Anti Hypertensive Drugs and Treatment of Hypertension – Flashcards
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What are the 5 classes of standard antihypertensive drugs?
answer
1. diuretics 2. ?-adrenoceptor antagonists (?-blockers) 3. Ca-channel blockers 4. inhibitors of angiotensin (ACE-inhibitors/AT1-blockers) 5. ?-adrenergic blockers
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what are the centrally acting antihypertensive drugs?
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1. clonidine 2. methyldopa 3. reserpine
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what are the vasodilators?
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1. nitrates 2. nitroprusside 3. dihydralazine
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what is a normal SBP?
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<120 mmHg
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what is a prehypertension SBP?
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120-139 mmHg
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what is a stage 1 hypertension SBP?
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140-159 mmHg
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what is a stage 2 hypertension SBP?
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>160 mmHg
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what is a normal DBP?
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<80mmHg
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what is a prehypertension DBP?
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80-89
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what is a stage 1 hypertension DBP?
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90-99
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what is a stage 2 hypertension DBP?
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>100
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what drugs are indicated for prehypertension without compelling indication?
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no antihypertensive drug indicated
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what is the initial drug therapy for stage 1 hypertension without compelling indication?
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Thiazide diuretics for most. May consider ACEI, ARB, BB, CCB, or combination.
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what is the initial drug therapy for stage 2 hypertension without compelling indication?
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2 drug combination for most: usually thiazide diuretic and ACEI or ARB or BB or CCB
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what is the initial drug therapy for prehypertensive and stage 1 hypertensive patients with compelling indications?
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drugs for the compelling indications
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What is the initial drug therapy for stage 2 hypertensive patients with compelling indications?
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1. drugs for the compelling indications 2. other antihypertensive drugs (diuretics, ACEI, BB, CCB) as needed.
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What is the relative risk of stroke in hypertensive vs. normotensive patients?
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7-fold
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what is the relative risk of CAD in hyptertensive vs. normotensive patients?
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2-3 fold
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what is the relative risk of heart failure in hypertensive vs. normotensive patients?
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2-3 fold
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what is the relative risk of peripheral vascular disease in hypertensive vs. normotensive patients?
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2-3 fold
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What type of compound is Reserpine?
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Rauwolfia alkaloid, obsolete but inexpensive
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what are the relevant pharmacokinetics of reserpine?
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p.o.: t1/2= 24h effect persists for up to 6 weeks
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what are the relevant pharmacodynamics of reserpine?
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depletes biogenic amines from neuronal vesicles by inhibition of re-uptake, CNS/peripheral
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what are the adverse effects of reserpine?
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1. denervation of sympathetic nervous system 2. parasympathetic system prevails 3. 60-80% nasal congestion, hypersecretion, bronchoconstriction 4. mental depression, may promote suicide 5. parkinsonism 6. ulcerogenic
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what is the use of reserpine?
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don't use in humans anymore
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what is the most common ROA of reserpine?
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PO
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what is the half life of reserpine?
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24h
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how long do the effects of reserpine persist?
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up to 6 weeks
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what kind of compound is clonidine?
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?2-sympathomimetic drug, 2nd choice in treatment of hypertension, with interesting off label uses
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what are the relevant pharmacokinetics of clonidine?
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p.o.; i.v.; transdermal patch: t1/2 = 8-12h mainly renal excretion
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what are the relevant pharmacodynamics of clonidine?
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1. centrally mediated hypotensive effects: a. reduction of cardiac output b. relaxation of capacitance vessels c. reduction of peripheral resistance 2. renal blood flow maintained 3. initial hypertensive episode may occur 4. various CNS effects 5. pronounced rebound effect after
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what are the adverse effects of clonidine?
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high doses/predisposition: 1. symptomatic bradycardia 2. AV-block 3. functional cardiac failure 4. dry mouth 5. drowsiness 6. sedation 7. constipation 8. mental depression
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What is the primary use of clonidine?
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second line treatment of hypertension
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what are the other (empirical) clinical uses of clonidine?
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1. symptomatic treatment of withdrawal syndromes (heroin, alcohol, benzodiazepenes) 2. prevention / treatment of alcoholic delirium 3. postmenopausal syndrome 4. refractory diarrhea (short bowel syndrome) 5. adjunct in analgo-sedation (dexmedetomidine)
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What type of compound is methyldopa?
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centrally acting antihypertensive drug
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is methyldopa safe for use in pregnancy?
