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5_2010 Endo
Endo
| 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 |
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ehstephns
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