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237 Cards in this Set
- Front
- Back
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How does ibuprofen decrease GFR?
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Ibuprofen, an NSAID, inhibits the production of prostaglandins (PGE, PGI), which normally counteract the effects of RAAS. Prostaglandins produced by the macula densa vasodilate the afferent arteriole, thus increasing GFR.
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What is one use of indomethacin in the newborn?
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Indomethacin promotes closure of patent ductus arteriosus.
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What are two uses of indomethacin in pregnancy?
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1) In polyhydramnios, indomethacin reduces fetal GFR and thus fetal urine (which is amniotic fluid). 2) To prevent premature labor, which is dependent on prostaglandins.
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What is the main pharmacologic action of NSAIDs?
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By inhibiting COX1/2, NSAIDs inhibit the production of prostaglandins from arachadonic acid.
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How are NSAIDs anti-inflammatory?
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By inhibiting the production of prostaglandins, which are involved in pain, swelling, and the immune response.
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What is the mechanism of NSAID-induced renal failure?
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Most commonly, acute tubular necrosis secondary to ischemia from decreased prostaglandin synthesis. Rarely, idiosyncratic reactions produce acute interstitial nephritis.
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Name the 3 NSAIDs we must know for Block 9.
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ibuprofen, indomethacin, naproxen
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What is the pharmacologic action of furosemide and where in the nephron does it act?
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Furosemide is a loop diuretic, meaning that it inhibits the Na-K-2Cl transporter in the thick ascending limb of the loop of Henle.
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How does long-term use of furosemide cause hypomagnesemia?
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Normally, the Na-K-2Cl transporter helps create the lumen-positive potential gradient, which promotes the passive absorption of magnesium (and calcium).
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Why doesn't furosemide usually cause hypocalcemia?
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Although furosemide inhibits calcium reabsorption in the thick ascending limb of the loop of Henle, calcium is also absorbed in the distal tubule.
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What is the major adverse effect of furosemide?
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Hypokalemia. Often, it is administered together with a K+-sparing diuretic like amiloride. (When used chronically, it can also cause hypomagnesemia.)
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How does furosemide cause hypokalemia?
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When furosemide inhibits the Na-K-2Cl cotransporter in the thick ascending limb, more Na+ is delivered to the distal tubule, where it is exchanged for K+. Thus, extra K+ is secreted and this can cause hypokalemia.
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Name the 4 K+-sparing diuretics we need to know for Block 9.
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spironolactone, eplerenone, amiloride, triamterine (SEAT--SE=aldosterone antagonists, AT=Na+ channel blockers)
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What is the mechanism of action of spironolactone?
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Spironolactone is an aldosterone antagonist.
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Aside from diuresis, what is one use of spironolactone (Block 7)?
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Anti-androgen, e.g. for hirsutism in PCOS
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Can you use spironolactone when you need to diurese someone quickly?
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No, spironolactone takes several days to work.
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How do spironolactone and eplerenone spare K+?
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These K+-sparing diuretics are aldosterone antagonists. Normally aldosterone increases reabsorption of Na+, which also increases secretion of K+. Thus, K+-sparing diuretics actually inhibit the secretion of K+.
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What is the major complication of eplerenone?
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Eplerenone is a K+-sparing diuretic and therefore can cause hyperkalemia.
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How do amiloride and triamterene spare K+?
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Amiloride and triamterene inhibit the Na+ transporter in the late distal tubule, thus decreasing K+ secretion.
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What drug is commonly combined with triamterene for diuresis?
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Hydrochlorothiazide. In addition to increasing diuresis, the triamterene protects against hypokalemia.
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Why is mannitol used in oliguric renal failure?
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Mannitol is freely filtered, but cannot be reabsorbed. Therefore, once in the tubule, it increases urine osmolality, thus reducing water and Na+ reabsorption.
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Besides renal failure, what is another use of mannitol?
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Mannitol is also used as an osmotic agent to reduce intracranial pressure.
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What Block 7 and 9 condition is treated with demeclocycline?
