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109 Cards in this Set
- Front
- Back
causes and tx of hypervolemic hyponatermia
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CHF, cirrhosis, nephrotic syndrome; tx with diuretics
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what is pseudohyponatremia?
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measurement artifact caused by elevated serum proteims or lipids; rare nowadays
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hormonal etiologies of hyponatermia
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TH and cortisol facilitate free water excretion ==> deficit --> retention of free water --> hyponatermia
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lab clues of SIADH
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low BUN, low uric acid levels
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tx of SIADH
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water restriction, +/- hypertonic saline if neurologic sx
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tx of hyponatermia
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HYPOVOL: 0.9% (normal) saline; EUVOL: H2O restric; if neurologic sx, give 3% (hypertonic) saline +/- diuretic (furosemide) to avoid volume overload
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what neuro syndrome if replenish Na too fast in hyponatermia?
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osmotic cerebral demyelination / central pontine myelinolysis ==> quadriplegia, pseudobulbar palsy, "locked-in" syndrome, coma, death
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what is a dissecting aneurysm?
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aneurysm CAUSED by dissection
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factors predisposing to aortic dissection (6)
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Connective tissue diseases (Marfan's, ED); HTN; Pregnancy; Valvular problems (AS, congenital bicuspid Ao valve); Atherosclerosis; Coarctation of the aorta
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timing of pain in MI vs aortic dissection
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MI: builds up over minutes; AD: maximal at onset
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2 types of Aortic dissection
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Type A: involves ascending aorta (+/- descending), dangerous, requires urgent surgery; Type B: descending aorta only (no ascending involvement), managed medically
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symptoms of AAA
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often asymptomatic, detected as midline pulsatile mass on PE
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major predictive factor for AAA rupture and recommended management
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size of aneurysm (>5.5cm recommended elective surgery, <5.5 recommended serial imaging)
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CXR finding with aortic dissection
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widened mediastinum
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causes of lung dz in AIDS pt
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PCP, TB, atypical mycobacteria, cryptococcus, histoplasmosis (disseminated), + usual causes of comm-acquired PNAs (S.Pneumo, mycoplasma, viruses)
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lab findings characteristic of PCP
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elevated LDH
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what CD4 count does presence of thrush suggest?
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<250
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how can ABG used to prognosticate PCP / guide therapy?
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PO2 < 70mmHg or A-a gradient > 35mmHg = BAD ==> corticosteroids followed by bactrim (TMP-SMX)
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what bugs at CD4 < 500?
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infections that "normal" people can get: zoster, TB, vaginal candidiasis, recurrent PNA
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what bugs at CD4 < 200?
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infections that "normal" people DON'T get: PCP, toxo, fungal (cryptococcosis, histoplasmosis, cryptosporidiosis)
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what bugs at CD4 < 50?
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disseminated histoplasmosis, MAC, CMV retintis/esophagitis, CNS lymphoma
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CXR findings in lung dz with AIDS pts
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TB presentation highly variable with CD4 < 200; DIFFUSE interstitial infiltrates: PCP, histo; PATCHY infiltrates: cryptococcus; CAVITARY lesions: PCP, coccidiomycosis
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most common cerebral mass lesion in AIDS pts
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toxoplasmosis
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toxo vs cns lymphoma
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CNS lymphoma: single mass, no improvement with empiric tx (sulfadiazine + pyrimethamine), 90% cases CSF positive for EBV DNA
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tx for MAC
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clarithromycin, ethambutol, rifabutin
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drugs in HAART
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3: 1) nnRTI/protease inhibitor, 2+3) nRI
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prophylaxis in AIDS
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CD4 < 200: BACTRIM (pcp, toxo); CD4 < 50: CLARITHYROMYCIN / AZITHROMYCIN (mac)
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most common sx a/w periph vascular dz
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intermittent claudication: pain, ache, fatigue, discomfort in legs a/w exercise, relieved with rest
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use of ankle-brachial index (ABI) in PAD (periph arterial dz)
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ABI: nl: >1.0; claudication: 0.41-0.90; critical leg ischemia: <0.4
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meds used to tx PAD
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treat RISK FACTORS (SMOKING, htn, hchol); ANTIPLATELET agents (aspirin, clopidogrel); PENTOXIFYLLINE (inc RBC elasticity --> dec bld viscosity); CILOSTAZOL (PDEi ==> vasodilat, antiplatelet)
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tx of critical leg ischemia
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?revascularization (eval via angioplasty / imaging), tx w/ balloon, stent, locally-delivered thrombolytic
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most important intervention for PAD
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smoking cessation
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hypertension workup
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LABS: gluc, Cr, Ca, fasting lipids (LDL, HDL, TG), U/A, ECG
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Stages of HTN
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Pre-HTN: <140/90; Stage I HTN: 140-160/90-100; Stage II HTN: >160/100
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prevalence of primary vs secondary htn
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1': 92-95%
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what clinical features raise suspicion of 2' HTN?
