5_2010 Endo Word Scramble
|
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Question | Answer |
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
Popular Midwifery sets