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233 Cards in this Set
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how often should you screen for HTN and what age begin screening?
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every 2 years, start at 3 yrs old
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accepted cut off value for normal BP; and how do you diagnose HTN
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140/90; 3 separate measurements on 3 separate occasions >140/90
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is 145/75 HTN?
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yes, it's isolated systolic HTN. systolic and diastolic HTN both decrease life expectancy
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when should you treat HTN immediately?
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pregger and severe HTN like >210/>120
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Initial drug tx for HTN depends on what?
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classification
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normal is what and what is initial drug tx?
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<120/<80; no tx
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Prehypertension
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120-139/80-89; no tx unless compelling indications (DM, chronic kidney dz)
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Stage 1 HTN
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140-159/90-99; tx is thiazides or combo
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Stage 2 HTN
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>160/>100; tx is thiazide plus at least one other agent
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what is stage if BP = 168/60?
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stage 2 b/c classification is based on the worst number
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what are the five first line antihypertensive medications?
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1. thiazide diuretics (preferred agent in pts wtihout additional comorbidities)
2. B blockers 3. ACEIs 4. ARBs 5. Ca2+ channel blockers |
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how do you choose which medication to give?
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based on comorbidities
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which medication is safe in pregnancy?
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hydralazine, labetalol or alpha-methyldopa
*in preeclampsia, mag sulfate lowers BP |
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define a hypertensive urgency and emergency
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urgency: BP >200/120 without end organ damage
emergency: BP >200/120 with acute end organ damage *tx with nitroprusside, nitroglycerin or B blocker (labetalol) emergently |
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what is evidence of end organ damage?
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acute L ventricular failure, unstable angina, MI, encephalopathy (HAs, mental status changes, vomiting, blurred vision, dizziness, papilledema)
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when would you use an ACEI?
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pts with: heart failure, DM, ACS or unstable angina, acute or prior MI, high risk of coronary artery dz or CVA, chronic kidney dz
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when should you avoid ACEIs?
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pregnancy, angioedema, renovascular HTN (can cause renal failure)
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When would you use an aldosterone receptor blockers (ie: spironolactone, eplerenone)?
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pt with: heart failure, prior MI
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when should you avoid aldosterone receptor blockers?
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hyperkalemia, pregger
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when would you use and angiotensin receptor blocker (ARB: ie. losartan, irbesartan)?
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heart failure, DM, chronic kidney disease
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when should you avoid ARBs?
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pregger, renovascular HTN (can cause renal failure)
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when would you use B blockers?
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stable angina, ACS, unstable angina, acute or prior MI, high risk of coronary artery disease, atrial tachycardia or fibrilliation, thyrotoxicosis, essential tremor, migraines
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when should you avoid B blockers?
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asthma, COPD, heart block, sick sinus syndrome
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when would you use Ca2+ channel blocker?
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raynaud's syndrome, atrial tachyarrythmias
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When should you avoid Ca2+ channel blockers?
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heart block, sick sinus syndrome, CHF, pregger
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when should you give thiazide diuretics?
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heart failure, DM, high risk of coronary artery dz or CVA, osteoporosis
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when should you avoid thiazides?
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gout, electrolyte disturbances (ie. hyponatremia), pregger
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what's the difference b/w nitroprusside and nitroglycerin?
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nitroprusside dilates arteries and veins; nitroglycerin is a venodilator only
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which HTN meds are arterial dilators only?
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hydralazine, alpha-1 antagonists, Ca2+ channel blockers
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venodilators reduce what?
arterial dilators reduce what? nitroprusside does what? |
veno- reduce preload
art- reduce afterload nitroprusside reduces preload and afterload |
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what are the benefits of lowering BP?
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lowers risk for CVA (HTN is most important CVA risk factor), heart dz, MI, atherosclerosis, and dissecting aortic aneurysm
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what is the most common cause of death among untreated hypertensive patients?
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coronary disease
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what is MCC of secondary HTN in female? what is the 2nd MCC?
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OCPs; renovascular HTN d/t fibrous dysplasia
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causes of secondary HTN in young man?
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ETOH, "exotic" conditions (pheochromocytoma, cushing's, conn's, polycystic kidney dz)
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causes of new onset secondary HTN in elderly?
