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109 Cards in this Set

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