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496 Cards in this Set
- Front
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the only 3 ways to lower BP
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1. dump some fluid
2. dilate vessels 3. decrease HR and contractility |
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what do the kidneys/adrenals and the renin-angiotensin-aldosterone system do to your attempts to lower BP?
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the kidneys and the RAAS will fight your attempts to lower BP
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what is essential HTN due to?
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"essential" vasoconstriction of the arterioles
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in essential HTN, what happens to TPR? to CO?
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TPR is increased due to vasoconstriction
CO stays normal |
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what happens when the LV begins to wear out from too many years of HTN?
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CO decreases and the pt goes into early LV failure
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how do NSAIDs interfere w/ the good effects of anti-HTN drugs?
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they increase renal Na retention
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for mild HTN, start with...
if HTN is not controlled by the above, add... |
thiazide diuretic
a beta-blocker |
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if HTN is not controlled by a beta blocker, add...
if HTN is not controlled by a beta blocker or the above drug, add... |
thiazide diuretic
vasodilator |
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which 2 anti-HTN drugs do blacks respond best to?
which 3 do the elderly respond best to? in whom are ACEIs most effective in lowering BP? |
blacks - thiazides and CCBs
elderly - thiazides, CCBs, and ACEIs ACEIs best in --> young whites |
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captopril
enalopril what drug class are these drugs? |
ACEIs
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when are ACEIs 1st-choice drugs for HTN?
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when there are contraindications to taking thiazides or BBs
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3 contraindications to taking thiazides for HTN
3 contraindications to taking BBs for HTN |
thiazides - gout, sulfa allergy, and creatinine clearance <50
BBs - elderly, asthma, and COPD |
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2 ways in which ACEIs lower BP
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1. block production of angiotensin II --> causes vasodilation
2. decreases aldosterone --> causes decrease in circulating fluid volume |
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which drug class is the preferred choice for the tx of HTN in diabetics? why?
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ACEIs, b/c they are renal protective
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explain why ACEIs are renal-protective
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dilate efferent arterioles --> decreases glomerular pressure
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what could happen if you dilate the glomerular efferent arterioles in someone who has bilateral or unilateral RAS
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can decrease the glomerular filtration pressure to the point of ARF
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angiotensin converting enzyme (ACE) normally metabolizes...
so, part of ACEIs vasodilatory effect is due to... in some pts, the above causes these 2 side effects |
bradykinin
the increase in bradykinin increase in bradykinin can cause: 1. dry cough 2. angioedema (laryngeal edema +/- hypoTN) |
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why does the 1st dose of an ACEI have to be given in the office?
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it can cause 1st dose syncope
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ACEIs can cause this electrolyte disturbance b/c it decreases aldosterone
b/c of this, what should you never give w/ ACEIs? |
hyperK
never give an ACEI w/ a K supplement or K-sparing diuretic |
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what is the upside to taking ARBs instead of ACEIs?
when would you switch a pt from an ACEI to an ARB? |
less chance of dry cough or angioedema
switch the pt when they complain of dry cough |
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any drug that causes significant arteriolar vasodilation may cause...
how? name 4 drug classes which could cause this |
edema
arterioles dilate --> permit higher BP to pervade the capillaries --> capillaries leak fluid into the tissues 1. alpha blockers 2. ACEIs 3. ARBs 4. CCBs |
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nifedipine
amlodipine verapamil diltiazem what drug class are these drugs? which are dihydropyridines? which are nondihydropyridines? |
CCBs
dihyropyridines - nifedipine and amlodipine nondihydropyridines - verapamil and diltiazem |
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do dihyropyridines (-ipines) or nondihydropyridines have much greater selectivity for the Ca channels of vascular smooth muscle?
what 3 things are they used to treat? |
dihydropyridines (-ipines)
used to treat: 1. HTN 2. peripheral vascular disease 3. Raynaud's |
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this CCB decreases HR and contractility more than it causes vasodilation
this CCB decreases HR and contractility about equally as it dilates the coronaries and arterioles |
verapamil
diltiazem |
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these anti-HTN drugs can be used to treat angina b/c they dilate coronary vessels
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CCBs (nifedipine, amlodipine, verapamil, and diltiazem)
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this CCB has a marked negative chronotropic effect on the SA and AV nodes
b/c of this, it is used to decrease HR in... |
verapamil
SVT |
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these anti-HTN drugs can be used as migraine prophylaxis
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CCBs
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4 side effects of CCBs due to their vasodilatory effects:
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1. peripheral edema
2. flushing 3. headache 4. constipation |
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1. this is the main internal regulator of both Na and K levels by causing an ion exchange across the tubule cells of the nephron
2. how does the ion exchange work? 3. in edematous states, is there too much or not enough aldosterone? what does this cause? |
1. aldosterone
2. Na is reabsorbed from the tubular fluid back into the tissues, while K and H are secreted into the tubular fluid for excretion 3. in edematous states, there is excess aldosterone, causing conservation of Na and water, expanding the total fluid volume, and dumping of K and H, causing alkalosis |
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hypoK potentiates the toxicity of...
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digoxin
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4 kinds of diuretics
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1. thiazide diuretics
2. loop " 3. K-sparing " 4. osmotic " |
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3 edematous states for which diuretics are used
2 nonedematous states for which diuretics are used |
edematous:
1. HF 2. hepatic ascites 3. nephrotic syndrome non-edematous: 1. HTN 2. Diabetes Insipidus |
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explain how HF causes edema
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HF --> decreased CO --> juxtaglomerular apparatus of kidneys detects hypovolemia --> increases renin secretion -->
1. increase in angiotensin --> increase in vasoconstriction --> increase in BP 2. increase in angiotensin --> increase in aldosteorne --> increase in renal Na and water retention --> increase in circulatory fluid volume --> edema and increase in BP Both 1. and 2. causes worsening HF w/ pulmonary and/or peripheral edema |
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explain what causes hepatic ascites
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1. cirrhosis --> increase in portal BP --> fluid exudes from liver 00> ascites
2. cirrhosis --> fewer plasma proteins --> decreases plasma osmolarity --> water leaks from vessles --> ascites |
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explain how nephrotic syndrome causes edema
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1. glomeruli damaged by DM, HTN, glomerulonephritis, etc. leak plasma proteins into urine --> decreases in plasma osmolarity --> water leaks out --> edema
2. glomerular leak plasma proteins into urine --> decreases plasma volume --> increases aldosterone --> increases Na and water retention --> edema |
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how do thiazide diuretics tx HTN short-term? long-term?
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short-term - dump fluid
long-term - causes arteriolar vasodilation |
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how do thiazides tx diabetes insipidus?
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thiazides --> decrease plasma volume --> increase aldosterone --> increase Na and water retention --> decrease polydipsia and polyuria
thiazides --> decrease plasma volume --> decrease glomerular filtration --> decrease fluid to distal tubule --> decrease polydipsia and polyuria |
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why are thiazides called "ceiling" diuretics?
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they cause their maximal diuretic and anti-HTN effects at relatively low doses w/ no extra effect at higher doses
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hydrochlorothiazide
chlorthalidone |
2 most commonly used thiazides
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thiazides decrease Na reabsorption in the...
loops decrease Na reabsorption in the... |
distal convoluted tubule
thick ascending limb of Henle's loop |
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at what GFR and creatinine clearance are thiazides not effective
what should you use instead? |
if GFR < 30 ml/min or
if Ccr < 50 ml/min use a loop diuretic |
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4 things that thiazides are used to treat/prevent
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HTN and CHF (by decreasing Na retention)
Osteoporosis and Ca stones (by increasing reabsorption of Ca) |
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3 side effects of thiazides (electrolyte imbalances)
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1. increased K excretion --> hypoK
2. increased H excretion --> metabolic alkalosis 3. decreased uric acid secretion --> hyperuricemia --> gout |
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how might you compensate for thiazide-induced hypoK?
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add a K-sparing diuretic (spironolactone for example), a K supplement, or bananas
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both thiazides and loop diuretics cause these electrolyte imbalances
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hypoK and metabolic alkalosis (from increased K and H secretion)
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furosemide (Lasix)
bumetanide ethacrynic acid |
loop diuretics
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thiazides increase the renal absorption of this from the urine
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Ca
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which diuretics work in a patient w/ severe renal impairment: thiazides or loops?
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loops
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what do loop diuretics do to renal vascular resistance? to renal blood flow?
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they decrease vascular resistance and increase blood flow
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drug of choice for reducing (mobilizing) pulmonary edema of HF
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loop diuretics
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which kind of diuretic is useful in an emergnecy b/c it works fast?
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loop diuretics
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loops increase the excretion of these 2 electrolytes
b/c of this, what can loops be used to treat? |
Ca and K
used to tx hyperCa and hyperK |
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loops + aminoglycoside antibiotic =
which loop is most likely to cause this? what is another side effect of loops? |
ototoxicity
ethacrynic acid severe rapid reduction in circulating fluid volume --> hypovolemia --> shock |
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triamterene
amiloride spironolactone |
K-sparing diuretics
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K-sparing diuretics may cause this electrolyte imbalance
should they be used w/ a K supplement? should you monitor K levels when on these? |
hyperK
no yes |
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1. spironolactone is a specific...
2. in what two states is it used? 3. it is also used like ACEIs and ARBs to... 4. is spironolactone effective in Addison's disease (primary adrenal insufficiency) |
1. aldosterone receptor antagonist
2. edematous states and hyperaldosteronism 3. prevent cardiac remodeling in CHF 4. no, b/c aldosterone isn't high in Addison's |
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2 side effects of spironolactone
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1. gynecomastia
2. menstrual abnormalities this is b/c it resembles sex steroids |
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1. most common osmotic diuretic
2. how does it work? 3. how must it be given and why? 4. what is a side effect of this and how can you prevent it? |
1. mannitol
2. increases water excretion: it is freely filtered into the tubular fluid and not reabsorbed, so it increases fluid osmolarity --> holds water in the tubular fluid --> increases urine 3. must be given IV b/c it is not absorbed from the GI tract 4. dehydration --> prevent it by maintaining PO and IV fluids |
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what is used to do the following 3 things:
1. maintain tubular fluid flow after ingestion of toxic substance that can clog the tubules and cause ARF 2. prevent ARF due to circulatory shock 3. lower increased ICP |
mannitol
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these 2 general things can decrease the rate of progression of atherosclerotic plaque and even reduce pre-existing plaque
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1. lifestyle changes
2. medication |
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CAD is positively correlated with...
CAD is negatively correlated with... |
high TC, and more so, high LDL
high HDL |
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total cholesterol =
VLDL = |
VLDL + LDL + HDL
TGs/5 |
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primary goal in cholesterol-lowering therapy
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decrease LDL
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what are the target levels of the following lipids:
1. TC 2. LDL 3. HDL 4. ratio of TC to HDL |
1. <200
2. <130 3. >60 4. as low as possible |
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what are the following mainly used for:
1. statins (HMG CoA reductase inhibitors) 2. fibrates 3. niacin 4. bile-acid binding resins |
1. decrease LDL
2. decrease TGs 3. increase HDL (about 35%) 4. decrease LDL (about 30%) |
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atorvostatin (Lipitor)
rosuvastatin (Crestor) |
statins that decrease LDL by about 50% (other statins decreased LDL less)
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how do statins decrease LDL?
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they inhibit the rate-limiting step in intracellular cholesterol synthesis (mostly hepatic) --> causes increase in number of extracellular LDL receptors --> increases cellular uptake of LDL --> decreases plasma LDL
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2 side effects of statins
what tests should be done regularly to monitor these side effects? |
1. myopathy (test CPK-MM regularly)
2. elevated liver enzymes (test AST and ALT regularly) |
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this penny-a-day drug decreases the incidence of CV events to the same degree as a statin costing $1-4/day
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aspirin
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fenofibrate (Lofibra)
gemfirozil (Lopid) what is a side effect of these drugs? |
1. fibrates - fenofibrate decreases TGs by about 50%; gemfirozil decreases TGs less
2. myopathy |
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fasting TG > 500 mg/dl can cause...