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yes
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what are the relevant pharmacokinetics of methyldopa?
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p.o.: t1/2= 4-6h, up to 24h including active metabolites
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what are the relevant pharmacodynamics of methyldopa?
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centrally mediated hypotensive effects quite comparable, but not identical to clonidine
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what are the adverse effects of methyldopa?
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mostly like clonidine coombs test may turn positive
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what are the important prototypical ?1-blockers and their half lives?
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1. prazosin (3-4h) 2. terazosin (12h) 3. doxazosin (22h)
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what are the relevant pharmacokinetics of the ?1-blockers?
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po or iv
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what are the relevant pharmacodynamics of ?1-blockers?
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1. blockade of ?1-receptors in arterioles/venules 2. NO effect on pre-synaptic ?2-receptors 3. NO effect on inhibitory feedback for NE release
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what are the adverse effects of ?1-blockers?
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1. first dose phenomenon 2. orthostatic hypotension 3. dizziness 4. palpitations 5. headache 6. tests for ANA may turn positive 7. reflex tachycardia
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what are the first choice diuretics in the treatment of hypertension?
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thiazides like HCTZ
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what are the second choice diuretics in the treatment of hypertension?
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K+ sparing diuretics: amiloride, triamterene spironolactone
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what is the choice diuretic for treatment of hypertension in patients with GFR ; 30ml/min or refractory hypertension?
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1. loop diuretic like furosemide 2. thiazide type metolazone
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what are the rules for routine use of thiazides?
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1. low dose thiazide, may already work at sub-diuretic doses within 2-4 weeks; to be taken in the morning 2. if hypokalemia is a problem, combine with K+ sparing diuretic but watch for hyperkalemia with this combination 3. keeping the patient "on dry weight" may be a good thing, BUT, dehydration may cause mental confusion, may aggravate COPD, or peripheral arterial occlusive disease 4. important adverse effects: hypokalemia, impaired glucose tolerance, hyperlipidemia
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what are the relevant pharmacokinetics of metolazone?
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1. oral bioavailability 65% 2. t1/2 = 8-10h 3. duration of action 12-24 h
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what are the pharmacodynamic of metolazone similar to?
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thiazide diuretics like HCTZ
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what is the difference in the pharmacodynamics of metolazone vs. HCTZ?
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also effective at GFR ;30ml/min
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what are the uses of metolazone?
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1. hypertension (low dose 1.25 - 2.5 - 5mg) also used in combination treatment 2. edema (10-20 mg) 3. can replace other thiazides in combination treatment of furosemide resistance
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what are the ?-adrenoceptor antagonists and their respective selectivities?
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1. propanolol (?1 + ?2, non selective) 2. atenolol (?1 ; ?2) 3. metoprolol (?1 ; ?2) 4. pindolol (partial agonist, ISA) 5. labetalol (4 isomers, ?-blocker ; ? blocker, ?2-agonist) 6. carvedilol (2 isomers, ?-blocker, ?-blocker) 7. esmolol (?1 ; ?2, short acting, emergency med)
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what is the specificity of propanolol?
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?1 and ?2, non-selective
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what is the specificity of atenolol?
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?1 ; ?2
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what is the specificity of metoprolol?
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?1 ; ?2
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what is the specificity of pindolol?
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partial agonist, ISA
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what is ISA?
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intrinsic sympathomimetic activity
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what is the specificity of labetalol?
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4 isomers, ?;?-blocker, ?2-agonist
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what is the specificity of carvedilol?
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2 isomers, ?-blocker, ?-blocker
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what is the specificity of esmolol?
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?1 ; ?2, short acting, emergency med
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when does one NEVER prescribe ?blockers and why?
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never use beta-blockers in asthma or COPD because ?1-selectivity is relative
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when are unselective ?blockers contraindicated?
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1. pregnancy 2. Diabetes Mellitus
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in what condition is the use of ?-blockers tricky?
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CHF
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what are some of the many conventional contraindications of ?-blockers?
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1. asthma 2. COPD 3. PAD 4. SA or AV-node abnormalities
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what effect do ?blockers have on LDL?
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increase
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what effect do ?blockers have on HDL?
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decrease
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what effect do ? blockers have on triglycerides?
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strong increase
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what effect do ?1blockers have on LDL?
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decrease
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what effect do ?1-blockers have on HDL?
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strong increase
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what effect do ?1blockers have on triglycerides?