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SIADH
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How does demeclocycline work?
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Demeclocycline is a tetracycline antibiotic. It also inhibits the ADH receptor and therefore can be used to treat SIADH.
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Should you take demeclocycline with food?
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No, particularly not with dairy products. When taken with calcium and magnesium, demeclocycline is not absorbed.
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What is the pharmacologic action of acetazolamide?
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Carbonic anhydrase inhibitor.
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Is acetazolamide used to treat acidosis or alkalosis?
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Metabolic and respiratory alkalosis. Acetazolamide inhibits carbonic anhydrase, thus reducing the secretion of H+ (alkalinizing the urine, acidifying the blood).
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What is the trade name for sodium polystyrene sulfonate suspension?
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Kayexalate. The generic name is never used.
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How does acetazolamide work as a diuretic?
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By inhibiting carbonic anhydrase, acetazolamide alkalinizes the urine and thus decreases the action of the Na+-H+ exchanger in the proximal tubule. This modest reduction in Na+ reabsorption leads to a mild diuresis.
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What is kayexalate used for?
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The treatment of hyperkalemia.
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What are the TWO effects of vasopressin (ADH) on the kidney?
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1) Increased aquaporins in the medullary collecting duct, thus increasing water reabsorption. 2) Increased permeability of the medullary loop of Henle to urea.
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How does norepinephrine affect blood pressure?
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Increases blood pressure as an alpha-adrenergic agonist.
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What are the specific effects of norepinephrine on the kidney?
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Norepinephrine binds alpha receptors on the afferent arteriole, which leads to 1) constriction of the afferent arteriole, decreasing GFR and 2) increased Na+ reabsorption
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What was midodrine used for before it was pulled from the market?
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orthostatic hypotension
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What is the mechanism of action of midodrine?
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Midodrine is an alpha-adrenergic receptor agonist. It causes generalized vasoconstriction, increasing blood pressure.
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Octreotide is an analog of what hormone?
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somatostatin
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What is one Block 9 use of octreotide?
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As a somatostatin analog, it decreases splanchnic vasodilation and thus can be useful in hepatorenal syndrome.
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What are some Block 7 uses of octreotide?
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Acromegaly, diarrhea in carcinoid syndrome and VIPoma
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What is the pharmacologic action of the vaptans?
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The vaptans are ADH receptor antagonists.
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What are the vaptans used for?
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The treatment of hyponatremia in SIADH, as they increase free water excretion.
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Name the two vaptans we need to know for Block 9.
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conivaptan, tolvaptan (ADH receptor antagonists)
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Which drug is FDA-approved for the treatment of hyponatremia in congestive heart failure: conivaptan or tolvaptan?
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Tolvaptan, although conivaptan is used off-label.
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What 1 drug is the first-line treatment for hypertension?
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hydrochlorothiazide
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Aside from HCTZ, what is another thiazide diuretic?
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chlorthalidone
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Where do thiazide diuretics act?
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inhibit the NaCl cotransporter in the distal tubule
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What class of drugs do you use for diabetes insipidus?
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diuretics
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HCTZ can cause hypokalemia, hyponatremia, hypochloremia, and hypomagnesemia, but it can raise the concentration of what 2 substances?
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calcium and uric acid
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What are two reasons why you might choose an ACE inhibitor over a thiazide diuretic for a diabetic?
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1) ACE inhibitors protect the kidneys of diabetics 2) HCTZ can cause hypokalemia, which can worsen glucose control.
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What acid-base abnormality might develop with the use of HCTZ?
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metabolic (contraction) alkalosis
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Name the 4 loop diuretics we must know for block 9.
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furosemide, bumetanide, ethacrynic acid, torsemide
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Should you use HCTZ or furosemide for hyponatremia?
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furosemide can be used therapeutically for hyponatremia, while HCTZ can cause hyponatremia
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Would you use HCTZ or furosemide to treat hypercalcemia?
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furosemide. HCTZ can cause hypercalcemia.
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Which class of diuretics is the most potent?