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renovascular HTN d/t atherosclerosis (ACEIs can precipitate renal failure)
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hints to secondary HTN and tests to order
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following 7 slides
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pheochromocytoma
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urinary catecholamines (vanillylmandelic acid, metanephrine) plus intermittent severe HTN, dizziness and diaphoresis
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Polycystic kidney disease
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flank mass, family hx, elevated creatinine, and elevated blood urea nitrogen (BUN)
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cushing's syndrome
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dexamethasone suppression test or 24 hour urine cortisol level
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renovascular HTN
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MR or CT angiogram, US, or ACEI nuclear renal scan, if there is a bruit on exam, tx with angioplasty and stenting
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where does fibromuscular dysplasia usually occur in the renal artery? what does it look like?
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mid-renal artery; beaded appearance; usually occurs without other evidence of atherosclerosis (young pts)
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conn's syndrome
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high aldosterone, low renin
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coarctation of aorta
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upper extremity HTN only, unequal pulses, radio-femoral delay, a/w turner's syndrome, rib notching on xray
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what are classic signs and symptoms of DM?
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polydipsia, polyuria, polyphagia, weight loss
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how do you dx DM?
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fasting plasma glucose of 126mg/dL or random glucose of 200mg/dL
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what is the goal of DM treatment?
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keep postprandial glucose <180-200 and fasting glucose <130. stricter control results in too many episodes of hypoglycemia (symptoms of sympathetic d/c and mental status changes)
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type I DM
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develop ketoacidosis, is HLA associated, <50% twin occurance, antibodies to insulin, insulitis (loss of most beta cells of pancreas), do NOT respond to oral hypoglycemics
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type II DM
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develop hyperosmolar state, no HLA assoc, >50% twin occurance, NO ketoacidosis, respond to oral hypoglycemics, NO antibodies to insulin, normal number of islet beta cells but with amyloid deposits
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how is C peptide important in DM?
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low C peptide = too much exogenous insulin (accidental overdose or factitious d/o)
high C peptide = insulinoma |
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what kind of imaging contrast should be used in DM pts?
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iodinated contrast ONLY when absolutely necessary b/c IV contrast agents can precipitate acute renal failure, and make sure pt is well hydrated before using contrast agents
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what constitutes the dx of DKA?
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hyperglycemia, hyperketonemia, and metabolic acidosis; seen in DM1
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what is tx for DKA?
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fluids, IV regular insulin, potassium and phosphorus replacement. do NOT use bicarb unless the pH is <7
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what is nonketotic hyperglycemic hyperosmolar state?
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seen in DM2, hyperglycemia, hyperosmolarity without ketonemia
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how do you tx nonketotic hyperglycemic hyperosmolar state?
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IV fluids, IV insulin and electrolyte replacement
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what are some long term complications of DM?
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atherosclerosis, retinopathy, nephropathy (ACEIs help prevent this), infections, neuropathy, foot ulcers/infection/gangrene, peripheral neuropathy, gastroparesis, charcot's joints, impotence from autonomic neuropathy and PVD, cranial nerve palsies, orthostatic hypotension, silent MI
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what is MCC of non-traumatic amputations?
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DM
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how much insulin is usually required in DM1?
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0.5-1.0 U/kg body weight per day
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if pt has high 7am glucose, what should you do?
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increased NPH insulin at dinner the night before
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if pt has high noon glucose, what do you do?
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increase morning regular insulin or increase before-breakfast lispro or aspart insulin
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if pt has high 5pm glucose, what do you do?
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increase morning NPH or increase before-lunch lispro or aspart insulin
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if pt has high 9pm glucose, what do you do?
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increase dinner time regular insulin or increase before dinner lispro or aspart insulin
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what are the ultra rapid acting insulins?
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insulin aspart and insulin lispro; give right before meals
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what is the rapid acting insulin?
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regular insulin; can give IV to inpatients, give 0.5-1 hour before meals for outpatients
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what are the intermediate acting insulins?
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NPH insulin (is usually part of standard regimens that mix with shorter-acting insulin: 70/30, 50/50 of NPH/regular) and lente insulin
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what is the long acting insulin?
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ultralente insulin; provide basal insulin level, supplement with short acting insulin
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what is the ultra long acting insulin?
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insulin glargine; provide basal insulin level, supplement with short acting insulin
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what is the somogyi effect?
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the body's reaction to hypoglycemia. ex. if too much NPH or other longer acting insulin preparation is give the day or night before, the 3am glucose will be low (hypoglycemia) and the body reacts by releasing stress hormones which cause the 7am glucose to be high. treatment is to decrease insulin
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what is the dawn phenomenon?