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null
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how do ?1 blockers affect insulin sensitivity?
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they do not affect insulin sensitivity
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what changes in cardiac output do ?1blockers produce?
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minimal changes in cardiac output
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do ?1 blockers cause cold extremity syndrome?
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they do not
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do ?-blockers cause orthostatic hypotension?
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they do not
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what are the prototypical calcium channel blockers?
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1. verapamil 2. diltiazem 3. nifepidine (and dihydropyridines)
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what are the relevant pharmacokinetics of calcium channel blockers?
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p.o.; i.v.: highly bound by serum proteins, hepatic metabolism, renal excretion
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how are calcium channel blockers eliminated?
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1. metabolized in liver 2. excreted by kidney
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what are the relevant pharmacodynamics of calcium channel blockers?
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1. block L-type calcium channels -->cardiodepressant effects 2. arteriolar vasodilation
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what are the adverse effects of dihydropyridines?
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due to excessive vasodilation: 1. dizziness 2. headache 3. flushing 4. digital dysaesthesia 5. nausea 6. peripheral edema 7. constipation 8. reflex tachycardia
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what are the adverse effects of verapamil and diltiazem?
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1. bradycardia 2. slow SA and AV conduction 3. increase digoxin levels in the blood
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how do short acting calcium channel blockers affect risk of myocardial infarction?
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the use of short acting Ca channel blockers nifedipine, diltiazem, and verapamil was associated with an increased risk of myocardial infarction
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what is the onset and duration of verapamil, nifedipine, and diltiazem?
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fast onset short acting
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what are the 1st generation Ca channel blockers?
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verapamil SR nifedipine GITS
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what are the second generation calcium channel blockers?
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1. amlodipine 2. felodipine 3. nisoldipine 4. isradipine
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what are the second generation ca channel blockers which are long acting?
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1. amlodipine 2. felodipine 3. nisoldipine
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what are the slow onset second generation ca channel blockers?
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1. amlodipine 2. felodipine
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what are the second generation ca channel blockers with increased vascular selectivity?
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nisoldipine
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what are the second generation ca channel blockers with increased potency?
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isradipine
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What are the 2 types of inhibitors of angiotensin?
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1. ACE- inhibitors 2. AT1- Blockers
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What are the prototypical ACE Inhibitors?
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1. captopril 2. enalapril 3. enalaprilat 4. lisinopril 5. benazepril 6. fosinopril 7. moexipril 8. quinapril 9. ramipril
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what are the ACE inhibitors used for?
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all used to treat hypertension some also labelled for use in CHF
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what are the prototypical AT1-blockers?
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1. losartan 2. valsartan
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what is losartan used for?
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labelled for hypertension and CHF
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what is valsartan used for?
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hypertension
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what are the relevant pharmacokinetics of captopril?
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po: renal elimination
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what are the relevant pharmacodynamics of captopril?
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Angiotensin II antagonism: - decrease vasoconstriction - decrease norepinephrine release - decrease aldosterone secretion - Vasodilation Bradykinin related: - no reflex tachycardia - no significant change in cardiac output - no water and sodium retention - some reduction of sympathetic tone
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how is captopril eliminated?
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renal elimination
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what are the effects of captopril on the vasculature?
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vasodilation, decrease vasoconstriction
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what are the effects of captopril on the sympathetic nervous system?
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decrease NE release some reduction of sympathetic tone
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what is the effect of captopril on aldosterone secretion?
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decrease aldosterone secretion
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is reflex tachycardia associated with captopril?
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no
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is a significant change in cardiac output associated with captopril?
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no
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is sodium/water retention associated with captopril?
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no
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what are the adverse effects of captopril?
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1. hypotension 2. dry cough, bronchospasm 3. skin rashes, angioneurotic edema 4. neutropenia, leukopenia 5. taste perversion 6. hyperkalemia 7. proteinuria
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what conditions are contraindications of captopril?
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1. renal artery stenosis 2. renal failure 3. history of angioedema (asthma, COPD) 4. pregnancy (oligohydramnion)
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what are the signs of captopril toxicity?
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hypotension without marked tachycardia
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what are the unwanted interactions associated with captopril?
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1. NSAIDs reduce antihypertensive response by inhibition of the bradykinin pathway 2. K+ sparing diuretics aggravate hyperkalemia 3. hypersensitivity reactions to other drugs may be aggravated 4. increased plasma levels of digoxin, lithium
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what are the wanted interactions associated with captopril?