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loop diuretics
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Why are loop diuretics so powerful?
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Because they act on the thick ascending limb of the loop of Henle, loop diuretics disrupt a major site of Na+ reabsorption. There are no high-capacity reabsorptive surfaces downstream.
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What is one way to reduce the effects of diuretics on glucose tolerance?
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Co-administer KCl. The K+ offsets the tendency towards glucose intolerance.
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Which would you use in an edematous patient with chronic kidney disease: HCTZ or furosemide?
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Furosemide! It's still effective in patients with low GFR.
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Is furosemide Ca2+ sparing or K+ sparing?
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Neither. Furosemide can cause both hypocalcemia and hypokalemia.
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What Block 9 drug can be used for altitude sickness?
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acetazolamide (carbonic anhydrase inhibitor)
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What is the treatment of choice for primary hyperaldosteronism, as from an adrenal adenoma?
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an aldosterone antagonist like spironolactone or eplerenone
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What is the mechanism of action of aliskiren?
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Direct renin inhibitor.
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What drugs should you combine with aliskiren for maximal effect?
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ACE inhibitors or ARBs
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What antihypertensives should not be used in patients with sulfa allergy?
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furosemide, acetazolamide, thiazides
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Although ACE inhibitors are named for their effects on the RAAS system, what are TWO more antihypertensive effects of ACE inhibitors?
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1) vasodilation 2) inhibit breakdown of bradykinin
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What rare side effect of ACE inhibitors seems to have increased prevalence in blacks?
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angioedema
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Why are ACE inhibitors contraindicated in pregnancy?
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They are potent teratogens, and can cause skull hypoplasia and fetal renal failure.
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Why are ACE inhibitors effective in congestive heart failure and myocardial infarction?
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they reduce cardiovascular remodeling
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Should you use captopril or benazepril in patients with liver failure?
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captopril (benazepril is hepatically metabolized)
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What is the suffix of angiotensin receptor blockers (ARBs)?
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-sartan
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How do ARBs work?
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They bind the AT1 angiotensin II receptor, inhibiting vasoconstriction, fibrosis, thrombosis, and aldosterone release.
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What happens to the concentration of angiotensin II when you use an ARB? An ACE inhibitor?
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Increases with ARB (facilitating stimulation of AT2 receptors, which are vasodilatory, antifibrotic, etc.). Decreases with ACE inhibitor.
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Name the 4 calcium channel blockers we need to know for Block 9.
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verapamil, amlodipine, nifedipine, diltiazem
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How do CCBs work?
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They block Ca-mediated smooth muscle contraction, thus resulting in less vasoconstriction.
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What is one side effect of CCBs that is unique among antihypertensives?
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bradycardia and heart block, which is exacerbated by concomitant use of beta blockers
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What are 2 advantages of CCBs?
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They do not affect electrolytes or the kidneys.
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What is one special use of hydralazine?
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It is particularly useful in African Americans with severe CHF uncontrolled by triple therapy (ACE inhibitor, beta blocker, and aldosterone antagonist).
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What is the first-line ("triple") therapy for CHF?
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ACE inhibitor, beta-blocker, and aldosterone antagonist (if severe)
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How does hydralazine work?
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It is an arteriolar vasodilator.
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In what patient populations should you avoid hydralazine?
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Patients with CAD or peripheral vascular disease (ischemic "steal" syndrome) .
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What is the arteriolar vasodilator that can cause hypertrichosis?
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minoxidil sulfate
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What is the suffix for alpha blockers?
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-sin
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Name three alpha blockers we need to know for Block 9.
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prazosin, dozasosin, terazosin
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What is one cardiovascular side effect of alpha blockers when used for BPH?
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orthostatic hypotension
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Name the 3 main sites of action of beta blockers.
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Cardiac (decrease contractility and heart rate); renal (reduce renin secretion); CNS (SNS regulation changes)
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What 3 beta blockers are approved for use in congestive heart failure?
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carvedilol, metoprolol, bisoprolol
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What receptors does carvedilol inhibit?