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pancreatitis
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side effect of fibrates
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myopathy
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single drug that causes the largest changes in all 3 lipids
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niacin
increases HDL and decreases LDL and TGs |
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2 side effects of niacin
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1. severe facial flushing (can be prevented by taking ASA or NSAID 30 minutes before taking niacin or by taking an extended-release niacin)
2. gout |
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cholestyramine (Questran)
colesevelam (Welchol) colestipol (Colestid) 5 side effects of these drugs |
bile acid binding resins - decrease LDL
1. bloating 2. flatulence 3. abdominal pain 4.decrease absorption of vitamins ADEK 5. decrease absorption of many drugs |
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ezetimibe (Zetia)
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directly decreases GI tract cholesterol absorption
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3 things that you may have to get on a patient for whom you prescribe one or a combination of antihyperlipidemic drugs
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1. baseline LFTs
2. regular liver enzymes while on the drug 3. regular CPK-MM levels while on the drug |
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important drug combo of antihyperlipidemic drugs that significantly changes all cardiac lipids in beneficial directions
2 other combinations that are common |
fenofibrate + statin
fenofibrate + niacin statin + niacin |
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antihyperlipidemic substance that has significant cardioprotective effects and is underutilized in clinical practice
what effect do they have? |
omega-3 fatty acids (from oily fish or dietary supplement)
decrease TGs |
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myocardial O2 demand exceeds coronary O2 supply
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angina
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some degree of atherosclerotic occlusion in the coronary vessels so that at some intensity of exercise, O2 demand becomes > O2 supply, leading to pain
how can this be relieved? |
stable angina
rest and nitro |
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unexplained temporary coronary vasospasm
is this more common in men or women? how can this be relieved? |
Prinzmetal (variant or vasospastic) angina
more common in women nitro |
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2 causes of unstable angina
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1. acute plaque change --> partial thrombus
2. atherosclerotic occlusion severe enough that sedentary changes in heart activity causes O2 demand to exceed O2 supply |
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4 general things you aim for in the tx of angina
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1. dilate coronaries
2. dilate systemic veins to decrease preload 3. dilate systemic arterioles to decrease afterload 4. decrease contractility |
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nitrolingual spray
nitrostat sublingual tabs what are these used for? |
used to dilate the coronary vessels for prompt relief of stable or Prinzmetal's angina; also dilates the systemic veins, decreasing VR --> decreases preload --> decreases cardiac work
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nitroglycerin patch (Nitro-Dur) ointment (Nitro-BID)
long-acting tabs (isosorbide mononitrate or dinitrate) what are these used for? |
used to dilate the coronaries and system veins LONG-TERM in order to prevent attacks of angina
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which drug class other than nitro can be used to prevent anginal attacks? how do they do this?
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dihydropyridine CCBs such as nifedipine (Procardia XL)
by dilating the coronaries and systemic arterioles |
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1. which 2 drug classes can you use to decrease cardiac contractility long-term in order to prevent anginal attacks? give examples of each
2. which drug is good for preventing variant angina? 3. which drug class cannot be used in pts with a "damaged heart" (MI, CHF)? |
1. BBs: propranolol (Inderal) and metoprolol (Toprol-XL)
non-dihydropyridine CCBs: verapamil (decreases HR and contractility) and diltiazem (decreases HR and contractility, dilates coronaries and arterioles) 2. diltiazem is good for variant angina 3. CCBs cannot be used; only BBs are beneficial in these pts |
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3 side effects of nitro
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1. headache
2. postural hypoTN 3. tolerance (prevent this by removing the patch or ointment at bedtime) |
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most common cause of HF
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left systolic dysfunction due to coronary artery disease
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ventricles less able to eject blood (decreased contractility) =
ventricles stiff, non-compliant, and can't fill properly = both cause a decrease in... |
systolic failure
diastolic failure CO |
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organ that tries to assure its own function in HF and in so doing most single-handedly makes HF worse
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kidneys
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3 compensatory mechanisms that help increase CO and maintain glomerular filtration pressure in HF
5 things these compensatory mechanisms cause |
1. sympathetic tone --> increases HR and contractility, causes vasoconstriction, and increases renin secretion
2. Renin --> angiotensin --> vasoconstriction and aldosterone --> increase in renal Na and water retention 3. cardiac hypertrophy --> dilated and globular shape (remodeling) -------------------------------------------------- 1. fluid overload 2. increased cardiac filling pressures 3. HTN 4. increased preload and afterload 5. increased cardiac work 6. worse HF |
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4 categories of drugs used to treat HF
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1. BBs and alpha blockers
2. ACEIs and ARBs 3. diuretics 4. inotropic agents (like digoxin) |
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6 causes of decompensation or exacerbation or acute HF in a pt w/ chronic HF
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1. increased Na intake
2. increased exertion 3. illness, fever, etc. 4. emotion 5. not taking meds 6. AMI |
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DOC for all stages of HF
why? |
ACEIs (captopril, lisinopril)
they prevent or limit cardiac remodeling and decrease M&M |
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how can ACEIs lead to acute renal failure in pts with RAS?
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stenosis chockes glomerular filtration pressure, so the glomerular efferent arterioles compensate by constricting --> the BP is okay --> add the ACEI --> arterioles dilate --> no filtration pressure --> ARF
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how do ACEIs and ARBs decrease cardiac remodeling?
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block aldosterone release --> decreases renal fluid retention --> decreases cardiac filling pressures
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which of the three is used in advanced HF? in mild HF? in significant pulmonary or pedal edema from HF and/or renal insufficiency (Ccr <50)?
1. thiazides 2. loops 3. spironolactone |
thiazides - mild HF
loops - pulm/pedal edema or renal insufficiency spironolactone - advanced HF |
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2 beta-blockers that are negative inotropes and improve systolic function in HF and decrease remodeling b/c they decreases renin --> decrease in aldosterone
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carvedilol
metoprolol |
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this beta-blocker is also an alpha-blocker
what effect does it have as an alpha-blocker? |
carvedilol
dilates arterioles --> decreases BP and cardiac work dilates veins --> decreases preload and cardiac work |
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what role do CCBs play in HF?
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none
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cardiac glycoside and positive inotrope (increases contractility) w/ very narrow therapeutic index
who is it reserved for? |
digoxin
reserved for HF pts not responding adequately to a combo of diuretic + BB + ACEI |
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which kind of HF is digoxin used for?
which kinds is it not used for? |
severe left systolic HF
not used for diastolic HF or right-sided HF |
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overdose of this drug includes:
1. severe potentially fatal dysrhythmias 2. N/V 3. headache and confusion 4. blurred vision, color distortion, and halos |
digoxin toxicity
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which 3 electrolyte disturbances predispose someone to digoxin toxicity?
what is the antidote for dig toxicity? |
hypoK
hypoMg hyperCa Digibind (a digoxin antibody) |
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prostacyclin
nitric oxide what are these and where are they made? |
inhibitors of platelet aggregation
made by healthy endothelial cells |
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4 things that can bind to external receptors on the platelet membrane
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1. exposed vascular collagen (from injury)
2. thromboxane A2 3. thrombin 4. ADP |
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when things bind the external receptors on platelets, what 5 things are released externally from the platelet? what do these things do? what is released internally? what does this do?
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externally:
1. thromboxane A2 2. thrombin 3. ADP 4. serotonin 5. PAF these 5 things activate other platelets' receptors internally: 1. calcium Ca activates this platelet's GP IIb/IIIa receptors --> bind fibrinogen in the plasma --> cross-links 2 platelets --> cross-linking cascade --> platelet plug |
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vessel injury and platelet chemicals start the coagulation cascade producing...
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thrombin + fibrinogen --> fibrin-platelet plug (thrombus)
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3 main classes of antiplatelet drugs
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platelet COX-1 inhibitors: ASA
platelet ADP receptor blockers: clopidogrel (Plavix) platelet GP IIb/IIIa receptor blockers: abciximab (ReoPro) and tirofiban (Aggrastat) |
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this drug irreversibly acetylates and inhibits COX-1 in platelets so that thromboxane A2 is not produced and cannot activate platelets
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ASA
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these drugs inhibit ADP-induced activation of GP IIb/IIIa receptors so that they don't bind fibrinogen
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ADP receptor blockers such as clopidogrel (Plavix)
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these drugs block fibrinogen from binding even activated GP IIb/IIIa receptors
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GP IIb/IIIa receptor blockers such as abciximab (ReoPro) and tirofiban (Aggrastat)
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ASA suppresses the synthesis of __________ irreversibly for the life of the platelet
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thromboxane A2
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do non-acetylated salicylates such as Disalcid have antiplatelet effects? do COX-2 inhibitors such as celecoxib (Celebrex)? does APAP?
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no, none of these do
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do COX-2 inhibitors interfere w/ the antiplatelet effects of ASA? what happens when these are taken alone? give an example of one of these
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no, it doesn't interfere w/ ASA
when taken alone, COX-2 inhibitors may cause CV events by shifting the balance of chemical mediators to produce more thromboxane A2 an example is rofecoxib (Vioxx) which was taken off the market for the above reason |
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this drug is used prophylactically against TIA/stroke and 1st and recurrent MIs
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ASA
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give 3 S&S of PAD
what should someone w/ PAD be taking routinely? |
1. claudication
2. visible arterial insufficiency 3. ankle-brachial index <0.9 they should be taking ASA for its cardioprotective effect |
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give 3 side effects of ASA
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1. prolongs bleeding time
2. increases risk of hemorrhagic stroke and GI bleed, esp. at high dose 3. causes Guaiac + stool even in the absence of a GI tract lesion or ulcer |
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this drug can be used in pts who are intolerant to ASA, for the same reasons as ASA, and during stent insertion for CAD
what is a side effect of this drug and other drugs in its class? |
clopidogrel (Plavix) which is an ADP receptor blocker
side effects of ADP receptor blockers include neutropenia - must monitor blood when on this |
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intrinsic and extrinsic pathways of coagulation eventually convert ________ to _________, which converts _________ to _________, which forms a thrombus
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prothrombin
thrombin fibrinogen fibrin |
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these 2 anticoagulants inhibits the action of thrombin by binding anti-thrombin
this anticoagulant inhibits the synthesis of thrombin |
heparins and lepirudin (Refludan)
warfarin |
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anticoagulants of choice in pregnancy b/c they don't cross the placenta
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heparin or LMWH
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4 things heparin is used for
name the main complication of heparin. name 2 others 5 contraindications for heparin or LMWH |
4 uses:
1. DVT/PE 2. AMI 3. Post-op hip replacement 4. in dialysis machines main complication: hemorrhage other complications: 1. hypersensitivity reactions (chills/fever, urticaria, anaphylaxis) 2. thrombocytopenia (+ thrombosis is serious, but rare - D/C heparin and replace w/ lepirudin) contraindications: 1. bleeding disorder 2. recent hemorrhagic stroke 3. GI ulcer 4. uncontrolled HTN 5. recent brain, spinal, or eye surgery |
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anticoagulant effect of this drug is monitored by the aPTT (1.5-2.5x normal)
anticoagulant effect of this drug is monitored by the PT (1.5-2.5x normal) |
IV heparin
oral warfarin |
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enoxaparin (Lovenox)
dalteparin (Fragmin) what are these? what are they replacing and why? |
LMWHs
replacing IV heparin b/c it can be given SC in the outpt setting and you usually don't need to monitor w/ aPPT |
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antidote for heparin-induced hemorrhage; is it a good antidote for LMWH?
antidote for Coumadin-induced hemorrhage? |
you can lower or D/C heparin or give protamine sulfate; doesn't work as well as an antidote for LMWH
oral Vitamin K; if severe can use IV Vitamin K or FFP |
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Vitamin K antagonist - deactivates and prevents reactivation of Vitamin K so that several coagulation factors, including factor II cannot be synthesized
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Coumadin
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this anticoagulant should never be used during pregnancy b/c it is teratogenic
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Coumadin
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alteplase (Streptase)
streptokinase (Streptase) what are these drugs and what do they do? |
thrombolytics
convert plasminogen to plasmin --> dissolves fibrin clot |
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this thrombolytic has greater affinity for plasminogen already bound to a fibrin clot, so it is considered "fibrin-selective" or "clot-selective"
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alteplase (Streptase)
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this thrombolytic binds free plasminogen in the plasma in addition to plasminogen already bound to fibrin in a clot
what does this induce? what does this drug increase the risk of? |
streptokinase
induces a "systemic fibrinolytic state" increases risk of hemorrhage |
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aminocaproic acid (Amicar)
what is this the antidote for? |
the fibrinolytic state induced by the thrombolytic streptokinase
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these drugs are contraindicated in pts w/:
1. healing wounds 2. pregnancy 3. recent CVA 4. metastatic CA |
thrombolytics
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these are used for acute (within 2-6 hours) thromboembolic disease (AMI, stroke, PE is controversial)
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thrombolytics
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which administration of a thrombolytic is most successful for an AMI? which administration is used most commonly?