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K+ wasting diuretics yield over-additive antihypertensive effect
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elalapril is the prodrug of what?
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enalaprilat
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how is enalapril converted into enalaprilat?
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intrahepatic conversion
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what are the relevant pharmacokinetics of enalapril?
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po: tmax=3-4h t1/2=11h renal elimination start with 2-5mg/d up to a maximum 40 mg/d
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what are the relevant pharmacokinetics of enalaprilat?
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iv: use in hypertensive emergencies
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what is the tmax of enalapril?
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3-4 h
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what is the t1/2 of enalapril?
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11h
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how is enalapril eliminated?
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renal elimination
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how is enalapril dosed?
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start with 2.5-5 mg and increase up to 40mg/d
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when is enalaprilat used?
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iv in hypertensive emergencies
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how do the pharmacodynamics and adverse effects of enalapril compare to captopril?
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enalapril is: more potent slower onset/longer duration of action compound contains no sulfhydryl group (no taste perversion)
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what proportion of ACE inhibitors are prodrugs?
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most are prodrugs
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what makes fosinopril and moexipril different than all other ACE inhibitors?
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fosinopril and moexipril are eliminated by the liver and all others are eliminated by the kidneys
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do ACE inhibitors have variable influence on tissue specific AG subsystems?
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this remains to be verified
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what are the indications for ACE inhibitors?
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1. hypertension 2. CHF 3. Myocardial Infarction 4. Progressive renal disease (DM nephropathy)
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what type of drug is losartan?
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Angiotensin II receptor subtype 1 blocker (AT1 blocker)
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what are the relevant pharmacokinetics of losartan?
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po: bioavailability=33% t1/2= 2h active metabolite t1/2= 6-9h hepatic elimination usual dose 50-100 mg/d
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what are the relevant pharmacodynamics of losartan?
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Like ACE inhibitors: - decrease vasoconstriction - decrease NE release - decrease aldosterone secretion Unlike ACE inhibitors: - NO effect on bradykinin
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what are the adverse effects of losartan?
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Like ACE inhibitors except for bradykinin related AE: -no cough - no angioedema
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what conditions are contraindicated in the use of losartan?
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1. renal artery stenosis 2. renal failure 3. pregnancy
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What is the first step in the guidelines for treatment for hypertension?
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1. Single drug therapy- THIAZIDE or ?BLOCKER... or Ca channel blocker or ACEI or Alpha Blocker
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what is the second step in the guidelines for the treatment for hypertension?
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2. Combination Therapy- a. combine a thiazide with a ?blocker/CaChannel blocker/ACEI (or ?1 blocker) b. combine Ca channel blocker with a ?blocker/ACEI
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what is the third step in the guidelines for treatment of hypertension?
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3. Triple therapy between drugs listed above (thiazide/?b/CaCB/ACEI/?B)or add furosemide or add clonidine
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Which antihypertensives are contraindicated in COPD, Asthma?
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? Blockers ACE inhibitors
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which antihypertensives are contraindicated in Bradycardia?
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clonidine ? blockers Verapamil/Diltiazem
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which antihypertensives are contraindicated in Diabetes Mellitus?
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Thiazides UNSELECTIVE ? Blockers
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which antihypertensives are contraindicated in Gout?
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thiazides
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which antihypertensives are contraindicated in CAD?
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hydralazine Prazosin Minoxidil
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which antihypertensives are contraindicated in peripheral artery occlusive disease?
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? blockers
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which antihypertensives are contraindicated in CHF?
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Ca++ antagonists HIGH DOSE ?Blockers
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which antihypertensives are contraindicated in Renal Failure?
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Amiloride Triamterene Spirololactone ACE Inhibitors
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why are ? Blockers contraindicated in COPD/Asthma?
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Induction of bronchospasm
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why are ACE Inhibitors contraindicated in COPD/Asthma?
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induction of cough, Use AT1 blocker
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why are clonidine, ?Blockers, Verapamil/Diltiazem contraindicated in Bradycardia?
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aggravation, risk of Adams-Stokes syndrome
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why are thiazides contraindicated in DM?
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reduce glucose tolerance
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why are unselective ? Blockers contraindicated in DM?
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blunt symptoms of hypoglycemia
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why are thiazides contraindicated in Gout?
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reduced excretion of uric acid
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why are hydralazine, prazosin, and minoxidil contraindicated in CAD?