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beta1, beta2, alpha1
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What receptors does clonidine agonize?
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alpha2 receptors
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How does methyldopa work as an antihypertensive?
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A metabolite stimulates central alpha receptors and produces a hypotensive effect via dilation of arterioles and veins
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Name 3 drugs you could use in a hypertensive emergency.
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Diazoxide, nitroprusside, nitroglycerine
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Say whether each drug acts on arterioles, veins, or both: diazoxide, nitroprusside, nitroglycerine
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diazoxide, arterioles; nitroprusside, both; nitroglycerine, veins
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What is alteplase?
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tPA (tissue plasminogen activator). Converts plasminogen to plasmin, which breaks down fibrin.
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Why might you prefer tenecteplase over alteplase for STEMI?
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Tenecteplase (TNK-tPA) has fewer bleeding complications, but does not improve mortality.
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What are two indications for streptokinase, and how does it work?
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STEMI and PE. Streptokinase activates plasminogen --> plasmin which breaks down fibrin.
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What class of drugs includes alteplase, tenecteplase, and streptokinase?
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Fibrinolytics, sometimes inappropriately called "thrombolytics" or just "lytics."
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Should you use fibrinolytics for non-STEMI ACS?
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Nope. The risk of bleeding outweighs the possible benefits.
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What are the contraindications to fibrinolytics?
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Anything that will increase the risk of hemorrhage - recent major surgery, recent stroke, leaking aneurysm, etc.
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Why can't you use fibrinolytics alone?
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Fibrinolysis generates more free thrombin and activates platelet aggregation, and fibrinolytics don't affect platelet-rich parts of clot. So you need to combine with antithrombins and antiplatelets.
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Do you use antithrombins for STEMIs or non-STEMIs?
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Both!
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What is the mechanism of action of heparin (UFH)?
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Antithrombin. Binds antithrombin to thrombrin, deactivating thrombin.
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What is the mechanism of action of enoxaparin (low molecular weight heparin)?
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Antithrombin. Binds antithrombin to factor Xa, deactivating Xa.
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What is the advantage of fondaparinux over enoxaparin?
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Both are LMW heparins, but fondaparinux does not interact with platelets. Enoxaparin (and UFH) can lead to the formation of antiplatelet antibodies, causing a hypercoagulable thrombocytopenia.
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How might enoxaparin (LMWH) and heparin (UFH) cause thrombocytopenia?
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They can lead to the creation of antiplatelet antibodies, causing a hypercoagulable thrombocytopenia.
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What are hirudin and argatroban?
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Direct thrombin inhibitors. 3rd line agent for MI. Useful for substitution for heparin in heparin-induced thrombocytopenia.
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What blood tests should be used to monitor anticoagulability during administration of heparin and direct thrombin inhibitors like hirudin and argatroban?
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PTT, platelet count
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Besides aspirin, what is another antiplatelet therapy useful for ACS?
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Clopidogrel (PO) and prasugrel (IV).
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What class of drugs includes abciximab and eptifibatide?
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G2b3a inhibitors, a type of antiplatelet therapy.
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How do G2b3a inhibitors work?
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They block the G2b3a receptor site, which is normally bound by fibrinogen, thus inhibiting platelet aggregation.
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What 3 classes of drugs are used to treat ACS?
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Fibrinolytics (STEMI only!), antithrombins, and antiplatelets
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If we have 3 classes of drugs to treat MI, why do we use PCI?
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20% of patients do not respond to pharmacological therapy alone.
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Why are beta-blockers useful in the treatment of ACS long-term?
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They reduce MVO2, thus reducing ischemia and infarct size. They also decrease reperfusion injury, remodeling, and rupture.
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Why are ACE inhibitors and ARBs useful in treating ACS long-term?
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They reduce the risk of heart failure, rupture, and remodeling.
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Can you use beta-blockers acutely in ACS?
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YES, as long as the patient is not in cardiogenic shock (pulmonary edema, hypotension, etc.)
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Should you use Ca2+ channel blockers in ACS?