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hyperglycemia caused by normal early AM growth hormone secretion. the 7am glucose is high without 4am hypoglycemia (glucose is normal or high at 4am). treatment is to increase insulin
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how do you follow compliance in DM pt?
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check hemoglobin A1c levels (overall control for previous 3 months). want it to be <7%
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how do you prepare DM pts for surgery?
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give 1/3 to 1/2 their normal insulin dose then monitor glucose closely through surgery and postop using D5W and IV regular insulin to maintain glucose control
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which drugs can mask manifestations of hypoglycemia (tachycardia, diaphoresis) and so can prevent early detection of DM?
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B blockers, but benefits might outweigh the risks
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when should you measure cholesterol (ie. fasting lipoprotein profile)?
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starting at age 20 and every 5 years after that
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what is the formula for calculating LDL?
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LDL = total cholesterol - HDL - (triglycerides/5)
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what is the goal for total cholesterol?
for triglycerides? for LDL? for HDL? |
total chol <200 (>240 = high)
triglycerides <150 (>200 = high) LDL <160 HDL >60 |
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which component is used in treatment decision making?
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LDL
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what are markers for familial hypercholesterolemia?
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xanthelasma, corneal arcus, lipemic-looking serum, obesity
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what is a marker for familial hypertriglyceridemia?
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pancreatitis with no risk factors (no alcohol, no gallstones)
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what are secondary causes of hyperlipidemia?
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uncontrolled DM, hypothyroidism, uremia, the nephrotic syndrome, obstructive liver dz, excessive ETOH intake (increases triglycerides), and medications (OCPs, glucocorticoids, thiazides and B blockers)
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what dz process is involved in ~1/2 of all deaths in US b/w ages 35-65 and is the most important cause of permanent disability and accounts for more hospital days than any other illness?
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atherosclerosis
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what are the risk factors for coronary heart disease?
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age (men 45, women 55), family hx of premature CHD, current cig smoking, HTN, low HDL (<40)
***these are the risk factors used when deciding whether to tx hypercholesterolemia ***HDL = 60 is cardioprotective and negates one risk factor |
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in a pt with NO CHD risk factors, and
a) LDL = <160, what is tx? b) LDL = 160-189? c) LDL = >190 |
a) no tx
b) diet +/- medications c) medications (+diet) |
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in pt with >/=2 CHD risk factors, and
a) LDL = <100, what is tx? b) LDL = 100-129 c) LDL = >130 |
a) none
b) diet +/- medications c) medications (+diet) |
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in pt with known CAD or equivalent, and
a) LDL = <100 b) LDL = >100, what is tx? |
a) none
b) medications (+diet) |
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in pt with very high risk, and
a) LDL = <70 b) LDL = 70-99 c) LDL = >100 |
a) none
b) diet +/- medications c) medications (+diet) |
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what are considered CAD equivalents?
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DM, peripheral arterial atherosclerotic disease, symptomatic carotid artery dz, abdominal aortic aneurysm
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which pts are considered "very high risk"?
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pts with CAD who have had a MI, DM, or other severe and poorly controlled risk factors (ie. metabolic syndrome, heavy smoking)
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what is the initial treatment in pt with hypercholesterolemia?
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if lower risk pt, give them 3-6 months to try lifestyle modification before initiating drug tx
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a) what increases HDL (good chol)?
b) what decreases it? |
a) exercise, estrogens, moderate ETOH intake (1-2 drinks/day)
b) smoking, androgens, progesterone, hypertriglyceridemia |
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what are the 1st line agents for hypercholesterolemia?
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niacin (poorly tolerated but effective, esp to raise HDL); bile acid binding resins (cholestyramine, colesevelam); HMG CoA reducatase inhibitors (statins- most effective, more expensive, potential liver/muscle damage); and ezetimibe (zetia- blocks cholesterol absorption and is often combined with a statin)
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what is the single most significant source of preventable morbidity and premature death in the US?
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smoking (whenever not sure which risk factor to eliminate, always pick smoking)
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what does a young person with emphysema but no smoking hx have?
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alpha-1 antitrypsin deficiency
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what is involved in 50% fatal car accidents, 67% of drownings and homicides, 70-80% of death in fires, and 35% of suicides and is also the MCC of cirrhosis and esophageal varices?
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alcohol
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what are symptoms of Wernicke's syndrome?