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intra-coronary delivery is most successful, but cardiac cath may not be possible within 2-6 hours
most common delivery is IV |
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tx of Fe-deficiency anemia
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oral ferrous sulfate (Feosol)
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how long are Fe supplements given for?
2 side effects of Fe supplements |
3-6 months
constipation and black stools |
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Iron Dextran (DexFerrum)
who is this reserved for? |
parenteral Fe-therapy, either IM or IV
reserved for pts who can't tolerate or absorb PO Fe, such as pts w/ IBD |
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3 possible causes of folate-deficiency anemia
how do you tx it? |
1. increased need in pregnancy or lactation
2. decreased absorption in alcoholism 3. folate-antagonist drugs, such as trimethoprim (Bactrim) and methotrexate tx - folic acid (generic) |
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2 causes of decreased IF causing B12-deficiency anemia
what is another cause of B12-deficiency? |
1. pernicious anemia
2. gastric resection another cause is dietary deficiency, but this is extremely rare |
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tx of dietary B12-deficiency
tx of pernicious anemia or other B12 malabsorption |
oral B12 (cyanocobalamin)
IM cyanocobalamin to normalize Nascobal nasal gel to maintain |
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in B12-deficiency anemia, _________ will correct the anemia, but the ________ effects will get worse
name 4 of these effects |
folic acid
neurological 1. parasthesias 2. tinnitus 3. decreased proprioception --> balance problems 4. decreased vibration sense |
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what should be done if a pt has a megaloblastic anemia but the specific cause cannot be or has not been determined?
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tx w/ both B12 and folic acid
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for severe anemia of ESRD, HIV, or CA, how should you treat?
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erythropoietin (Epogen) + Fe supplement
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used to treat sickle cell disease b/c it dilutes HbS by stimulating production of HbF; reduces painful crises by delaying polyermization of HbS, decreasing sickling
is there long-term safety w/ this drug? |
hydroxyurea
long-term safety is not yet known |
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2 drugs to treat A-flutter
2 drug combos to treat A-fib 2 drugs to treat SVTs 2 drugs to treat acute V-tach in AMI 2 drugs to treat V-fib not responding to defibrillation |
propranolol or verapamil/diltiazem
propranolol or amidoarone + Coumadin propranolol or verapamil/diltiazem lidocaine/epinephrine or amiodarone amiodarone or lidocaine/epinephrine |
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vancomycin (glycopeptides)
beta-lactams (PCNs, cephalosporins, and carbapenems) what is their mechanism of action? |
inhibitors of cell wall synthesis
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macrolides
aminoglycosides streptogramins tetracyclines what is their mechanism of action? |
protein synthesis inhibitors
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fluoroquinolones
what is their mechanism of action? |
DNA replication inhibitors
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sulfamethoxazole
trimethoprim what is their mechanism of action? |
folate antagonists
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urinary tract antiseptic
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nitrofurantoin (Macrobid)
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2 times when you should use broad-spectrum abx
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1. critically ill patients - give empiric treatment before getting the C&S results
2. when the infx is likely polymicrobial |
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should the broad-spectrum abx given to critically ill pts be bactericidal or bacteriostatic?
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bactericidal
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the BBB prevents penetration of which kind of drugs into the CNS
when might these be able to get past the BBB? |
non lipid-soluble
they may get past when there is CNS inflammation b/c of capillary leakiness |
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4 questions you should ask yourself before prescribing any drug to a pt
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1. is she or could she be pregnant?
2. does he/she have drug allergies? 3. is he/she old? 4. does he/she have decreased liver or kidney function? |
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4 traditional uses for prophylactice abx or antivirals
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1. before bowel surgery, joint replacement, etc.
2. before dental procedures in those w/ artificial heart valves 3. against TB and meningitis in those exposed 4. zidovudine (AZT or Retrovir) before HIV+ mothers give birth |
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these 2 things can cause superinfx of one unaffected organism
these superinfx usually occur in one of these 3 parts of the body what is a classic superinfx? what is it often caused by? name another classic superinfx/opportunistic infx |
1. broad-spectrum abx
2. combos of abx 1. respiratory tract 2. GI tract 3. GU tract pseudomembranous (C. diff) colitis, often caused by clindamycin or some other broad-spectrum abx Candida albicans or other fungi |
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explain the following pregnancy contraindication categories of drugs:
1. A 2. B and C 3. D 4. X |
A - show to be safe in human studies, at least for 1st trimester
B-D - sometimes the drug benefit outweighs the risk D - known fetal risk X - known risk outweighs benefit always |
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main uses of PCN G (IV) and PCN VK (oral)
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most bacteria are resistant, but main uses are:
1. susceptible strep infx 2. all stages of syphilis (T. pallidum) |
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cloxacillin
dicloxacillin nafcillin methicillin what are these and what are their main uses? which one is not used b/c it is too toxic? |
penicillinase resistant PCNs
main uses: 1. susceptible staph infx - cellulitis, endocarditis methicillin is too toxic for use |
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amoxicillin
ampicillin what are these and what are the 3 main uses of these? what is ampicillin famous for causing? |
aminopenicillins
3 main uses: 1. URIs 2. UTIs 3. PUD (h. pylori) side effect of ampicillin is nasty rash reaction |
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piperacillin
carbenicillin ticarcillin what are these and what are 2 main uses of these? what are they susceptible to? which is the only one that is PO? |
antispeudomonal PCNs
main uses: 1. Pseudomonas 2. hospital-acquired pneumonia and other nosocomial infx susceptible to beta-lactamases carbenicillin is the only PO drug |
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piperacillin + tazobactam =
amoxicillin + clavulanate = ampicillin + sulbactam = what are these? what do they treat? which one is antipseudomonal? |
Zosyn
Augmentin Unasyn beta-lactam + beta-lactamase combos they are broad-spectrum and good for empiric coverage of nosocomial infx main uses: 1. GI infx 2. abscesses 3. HAP 4. diabetic wounds only Zosyn is anti-pseudomonal |
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are cephs more or less beta-lactamase susceptible than PCNs?
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less susceptible
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cephalexin (Keflex)
which generation is this? 2 main uses |
1st generation
1. cellulitis 2. surgical prophylaxis |
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cefaclor (Ceclor)
which generation is this? what kind of coverage does it have? 2 main uses |
2nd generation
better Gram(-) coverage than 1st generation 1. gonorrhea 2. surgical prophylaxis |
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cefixime (Suprax)
ceftriaxone (Rocephin) what generation are these? what kind of coverage do they have? 4 main uses |
3rd generation
better Gram (-) coverage than 2nd generation 4 uses: 1. meningitis 2. HAP 3. Lyme disease 4. febrile neutropenia |
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cefepime (Maxipime)
what generation is this? 3 main uses |
4th generation
3 uses: 1. anti-pseudomonal 2. HAP/nosocomial 3. febrile neutropenia |
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imipenem/cilastatin
meropenem ertapenem what are these? 3 main uses |
carbapenems
they are not 1st-line, but can be used as broad-spectrum; they are stable against most beta-lactamases 3 main uses: 1. mixed aerobic/anaerobic infx 2. nosocomial infx 3. febrile neutropenia |
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side effect of imipenem
side effect of vancomycin and dalbavancin |
seizures (in high doses)
Red Man syndrome |
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vancomycin
dalbavancin what kind of abx are these? how are they usually administered? why? 2 main uses 1 side effect |
glycopeptides
usually given IV b/c they have poor bioavailability PO 2 main uses: 1. IV DOC for MRSA 2. given PO for C. diff colitis, only if Flagyl fails |
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gentamicin
streptomycin neomycin tobramycin what kind of abx are these? what other kind of abx do they synergize well with? 2 main uses 2 side effects which one can only be used topically b/c of toxicity |
aminoglycosides (they are protein synthesis inhibitors)
synergize well w/ beta-lactams (cell wall inhibitors) 3 main uses: 1. aerobic Gram (-) bacilli (such as Pseudomonas) 2. enterococci 2 side effects: 1. nephrotoxicity 2. ototoxicity neomycin can only be used topically |
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clindamycin
lincomycin what kind of abx are these? 2 main uses common side effect |
lincosamides
2 main uses: 1. acne 2. aspiration pneumonia side effect: C. diff colitis |
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erythromycin
clarithromycin azithromycin what kind of abx are these? what organ do they penetrate well? 4 main uses common side effects |
macrolides
excellent lung penetration 4 main uses: 1. strep CAP and URIs 2. atypicals: Mycoplasma & Chlamydia 3. PUD (clarithromycin) 4. Mycobacterium avium intracellulare in AIDS side effects: N/V/D |
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telithromycin
what kind of abx is this? what is it an analogue to? main use |
ketolide
it is a macrolide analogue main use: macrolide-resistant Strep pneumo infx |
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tetracycline
doxycycline what kind of abx are these? 2 main uses 2 side effects |
tetracyclines
2 main uses: 1. Mycoplasma & Chlamydia 2. tick-borne diseases 2 side effects: 1. tooth discoloration in <12 y/o 2. photosensitivity |
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this abx has good CNS penetration, but may cause Gray Baby syndrome
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chloramphenicol
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quinupristin/dalfopristin (Synercid)
what kind of abx is this? 2 main uses which does it kill: VRE faecium or VRE faecalis? |
streptogramins
2 main uses: 1. VRE (vanco-resistant enterococcus) 2. MRSA when pt can't take other abx kills VRE faecium |
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linezolid
what kind of abx is this? 2 main uses |
oxazolidinone
2 main uses: 1. MRSA 2. VRE |
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metronidazole
what kind of abx is this? 3 main uses side effect |
nitroimidazole
3 main uses: 1. C. diff colitis 2. PID 3. Protozoa such as Giardia side effect: Antabuse reaction w/ ETOH |
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ciprofloxacin
levofloxacin gatifloxacin what kind of abx are these? 4 main uses |
fluoroquinolones
4 main uses: 1. CAP (Strep pneumo) 2. Anthrax (Cipro) 3. traveler's diarrhea (Cipro) 4. STDs and prostatitis, but not syphilis |
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Bactrim
Septra what kind of abx are these? 3 main uses |
trimethoprim/sulfamethoxazole - folic acid antagonists
3 main uses: 1. UTIs 2. opportunistic infx like pneumocystis 3. Toxoplasma gondii |
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macrodantin
what kind of abx is this? main use |
nitrofurantoin
main use: UTIs |
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slender rod-shaped bacteria that are
acid-fast, because they take stain well but do not decolorize with acid solvents 2 kinds of infx caused by these bacteria |
Mycobacteria
TB and leprosy |
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5 1st line drugs for TB
which is the most potent anti-tubercular drug? which is the most potent anti-leprosy drug? 2 2nd line drug classes for Mycobacteria why are they considered 2nd line? |
Rifampin
Isoniazid Pyrazinamide Ethambutol Streptomycin most potent anti-TB: isoniazid most potent anti-leprosy: rifampin fluoroquinolones (i.e. Cipro) and macrolides (i.e. azithromycin) they are less effective and more toxic than 1st line drugs |
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to combat drug resistance, how is TB treated?
what is the traditional short-course therapy for TB |
multi-drug therapy for months
isoniazid + rifampin + pyrazinamide x 2 months, then isoniazid + rifampin x 4 months |
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this TB drug causes pyridoxine deficiency which causes peripheral neuritis (paresthesias)
how do you treat it? |
isoniazid
tx w/ pyridoxine (vitamin B6) |
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this TB drug may cause optic neuritis, so you must monitor visual acuity
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ethambutol
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rifampin + dapsone + clofazimine
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triple drug therapy for leprosy recommended by the WHO
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Blastomycosis
Candidiasis Cryptococcus Histoplasmosis |
tx w/ antifungals
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are fungal infx usually chronic or acute?
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chronic
l |
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4th most common cause of septicemia
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Candidemia
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systemic mycoses are often...
what is the DOC for these mycoses? what 3 other antifungals may be used? |
ife-threatening
DOC for tx of these is amphotericin-B, which has toxic side effects other drugs: ketoconazole (Nystatin), itraconazole (Sporonox), and fluconazole (Diflucan) |
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this antifungal has largely replaced ketoconazole (Nystatin)
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itraconazole (Sporonox)
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Trichophyton species are fungi that cause the superficial skin infx called Tineas. what are these fungi called?
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dermatophytes
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where are protozoal infx common?