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provocation of angina pectoris (reflectory tachycardia)
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why are ? Blockers contraindicated in peripheral artery occlusive disease?
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aggravation/manifestation
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why are Ca++ antagonists and high dose ? Blockers contraindicated in CHF?
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negative inotropic
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why are amiloride, triamterene and spironolactone contraindicated in renal failure?
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may cause hyperkalemia
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why are ACE inhibitors contraindicated in Renal failure?
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plasma concentration increases--> side effect
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what are the positive criteria for the selection of Diuretics for Tx of hypertension?
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old age black race CHF chronic renal failure (loop diuretics)
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what are the positive criteria for the selection of ? blockers in the Tx of hypertension?
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youth white race post-MI migraine senile tremor atrial fibrillation PSVT
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what are the positive criteria for selection of long acting Ca channel blockers in the Tx of hypertension?
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old age black race migraine
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what are the positive selection criteria for the selection of ACE inhibitors in the Tx og hypertension?
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youth white Diabetes Mellitus Type I w/ nephropathy impotence from other drugs NOT IN PREGNANCY
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what are the positive criteria for selection of AT1-blockers in the Tx of hypertension?
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conditions for which ACEI are indicated, but can't be used due to hypersensitivity or cough NOT IN PREGNANCY
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what are the positive criteria for selection of ? blockers in the Tx of hypertension?
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prostatism DM dyslipidemia
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What are the favorable combinations of antihypertensives?
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1. Thiazide + ACEI 2. Dihydropyridine + ? Blocker 3. K wasting diuretic + K sparing diuretic
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why is Thiazide + ACEI a favorable combination?
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more effective and reduction of adverse effects
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why is dihydropyridine + ?blocker a favorable combination?
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more effective
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why is a K wasting + a K sparing diuretic a favorable combination?
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reduction of adverse effects
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what factors contribute to cardiac output?
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HR SV
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what does the PSNS do to HR?
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decreases it
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what does the SNS do to HR?
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increases it
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what do catecholamines do to HR?
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increases HR
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what factors contribute to blood pressure?
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Cardiac output and systemic vascular resistance
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what factors contribute to SVR?
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direct innervation circulating regulators local regulators
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what is the effect of ?1Adrenergic receptors on SVR?
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increases it by direct innervation
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what are the circulating regulators that affect SVR?
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catecholamines ATII
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how do catecholamines affect systemic vascular resistance?
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increase it
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how does ATII affect SVR?
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increases it
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what are the local regulators that affect SVR?
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NO prostacyclin endothelin ATII O2 H+ Adenosine
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what is the effect of NO on SVR?
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decreases it
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what is the effect of prostacyclin on SVR?
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decreases it
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what is the effect of endothelin on SVR?
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increases it
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how does ATII affect SVR as a local regulator?
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increases it
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what is the effect of O2 on SVR?
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increases it
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what is the effect of H+ on SVR?
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decreases it
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what is the effect of adenosine on SVR?
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decreases it
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which drugs affect BP by affecting CO by affecting HR?
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?B CCB
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which drugs affect BP by affecting CO by affecting SV by affecting contractility?
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?B CCB
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which drugs affect BP by affecting CO by affecting SV by affecting Preload by affecting venous tone?
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?1B sodium nitroprusside ACE inhibitors AT1 Antagonist
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which drugs affect BP by affecting CO by affecting SV by affecting Preload by affecting Intravascular volume by affecting Na+/H2O retention?
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Diuretics ACE inhibitors AT1 Antagonists
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which drugs affect BP by directly affecting SVR?
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CCB Direct Arterial Vasodilators
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which drugs affect BP by affecting SVR by affecting direct innervation?
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?1B Central ?2 agonists
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which drugs affect BP by affecting SVR by affecting circulating regulators?
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?1 B central ?2 agonists ACE inhibitors AT1 antagonists
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which drugs affect BP by affecting SVR by affecting local regulators?
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endothelin antagonists sodium nitroprusside ACE inhibitors AT1 antagonists
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what is a hypertensive emergency?
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clinical situation that requires immediate BP- reduction to prevent or limit target organ damage
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what is hypertensive urgency?
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any situations in which BP should be lowered within a few hours
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what is the general strategy for treating hypertensive emergency?
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intensive care monitoring pareneral drugs
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what is the general strategy for treating hypertensive urgency?
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oral therapy
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what is the goal for BP reduction in crisis?
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generally no immediate reduction of BP to 'normal' levels
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the endothelium modulates vascular resistance through what?