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opthalmoplegia, nystagmus, ataxia, confusion; it is acute and often reversible and can be fatal
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what are symptoms of Korsakoff's syndrome?
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anterograde amnesia and confabulation, is chronic and irreversible
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wernicke's and korsakoff's syndromes are both caused by?
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thiamine deficiency and damage to mamillary bodies and thalamic nuclei
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What is stage 1 alcohol withdrawal?
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acute withdrawal syndrome: 12-48 hrs after last drink, tremors, sweating, hyperreflexia, and seizures ("rum fits")
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what is stage 2 alcohol withdrawal?
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alcoholic hallucinations: auditory and/or visual hallucinations and illusions with or without autonomic symptoms
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what is stage 3 alcohol withdrawal?
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delirium tremens: 2-4 days after last drink, hallucinations and illusions plus confusion, poor sleep and autonomic lability (sweating, increased pulse and temp); is occasionally fatal
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how do you treat alcohol withdrawal on inpatient basis?
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benzodiazepines and gradually taper dose over days
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signs of chronic liver dz in alcoholics?
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varices, hemorrhoids, caput medusae, jaundice, ascites, palmar erythema, spider angiomas, gynecomastia, testicular atrophy, encephalopathy, asterixis, prolonged prothrombin time, hyperbilirubinemia, spontaneous bacterial peritonitis, hypoalbuminemia and anemia
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common conditions caused by alcohol abuse?
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gastritis, mallory-weiss tears, pancreatitis, peripheral neuropathy (via thiamine deficiency), brain damage (cerebellar degeneration), and cardiomyopahty
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what is best treatment for alcoholism?
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AA or other support group, also disulfiram can be tried (makes pts sick when they drink b/c of alcohol dehydrogenase enzyme inhibition)
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what are symptoms of fetal alcohol syndrome?
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mental retardation, microcephaly, microphthalmia, short palpebral fissures, midfacial hypoplasia and cardiac defects
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what is MCC of preventable mental retardation?
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fetal alcohol syndrome
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what kind of pneumonia is common in "skid row" alcoholics (homeless)?
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aspiration pneumonia via klebsiella (currant jelly sputum), anaerobes, e. coli, streptococci, staphylococci
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what are the most common vitamin and mineral deficiencies in alcoholics?
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folate, magnesium, and thiamine
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what should you give before glucose in alcoholics to prevent wernicke's encephalopathy?
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thiamine
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how do you treat bleeding varices?
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stabilization (IV fluids, blood), then upper endoscopy and sclerotherapy with cauterization, banding or vasopressin. for intractable cases, try transjugular intrahepatic portosystemic shunt (TIPS)
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what does high CO2 tell you?
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pt either has respiratory acidosis (pH <7.4) or is compensating for metabolic alkalosis (pH >7.4)
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what does low CO2 tell you?
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pt either has respiratory alkalosis (pH >7.4) or is compensating for metabolic acidosis (pH <7.4)
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what if pt has high bicarb?
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pt either has metabolic alkalosis (pH >7.4) or is compensating for respiratory acidosis (pH <7.4)
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what if pt has low bicarb?
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pt either has respiratory acidosis (pH <7.4) or is compensating for respiratory alkalosis (pH >7.4)
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common causes of respiratory acidosis?
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COPD, asthma, drugs (opoids, benzos, barbs, alcohol, and other respiratory depressants), chest wall problems (paralysis, pain), sleep apnea
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common causes of respiratory alkalosis?
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anxiety or hyperventilation, ASA or salicylate overdose
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common causes of metabolic acidosis?
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ethanol, DKA, uremia, lactic acidosis (sepsis or shock), methanol or ethylene glycol poisoning, ASA or salicylate overdose, diarrhea, carbonic anhydrase inhibitors
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common causes of metabolic alkalosis?
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diuretics (except carbonic anhydrase inhibitors), vomiting, volume contraction, antacid abuse, or milk-alkali syndrome, hyperaldosteronism
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what are two primary disturbances caused by salicylate overdose?
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respiratory alkalosis and metabolic acidosis; look for coexisting tinnitus, hypoglycemia, vomiting, and hx of swallowing several pills. alkalinization of the urine (with bicarb) speeds excretion
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what should you do first before trying bicarb to treat low pH?
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correct underlying cause and/or saline (do use bicarb is pH <7.0)
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what are signs and symptoms of hyponatremia?