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underdeveloped tropical countries
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are bacteria prokaryotes or eukaryotes? how about protozoa (amoebas)?
which are more difficult to tx? |
bacteria --> prokaryotes
protozoa --> eukaryotes protozoa are more difficult to tx b/c they have metabolic processes closer to humans since they are eukaryotic |
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2 most important GI tract protozoa
how do you tx these? |
1. Giardia lamblia
2. Entamoeba histolytica (amebic dysentery or amebiasis) metronidazole (Flagyl) |
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protozoa that is found in cat poop and infected meat and commonly infects humans
how do you tx this? |
Toxoplasma gondii
pyrimethamine |
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Plasmodium falciparum
what 2 parts of the body does it infect? |
protozoa that causes malaria
infects RBCs (erythrocytic stage) and the liver (exo-erythrocytic stage) |
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DOC for malaria that treats the erythrocytic stage
what is used to tx resistant P. falciparum? what is used to tx the exo-erythrocytic stage? |
chloroquine (DOC)
quinine primaquine |
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worms w/ a complete GI tract, mouth to anus
worms that look like a leaf |
nematodes
trematodes, aka flukes |
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mebendazole (Vermox)
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used to tx nematode infx
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thiabendazole (mintezole)
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used to tx the nematode that causes visceral larva migrans
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Schistosoma
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trematode that causes schistosomiasis
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Praziquantel
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used to tx all trematode infx
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4 classes of viral diseases for which anti-viral drug tx is available
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1. respiratory infx (influenza A & B, RSV)
2. Hep B&C 3. Herpes: HSV 1&2, herpes zoster, CMV 4. HIV/AIDS |
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amantadine (Symmetrel)
rimantadine (Flumadine) what are these used to tx? who are these useful in? what is preferred over these? |
prevention and tx of influenza A
useful in pts who are at high risk of infx, who have not been vaccinated, or during epidemics vaccination is preferred |
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oseltamivir (Tamiflu)
what is this and what is it used to tx? |
a viral neuraminidase inhibitor
used to tx influenza A & B |
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when must antivirals be given in order to be effective?
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way in advance (prophylactic) or within 48 hours of suspected infx
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ribavirin (Rebetol)
what is it? what is it used to tx in children? what is it used to tx in adults? |
antiviral
tx RSV in infants and children tx Hep C in adults |
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2 most common causes of chronic hepatitis
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hep B and C
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Intron-A (interferon-alpha) is used to tx...
interferon-alpha + ribavirin us used to tx... |
chronic hep B
chronic hep C |
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DOC for Herpes encephalitis
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acyclovir (Zovirax)
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acyclovir (Zovirax)
valacyclovir (Valtrex) what are these used to tx? which is more potent? why? |
tx acute herpes (genital, labial, zoster)
supress herpes (genital, labial) valacyclovir (Valtrex) is more potent b/c it had much greater oral bioavailability |
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ganciclovir (Cytovene)
what is this approved to tx? |
CMV only (CMV retinitis)
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econazole (Spectazole)
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antifungal for:
tinea corporis tinea cruris tinea pedis tinea versicolor cutaneous candidiasis |
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ketoconazole (Nizoral Shampoo)
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antifungal for tinea capitis
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2 antifungals used to tx tinea unguium (onychomyosis)
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itraconazole (Sporonox)
terbinafine (Lamisil) |
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tx of oral thrush
tx of vulvar/vaginal candidiasis |
fluconazole (Diflucan) oral suspension
fluconazole (Diflucan) or clotrimazole (Gyne-Lotrimin) vaginal suppository |
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diphenhydramine (Benadryl)
doxepin (Zonalon) what derm condition can these 2 drugs tx? |
pruritus
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Aveeno
Lac-Hydrin |
tx dry skin
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alclometasone (Aclovate)
pimecrolimus (Elidel) what derm condition do these tx? |
atopic dermatitis (eczema)
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tx of acne vulgaris
2 options for tx of acne rosacea tx of impetigo |
clindamycin (Clindagel)
clindamycin (Clindagel) or metronidazole (Metrogel) mupirocin (Bactroban) |
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Calamine lotion
fluocinonide (Lidex) what derm condition can these tx? |
allergic contact dermatitis
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how should you tx bad poison ivy (large patch)
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oral prednisone
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hydroxyzine (Atarax)
ceterizine (Zyrtec) what 2 derm conditions can these tx? |
urticaria
angioedema |
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liquid nitrogen
imiquimod (Aldara) salicyclic acid (Duofilm) |
tx for warts
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tx of scabies
tx of pediculosis (head & body lice) |
permethrin (Elimite)
permethrin (Nix) |
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etanercept (Enbrel)
calcipotriene (Dovonex) acitretin (Soriatane) methotrexate (Rheumatrex) |
tx of limited psoriasis
tx of generalized psoriasis |
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tx of varicella (chicken pox)
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Benadryl or Calamine lotion for pruritus
APAP for fever |
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tx of facial and genital herpes, and herpes zoster (shingles)
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valacyclovir (Valtrex)
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capsaicin (Zostrix)
gabapentin (Neurontin) what complication of a derm condition can these 2 drugs tx? |
herpetic neuralgia
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in common allergies, prior exposure to an allergen causes these 2 things to happen in the body
what occurs during the early phase response? what occurs during the late phase response? |
1. mast cell growth
2. IgE production by B cells --> mast cell degranulation --> release of histamine early phase - histamine causes: 1. arteriolar dilation 2. capillary & venule leakiness 3. increased mucus production 4. smooth muscle contraction - bronchoconstriction late phase - eosinophils |
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if an allergen is ingested (drug or food), what 2 things can occur?
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urticaria
intestinal smooth muscle contraction --> abdominal cramps and diarrhea |
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3 effects that occur from 1st generation antihistamines that don't occur w/ 2nd generation antihistamines
what is the prototype 1st generation drug |
1. sedative effects b/c they cross the BBB and enter the CNS --> central anticholinergic effects --> fatigue and sleepiness
2. peripheral anticholinergic effects (dry mouth and eyes, blurred vision, urinary retention, constipation) 3. anti-emetic activity prototype - diphenhydramine (Benadryl) OTC |
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hydroxyzine (Vistaril)
promethazine (Phenergan) meclizine (Antivert) which has a strong anti-emetic effect? which has anti-emetic and anti-vertigo effects? |
1st generation antihistamines
anti-emetic - promethazine (Phenergan) anti-emetic + anti-vertigo - meclizine (Antivert) |
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akathisia
acute dystonic reactions tardive dyskinesia what are each of these and what are they forms of? what can cause these to occur? how might you tx these? |
akathisia - uncontrollable restlessness
acute dystonic reactions - spastic torticollis tardive dyskinesia - incessant mouth, tongue, and jaaw movements these are forms of EPS caused by Parkinson's or antipsychotics tx w/ 1st generation antihistamines (Benadryl) or benztropine (Cogentin) which is a anticholinergic |
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meclizine (Antivert)
dimenhydrinate (Dramamine) scopolamine (Transderm Scop patch) what kind of drug are each of these? what do they tx? |
Antivert and Dramamine are antihistamines
scopolamine is a specific antimuscarinic both tx motion sickness and vertigo |
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sedative antihistamine + other CNS-depressing drug (ETOH, benzos, barbituate, opioids) =
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additive effects - bad news
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should 1st generation antihistamines be given to a pt w/ narrow angle glaucoma? why or why not?
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no, it can cause the pupil to dilate for too long, closing the angle even more
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3 major categories of anti-emetics
what are each usually used for |
1. antihistamines/anticholinergics - for motion sickness and vertigo
2. dopamine antagonists - for chemo, radiation, or surgery 3. serotonin antagonists (5-HT3 receptor blockers) - for chemo, radiation, or surgery |
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promethazine (Phenergan)
prochlorperazine (Compazine) what class of drug are these? what are they used to tx? possible side effect at high doses |
dopamine antagonists
used to tx nausea, usually from chemo, radiation, or surgery side effect at high doses - EPS |
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dolasetron (Anzemet)
ondasetron (Zofran) what class of drug are these? what are they used to tx? |
anti-emetic 5-HT3 antagonists
used to tx nausea due to chemo, radiation, or surgery |
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best anti-emesis against chemo
drug of choice for anticipatory nausea |
5-HT3 antagonist + corticosteroid (methylprenisolone or dexamethasone)
lorazepam (Ativan) |
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desloratadine (Clarinex)
cetirizine (Zyrtec) what class of drug are these? |
2nd generation antihistamines
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doxepin (Zonalon) cream
what is it used to tx? ketorolac (Acular) oph. soln. what is it used to tx? azelastine (Astelin) what is it and what does it tx? |
pruritus due to atopic dermatitis
acts as an NSAID for the ocular itch of allergic conjunctivitis 1st generation antihistamine nose spray to tx nose itch of allergic rhinitis |
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decongestants (sympathomimetics) - what kind of drugs are these? what do they do?
side effects? how do you prevent these side effects? |
alpha-1 agonists
cause vasoconstriction to decrease nasal congestion side effects include systemic vasoconstriction --> increases BP; aos can bind at the beta-1 receptors in the heart --> increased rate and palpitations prevent these side effects by using a nasal spray rather than an oral drug |
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what should you not give a pt w/ sinusitis?
what should you not give to a person w/ a productive cough? |
antihistamine
antitussive |
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fluticasone (Flonase)
mometasone (Nasonex) what kind of drugs are these? possible side effects |
nasal steroids
side effects: 1. local irritation 2. Candida overgrowth (very rare) 3. systemic side effects (only w/ too frequent use of very high doses) |
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best 2 starting abx for sinusitis
2 others that can be used |
best:
1. amoxicillin +/- clavulanate 2. Bactrim others: 1. azithromycin (Zithromax) 2. clarithromycin (Biaxin) |
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mild intermittent asthma =
mild persistent asthma = moderate persistent = severe persistent = what is the rescue drug for each? long-term drug for each? |
< 2 attacks/week; peak flow > 80% (NL)
>2 attacks/week; peak flow >80% (NL) daily attacks; peak flow 60-80% continual attacks; peak flow <60% rescue drug for all asthma is short-acting beta-2 agonist MI - none MiP - low dose inhaled steroid MoP - medium dose inhaled steroid + long-acting beta-2 agonist SP - high dose inhaled steroid + long-acting beta-2 agonist |
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albuterol (Proventil HFA)
terbutaline (Brethine) what are these? how do they work? they are the DOC for... they are the rescue drug for... |
short-acting beta-2 agonists
they stop bronchospasm; work in 15-30 minutes, lasting 4-6 hours; no anti-inflammatory effect and little or no alpha1 or beta1 agonism DOC for mild asthma rescue drug for all asthma |
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salmeterol (Serevent)
formoterol (Foradil) what are these? how do they work? |
long-acting beta-2 agonists
slow-onset, not for rescue; work for >12 hours |
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DOC for mild asthma
DOC for moderate-severe asthma |
short-acting beta-2 agonists
inhaled glucocorticoids (they are anti-inflammatory and reduce airway reactivity to allergens, irritants, cold air, and exercise) |
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fluticasone (Flovent HFA)
triamcinolone (Azmacort) what are these? |
inhaled steroids
|
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best combination tx for moderate and severe asthma
|
long-acting beta-2 agonist + inhaled steroid
|
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tx of severe asthma exacerbation or status asthmaticus
|
po steroid (prednisone) or IV steroid (methylprenisolone)
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is growth retardation a big risk in children who use inhaled steroids?
what is another side effect of inhaled steroids? |
no
oral candidiasis |
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po anti-leukotrienes
inhaled anticholinergics po theophylline inhaled cromolyn and nedocromil subq injection of monoclonal Ab to IgE what are these alternative drugs for? |
moderate/severe asthma when beta-2 agonist + inhaled steroid combo is inadequate or not well tolerated
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montelukast (Singulair)
what is this? ipratropium (Atrovent) what is this? what does it do? |
anti-leukotriene that can be used to treat moderate/severe asthma
inhaled anticholinergic; causes bronchodilation and decreases mucus secretion |
|
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bronchodilator w/ slight anti-inflammatory effect that can be used to tx moderate/severe asthma
|
theophylline (Theo-24)
|
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cromolyn
nedocromil what are they and what are they used to tx? |
mast cell stabilizers used to blocke both allergen- and exercise-induced bronchospasm
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|
omalizumab (Xolair)
what is this and what does it tx? |
monoclonal Ab that binds to IgE and prevents it from binding to mast cells
tx asthma (not first line) |
|
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airway obstruction that is only partially reversible by bronchodilators
|
COPD
|
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|
tiotropium (Spiriva)
what is this and what does it tx? |
long-acting anticholinergic
tx COPD |
|
|
combination of long-acting anticholinergic + long-acting beta-2 agonist (tiotropium + salmeterol)
what is this a tx for? |
COPD
|
|
|
are inhaled steroids used regularly in the tx of COPD?