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age of onset (<25 or >55); presenting with malignant HTN; requiring >=3 HTN meds; suddenly uncontrolled; rising Cr with ACEi
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hormonal causes of HTN
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Cushings, Hyperthyroidism, Hyper aldo
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tx of HTN by stage
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Pre-HTN: lifestyle mod; Stage I: one med; Stage II: >= 2 meds
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target BP in HTN
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135/85, unless DM/Renal dz --> 130/80
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Which drugs are first line for HTN?
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Thiazides (dec mortality in ALL pts) and beta-blockers; ACEi in diabetes or heart failure
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lab findings in hyperaldo
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hypokalemia
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obstructive sleep apnea and HTN
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hypoxia/hypercarbia --> systemic vasoconstriction --> systolic and pulmonary hypertension
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signs of hyperthyroidism --> 2' HTN
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hyperthyroid signs (nervousness, tremor, weight loss, heat intol, etc.) + WIDENED PULSE PRESSURE (increased systolic BP, decreased diastolic BP)
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hypertensive emergencies and clonidine
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clonidine = alpha2 agonist --> increased symp sensitivity; clonidine withdrawal can cause reflex sympathetic surge --> HTN
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how do blood vessels react to hypertension?
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vasodilation (mediated by NO)
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in what range does cerebral autoregulation work?
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maintains constant cerebral perfusion with MAP 60-120 (range shifts in hypertensive patients ==> focus on SYMPTOMS not NUMBERS)
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what happens if MAP exceeds the limit of cerebral autoregulation?
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endothelial dysfunction --> vasogenic edema --> microhemorrhages --> encephalopathy
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BP goal in hypertensive emergency
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25% decrease or diastolic of 100-110 over minutes-hours
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agents used to tx hypertensive crisis
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either vasodilator (eg nitroprusside + beta blocker (to prevent reflex tachy) or combined alpha/beta anatagonist (eg labetalol)
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treatment for pheo
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surgical resection after reversal of excess catecholamine effect (alpha blockers like phenoxybenzamine, sometimes FOLLOWED by beta blocker)
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why not use beta blocker alone (or first) in pheo?
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can cause unopposed alpha stimulation --> vasoconstriction --> worsened HTN
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in what cases would you not treat hypertensive crisis?
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possible stroke -- decreasing cerebral perfusion will exacerbate ischemia
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transaminase levels in alcoholic hep vs hepatic necrosis
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alcoholic hep: levels elevated but < 500; hepatic necrosis: levels > 1000 (toxic injury, viral help, ischemia)
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clinical findings in acute hep
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prodrome of nonspecific constitutional symptoms; jaundice, hepatomegaly, dark urine (bilirubinuria)
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most common cause of acute viral hep in US
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Hepatitis A
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Hep B outcome
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depends on age; 90% of infected newborns --> chronic hep B --> ?HCC; 95% adults with new infection --> complete recovery w/o sequelae
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tx of viral hep
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acute viral hep usually self limited --> supportive tx; fulminant hepatic failure --> requires liver xplant
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findings in fulminant hepatic failure
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massive necrosis, encephalopathy, worsening coagulopathy, increasing PTT, ascites, peripheral edema, hypoglycemia, hyperammonemia, lactic acidosis
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how to use HBeAg to establish infection as chronic?