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confusion, lethargy, mental status changes, anorexia, seizures, disorientation, cramps, and coma
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what is first step in determining the cause of true hyponatremia?
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look at the volume status
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what are common causes of SIADH?
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head trauma, surgery, meningitis, small cell lung CA, painful states (trauma, postop), pulmonary infections, opoids or chlorpropamide
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what is treatment for SIADH?
|
water restriction
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when can you expect potassium to be elevated?
|
addison's disease and hypoaldosteroniam
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how do you treat
a) hypovolemic hyponatremia? b)euvolemic and hypervolemic hyponatremia? |
a) saline
b) free water restriction and possibly diuretics for hypervolemia |
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why shouldn't you correct hyponatremia rapidly?
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can cause brainstem damage (central pontine myelinolysis). only use hypertonic saline when pt has seizures due to hyponatremia (always pick normal saline for hypovolemic hyponatremia on boards!!!)
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what are causes of hypovolemic hyponatremia?
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dehydration, diuretics, DKA or DM, addison's dz, hypoaldosteronism (treatment is saline)
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what are causes of euvolemic hyponatremia?
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SIADH, psychogenic polydipsia, oxytocin use (tx: free water restriction)
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what are causes of hypervolemic hyponatremia?
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CHF, nephrotic syndrome, cirrhosis, toxemia, renal failure (tx: free water restriction and possibly diuretics)
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once glucose reaches 200mg/dL, how much does Na+ decrease by for each increase of 100mg/dL glucose?
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decreases by 1.6 mEq/L
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which two disease states can cause false (spurious) hyponatremia by their osmotic effect?
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hyperlipidemia and hyperproteinemia
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what is the MCC of hyponatremia in surgical pt?
|
inappropriate or excessive fluid administration
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what are signs and symptoms of HYPERnatremia?
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confusion, mental status changes, hyperreflexia, seizures, coma
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what are common causes of hypernatremia?
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dehydration, inability to drink (dementia, paralysis), diuretics, DI, diarrhea, renal dz, iatrogenic administration of excessive salt
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what is treatment of hypernatremia?
|
water replacement; may start with normal saline if pt very dehydrated and then switch to 1/2 normal
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distinguish between pituitary and nephrogenic DI
|
pituitary DI responds to vasopressin, nephrogenic DOES NOT
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what are some causes of nephrogenic DI? and what is treatment?
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medications (lithium, demeclocycline, methoxyflurane, ampho B); tx is thiazide diuretic (paradoxical effect)
|
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what are causes of central DI (pituitary DI)?
|
tumor, trauma, sarcoidosis, often idiopathic
|
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what are the symptoms of hypokalemia?
|
muscle weakness (including smooth muscles) (and can lead to paralysis/death); can have ileus and/or hypotension
|
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what are the EKG changes in hypokalemia?
|
loss of T wave, presence of U waves, PVCs, PACs, ventricular and atrial tachyarrhythmias
|
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Explain the process used to assist someone who is considering suicide.
|
Be actively concerned and listen carefully. Be very positive without being condescending and try to utilize peer support for encouragement and acceptance. Do your best to get the person to the proper referral agency as soon as you can. In all cases do not leave the person alone.
|
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what cardiac drug causes the heart to be especially sensitive to hypoK?
|
digitalis (watch K carefully)
|
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should you replace K fast? and what is best method of replacement?
|
NO, oral, if have to give IV, don't exceed 20 mEq/hr
|
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what can cause a false hyperK?
|
hemolyzed specimen
|
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what are signs and symptoms of hyperK?
|
tall, peaked T waves, widening of QRS, PR interval prolongation, loss of P waves and a sine wave pattern;
arrhythmias include asystole and ventricular fib |
|
what are common causes of hyperkalemia?
|
renal failure (acute or chronic), severe tissue destruction, hypoaldosteronism, medications (K sparring diuretics, B blockers, NSAIDs, ACEIs), adrenal insufficiency
|
|
what is treatment for hyperK?
|
decrease intake or sodium polystyrene resin; unless it's severely increased, then start with calcium gluconate (for cardioprotection) and then give sodium bicarb (alkalosis causes K+ to shift to inside of cells, and glucose with insulin (also forces K+ into cells). If pt has renal failure or initial tx is ineffective, emergent dialysis needed
|
|
what is most common finding in hypocalcemia?