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NO, they increase mortality!
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Why do you use nitroglycerin in ACS?
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It relieves the pain. According to Dr. Goldhaber, no good trial has demonstrated its efficacy at reducing mortality.
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List all the drugs you would place someone on at discharge for ACS.
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ASA; clopidogrel; beta-blocker; ACE inhibitor or ARB; statin; +/- fish oil (1g/day)
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Which beta-blocker would you suggest for long-term treatment after ACS if someone has a low ejection fraction?
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carvedilol
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Describe the 3 types of Class I antiarrhythmics.
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Class I antiarrhythmics are Na+ channel blockers. They are divided into Class Ia (intermediate potency), Ib (low potency), and Ic (high potency).
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Quinidine, procainamide, and disopyramide are Class ___ antiarrhythmics.
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Class Ia (intermediate potency Na+ channel blocker)
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Lidocaine is a class ___ antiarrhythmic?
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Class Ib (low potency Na+ channel blocker)
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Flecanide and propafenone are Class ___ antiarrhythmics.
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Class Ic (high potency Na+ channel blockers)
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What are Class II antiarrhythmics?
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beta-blockers
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Name 3 Class III antiarrhythmics.
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amiodarone, ibutilide, dofetilide (K+ channel blockers)
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What drug is the first line agent for V-tach?
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amiodarone (Class III antiarrhythmic, K+ channel blocker)
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What are Class IV antiarrhythmics? Name 2.
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Ca2+ channel blockers. Verapamil, amlodipine, nefedipine, diltiazem
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Quinidine is a Class ___ antiarrhythmic with 3 side effects we must know for block 9.
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Class Ia, SEs = cinchonism (just means quinine overdose, includes tinnitus, headache, flushing); syncope; thrombocytopenia
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Procainamide is a Class ___ antiarrhythmic which, if given orally, can produce drug-induced ___.
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Class Ia, lupus
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Disopyramide is a Class ___ antiarrhythmic with what autonomic side effect?
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Class Ia, anticholinergic
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When given systemically, lidocaine (Class ___) can cause what neurological side effects?
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Class Ib, peri-oral numbness, parasthesias, seizures, coma
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Flecainide, like all antiarrhythmics, is particularly ...
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arrhythmogenic. Flecainide = Class Ic
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Propafenone, a Class ___ antiarrhythmic, has effects on what organ system?
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Ic, GI tract
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Name a hematologic side effect of amiodarone.
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Agranulocytosis
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Name a pulmonary side effect of amiodarone.
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Pulmonary fibrosis
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Name 2 Block 7 side effects of amiodarone.
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hepatotoxicity, hyperthyroidism
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What commonly used drug interacts with amiodarone?
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warfarin
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Amiodarone turns your skin ___ after exposure to sunlight.
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blue
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Amiodarone causes this ophthalmalogic side effect.
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corneal deposits
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What classes of antiarrhythmics are used for supraventricular tachycardias?
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Classes Ia, Ic, III
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What class of antiarrhythmics is SECOND line therapy for v-tach?
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Class Ib, lidocaine
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Adenosine is particularly useful in treating what type of arrhythmia?
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AVNRT
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Adenosine acts as a "reset button" for the ______.
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AV node
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What immediate side effects might someone experience if you give them adenosine?
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Since adenosine produces asystole for a few seconds, it may cause chest pain and an impending sense of doom.
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Deficiency of what 2 ions can lead to arrhythmias?
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Potassium, magnesium
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In what arrhythmia is it important to prescribe warfarin?
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atrial fibrillation, if CHADS score > 1
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What are two alternatives to warfarin?
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dabigatran, rivaroxaban
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If a patient with a-fib cannot take anticoagulation therapy, what do you do?
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Block or remove the LA appendage.
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For a-fib, you want to use antiarrhythmics to control the ___ but not the ___.
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rate but not the rhythm. Use Class II or IV (beta-blocker, Ca2+ channel blocker)
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What is paclitaxel and what does it have to do with Block 9?
