambiguous genitalia, nml ovaries and uterus; males=macrogenitosomia, precocious puberty
describe salt-wasting form of congenital adrenal hyperplasia this more severe form has dehydration, hypotension, lack aldost causes decrsd Na and incrsd K, hypogly
dx of congenital adrenal hyperplasia 17-OH-progesterone incrsd in serum
tx of congenital adrenal hyperplasia cortisol and mineralcorticoids
general features of DMI, pathophysiol, presentation, genetic component autoimmune destruction of pancreatic b cells, symptoms develop rapidly sometimes appearing after illness or w DKA, usu present <20yo; less genetic component than DMII (HLADR 3, 4)
pathophysiol of DMII nml/hi insulin, but body insulin resistant (often related to obesity), develops over yrs, more genetic component
how do free fatty acids relate to insulin resistance free fatty acids make mscls more insulin resistant and decrs glu uptake; ffa make liver incrs glu production; body doesn't compensate by incr insulin and b cells become more desensitized to incrsd glu
risk factors DMII (3) **obesity, genetics, age (insulin decrs w age)
what's protocol for screening for DM adults >45 q 3yrs; if risk factors (obesity, fam hx, gestational DM) start screening earlier
diagnosis criteria for DM (random glu, fasting, 2hr post-prandial) random: >200 w sympt; fasting: >126 x2; post-prandial: >200
diagnosis criteria for impaired glu tolerance (random glu, fasting, 2hr post-prandial) random: NA; fasting: 110-126; post-prandial: 140-200
DMII pts often present w polyuria/polydipsia, polyphagia, fatigue, blurry vision, candidal vaginitis
when evaluating DM pt pay attn to feet, vascular dz, neuropathies, retinopathy, renal dz, ID
if DM pts present later what can they present w MI, intermittent claudication, perinpheral neuropathy, proteinuria, retinopathy, impotence
outpatient management of DM at home: if on insulin check blood glu before meals and bedtime +/- 90-120 min after meals; q3mo: Hb1AC <7 to prevent microvasc; q6mo: neuropathy; q1yr: urinalysis (microalbuminuria), BUN, Cr, Chol, eye screening; every visit: BP, feet
differentiate bw Dawn and Somogyi syndrome, cause, dx, how tx Dawn: cause incrsd GH at night, 3am hi Glu, tx: incrs pm insulin; Somogyi: cause rebound hypogly at night, 3am low Glu, tx: decrs pm insulin
general regimens for insulin, usu dosage 0.5-1u/kg/d; 2/3 in am (2/3 NPH, 1/3 reg), 1/3 in pm (1/2 - 2/3 NPH, 1/2 - 1/3 reg)
levels of HbA1c glu control; measurement of glu control over what time frame measures glu over last 2-3 mos; >10=poor control, 8.5-10=fair, 7-8.5=good, <7=ideal
goal of fasting glu, post-prandial glu for DM fasting <130, post-prandial <180
goal of BP, LDL, TG for DM BP <130/75, LDL<100, TG<150
name 6 types of insulin human insulin Lispro, regular, NPH/Lente, Ultralente, 70/30 (70NPH, 30Lente), Glargine/Lantus
which insulin is the only one that can be given IV? What is the time for its onset and how long it lasts? regular; 30-60 min onset, duration of 4-6hrs
name the 2 shorter acting insulins, timing of onset and duration human insulin Lispro (15min, 4h), regular (30-60min, 4-6h)
name 4 longer acting insulins, time of onset and duration NPH/Lente (2-4h, 10-18h), Ultralente (6-10h, 18-24h), 70/30 (30min, 10-16h), Glargine/Lantus (3-4h, 24h)
how is intensive insulin control structured; who used in; risks a long acting insulin 1xd at night, then reg insulin before ea meal based on preprandial measure; use in preg and for better glu control; risk hypogly
what are the 4 types of oral hypoglycemics sulfonylureas, metformin, acarbose (alpha-glucosidase inhib), thiazolidinediones
name some sulfonylureas, their mech, and disadv glyburide, glipizide, glimepride; stimulates pancreas to make more insulin; hypoglycemia and wgt gain
metformin: mechanism, adv, disadv incrs insulin sensitivity, may descr wgt and doesn't cause hypogly; SE: GI upset (diarrhea, nausea, pain), lactic acidosis, metallic taste, can't use if Cr=1.5 men or 1.4 women, or >80yo
in which pts can metformin not be used can't use if Cr=1.5 men or 1.4 women, or >80yo
what's the mech of acarbose (alpha-glucosidase inhib), SE decrs glu absorption GI, SE: GI upset (abd cramp and flatulance), so not used much
name some thiazolidinediones, their mech of action, adv and disadv rosiglitazone, pioglitazone; decr insulin resistance by fat and mscl; adv: decrs insulin levels; disadv: hepatotoxicity so have to monitor LFTs
if a pt is on a thiazolidinediones (name some), what blood test do they need rosiglitazone, pioglitazone; monitor LFTs
name/describe 2 types of retinopathies seen in DM 1) nonproliferative (majority): hemorr, exudate, microaneurysm; edema macula is leading cause of vision loss; 2) proliferative: neovasc, cxns: vitreal hemorr and retinal detach
describe 4 types of neuropathies seen in DM 1)peripheral lack of sensation, symmetric starting feets then hands; 2)painful w severe burning; 3) mononeuropathies due to infarct, ie CNIII (eye pain, diplopia, can't addct, spares pupil; 4) autonomic-impotence in men, neurogenic bladder, gastroporesis