|
tetany (tap on facial nerve/Chvostek's sign) or apply tourniquet or BP cuff and inflate to elicit hand muscle spasms (carpopedal spasms/trousseau's sign); other findings: depression, encephalopahty, dementia, laryngospasm, convulsions
|
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what does EKG show in hypocalcemia?
|
QT interval prolongation
|
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What are the common causes of hypocalcemia?
|
digeorge's syndrome (tetany shortly after birth, absent thymic shadow); renal failure (b/c of kidney's role in vit D metabolism), hypoparathyroidism (watch for post-thyroidectomy pts), vit D def, pseudohypoparathyroidism, acute pancreatitis
|
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which two electrolyte disturbances are hard to correct when coupled with hypomagnesemia?
|
hypoK and hypoCa
|
|
what are the skeletal effects of vitamin D deficiency in:
a) children b) adults |
a) rickets
b) osteomalacia |
|
how do phosphorus and calcium levels correspond usually?
|
in opposite directions
|
|
what are symptoms of hypercalcemia?
|
usually asymptomatic, but when are present: bones, stones, groans, and psych overtones (ie. osteopenia or pathologic fx, kidney stones, polyuria, abd pain, anorexia, constipation, ileus, N/V, depression, psychosis, delirium, confusion
|
|
what does EKG show in hypercalcemia?
|
QT interval shortening
|
|
what are common causes of hypercalcemia?
|
hyperparathyroidism (MCC in outpts), malignancy (MCC in inpts), vitamin A or D intoxication, sarcoidosis, thiazide diuretics, familial hypocalciuric hypercalcemia (low urinary calcium which is usually rare with hypercalcemia), immobilization
|
|
what can cause hypercalcemia because of an increase in the protein-bound fraction of calcium, but pt will be asymptomatic b/c the ionized (unbound) fraction is unchanged?
|
hyperproteinemia
|
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how do you treat hypercalcemia?
|
IV fluids first, once hydrated give furosemide to cause calcium diuresis (thiazides are CONTRAINDICATED). other txs: phosphorus administration, calcitonin, diphosphonates, plicamycin and prednisone (for malignancy induced hyperCa2+)
|
|
what can severe prolonged hypercalcemia cause?
|
nephrocalcinosis, urolithiasis, renal failure from calcium salt deposits in kidneys
|
|
when do you most often see hypoMg?
|
alcoholics
|
|
what is a classic cause of hyperMg?
|
iatrogenic d/t preggers tx'd with magnesium sulfate for preeclampsia; on boards, often d/t renal failure. (should look for decreased DTRs, hypoTN, and resp depression)
|
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how do you treat hypoMg?
|
oral replacement
|
|
how do you treat hyperMg?
|
stop mag sulfate tx if it is being given and supportive; IV hydration, furosemide, and dialysis as last resort
|
|
when do you usually see hypophasphatemia and what are the signs and symptoms?
|
pts with DKA and in alcoholics; neuromuscular disturbances (encephalopathy, weakness), rhabdomyolysis (esp in alcoholics), anemia with WBC and platelet dysfxn
|
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when do you see hyperphosphatemia; and how do you treat it?
|
almost always seen in pts with renal failure; tx with phosphate restriction, dialysis, and possibly phosphate binding resins (calcium carbonate)
|
|
what is the fluid of choice in trauma pts? what is the 2nd choice?
|
ringer's lactate; normal saline
|
|
what is maintenance fluid in NPO patient?
|
D5W in 0.45% NS. and since hypoK can develop acutely in NPO pts, give K+ supplements (10 mEq KCl in the first liter of fluid each day)
|
|
what are the fat soluble vitamins?
|
A, D, E, K
|
|
deficiency of fat soluble vitamins is often d/t what?
|
malabsorption (ie: CF, cirrhosis, celiac dz, duodenal bypass, bile duct obstruction, pancreatic insufficiency, chronic giardiasis (tx with high dose oral supplements)
|
|
alcoholics can have almost any vitamin deficiency, but which ones should you look for?
|
folate, thiamine, magnesium
|
|
what is MCC of B12 deficiency?
|
pernicious anemia (antiparietal cell Abs destroy the ability to secrete instrisic factor)
|
|
what conditions are associated with vitamin B12 def (pernicious anemia)?
|
hypothyroidism and vitiligo
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how do you diagnose the cause of B12 def?
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Schilling's test (bunch of crazy stages where you give pt B12 and intrinsic factor, etc); can tell you if the B12 def is d/t pernicious anemia or malabsorption
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what are some other causes of B12 def?