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Paclitaxel is Taxol, the chemotherapy drug that stabilizes microtubules, thus inhibiting mitosis. It is used on coronary stents to prevent fibrosis and remodeling around the stent.
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What are sirolimus and everolimus and what do they have to do with MI?
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Sirolimus (aka rapamycin!) and its derivative, everolimus, are immunosuppressants used in organ transplantation. They are also used as coatings for drug-eluting stents. They are antiproliferative and prevent restenosis.
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What is dobutamine?
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A positive inotrope (B1-agonist)
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What is milrenone?
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A positive inotrope (enhances Ca2+ uptake into the SR) that is used when vasodilator therapy for cardiogenic shock has failed.
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How does levosimendan work to treat cardiogenic shock?
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Levosimendan is a calcium sensitizer (positive inotrope) and a vasodilator.
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How do statins work?
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Inhibiting HMG-CoA reductase, which performs the rate-limiting step of cholesterol synthesis in the liver. (HMG-CoA --> mevalonate)
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What is the most dangerous side-effect of statins?
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Rhabdomyolysis
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Statins reduce LDL by approximately ___ %.
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20-35%, depends on the statin
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Which lipid-lowering medication works by inhibiting the sterol transporter in the intestinal brush border?
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ezetimibe
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Which class of lipid-lowering medication works by binding and sequestering a cholesterol product in the intestinal lumen?
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bile acid sequestrant (resin), e.g. cholestyramine
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What is one nutritional side-effect of cholestyramine?
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deficiencies of fat-soluble vitamins (A, D, E, K)
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How does cholestyramine lower LDL cholesterol?
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By sequestering bile acids in the intestinal lumen, resins prevent their reabsorption. The liver is forced to synthesize more using cholesterol. This depletes the body's stores of cholesterol, lowering serum LDL.
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What drug is best for raising HDL?
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niacin
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What is the limiting side effect of niacin?
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Flushing, which usually goes away in a few weeks.
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Which lipid-lowering medication works by inhibiting hepatic synthesis of VLDL?
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niacin
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What is the drug of choice for lowering triglycerides, for example in a patient at risk of pancreatitis?
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niacin or fibrates
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What are fibrates used for? Name two.
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Fenofibrate and gemfibrozil are used to lower triglycerides and LDL and raise HDL.
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What class of lipid-lowering medications works by agonizing PPAR-alpha?
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fibrates
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What does agonism of PPAR-alpha do?
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increases beta-oxidation in the liver; decreases hepatic triglyceride secretion; increases LPL activity which clears VLDL, increases HDL
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Which class of anti-asthmatics has largely replaced cromolyn sodium?
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leukotriene receptor antagonists
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What is the mechanism of action of cromolyn sulfate and nedocromil?
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mast cell stabilizers, meaning they inhibit mast cell degranulation
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Name two methylxanthines used to treat asthma. How do they work?
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Aminophylline and theophylline. In addition to being adenosine receptor antagonists, the methylxanthines are nonspecific inhibitors of phosphodiesterase. Thus, they inhibit the synthesis of leukotrienes.
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What are the major side effects of beta-2 agonists like albuterol?
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tremor, tachycardia
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Which beta-2 agonist anti-asthmatics are rapid onset?
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albuterol, formoterol. Albuterol is short-acting, whereas formoterol is long-acting.
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Which two beta-2 agonists are long-acting with slow onset?
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salmeterol (lasts 12 hr) and indacaterol (lasts 24 hr)
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In addition to use as a rapid-onset bronchodilator, terbutaline is used to prevent what?
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tocolytic, prevents the onset of premature labor
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Name two anticholinergics used for the treatment of COPD.
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ipatropium, tiotropium
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What class of drugs includes montelukast?
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antileukotrienes, used for asthma
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What is the proposed mechanism of action of inhaled anesthetics?
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stimulation of GABA-A receptors and inhibition of excitatory receptors
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What is the minimum alveolar concentration (MAC)?
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The alveolar concentration (%) that produces immobility to noxious stimulation in 50% of subjects
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Does MAC increase or decrease with age? Temperature?