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endocrine or paracrine release of vasoactive molecules such as NO and PGI2
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acute changes in vascular resistance occur in response to what?
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excess production of: 1.CAT 2. ATII 3. ADH 4. Aldosterone 5. TXA2 6. ET1 or low production of vasodilators
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acute severe rises in BP may promot the expression of what?
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cellular adhesion molecules
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in a hypertensive emergency, endothelial control of vascular tone may be overwhelmed, leading to what?
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1. end-organ hyperperfusion 2. arteriolar fibrinoid necrosis 3. increased endothelial permeability with perivascular edema
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loss of endothelial fibrinolytic activity coupled with activation of coagulation and platelets promotes what?
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DIC
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what are the causes of hypertensive emergencies?
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1. essential hypertension 2. renal parenchymal disease 3. renovascular disease 4. pregnancy 5. endocrine 6. drugs 7. drug withdrawal 8. central nervous disorders 9. autonomic hyperreactivity
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what is the term for hypertensive emergency associated with pregnancy?
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eclampsia
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what endocrine disorders can cause hypertensive emergency?
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pheochromocytoma cushings renin-producing tumors
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which drugs can cause hypertensive emergencies?
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cocaine crack sympathomimetics amphetamines CsA MAO-I+Tyramine
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withdrawal of which drugs can cause hypertensive emergency?
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clonidine nifedipine
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which central nervous disorders can cause hypertensive emergencies?
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injury stroke tumor
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what are the important History items to cover in hypertensive crisis?
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1. severity/duration of pre-existing hypertension, details of therapy 2. presence of previous end organ damage 3. drug intake 4. illicit drugs
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what are the important Symptoms to cover in hypertensive crisis?
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1. CP (MI, aortic dissection) 2. back pain (aortic dissection) 3. dyspnea (CHF, pulmonary edema) 4. neurology, seizures, altered consciousness (hypertensive encephalopathy)
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what are the 5 key parts of an initial assessment of hypertensive crisis?
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1. BP 2. Fundoscopic exam 3. CV 4. Neuro 5. Lab
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what should be considered about BP taken in hypertensive emergency?
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take supine and standing take on both arms
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what should be considered in fundoscopic exam during hypertensive emergency?
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new hemorrhages exudates papilledema
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what should be considered in CV assessment during hypertensive emergency?
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evidence of CHF
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what should be considered in a neuro exam during hypertensive crisis?
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consciousness vision visual fields meningeal irritation focal signs
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what labs should be checked during assessment of hypertensiv crisis?
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urea electrolytes creatinine CBC (hemolysis, schistiocytes) ECG CXR UA plasma renin/aldo
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what are the consensus recommendations for Tx of hypertensive crisis?
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1. admit ICU, IV drugs 2. arterial BP measure line 3. therapy: a. lower BP =100-110 mmHg c. further reduction of BP within days
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which hypertensive crisis drug is toxic in pts with renal impairment?
answer
sodium nitroprusside
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what is the onset of sodium nitroprusside?
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immediate
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what is the onset of labetalol?
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5-10 min
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what is the onset of hydralazine?
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10 min
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what is the onset of fenoldopam?
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5-10 min
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what is the onset of GTN?
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1-3 min
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what is the onset of enalaprilat?
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15 min
question
what is the onset of nicardipine?
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5-10 min
question
what is the onset of phentolamine?
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1-2 min
question
what is the duration of sodium nitroprusside?
answer
1-2 min
question
what is the duration of labetalol?
answer
2-6 h
question
what is the duration of hydralazine?
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2-6 h
question
what is the duration of fenoldopam?
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10-15 min
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what is the duration of GTN?
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5-15 min
question
what is the duration of nicardipine?
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2-4h
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what is the duration of phentolamine?
answer
3-5 min
question
what are the adverse effects of sodium nitroprusside?
answer
hypotension nausea vomiting cyanate toxicity
question
what are the adverse effects of labetalol?
answer
nausea vomiting heart block bronchospasm
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what are the adverse effects of hydralazine?
answer
reflex tachycardia
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what are the adverse effects of fendolopam?
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hypotension headache
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what are the adverse effects of GTN?
answer
headache, vomiting
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what are the adverse effects of enalaprilat?
answer
hypotension renal failure
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what are the adverse effects of nicardipine?
answer
reflex tachycardia flushing
question
what are the adverse effects of phentolamine?
answer
reflex tachycardia