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diphyllobothrium latum (tapeworm) and removal of the ileum
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what vitamin deficiency is a/w use of isoniazid?
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B6 (pyridoxine) deficiency; must give pts on this supplemental B6
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which class of drugs can cause folate deficiency?
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anticonvulsants (especially phenytoin)
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which vitamin is a teratogen and female pt must have pregger test before starting tx with meds containing this vitamin and must stay on birth control during tx?
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vitamin A (isotretinoin); acne med
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what are the physical findings a/w rickets (vit D def in kids)?
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craniotabes (poorly mineralized skull and bones that feel like a ping pong ball, rachitic rosary (costochondral beading with small round masses on the anterior rib cage, delayed fontanelle closure, bossing of skull, kyphoscoliosis, bowlegs, knock knees. bone changes first appear at the lower ends of the radius and ulna (xrays)
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what vitamin is given to all newborns as prophylaxis against hemorrhagic dz of the newborn
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vitamin K since it is required for synthesis of factors II, VII, IX and X and proteins C and S
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prothrombin time may be prolonged in cirrhosis b/c can't synthesize clotting factors, but vitamin K won't work with this condition. how do you tx?
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fresh frozen plasma
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what are symptoms of vit A deficiency?
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night blindness, scaly rash, xerophthalmia (dry eyes), bitot's spots (debris on conjunctiva), increased infections
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what are signs and symptoms of vitamin A toxicity?
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pseudotumor cerebri, bone thickening, teratogenicity
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what are signs and symptoms of vitamin D deficinecy?
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rickets, osteomalacia, hypocalcemia
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what are signs and symptoms of vitamin D toxicity?
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hypercalcemia, N/V, renal effects
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what are S&S of vit E def?
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anemia, peripheral neuropathy, ataxia
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what are S&S of vit E toxicity?
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necrotizing enterocolitis (infants)
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what are S&S of vitamin K def?
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hemorrhage, prolonged prothrombin time
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what are S&S of vit K toxicity?
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hemolysis (kernicterus)
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what are S&S of vitamin B1 (thiamine) def?
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wet beriberi (high output cardiac failure), dry beriberi (peripheral neuropathy), wernicke's and korsakoff's syndromes
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what are S&S of vitamin B2 (riboflavin) deficiency?
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cheilosis, angular stomatitis, dermatitis
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what are S&S of vitamin B3 (niacin) deficiency?
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pellagra (dementia, dermatitis, diarrhea), stomatitis
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what are S&S of vitamin B6 (pyridoxine) deficiency?
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peripheral neuropathy, cheilosis (scaling and fissures in corner of mouth), stomatitis (inflammation of mucous lining in any part of mouth), convulsions in infants, microcytic anemia, seborrheic dermatitis
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what are S&S of vit B6 toxicity?
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peripheral neuropathy (is the only B vitamin with toxicity)
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what are S&S of vit B12 deficiency?
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megaloblastic anemia plus neurologic symptoms
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what are S&S of folic acid deficiency?
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megaloblastic anemia WITHOUT neurologic symptoms
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what are S&S of vitamin C deficiency?
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scurvy (hemorrhages- skin petechiae, bone, gums, loose teeth, gingivitis), poor wound healing, hyperkeratotic hair follicles, bone pain (from periosteal hemorrhages)
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what are S&S of iron def?
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microcytic anemia, koilonychia (spoon fingernails)
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what are S&S of iron toxicity?
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hemochromatosis
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what are S&S of iodine deficiency?
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goiter, cretinism, hypothyroidism
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what are S&S of iodine toxicity?
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can cause myxedema
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what are S&S of fluorine def?
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dental caries (cavities)
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what are s&s of fluorine toxicity?
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fluorosis with mottling of teeth and bone exostoses
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what are S&S of zinc deficiency?
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hyposeugia (decreased taste), rash, slow wound healing
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what are s&s of copper deficiency?
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menke's disease (X-linked, kinky hair, MR)
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what are s&s of copper toxicity?
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Wilson's dz
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what are s&s of selenium deficiency?
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cardiomyopathy and muscle pain
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what are s&s of selenium toxicity?
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loss of hair and nails
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what are s&s of manganese toxicity?
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"manganese madness" in miners of ore
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what are s&s of chromium deficiency?