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Decreases with age, decreases with temperature
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If you increase your cardiac output, is the onset of action of inhaled anesthetics delayed or hastened?
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Increasing CO delays onset of action of inhaled anesthetics
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As an inhaled anesthetic becomes more lipophilic, MAC (increases/decreases). Conversely, as it becomes more hydrophilic, MAC (increases/decreases).
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lipophilicity --> decreased MAC (higher potency); hydrophilicity --> increased MAC (lower potency)
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Why does a longer duration of exposure to an inhaled anesthetic result in a decreased rate of elimination?
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As you are exposed to inhaled anesthetics over time, they accumulate in poorly perfused tissues (fat, skeletal muscle, etc.) Therefore it takes longer to eliminate the drug if you have been exposed longer.
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What is the effect of nitrous oxide on closed gas spaces?
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Enlargement of airspaces, e.g. bowel, inner ear, pneumothoraces, air emboli
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In what population might you use inhaled anesthetics more often than intravenous anesthetics?
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Children, to avoid the needle stick.
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The -fluranes are (inhaled/intravenous) anesthetics?
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inhaled
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What is the most frequently used IV anesthetic?
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propofol
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Propofol has great ___ effect but little ___ effect.
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great hypnotic effect, little analgesic effect
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Intravenous anesthetics often affect the intracranial pressure. Which drugs increase ICP and which decrease ICP?
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Increase: ketamine; decrease: propofol, etomidate
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Why is propofol an anti-emetic?
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It reduces seretonin in the area postrema (the vomiting center).
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What is the mechanism of action of propofol and etomidate?
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GABA agonists
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What is the mechanism of action of ketamine?
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inhibits NMDA glutamate receptors
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Which anesthetic is related to PCP?
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ketamine ("special K")
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Why might you use benzodiazepines after giving ketamine?
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to prevent horrific nightmares
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Which intravenous anesthetic has the fewest cardiovascular side effects?
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etomidate
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What is the mechanism of action of dexmedetomidine?
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alpha2 receptor agonist (like clonidine)
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Which intravenous anesthetic would you use to sedate an intubated ICU patient?
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dexmedetomidine
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One of the following drugs increases BP, while the other decreases it. Which is which? Propofol or ketamine?
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Propofol decreases BP. Ketamine increases BP.
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What is the mechanism of action of all local anesthetics?
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Blockade of Na+ channels on peripheral nerves, thus inhibiting depolarization
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Are small or large fibers more sensitive to the action of local anesthetics? What results from this difference?
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Small fibers are more sensitive, including pain fibers. Large fibers transmit pressure and vibration, which may remain intact under local anesthesia.
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How can you remember which local anesthetics are esters and which are amides?
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Amides have more than 1 i in their names. Esters have only 1. You can remember which is which because the word amides has an i in it.
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Are allergic reactions more likely with ester or amide local anesthetics?
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esters
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How are ester and amide local anesthetics metabolized?
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Esters are metabolized by pseudocholinesterase (in the blood) and amides are metabolized by the liver.
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Increased lipophilicity increases or decreases the potency of local anesthetics?
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Increases. They must traverse the cell membrane to act on the inner part of the Na+ channel.
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If a local anesthetic is highly bound to plasma proteins, is it more likely or less likely to have high affinity for the Na+ receptor?
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More likely to have high affinity.
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Why do we add bicarbonate to local anesthetics?
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To induce more of the neutral form of the anesthetic, which speeds the onset of action because it can cross the cell membrane.
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Why do we add epinephrine to local anesthetics?
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To cause local vasoconstriction, prolonging the duration of action and reducing systemic toxicity.
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Why do some doctors add hyaluronidase to local anesthetics?
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Theoretically, the tissue destruction caused by hyaluronidase helps local anesthetics penetrate the tissue. Its use is controversial.
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With the exception of bupivicaine, do local anesthetics have systemic CNS or CV effects first?
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Systemic CNS effects are seen before CV effects, except with bupivicaine.