|
no, they have little use except in severe exacerbation
|
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|
3 causes of PUD
|
1. H. pylori
2. increased gastric HCl secretion 3. inadequate mucosal defense |
|
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3 ways to confirm H. pylori infx
|
1. endoscopic bx
2. urease breath test 3. serologic test |
|
|
4 abx used to tx H. pylori
how do you tx it? what can be added to increase the secretion of GI mucus? |
1. clarithromycin
2. amox 3. Flagyl 4. tetracycline use 2 of these + a H2-blocker or PPI bismuth subsalicylate |
|
|
what is Pylera?
|
combination drug of Flagyl + tetracycline + bismuth to tx H. pylori
|
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is GERD associated w/ H. pylori? does it respond to abx?
|
no
|
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3 enzymes which stimulate gastric acid secretion
this is secreted by the gastric mucosa to protect it these drugs can block the production of this |
1. Ach
2. gastrin 3. histamine prostaglandin NSAIDs --> block prostaglandins --> PUD |
|
|
cimetidine (Tagamet)
ranitidine (Zantac) what are these and what do they do? which of the above inhibits the liver's mixed function oxidase system, affecting the metabolism of many other drugs? |
H2 blockers
block 90% of all gastric acid secretion (basal, food-stimulated, and nocturnal) cimetidine ranitidine does not do this |
|
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how long do H2-blockers and PPIs take to work? what should be taken for immediate relief?
|
45 minutes
take anatacid or 1/2 glass of skim milk |
|
|
DOC for GERD, PUD, erosive esophagitis, and ZE syndrome
why? |
PPIs
H2-blockers fail in about 50% of pts |
|
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which reduced the the risk of bleeding from ulcers caused by ASA or NSAIDs: H2 blockers or PPIs?
|
PPIs
|
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|
rabeprazole (Aciphex)
|
PPI
|
|
|
misoprostol (Cytotec)
what is this and what is it used for? carafate (Sucralfate) and colloidal bismuth what are these and what are they used for? |
prostaglandin analogue (cytoprotectant)
used to prevent PUD in those who must take NSAIDs other cytoprotectants used for PUD by coating the mucosa |
|
|
loperamide (Immodium)
what's it used for? who should not be given this? |
diarrhea-predominant IBS
anyone w/ diarrhea unless you have proved the pt does not have C. diff colitis |
|
|
tx of C. diff colitis
|
Flagyl
vancomycin if Flagyl fails |
|
|
tx of constipation-dominant IBS
what tx can cause gas, bloating, and discomfort? |
osmotic laxatives such as Milk of Magnesia
fiber supplements |
|
|
hyoscyamine (Levsin)
what is it and what is used to tx? |
anticholinergic/antispasmodic to tx IBS pt w/ crampy abdominal pain
|
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|
docusate sodium (Colace)
senna (Senokot) docusate + senna (Peri-Colace) methylcellulose (Citrucel) lactulose (Kristalose) these are all OTC laxatives - what kind of laxatives are each? |
Colace - stool softener
senna - stimulant Peri-Colase - softener+stimulant Citrucel - bulk-forming Kristalose - osmotic |
|
|
mesalamines - what are these and what do they tx?
how do they work? |
5-ASA agents (anti-inflammatory drugs similar to aspirin
1st line tx for IBD they work topically on the bowel and then are systemically absorbed from the bowel |
|
|
Pentasa
Asacol Rowasa sulfasalazine (Azulfidine) balsalazide (Colaza) what are these? which is an enema for the rectum and sigmoid colon? |
the first 3 are mesalamines
the last 2 are Azo compounds both are types of 5-ASA agents tx of IBD Rowasa is the enema |
|
|
what are hydrocortisone enemas, foams, or suppositories used to tx?
|
UC/proctatitis
|
|
|
how should you tx severe flare-ups of UC or Crohn's?
|
po or IV steroids
|
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|
Flagyl or Cipro
infliximab (Remicade) what are these used to tx? |
specifically used to tx Crohn's
the abx are used for their anti-inflammatory effects Remicade is a TNF-alpha blocker |
|
|
development and progression of diabetic complications (nephropathy, neuropathy, and retinopathy) are directly related to...
this is proportional to average blood glucose over the past 3-4 months what is the target level? |
glycemic control
HgbA1c - target level is 7% |
|
|
2 things that decrease insulin resistance in type 2 DM
how do they do this? |
1. exercise
2. weight loss skeletal muscle is the largest bulk of tissue that uses glucose, and therefore has the most insulin receptors; the more you exercise, the more receptors are made and maintained |
|
|
2 physiological problems in DM II
|
1. insulin resistance
2. decline in beta cells |
|
|
constant danger of insulin and oral hyperglycemic agents
the tighter the glycemic control... |
hypoglycemia --> neuroglycopenia --> coma
the higher the risk of hypoglycemia |
|
|
3 classes of oral hyperglycemic agents and how they work
|
1. insulin secretagogues - help the beta cells secrete more insulin
2. insulin sensitizers - make existing insulin work better, decreasing insulin secretion 3. alpha-glucosidase inhibitors - inhibit the hydrolysis of oligosaccharides to glucose and other sugars, blunting the postprandial increase in BG |
|
|
tolbutamide (1st generation)
glimepirimide glipizide glyburide nateglinide repaglinide what are these? 2 side effects? |
insulin secretagogues used to tx DM II
tolbutamide and the -gli-, -gly- drugs are sulfonylureas the -glinides are meglitinide analogs side effects - weight gain and hypoglycemia |
|
|
metformin
piogitazone rosiglitazone what are these? side effects? beneficial effect? what else can they be used to tx? |
insulin sensitizers
cause less weight gain and hypoglycemia than secretagogues increase HDL can treat PCOS to induce ovulation |
|
|
DOC for newly dx DM II
how does it work? side effect? |
metformin
it is an insulin sensitizer and it decreases hepatic gluconeogenesis, which is a source of high BG side effect - fatal lactic acidosis |
|
|
original glitazone was taken off the market because...
what levels must be checked in a pt on a glitazone? |
death due to hepatoxicity
liver function must be monitored |
|
|
acarbose
miglitol what are these? what do they not cause that other oral hyperglycemic agents will cause? side effect? |
alpha-glucosidase inhibitors
do not cause hypoglycemia do cause GI distress |
|
|
tx of symptomatic hypoglycemia
what if they can't take anything po? |
sucrose or fructose:
- soda or juice - orange - candy or sugar call 911 give glucagon IM or glucose IV |
|
|
if a glucosidase inhibitor is given with other agents such as insulin or sulfonylureas and the pt becomes hypoglycemic, how do you tx them?
|
glucose itself rather than sucrose or fructose b/c the glucosidase inhibitor will prevent or delay the absorption of those sugars
|
|
|
2 kinds of physiologic insulin secretion
how should insulin be given in type I DM? |
1. basal
2. prandial divided doses |
|
|
detimir
glargine what are these and what are they used for? how long do they last? NPH Lente Ultralente what are these and what are they used for? |
prolonged-acting insulin; currently used for basal insulin
last 24 hours and considered "peakless" intermediate-acting insulin; traditionally used for basal insulin |
|
|
standard tx for type I DM? what HgbA1c level is associated?
intensive tx for type I DM? what HgbA1c level and BG level are associated? with which of the above is there higher incidence of hypoglycemia, seizures, and coma? |
insulin bid - HgbA1c of 9%
insulin 3-5x/day - HgbA1c of 7% and average BG of 154 higher incidence w/ intensive tx |
|
|
regular insulin
what is it and what is it used for? Lispro Aspart Glulisine what are these and what are they used for? |
short-acting insulin, traditionally used for prandial insulin
ultrashort-acting insulins; currently used for prandial insulin |
|
|
3 most common causes of hypoglycemic events in diabetics
|
1. delayed meals
2. physical activity 3. alcohol |
|
|
N/V
abdominal pain signs of severe dehydration fruity breath Kussmaul breathing stuporous or comatose slight hypothermia hypoTN and tachycardia 4+ glucosuria and ketonuria BG 250-1000 leukocytosis w/o infx acidosis low bicarb high K high serum osmolarity |
DKA
|
|
|
why is a DKA pt hypotensive and tachycardic?
why do they have acetone breath? why do they have Kussmaul breathing? why do they have high serum K? do these pts have too much K or K depletion? |
from dehydration due to osmotic diuresis and polyuria
from ketogenesis ketones --> metabolic acidosis --> trying to compensate by breathing off CO2 because as hydrogen ions move into cells, K moves out they have K depletion from vomiting and new urinary loss of K |
|
|
tx of DKA (5 possible steps)
|
1. regular insulin IV - bolus and infusion
2. NS IV to replace fluids 3. K replacement after about 2-3 hours b/c correcting the acidemia causes K to go back into cells 4. glucose IV when BG gets to <250 5. bicarb IV only if pH falls to <7.0 |
|
|
for erection:
sexual stimuli become integrated in the ________ --> efferent action potential in certain fibers (________) within the __________ release _________ w/in the penis --> NO --> activates __________ --> _____ --> penile arteriolar smooth muscle relaxation --> penile arteriolar vasodilation --> corpus cavernosum engorgement --> erection what goes wrong in ED? |
lumbar spinal cord
nervi erigentes pelvic splanchnic nerves nitric oxide synthase guanalyl cyclase cGMP type 5 phosphodiesterase (PDE-5) enzyme inactivates cGMP, inhibiting erection |
|
|
sildenafil (Viagra)
tadalafil (Cialis) what kinds of drugs are these? how do they work? do they have effect w/o prior sexual stimulation? how long do each work? |
PDE-5 inhibitors, blocking the enzyme from inactivating cGMP and allowing erection
no, not at recommended doses Viagra - 4 hours Cialis - 36 hours |
|
|
these 2 drug classes are contraindicated in combination w/ PDE-5 inhibitors
why? |
1. nitrates
2. alpha-blockers (-zosins) these drugs are also vasodilators, so in combination, they can cause hypoTN |
|
|
tamsulosin (Flomax)
what is this? where is its action? what can it be taken with? |
alpha-blocker
selective for prostate arteriolar smooth muscle the only alpha-blocker that can be used with a PDE-5 inhibitor |
|
|
alendronate (Fosamax)
ibandronate (Bonvia) zoledronic acid (Reclast) what are they and what do they tx? how often are each given? how do they work? side effect? how should they be taken? |
bisphosphonates for the tx of osteoporosis (post-menopausal, steroid-induced, Paget's disease)
Fosamax - once daily po Boniva - once monthly po Reclast - once yearly IV decrease osteoclast activity side effect - esophageal ulcers should take w/o food and should not lie down for 30 minutes after taking |
|
|
teriparatide (Forteo)
what is it, what does it tx, and how does it work? salmon calcitonin (Miacalcin) what does it tx? raloxifene (Evista) what is it and what does it tx? risks? |
form of human parathyroid hormone
drug for osteoporosis works by stimulating bone formation treats OP also; tx bone pain SERM that tx OP risk of DVT |
|
|
most effective therapy to prevent osteoporosis
this increases risk of what 3 things? |
HRT in early menopause
1. breast and uterine CA 2. stroke and CAD 3. DVT |
|
|
which abx can elevate the anticoagulant effect of warfarin when given with it?
|
Bactrim
|
|
|
which abx class should not be taken with dairy products?
|
fluoroquinolones
|
|
|
abnormal activity in one limb or muscle group w/ no LOC
what is the initial DOC? |
simple partial seizure
DOC = phenytoin in adults |
|
|
LOC, but pt keeps upright posture; bizarre behavior or mouth movements and sensory hallucinations
what is the initial DOC? |
complex partial seizure
DOC = phenytoin in adults |
|
|
LOC, falling, motor convulsion, followed by post-ictal depression (confusion)
what is the initial DOC? |
grand mal tonic-clonic seizure
DOC = phenytoin in adults |
|
|
is an absence seizure considered focal or generalized?