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if HBeAg elevated after 6 wks of illness --> chronic, high infectivity (in acute, would develop Anti-HBe)
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Hepatitis vaccines
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only for A and B, both > 90% efficacious
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what to do with HepB needle stick?
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give hepatitis B immune globulin (HBIg); also given to newborn of infected mother
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tx for hep b
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alpha-INTERFERON (for hep B and C); LAMIVUDINE for chronic hep B
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how much acetaminophen needed to cause hepatocellular injury?
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10g
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what drugs exacerbate acetaminophen injury, and how?
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INDUCTION of P450: ethanol, phenobarbital; or DEPLETION of glutathione: malnutrition, alcoholism, AIDS
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how to evaluate whether or not acetominophen toxicity has occurred?
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evaluate serum acetaminophen levels relative to time since ingestion (using nomogram)
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tx for acetaminophen tox
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gastric decontamination with charcoal + administration of N-acetylcysteine
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uses of oral lamivudine
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tx for chronic hep B + antiretroviral prophylaxis for HIV positive patients
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three most common causes of acute hep w/ transaminase > 1000
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viral infection, toxic exposure, and ischemic injury
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what labs first show acute hepatic injury?
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elevated PT evident before decreased albumin (because PT has shorter half life)
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main clinical findings in polycystic ovarian syndrome (PCOS)
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infertility, virilization, hirsutism, obesity, amenorrhea/oligomenorrhea
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hypothyroidism can cause what other pituitary abnormality?
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hyperprolactinemia
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primary vs secondary ameonorrhea
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PRIMARY: absence of menarche by age of 16 (usually genetic/congenital); SECONDARY: absence of menstruation for >= 3mo in woman with normal past menses
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oligomenorrhea
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infrequent menses (intervals > 40d) or < 9 menses/yr
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main causes of amenorrhea
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1) Pregnancy; 2) problems of genital outflow; 3) hypothal-pit-ovarian axis (eg PCOS, hypothyroidism)
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types of hypothal-pit-ovarian axis disorders resulting in amenorrhea
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45% hypothalamus (nutrition, excess exercise, stress, infiltrative diseases); 30% PCOS; 18% pituitary (neoplasms, empty sella syndrome, sheehan syndrome)
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causes of hypothyroidism
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95% primary thyroid failure (hashimoto's -- most common in US; surgical/radioactive; graves); IODINE deficiency (worldwide)
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what causes and characterizes myxedema?
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often caused by severe hypothyroidism; accumulation of hydrophilic polysaccharides in dermis --> dull facies, swollen eyes, doughy extremities, enlarged heart, ileus, delayed relaxation of DTR
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what causes excess thyroid binding globulin (TBG)?
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pregnancy, oral contraceptives
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how does T3RU relate to TBG?
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inverse relationship -- as TBG increases, more of the radioactive T3 is bound --> dec T3RU
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what T4 and T3RU levels suggest hyperthroidism? Hypothyroidism?
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hyperthyroidism: elevation of both T4 and T3RU; hypothyroidism: decrease of both T4 and T3RU;
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what effect does thyroid hormone have on lipids?
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dec thyroid --> elevated total chol and LDL
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levothyroxine vs dessicated thyroid extract to tx hypothyroidism
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levothyroxine (T4) preferred because less bolus effect -- thyroid extract can be varying ratios of T3:T4, unpredictable effects, tachyarrhythmia risk
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what antibody looked for in hashimoto's?