key features of DKA hypergly (>250), ketones in serum or urine, metabolic acidosis (pH<7.3, HCO3<15), volume depletion
if EtOH is part of DKA, what expect for Glu Glu may actually be nml
what to watch for w K for DKA and its treatment K might be incrsd bc acidosis, but as insulin is given it will decrs so will need to replenish
what lytes seen w DKA low P and Mg, psudo hypoNa bc of high glu, K may be high bc of acidosis
clinical features of DKA altered consciousness, N/V, acute abd pain, Kussmaul's respir (deep, rapid breathing bc of acidosis)
tx DKA 1) insulin (first make sure not hypoK) 0.1u/kg + 0.1u/kg/hr until AG closes and acidosis corrects, 2) Fluids (NS, add 5%glu once get to 250glu), 3) K **monitor K, Mg, P very closely, if glu levels decrs too rapidly can get cerebral edema
differential for DKA 1) EtOH ketoacidosis, 2) hyperosmolar hyergly nonketotic syndrome, 3) hypogly (can also cause altered mental status, abd pain, acidosis), 3) sepsis, 4) intoxication (EtOH, MetOH, Paradlehyde, Ethylglycl, ASA, IPA)
describe key features of hyperosmolar hypergly nonketotic syndrome very high Gly (>600), hyperosmol (>320 **not in DKA), pH >7.3, no ketone, very dehydrated
tx hyperosmolar hyperGly nonketotic syndrome fluids is key (1L in 1st hr, 1L in next 2hr), w small amts insulin (5-10 u bolus, 2-4u/hr)
nml pathophysiol when blood glu decrs when glu gets ~80, decrs in insulin, as decrs further glucagon incrses, then epinephrine and catecholamines increase; start symptoms glu<50
differential for hypoglycemia (6) DM/insulin Rx related, insulinoma, EtOH, post-op rapid gastric emptying, adrenal insuffic, liver failure
evaluation for hypoglycemia plasma insulin and C-peptide, anti-insulin Abs, plasma and urine sulfyl urea
clinical features of hypogly incrs epi: sweating, tremors, tachycardia, incrsd BP; neurogly: wkness, confusion, convulsions, coma
tx hypogly glu, but if suspected EtOH must give thiamine first
how differentiate bw insulinoma, Rx insulin problem and sulfonyl urea in hypogly pt insulinoma-C peptide and pro-insulin are high; too much Rx insulin: insulin very incrsd, C peptide incrsd some, proinsulin decrsd; sulfonyl urea: insulin incrsd, C-peptide incrsd, proinsulin nml
dx of insulinoma 72 hr fast, insulin lvls are too high
pathophys, prognosis and tx of insulinoma from beta cells, assoc MENI, 90% benign; tx: surgery (80% cure)
pathophys of ZES (zollinger-ellison syndrome) pancreatic islet cell tumor that secretes gastrin leading to ulcers and diarrhea
prognosis ZES, assoc dzs 60% malignant, 20% assoc MENI
dx ZES/gastrinoma secretin incrses gastrin (should decrs it); resting lvls of gastrin high
tx ZES/gastrinoma hi dose PPI, attempt curative resxn (20% cure if complete resxn)
what's a cxn of glucagonoma necrotizing migrating erythema (usu below waist)
lab values and clinical features of glucagonoma hi glucagon, hi glu, glossitis, stomatitis, +/- necrotizing migrating erythema (usu below waist)
tx glucagonoma surgical resxn
key features, prognosis of somatostatinoma rare malignant pancreatic tumor, usu met by time of dx, poor px; key features: gallstones, DM, steatorrhea
key features, prognosis, tx of VIPoma watery diarrhea, achlorydia, incrsd glu and Ca++; malignant 50%; tx: surgical resxn
what's the MC cause of 2 hyperaldost? How difft from primary hyperaldoster CRF, incrsd renin
what 4 things can cause incrsd cortisol? How difft? 1) Cushings (pituit adenoma, hi ACTH), 2) primary adrenal hyperplasia/neoplasia cortisol producing tumor (low ACTH), 3) ectopic ACTH production (ie. small cell lung cancer, hi ACTH), 4) Rx steroids (low ACTH)
how ACTH or cortisol tumors respond to dexamethason suppression test? V Cushings? incrsd cortisol at low and hi doses (Cushings: incrsd cortisol in response to low dose, decrsd in response to high dose)
what are 2 causes of hi cortisol and hi ACTH Cushings (pituit adenoma), cancer like small cell lung cancer that's producing ACTH
Sheehan's syndrome postpartum hypopituitarism (infarct of pituit)--fatigue, anorexia, poor lactation
define pheochromocytoma; dx? MC tumor of adrenal medulla, secrete NE, eppi, dopamine--VMA in urine
rule of 10s in pheochromocytoma 10% malignant, bilateral, extra adrenal, calcify, occur in kids, familial
symptoms pheochromo episodic HTN w headache, sweating tachycardia
what is pheochromocyt assoc w? tx? MEN II, III and NF; phenoxybenzamine
what is the other major tumor of the adrenal medulla? neuroblastoma, MC adrenal medulla tumor in kids, less likely HTN **HVA in urine
MENI (mltpl endocrine neo) 3 Ps: pancreas (Zollinger-Ellison syn, insulinoma, VIPoma), parathyroid, pituitary
MENII thyroid medullary carcinoma, pheochromo, parathyroid (think of acryonym PPT)
MENIII thyroid medullary carcinoma, pheochromo, mucosal neuroma (think of acronym PMT)
MENII and III assoc with what gene ret
which MEN has parathyroid? Thyroid? Pheo? parathyroid: I,II; thyroid: II, III; pheo: II, III
diff MEN II and III MEN II has parathyroid, III has mucosal neuromas
how MEN I difft from others has pancreas (Zollinger-Ellison syn, insulinoma, VIPoma), parathyroid (but also MENII), pituitary
MEN II aka Sipples syndrome
Created by: ehstephns