who does it occur in? DOC? is a febrile seizure focal or generalized? who does it occur in? DOC? |
generalized
3-5 y/o, lasting until puberty DOC is ethosuximide (Zarontin) generalized (tonic-clonic) 3-5 y/o w/ high-fever illness no medication is needed |
|
|
DOC for seizures during pregnancy
DOC for seizures of eclampsa (2 drugs) DOC for status epilepticus (2 drugs) which lasts longer? what is started for longterm control? |
phenobarbitol
magnesium sulfate or diazepam (Valium) IV diazepam (Valium) or IV lorazepam (Ativan) Ativan lasts longer IV drip of phosphenytoin is started for longterm control |
|
|
2 side effects of phenytoin, esp. in children
|
1. gingival hypertrophy
2. coarsening of facial features |
|
|
2 other uses for the anticonvulsant carbamazepine (Tegretol)
1 other use for anticonvulsant topiramine (Topamax) |
1. trigeminal neuralgia
2. bipolar disease 1. migraines |
|
|
loss of cholinergic neurons in the nucleus basalis of Maynert, and then widespread in other areas of the cortex
loss of dopaminergic neurons in the substantia nigra degeneration of the frontal lobes and of the caudate and putamen (of the basal ganglia) degeneration of the UMN (CS tract) and LMN (alpha motor neurons) |
Alzheimer's
Parkinson's Huntington's ALS |
|
|
tremor
muscle rigidity masked face bradykinesia posture and gait abnormalities |
Parkinson's
|
|
|
substantia nigra --> sends inhibitory input via dopaminergic neurons --> to the excitatory cholinergic neurons of the striatum (caudate nucleus + putamen)
what are all of these structures part of? what does this do? what happens when there is a problem here? UMN down through medullary pyramids --> down the spinal cord --> synapse w/ cell bodies of alpha motor neurons |
EMS (extrapyramidal motor system) - plans, initiates, and smooths our motor actions; when there's a problem, you get tremors, discoordination, and/or involuntary movements (dyskinesias)
in Parkinson's, the inhibitory dopaminergic neurons die off, so the excitatory cholinergic effect of the striatum is no longer balanced --> dyskinesias CS tract |
|
|
what is secondary Parkinson's due to? why?
what drugs cause the worst EPS (there are 3)? what drugs cause the least severe EPS (there are 2)? |
antipsychotic drugs - they bloick dopamine receptors --> EPS
typical antipsychotics: 1. haloperidol (Haldol) 2. chlorpromazine (Thorazine) 3. thioridazine (Mellaril) atypical antipsychotics: 1. clozapine (Clozaril) 2. risperidone (Risperdal) |
|
|
2 strategies for tx of Parkinson's
give drug examples |
1. restore dopaminergic transmission
- levodopa+carbidopa (Sinemet) - MAO-B inhibitor - COMT inhibitor - dopamine receptor antagonist 2. anticholinergics |
|
|
precursor of dopamine
why isn't dopamine just given for Parkinson's? what happens to the precursor when given for tx of Parkinson's? what is given to prevent this? when do Parkinson's pts stop benefiting from tx? |
levodopa
dopamine doesn't cross the BBB, so the precursor must be given levodopa is decarboxylated to dopamine in other tissues to prevent this, give carbidopa (a dopa-decarboxylase inhibitor) - give combo drug (Sinemet) after 3-5 years, enough neurons have died in the substantia nigra, so levodopa no longer works |
|
|
selegiline
what is it? what does it tx? |
MAO-B inhibitor, which is the enzyme that metabolizes dopamine; so the drug increases dopamine levels in the brain
tx Parkinson's |
|
|
what is MAO-B?
what is MAO-A? |
B - enzyme that metabolizes dopamine - inhibitors of MAO-B are used to tx Parkinson's
A - enzyme that metabolizes NE and serotonin - inhibitors of MAO-A are used as antidepressants |
|
|
phenelzine (Nardil)
tranylcypromine (Parnate) |
MAOIs
work by blocking the break down of NE and serotonin, increasing their levels |
|
|
MAOI + SSRI or TCA -->
|
too much NE and serotonin --> HTN crisis
|
|
|
entacapone
what is this? how does it work? what does it tx? |
COMT inhibitor
when carbidopa is given, levodopa gets metabolized by COMT (instead of MAO-B) into 3-O-methyldopa, which competes w/ levodopa for transport into the brain, leading to a wearing-off phenomenon of the benefit of levodopa enatacapone inhibits the above from happening |
|
|
bromocriptine
pergolide what are these and what do they tx? what side effect do they have? |
ergotamines and dopamine receptor agonists
used to tx Parkinson's sx b/c they are ergotamines, they are vasoconstrictors which can exacerbate PVD (such as Raynaud's) |
|
|
ropinirole
pramipexole what are these and what do they tx? what else can ropinirole be used to tx? |
non-ergotamine dopamine receptor agonists used to tx Parkinson's w/o causing vasoconstriction (like bromocriptine and pergolide do)
ropinirole can also be used to tx restless leg syndrome |
|
|
amantadine is an antiviral drug for Influenza A that also has these effects
|
anti-Parkinson's effects
|
|
|
benztropine
trihexyphenidyl what are these and what are they used to tx? side effects include: |
anticholinergics (antimuscarinics) used to tx Parkinson's by eliminating the cholinergic overbalance
side effects: 1. dry mouth 2. blurred vision 3. constipation 4. urinary retention 5. mydriasis |
|
|
donepezil (Aricept)
rivastigmine (Exelon) what are these? what do they tx? side effects? |
anticholinesterases aka acetylcholinesterase inhibitors aka indirect cholinomimetics
they prolong the action of Ach, increasing brain cholinergic function for thinking, memory, and ability to recognize loved ones tx Alzheimer's side effects - N/V/D |
|
|
tension
migraine cluster hangover caffeine withdrawal rebound |
primary benign headaches
|
|
|
4 types of emergent secondary headaches (non-benign)
4 other types of secondary headaches that aren't necessarily emergent |
1. glaucoma
2. temporal arteritis 3. meningitis 4. intracranial (hemorrhage, abscess, mass lesion) 1. sinusitis 2. severe HTN 3. Lyme or other bite 4. influenza |
|
|
2 things you must do if a pt presents w/ a headache
why? |
1. get good hx
2. full neuro - if it is serious, often find a neuro deficit; if no deficit, it is 85% probable it is benign |
|
|
pt c/o recurrent headaches w/ no hint of etiology and/or they don't respond to tx, what should be done?
|
head CT
|
|
|
3 common drugs for tx of tension H/A
what if these don't work? what if these don't work? what should be done if there is evidence of pericranial or neck muscle tension? what should be given if none of this works? side effects? what can be tried lastly if tension H/A persist? |
1. ASA
2. APAP 3. NSAIDs given naproxen (Anaprox) or some other prescription NSAID sedative antihistamine - diphenhydramine (Benadryl) sedative anti-emetic - prochlorperazine (Compazine) muscle relaxant like cyclobenzaprine (Flexeril) barbiturate combo - butalbital + APAP + caffeine (Fioricet) side effect is rebound H/A migraine drug like Imitrex |
|
|
considered to be "vascular" H/As
|
migraines
|
|
|
what physiologic change is said to be correlated w/ auras of migraines
what causes the throbbing H/A following the aura? what causes the pain itself? why do NSAIDs work? which works best? drug-induced _________ seems to prevent and/or relieve migraines which drugs are used? |
arteriolar constriction
spontaneous re-dilation of the arterioles release of neuropeptide inflammatory mediators --> irritate pain endings of the trigeminal nerve in the meninges b/c it is an inflammatory process Toradol vasoconstriction - ergotamines or triptans |
|
|
what should be done first in assessment of migraines?
what are these pts encouraged to do? what should you do if a pt comes in w/ a known migraine in progress? |
identify any triggers
keep a daily long of activities and foods ask what works and give it to him/her |
|
|
tx of mild/moderate migraine (3)
tx of moderate/severe migraine that doesn't respond to the above |
1. NSAIDs
2. Excedrin Migraine 3. Midrin Ergotamines: - Cafergot (ergotamine + caffeine) Triptans: - sumaptriptan (Imitrex) - tabs, injection, or nasal spray - zolmitriptan (Zomig) - tabs and nasal spray |
|
|
when do ergotamines work in tx of migraines?
|
usually only early in the attack
|
|
|
contraindications to taking ergotamines or triptans
why? |
CV conditions: pregnancy, uncontrolled HTN, CAD & PAD, variant angina, cerebrovascular disease
they are serotonin (5-HT) agonists, causing vasoconstriction in the brain and elsewhere |
|
|
Godzilla of NSAIDs
what can it be used to tx? |
ketorolac (Toradol) IM
migraines in the ED |
|
|
Toradol + Benadryl + Reglan
|
cocktail for migraine termination
|
|
|
all of the following can be used to tx what?
BB - propranolol CCB - verapamil TCA - amitryptiline anticonvulsants - Depakote and Topamax |
migraines
|
|
|
chronic H/A is caused by...
most common cause? other causes? critical factor in rebound H/A? tx? exception? how can you ameliorate intolerable H/A? |
chronic use of any type of analgesic, typically >/= 3x/week
transformed migraine-substance overuse - increased frequency of migraines causes the pt to take analgesic >3x/week; over time, not taking it causes the H/A and then the H/A becomes refractory to the drug traumatic injury, low back pain, surgery, flu-like illness - all of which they start taking chronic analgesics for not the amount of analgesic/day, but how many times/week tx - stop all analgesics immediately - the one exception is the abrupt cessation of any butalbital formulary can cause a generalized seizure, so cannot stop this abruptly after stopping the analgesic, can take D.H.E 45 (dihydroergotamine) IM self-injection |
|
|
all of the following can cause what?
APAP ASA and NSAIDs All opioids barbituates ergotamines triptans |
rebound H/A
|
|
|
H/A often awakens pt, usually starting in or around the eye and causing tearing, corneal injection, nasal congestion, facial flushing, and Horner's syndrome
tx? this can abort this H/A |
cluster H/As
DHE 45 (dihydroergotamine) self injection Imitrex self injection O2 via mask |
|
|
2 classes of drugs used as sleep aids
|
1. anxiolytics
2. hypnotics (sedatives) |
|
|
main class of anxiolytics
which receptors do they bind to in the CNS? what does this receptor do? how do these drugs work? which part of the brain do these drugs cause anxiolysis? how long should they be used for? |
benzos
GABAa receptors (gamma-aminobutyric acid) it is the main inhibitory neurotransmitter in the CNS bind to GABA receptors, opening membrane Cl channels --> hyperpolarizes the membranes --> fewer anxiety APs limbic system aka the emotional brain not long b/c they are addictive |
|
|
-zolam or -zepam
|
benzos
|
|
|
5 physiological changes driven by increased sympathetic activity during anxiety
|
1. tachycardia
2. palpitations 3. tachypnea 4. sweating 5. trembling |
|
|
do benzos have analgesic or antipsychotic activity?
|
no
|
|
|
used to tx the anxiety accompanying depression or schizophrenia
|
benzos
|
|
|
which benzos should be used to treat each of the following:
1. chronic stress 2. panic disorder 3. unruly and delirious pt in the ED |
chronic - long-acting diazepam (Valium)
panic disorder - short-acting alprozolam (Xanax) unruly and delirious - lorazepam (Ativan) |
|
|
non-benzo that is as effective as benzos for generalized anxiety, but has a slow onset of action of days to weeks
sedative H1 antihistamine w/ little potential for abuse; used for anxiety in pts w/ h/o drug abuse |
buspirone (Buspar)
hydroxyzine (Atarax) |
|
|
another indication for benzos besides anxiety
|
insomnia
|
|
|
flurazepam (Dalmane)
temazepam (Restoril) triazolam (Halcion) what are these and what are they used to tx? duration of action of each? 2 side effects? |
benzos used to tx insomnia
flurazepam - may cause daytime sedation (long-acting) Restoril - used when pt can't stay asleep (intermediate-acting) Halcion - used when pt has trouble getting to sleep (short-acting) side effects - daytime sedation or rebound insomnia |
|
|
3 reasons benzos should be taken short-term or withdrawn slowly
|
1. addition
2. withdrawal sx 3. mix well w/ ETOH |
|
|
flumazenil (Romazicon)
|
antidote for benzo OD
a GABA receptor blocker |
|
|
zolpidem (Ambien)
zaleplon (Sonata) what are these and what do they tx? 3 reasons why they are used over benzos? |
non-benzo hypnotics for insomnia
less disturbance of sleep architecture less next-day sedation less rebound insomnia |
|
|
eszopiclone (Lunesta)
rameteon (Rozerem) what are these and what are they used for? |
hypnotics that can be used long-term (6 months); used to decrease sleep latency (help the pt fall asleep)
Rozerem is a melatonin receptor agonist |
|
|
all antidepressants potentiate the effects of _________ and/or _________ in the brain
|
serotonin
NE |
|
|
these have replaced TCAs and MAOIs as antidepressants
why? |
SSRIs
1. fewer and less severe side effects 2. much safer in overdose |
|
|
which antidepressants cause orthostatic hypoTN, sedation, and dry mouth and blurred vision?