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antimicrosomal antibody (aka antithyroperoxidase antibody)
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causes of ascites
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CIRRHOSIS (--> portal htn); OTHERS: malignancy, etc. (differentiated by paracentesis)
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MCC chronic hep
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viral (B, C), EtOH, drugs/toxins, AIH; less common: metabolic (hemochromatosis, Wilson's, alpha1-antitrypsin deficiency)
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tx for hep C
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alpha-interferon + ribavirin
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tx of portal htn
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non-selective betablockers (eg propanalol) to lower portal pressure; octreotide if variceal bleed (constricts splanchnic circ)
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tx of ascites
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sodium restriction, spironolactone/furosemide, therapeutic paracentesis
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causes of ascites with SAAG > 1.1
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PORTAL HYPERTENSION (cirrhosis, portal vein thrombosis, budd-chiari, CHF, constrictive pericarditis)
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causes of ascites with SAAG < 1.1
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peritoneal carcinomatosis, tuberculous peritonitis, pancreatic ascites, bowel obstruction / infarction, serositis (eg lupus), nephrotic syndrome
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spontaneous bacterial peritonitis (SBP) vs secondary peritonitis (eg 2/2 to intestinal perforation)
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SBP usu 1 org in fluid; 2/2 peritonitis usu polymicrobial
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PBC epi and clinical presentation
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epi: mid-aged women; clin: pruritis, fatigue, 2-5x alkphos
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most common causes of acute pancreatitis in the US (3)
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1) EtOH, 2) biliary tract dz (incl gallstones), 3) hypertryglyceridemia (>1000)
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causes of acute pancreatitis
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GET SMASHeD (Gallstones, EtOH, Trauma, Steroids, Mumps/CMV, Autoimmune, Scorpion sting, Hypercalcemia/Hyperlipid/HyperTG, Drugs (sulfas, furosemide, thiazides etc)
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most common cause of "idiopathic" pancreatitis (no gallstones on ultrasound, no predisposing factors)
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BILIARY TRACT DISEASE (biliary sludge [microlithiasis] or sphincter of Oddi dysfunction)
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describe the pain in pancreatitis
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severe upper abdominal pain radiating to back, relieved by sitting up/bending forward, exacerbated by food, often accompanied by n/v, low grade fever, volume depletion
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two labs for pancreatitis and the difference
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AMYLASE and LIPASE; amylase elevated within hours, stays for 3-4d (longer in urine), not specific to liver; lipase elevated longer, more specific to pancreas
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tx of pancreatitis
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mostly supportive, keep pt NPO, IVF; narcotics like meperidine given for pain (no biliary colic)
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why is pancreatitis patient hypovolemic? (3)
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1) Inflammation --> third spacing; 2) pulm edema (2/2 ARDS or myocardial dysfunction); 3) dec PO intake, vomiting
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what is a phlegmon?
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a solid mass of inflamed pancreas with patchy areas of necrosis, can become abscess (suspect if fever/leukocytosis)
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characteristics of acute cholecystitis on ultrasound
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gallbladder wall thickening, pericholecystic fluid
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amylase levels and severity of pancreatitis
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unrelated
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when to suspect complication of pancreatitis?
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abd pain, mass, persistent hyperamylasemia in pt w/ prior pancreatitis ==> PHLEGMON / NECROSIS / ABSCESS / PSEUDOCYST
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temporary management of AV node block
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atropine or isoproterenol (sympathomimetic)
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neurogenic causes of syncope
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disturbance of autonomic function --> orthostatic hypotension (eg DM, parkinsonism); also, seizures
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main causes of syncope
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excess vagal activity (vasovagal); orthostatic hypotension (volume depletion, neurogenic, drug induced); cardiogenic (arrhythmias, outflow obstruction, PE, severe pHTN)
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MCC syncope
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vasovagal (usu preceeded by prodrome of nausea, yawning, diaphoresis -- think of someone fainting at sight of blood)
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causes of 2nd degree heart block
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Mobitz I (wenckebach): results from inferior MI; Mobitz II: block within bundle of His
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what is carotid sinus hypersensitivity
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vagally mediated cause of syncope in older men, often occurs when head turned to side, when wearing tight collar, or shaving neck over area
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