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impaired glucose tolerance
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name the 4 types of shock
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hypovolemic
cardiogenic septic neurogenic |
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what's the first thing you always do with pt in shock?
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give fluids; and if pt doesn't respond to fluid bolus, use invasive hemodynamic monitoring (swan-ganz catheter) to help make diagnostic and therapeutic decisions
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describe hypovolemic shock
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hx of fluid loss (blood, diarrhea, vomiting, sweating, diuretics, inability to drink water), cold/clammy skin, pale, fluid loss can be internal (ruptured AAA or spleen, with pancreatitis or after surg); other signs: orthostatic hypoTN, tachycardia, sunken eyes, skin tenting, sunken fontanel (in baby)
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describe cardiogenic shock
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hx of MI, chest pain, CHF or several risk factors for CAD; cold/clammy skin, pale; other signs: distended neck veins, pulmonary congestion. pts usually need diuretics (IV fluid can make them worse)
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describe neurogenic shock
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hx of severe CNS trauma or bleed, flushed skin. HR may be normal
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describe septic shock
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fever, changes in WBC count, flushed skin, warm to touch, extremes of age. use broad spectrum AbRx after pan-culturing pt (blood, sputum and urine cultures)
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what are the hemodynamic parameters (CO, PCWP, SVR, SVO2) of hypovolemic shock
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SVR is high; all others are low
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hemodynamic parameters of cardiogenic shock?
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PCWP and SVR are high, CO and SVO2 are low
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hemodynamic parameters of septic shock?
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high CO, high SVO2, low PCWP and low SVR
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hemodynamic parameters of neurogenic shock?
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all (CO, SVO2, SVR and PCWP) are low
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describe anaphylaxis
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look for bee stings, peanuts and shellfish and PCN, sulfa or other meds, tx with epinephrine and fluid and O2 (intubate if necessary). antihistamines help with mild cases, corticosteriods used when rxn is prolonged or severe, monitor all pts x 6 hrs after initial reaction
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describe pulmonary embolus
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look for risk factors for DVT (virchow's triad: endothelial damage, stasis, hypercoaguable state), hx of recent delivery (amniotic fluid embolus), fractures (fat emboli), DVT (+ homan's sign), recent surgery (esp ortho or pelvic surg) pts have CP, tachypnea, SOB, parasternal heave, right axis shift on EKG, and/or + ventilation/perfusion scan
tx with heparin to prevent further clotting and emboli |
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what is common hx in pericardial tamponade and what is tx?
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stab wound in left chest, distended neck veins; do pericardiocentesis emergently
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describe toxic shock syndrome
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classic is woman of reproductive age who leaves tampon in too long, look for skin desquamination. c/t staph aureus
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What is first thing to think of in pt with shock?
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ABC's: airway, breathing, circulation. intubate at drop of a hat, keep NPO, avoid narcotics if possible (mental status changes are important clue to impending doom). Monitor EKG, vitals, Swan-Ganz parameters, urine output, ABGs, CXR, Hgb and Hct
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what is standard bolus to give most pts in shock?
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10-20 mL/kg of normal saline (roughly 1-2 L as fast as possible), can bolus again if first bolus doesn't work. watch for fluid overload esp in CHF or don't cause CHF
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what is a cause of shock especially in post-op pt who has taken steroids in past year and got NO steroids perioperatively. and what is tx?
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addison's disease. give pt steroids
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name some IV meds used to support blood pressure
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dobutamine, dopamine, NE, phenylepherine, epinephrine, and milrinone/amrinone
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what is MoA of dobutamine?
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B1 agonist to increase CO by increasing contractility (IV equivalent of digoxin)
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what is MoA of dopamine?
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low doses of dopamine hit dopamine receptors in renal vasculature to keep kidney perfused. high doses have B1 agonist effects to increase ocntractility, highest doese have alpha-1 effects and cause vasoconstriction
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what is MoA of NE?
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alpha-1 agonist, given in hypoTN to increase peripheral resistance so perfusion of vital organs can be maintained; also has B-agonist effects
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what is MoA of phenylephrine?
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alpha-1 agonistwha
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what is MoA of ephinephrine?
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used for cardiac arrest and anaphylaxis
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what is MoA of milrinone and amrinone?
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phosphodiesterase inhibitors used in refractory heart failure (NOT first line agents) b/c they have + ionotropic effect
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what do you do if you can't intubate pt d/t laryngeal edema?
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tracheostomy or cricothyroidotomy
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