|
TCAs
|
|
|
these antidepressants have little effect at muscarinic, alpha-adrenergic, and histamine receptors
|
SSRIs
|
|
|
how long does it take for SSRIs to cause improvement? to take full effect?
what should you do if a pt does not respond to an SSRI? |
improvement - 2 weeks
full effect - >/= 12 weeks try another SSRI |
|
|
5 disorders that SSRIs are used to tx other than depression
2 side effects of SSRIs how can you prevent the 1 side effect? |
1. GAD
2. OCD 3. PMDD (post-menopausal dysphoric disorder) 4. bulimia 5. panic disorder sexual dysfunction sleep disturbances sexual dysfunction: 1. lower SSRI dose 2. add Viagra 3. switch to bupropion (Wellbutrin) or mirtazapine (Remeron) |
|
|
bupropion (Wellbutrin)
mirtazapine (Remeron) what are these used to tx? side effects of bupropion? |
depression (if SSRIs cause sexual dysfunction)
bupropion - seizures, decreased craving for nicotine |
|
|
paroxetine (Paxil)
fluoextine (Prozac) what are these? what do they tx? other effects of each? |
SSRIs
depression Paxil - sedation - may help people sleep Prozac - activating: helps fatigue, but may cause anxiety |
|
|
SSRI + MAOI =
sx? |
serotonin syndrome
sx: hyperthermia, myoclonus and rigidity, change in mental status |
|
|
are SSRIs effective against neuropathic pain?
are SNRIs? are TCAs? |
no
yes yes |
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|
venlafaxine (Effexor)
duloxetine (Cymbalta) what are these? what are they used to tx? |
SNRIs
tx depression in the pt for whom a SSRI fails |
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atypical antidepressant w/ no sexual disturbances and also used for smoking cessation
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bupropion (Wellbutrin) - antidepressant
bupropion (Zyban) - smoking cessation |
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which neurotransmitter(s) do TCAs block the reuptake of?
what else do they block? what side effects does this cause? |
serotonin and NE
alpha-adrenergic, muscarinic, and histamine H1 receptors orthostatic hypoTN glaucoma aggravation |
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which class of antidepressants causes glaucoma aggravation?
which should be used w/ caution in bipolar disease b/c they may unmask mania? |
TCAs
TCAs |
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amitryptiline (Elavil)
class of drug? what else can it be use for? |
TCA
neuropathic pain or migraine prophylaxis |
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the enzyme MAO normally inactivates excess what in the synaptic spaces, making MAOIs good as antidepressants?
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NE, dopamine, and serotonin
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phenelzine (Nardil)
tranylcypromine (Parnate) what class of drug? what do they tx? |
MAOIs
atypical depression |
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tyramine, found in aged cheeses, red wine, and beer, causes release of large amounts of _________ from nerve terminals everywhere
people taking this drug should not eat things w/ tyramine 5 side effects if they are taking together |
catecholamines
MAOIs side effects: 1. H/A 2. tachycardia 3. HTN crisis 4. arrhythmias 5. stroke |
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prazosin (Minipress)
class of drug? what is it used to tx? |
alpha-blocker
MAOI-induced HTN crisis |
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when switching from an MAOI to any other antidepressant or vice versa, how long must you D/C the first drug before starting the other?
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2-6 weeks
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used prophylactically and acutely against mania in bipolar
mechanism of action? wide or narrow therapeutic index? overdose causes these 2 sx what 2 anticonvulsants can be used in place of this? |
lithium
unknown very narrow ataxia and tremors carbamazepine (Tegretol) valproic acid (Depakote) |
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what class of drugs is used to tx:
1. schizophrenia 2. mania 3. delirium what are the 3 categories of these drugs? how long does it take for these to work? |
neuroleptics/anti-psychotics
1. low potency typicals 2. high potency typicals 3. atypicals take several weeks to work |
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what sx do anti-psychotics decrease in schizophrenics?
which are not eliminated? |
1. hallucinations
2. delusions thought disorders remain |
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chlorpromazine (Thorazine)
haloperidol (Haldol) what are these? what category are they? how do they work? side effects? how can the side effects be treated? |
Thorazine - low potency typical anti-psychotic
Haldol - high potency typical anti-psychotic block dopamine D2 receptors in the mesolimbic system they also block dopamine D2 receptors in the nigrostriatal pathway --> Parkinson's-like EPS benztropine (Cogentin) diphenhydramine (Benadryl) |
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akathisia
dystonia tardive dyskinesia what are each of these? what kind of sx are they? |
akathisia - inner restlessness
dystonia - twitching and repetitive movements tardive dyskinesia - repetitive involuntary movements EPS that can be caused by typical anti-psychotics |
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benztropine (Cogentin)
diphenhydramine (Benadryl) what class of drug are each of these? what are they used to tx? |
Cogentin - anticholinergic
Benadryl - antihistamine w/ anticholinergic properties tx EPS due to anti-psychotics b/c it treats the cholinergic overbalance due to the blocking of the dopamine D2 receptors |
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which sx of schizophrenia do typical anti-psychotics alleviate?which do they not alleviate well?
which sx of schizophrenia do atypical anti-psychotics alleviate? |
positive sx - hallucinations and delusions; don't alleviate negative sx - blunted affect, apathy, impaired attention
positive and negative sx |
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clozapine (Clozaril)
risperidone (Risperdal) what are they? how do they work? side effect of Clozaril? b/c of this, who is it reserved for? |
atypical anti-psychotics
mixed blocking effects on dopamine and serotonin (5-HT) receptors --> little or no EPS side effect - fatal agranulocytosis reserved for severe schizophrenia or that which is refractory to other drugs |
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pt taking an anti-psychotic and develops muscle rigidity and fever
how do you tx? |
Neuroleptic Malignant Syndrome
tx - stop the drug and give the muscle relaxant dantrolene |
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drug which agonizes the muscarinic cholinergic (M2 or M3) receptors on the parasympathetic target organ
drug which antagonizes acetylcholinesterase |
direct-acting cholinomimetics
cholinesterase inhibitor/anticholinesterase - indirect-acting cholinomimetic |
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bethanechol (Urecholine)
carbachol (Miostat) pilocarpine (Pilocar) what are these? |
direct-acting cholinomimetics
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edrophonium (Tensilon)
donepezil (Aricept) galantamine (Reminyl) carbamates: -neostigmine (Prostigmin) -physostigmine what kind of drugs are these? which are used to tx Alzheimer's? organophosphates what kind of drugs are these? |
reversible anticholinesterases (indirect-acting cholinomimetics)
Aricept and Reminyl tx Alzheimer's organo - irreversible anticholinesterases |
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the _______ produces aqueous humor at a regular rate, which moves toward the pupil in the _________. it then flows thorugh the pupil to the ________. to exit, it is absorbed by a network of ________ at the angle formed where the back of the cornea meets the front. these lead to a ________ called the __________ which drains it into the conjunctival venous blood
most irises are _______ allowing the angle to be _______ in narrow-angle glaucoma, what happens to the iris? how can you look for this on PE? what can precipitate rapid build-up of fluid pressure in the narrow angle? give 4 examples |
ciliary body
posterior chamber anterior chamber trabeculae conjunctival vein canal of Schlemm flat wide/open it bulges forward penlight from the lateral side; the iris will cast a shadow on the medial side significant dilation of the pupil for several hours 1. mydriatic drugs used during eye exam: tropicamide (Mydriacyl) or cyclopentolate (Cyclogyl) 2. pre-op atropine (anticholinergic) 3. antidepressants 4. nebulized beta2-agonists - cross react w/ alpha1 receptors of radial muscles of iris |
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acute eye pain
blurred vision and halos around lights nausea, abdominal pain conjunctivitis, steamy cornea, pupil dilated and unreactive to light permanent vision loss w/in 2-5 days tx? |
acute narrow-angle glaucoma
reconstrict the pupil and reopen the angle w/ muscarinic agonist - pilocarpine drops or carbachol drops + anticholinesterase like physostigmine ophth. ointment -both of these drugs cause ciliary muscle contraction can also give a carbonic anhydrase inhibitor to decrease fluid production: acetazolamide (Diamox) brinzolamide (Azopt) |
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which kind of glaucoma is more commonly bilateral?
|
chronic open angle glaucoma
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tx of this includes alpha-agonists, BBs, carbonic anhydrase inhibitors, prostaglandins, and cholinomimetics
|
chronic open angle glaucoma
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dipivefrin (Propine)
aproclonidine (Iopidine) brimonidine (Alphagan) what are these and what are they used for? how do they work? |
Propine is a non-selective alpha-agonist
Iopidine and Alphagan are alpha2-agonists they are all used to tx open angle glaucoma Propine increases drainage the other 2 decrease humor production |
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acetazolamide (Diamox)
brinzolamide (Azopt) what are these and what are they used for? how does it work? |
carbonic anhydrase inhibitors
used to tx glaucoma (both kinds) decrease humor production b/c it has high bicarb |
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brimatoprost (Lumigan)
what is this and what does it tx? |
prostaglandin used to increase drainage in chronic open angle glaucoma
|
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betaxolol (Betoptic)
what is it and what does it tx? |
BB
tx open angle glaucoma by decreasing humor production |
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which muscarinic agonist and anticholinesterase can be used to tx these?
post-op ileus urinary retention (post-op, postpartum, or after spinal cord injury) GERD |
muscarinic agonist - bethanechol (Urecholine)
neostigmine (Prostigmin) |
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how do you tx the dry mouth of Sjogren's?
|
muscarinic agent
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Ab-mediated reduction in the # of functional nicotinic Nm receptors in the NM junction
how do you dx? tx? |
myasthenia gravis
dx - edrophonium (Tensilon) IM or IV - see improvement in fatiguability w/in 5 minutes if pt has MG tx - long-term anticholinesterase: pyridostigmine (Mestinon) or neostigmine (Prostigmin) |
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how do you reverse a neuromuscular blockade used for surgery? give 2 examples
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anticholinesterase, which increases the amount of Ach and its half-life at the motor endplate
neostigmine (Prostigmin) pyridostigmine (Mestinon) |
|
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organophosphates are found in what?
what sx can occur if these are ingested? (DUMBELS) what can you use as an antidote? |
insecticides
Diarrhea Urination Miosis Bronchorrhea Bronchospasm Bradycardia Excitation (anxiety, fasciculations, seizures) Lacrimation Salivation antidote - atropine - blocks all muscarinic receptors |
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block transmission b/w the parasympathetic postganglionic fiber and the target organ (salivary glands, heart, GI tract, etc.)
side effects? |
antimuscarinics (a kind of anticholinergic)
dry mouth, blurred vision, constipation (the opposite of DUMBELS) |
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the prototype antimuscarinic
what does it do? |
atropine
causes reversible, competitive blockade of muscarinic receptors, which can be overcome by greater [Ach] or an equivalent muscarinic agonist |
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dicyclomine (Bentyl)
tropicamine (Mydriacil) what are the semisynthetic tertiary ammonium analogues of? |
atropine
|
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3 categories of drugs that are not anticholinergic per se, but that have similar side effects
|
1. TCAs - amitryptiline (Elavil)
2. antipsychotics - haloperidol (Haldol) 3. antihistamines - dimenhydrinate (Dramamine) and diphenhydramine (Benadryl) |
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tropicamide (Mydriacil)
cyclopentolate (Cyclogyl) what are these and what are they used for? |
antimuscarinics used as mydriatics and cycloplegics for the fundoscopic exam
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used as adjuncts in tx of IBS and PUD if an H2 blocker is not fully effective
why are quaternary compounds preferred? |
antimuscarinics
they don't cross the BBB so they don't cause CNS effects; they still cause peripheral effects like blurred vision, dry mouth, and constipation |
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dicyclomine (Bentyl)
hyoscyamine (Levsin) what are these and what can they be used to tx? |
antimuscarinics
used as adjuvant therapy for IBS or PUD |
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atropine + diphenoxylate (an opioid) = Lomotil
loperamide (Imodium A-D) OTC what are they and what do they tx? |
Lomotil is an antimuscarinic and opioid
loperamide is only an opioid used to tx traveler's diarrhea and other mild GI tract hypermotility |
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tolterodine (Detrol LA)
what is this and what is it used for? |
antimuscarinic used to tx overactive bladder and urge incontinence
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parasympathetic muscarinic activity int he bronchial tree causes...