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Which local anesthetic can cause methemoglobinemia?
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benzocaine
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What are the systemic cardiovascular effects of local anesthetics?
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negative inotropy --> bradycardia, ventricular fibrillation, asystole
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What are the CNS effects of local anesthetics?
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first: local effects like tinnitus, circumoral numbness, metallic taste, double vision; second: general effects like drowsiness, slurred speech, nystagmus
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What is the unique side effect of 2-chlorprocaine?
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back pain
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What are two purposes of neuromuscular blockade in anesthesia?
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To facilitate endotracheal intubation and to provide muscle relaxation as needed for certain surgeries.
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What is the only depolarizing neuromuscular blocker?
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succinylcholine
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What is the mechanism of action of succinylcholine?
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Binds the 2 alpha subunits of nicotinic AChR and holds the channel open. This causes uncoordinated fasciculations followed by relaxation.
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What enzyme breaks down succinylcholine?
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pseudocholinesterase
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What is one common side effect of succinylcholine?
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hyperkalemia
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Does succinylcholine increase or decrease intracranial, intraophthalmic, and intragastric pressure?
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Increase
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What is one potentially deadly side effect of succinylcholine (besides hyperkalemia)?
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malignant hyperthermia
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How do you remember which non-depolarizing neuromuscular blockers are benzylisoquinolines and which are aminosteroids?
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AmiNOsteroids end in curONium; benzylisoquinolones end in curium.
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What percentage of nicotinic AChR's do you need to block in order to thwart neuromuscular transmission?
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80-90%
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What is a short-acting non-depolarizing neuromuscular blocker?
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mivacurium
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What are 3 intermediate acting non-depolarizing neuromuscular blockers?
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cisatracurium, vecuronium, rocuronium
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What is 1 long-acting non-depolarizing neuromuscular blocker?
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pancuronium
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What is the major side effect of non-depolarizing neuromuscular blockers?
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histamine release leading to bronchospasm, flushing, peripheral vasodilation, anaphylaxis, etc.
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What TWO drugs do you give to reverse neuromuscular blockade?
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An AChE inhibitor AND a muscarinic antagonist
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What are 2 examples of muscarinic antagonists commonly used to reverse neuromuscular blockade?
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atropine, glycopyrrolate
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What are some examples of AChE inhibitors used to reverse neuromuscular blockade?
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neostigmine, pyridostigmine, physostigmine, edrophonium
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What is sugammadex?
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A neuromuscular reversal agent that does not rely on ACh; instead, it simply binds up rocuronium and inactivates it.
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Why must you give a muscarinic antagonist when you give an acetocholinesterase inhibitor to reverse a neuromuscular blockade?
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AChE inhibitors increase ACh concentrations at both nicotinic and muscarinic synapses. You want the nicotinic effects, but not the muscarinic effects.
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What are the symptoms of cholinergic crisis?
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SLUDGE. Salivation, lacrimation, urination, defecation, GI upset, emesis (and bradycardia and myosis)
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What class of drugs includes sacrolimus and cyclosporine?
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calcineurin inhibitors
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What is the most common serious side effect of the calcineurin inhibitors tacrolimus and cyclosporine?
|
nephrotoxicity
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Inhibition of calcineurin is useful in preventing what?
|
Calcineurin dephosphorylates and activates NFAT, which is the transcription factor that promotes T cell activation.
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What two immunosuppressive drugs block mTOR?
|
sirolimus, everolimus
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What is the mechanism of action of azathioprine?
|
Azathioprine is a purine analogue. It inhibits rapid cell division, thus suppressing the immune system.
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What was the first immunosuppressive drug developed for organ transplantation?
|
azathioprine
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What is mycophenylate mofetil?
|
An antimetabolite that blocks guanine synthesis, thus preventing the rapid cell division necessary for an immune response.
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Which causes hirsutism, cyclosporine or tacrolimus?
|
Cyclosporine. Tacrolimus causes hair loss.
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Is tacrolimus nephrotoxic?
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Yes.
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