how can you tx this? |
bronchoconstriction
inhaled antimuscarinic like ipratropium (this decreases systemic antimuscarinic effects) |
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ipratropium (Atrovent)
tiotropium (Spiriva) |
inhaled antimuscarinics for tx of asthma and COPD
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these 2 drugs can be used as adjunctive therapy for Parkinson's disease
|
antimuscarinic benztropine (Cogentin)
antihistamine diphenhydramine (Benadryl) |
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scopolamine (Transderm Scop)
dimenhydrinate (Dramamine) meclizine (Antivert) what are these and what do they tx? |
scopolamine is an antimuscarinic
the other 2 are antihistamines w/ antimuscarinic properties tx motion sickness |
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tx of insecticide or poisonous mushroom ingestion
|
atropine or some other tertiary antimuscarinic (needs to cross the BBB)
|
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trimethaphan (Arfonad)
|
ganglion-blocking drug
|
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|
location of the following adrenergic receptors:
alpha1a alpha1b alpha2 beta1 beta2 |
alpha1a - prostate smooth muscle
alpha1b - arterioles and veins alpha2 - medullary vasomotor center beta1 - heart and kidney beta2 - airways and arterioles |
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tamsulosin (Flomax)
what is it and what does it do? side effect? |
alpha1a antagonist
increases urinary stream may block alpha1b, causing vasodilation --> postural hypoTN |
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doxazosin (Cardura)
what is it and what does it do? side effects? |
alpha1b antagonist
vasodilation also block alpha1a --> increases urinary stream in BPH may cause postural hypoTN b/c it blocks alpha1b blocks alpha1b in the nose --> congestion |
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clonidine (Catapres)
what is it and what does it do? |
alpha2 agonist
decreaes sympathetic tone in the medullary vasomotor center --> decreases HR and increases vasodilation |
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propranolol (Inderal)
what is it and what does it do side effect? |
beta1 blocker
decreases HR and contractility; decreases renin secretion from the kidneys, which decreases BP can antagonize beta2 in the airways --> bronchoconstriction --> SOB |
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albuterol
what is it and what does it do? side effect? |
beta2-agonist
causes bronchodilation can agonize beta1 in the heart --> palpitations |
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epi/NE are agonists of which adrenergic receptors? what do they do at each?
|
alpha1b - causes vasoconstriction of the arterioles and veins
beta1 - increases HR and contractility; increases renin (only NE) beta2 - increases vasodilation of the arterioles |
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which adrenergic receptors do decongestants (pseudoephedrine, phenylephrine) agonize?
|
alpha1b --> vasoconstriction --> decongestion, increased BP
beta1 in the heart --> palpitations |
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decrease TPR and BP by binding alpha1b receptors --> arteriolar dilation
block alpha1b in the veins --> venodilation --> decreased VR --> decreased BP 3 side effects |
-azosin drugs (alpha blockers)
1. reflex tachycardia 2. postural hypoTN 3. syncope not first-line for HTN |
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2 most common alpha agonists
|
clonidine
methyldopa |
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alpha2 agonists are actually sympathoplegic - explain
what do they imitate? |
agonize alpha2 receptors in the medullary vasomotor center, but the effect is to decrease sympathetic tone --> sympathoplegic
imitate the carotid sinus reflex when BP gets too high |
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alpha2 agonists bind in the MVC, resulting in output from down the ________ tract in the spinal cord; axons make ________ synaptic contact w/ preganglionic __________ in the __________. this decreases sympathetic output to the heart and blood vessels
what is the result? |
reticulospinal
inhibitory sympathetic cell bodies intermediolateral cell column decreased HR, increased vasodilation --> decreased BP |
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which cause postural hypoTN, alpha blockers or alpha agonists?
|
alpha blockers
|
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non-selective beta-blocker
selective beta-blockers (block beta1 > beta2) combined alpha1 blocker and non-selective beta-blocker |
propranolol
atenolol and metoprolol labetalol and carvedilol |
|
|
which kinds of BBs have the following:
negative chronotropic effects --> decreases HR negative inotropic effects --> decreases contractility leads to decreases cardiac work, CO, O2 consumption, and BP 4 common uses |
selective and non-selective BBs
(propranolol, atenolol, and metoprolol) 1. chronic angina 2. s/p MI 3. migraine prophylaxis 4. hyperthyroid sx |
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beta blocker used in open angle glaucoma
|
timolol
|
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why are BBs a good choice for HTN?
|
they decrease HR and contractility as well as blocking the beta receptors in the juxtaglomerular apparatus --> decreased renin --> decreased angiotensin II and aldosterone
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pts w/ which 3 conditions should not get a non-selective BB?
who should get no BB? what can happen if a BB is stopped abruptly? 3 adverse effects of BBs |
asthma, emphysema, and Raynaud's - can block beta2 receptors in the airways or arterioles causing broncho- and peripheral vasoconstriction
diabetic pt - may mask sympathetic warning signs like tremor or tachycardia of hypoglycemia dysrhythmia 1. increased TGs and decreased HDL 2. ED 3. exercise intolerance |
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what are labetalol or carvedilol sometimes used for
|
HF
|
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this BB works fast and can be used for HTN emergency or can be used in place of hydralazine in pregnant pts w/ HTN
side effects? |
labetalol
postural hypoTN due to the alpha blockade |
|
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this has antiplatelet, analgesic, and antipyretic effects at low doses, but has anti-inflammatory effects only at high doses
|
ASA
|
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|
premanently acetylates COX-1 for the life of the platelet
what does this do to COX-1, TBX-2, and clots |
ASA
disable COX-1, prevents TBX-2, and prevents clots |
|
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do NSAIDs need to be used at low or high doses for anti-inflammatory effect?
|
high
|
|
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2 hypersensitivity reactions to ASA
why shouldn't it be used in children? what should be used instead? |
1. urticaria
2. bronchospasm Reyes' syndrome APAP |
|
|
antipyretic and analgesic, but not anti-inflammatory or antiplatelet
what happens at high doses? antidote for overdose? |
APAP
hepatic necrosis N-acetylcysteine |
|
|
moderate overdose of ASA causes...
toxic overdose of ASA causes |
salicyclism - N/V, tinnitus, hyperventilation --> resp. acidosis
salicylate intoxication - convulsions, hypoventilation --> resp and metabolic acidosis |
|
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NSAID generally used for gout
why shouldn't ASA be used for gout? |
indomethacin (Indocin)
at low-dose it decreases renale urate excretion |
|
|
powerful NSAID that can be given IM and is used in the ED for migraine
|
ketorolac (Toradol)
|
|
|
what do prostaglandins produced by COX-1 do to the gastric mucosa?
because ASA and traditional NSAIDs inhibit COX-1 and COX-2, what can they cause? |
protects it
no prostaglandins to protect the mucosa --> ulcers |
|
|
celecoximib (Celebrex)
|
COX-2 inhibitor that doesn't cause irritation to the gastric mucosa
no antiplatelet effect |
|
|
which is better for the following, ASA/NSAIDs or opioids:
1. MSK pain 2. inflammation pain 3. visceral pain |
ASA/NSAIDs
ASA/NSAIDs opioids |
|
|
montelukast (Singulair)
what is it? what does it do? |
leukotriene modifier, inhibits lipoxygenase or blocks leukotriene receptors
|
|
|
anti-inflammatory agents that inhibit phospholipase-A2 and inhibit lymphocytes
|
steroids
|
|
|
good first choice drug for OA
tx of RA or arthritis due to lupus |
APAP
NSAIDs or DMARDs (usually combo of methotrexate (Rheumatrex) and another DMARD) |
|
|
etanercept (Enbrel)
what is it and what 3 things is it approved to tx? |
TNF-a antagonist
1. RA 2. psoriatic arthritis 3. skin psoriasis |
|
|
tx of RA or psoriatic arthritis
|
methotrexate + Enbrel
|
|
|
this is used prophylactically in tx of gout, esp after starting allopurinol
this is used prophylactically during chemo b/c the purines of cancer cells that are killed are made into excess uric acid |
colchicine
allopurinol |
|
|
inhibits xanthine oxidase, blocking the production of uric acid and preventing gout by lowering serum uric acid
when should it not be given? |
allopurinol (Zyloprim)
during an acute gouty attack |
|
|
Probenecid
Sulfinpyrozone |
urosuric drugs which increase renal secretion of uric acid, and are therefore used in the tx of gout
|
|
|
used for trauma pain, cancer, or other visceral pain for which NSAIDs are inadequate
|
opioids
|
|
|
morphine
methadone meperidine fentanyl sufentanil |
strong opioid agonists
|
|
|
codeine
oxycodone hydromorphone |
medium potency opioid agonists
|
|
|
2 opioid antagonists which reverse the effects of opioids w/in 60 seconds
most common cause of death from opioid overuse common side effect of opioids, even in the short term; what can you do to avoid this? what effect do opioids have on the eyes? |
naloxone
naltrexone respiratory depression major constipation b/c they are strong GI anti-motility agents add a laxative pinpoint pupils (miosis) |
|
|
analgesic effect of opioids is mediated by which receptors?
what are the 2 ways that opioids relieve pain |
mu receptors
1. raising the threshold for pain neurotransmission in the spinal cord and elsewhere 2. changing the brain's perception of pain such as the affective component of pain (feel the pain, but they don't care) |
|
|
most drug overdoses and other causes of coma cause pupillary....
|
dilation - which is different from opioids which cause constriction
|
|
|
synthetic opioid preferred for labor pain b/c of its shorter action
synthetic opioid whose transmucosal formulary is used for breakthrough pain in cancer |
meperidine (Demerol)
Fentanyl |
|
|
better antitussive than morphine, but less analgesic/euphoric effect
in most OTC anti-tussives, this replaces the above drug |
codeine
dextromethorphan |
|
|
codeine + APAP =
used for? |
Tylenol #3
mild-moderate pain |
|
|
the following are withdrawal sx of what?
extreme anxiety vomiting hyperventilation hyperthermia diarrhea, rhinorrhea, and lacrimation |
opioid addiction
|
|
|
used for detoxification of heroin or other opioid addicts
why? what is special about its administration? |
methadone
more mild but more prolonged withdrawal sx can only be given at special clinics |
|
|
buprenorphine (Suboxone)
|
used for opioid detox and can be given at any practice office; given b/c it has shorter and less severe withdrawal sx than methadone
|
|
|
tx of aching black, areas of localized muscle spasm, and generalized spasticity from stroke, cerebral palsy, or MS
|
muscle relaxants
|
|
|
used as sedative/anxiolytic for general anxiety
DOC for status epilepticus used as muscle relaxant, but commonly causes sedation it has effects of what neurotransmitter? |
diazepam (Valium)
GABA |
|
|
baclofen (Lioresal)
what is it? what is it used for? side effect? |
muscle relaxant
used in place of Valium b/c has much less sedation side effect - lowers seizure threshold in epileptics, so needs to be withdrawn slowly |
|
|
tizanidine (Zanaflex)
what is it? what is it used for? 3 side effects? |
alpha-2 agonist similar to clonidine
used as a muscle relaxant side effects: sedation, dry mouth, hypoTN |
|
|
Valium Lioresal, and Zanaflex are all considered...
|
centrally acting muscle relaxants
better at stopping spasticity, not as good at returning the muscles to normal function |
|
|
dantrolene (Dantrium)
what is it? how does it work? what is it used to tx? |
muscle relaxant that is not centrally acting
inhibits exictation-contraction coupling within muscle fibers themselves tx malignant hyperthermia use IV Dantrium promptly |
|
|
cyclobenzaprine (Flexeril)
metaxalone (Skelaxin) what are they? what do they treat? |
muscle relaxants
recommended for acute muscle spasm rather than spasticity |
|
|
effect of leukotrienes and prostaglandins on tissues and in airways
|
tissues - dilation and vascular leakage
airways - bronchospasm and increased mucus |
|
|
arachidonic acid --> COX-1 and COX-2 --> prostaglandins and thromboxane-2:
what secretes thromboxane-2? what does this lead to? |
platelets
leads to platelet aggregation --> clot |
|
|
steroids inhibit this which comes from membrane phospholipids of all tissue cells and platelets
|
phospholipase-A2
|
