Apharm- anti hypertensives- CCB's

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Anonymous
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226346
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Apharm- anti hypertensives- CCB's
Updated:
2013-07-08 17:07:16
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aa emory pharm
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CCBs
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  1. CAB's selectively inhibit _-type channels.  They reduce _________ __ ______ by decreasing _________ and causing coronary ____________.
    • L
    • myocardial O2 demand
    • afterload
    • vasodilation
  2. What are the 3 classes of CAB's? name a drug in each.
    • PHENYLALKYLAMINES- verapamil
    • DIHYDROPYRIDINES- nicardipine
    • BENZOTHIAZEPINES- Diltiamzem
  3. name the 6 types of antihypertensives:
    • sympatholytics
    • CAB's
    • Vasodilators
    • ACE- I
    • ARBs
    • Diuretics
  4. pharmacologic fx of CCB's: (7)
    (hint: the first 6 are decreases)
    • ↓ contractility, HR, SA node activity, AV Node conduction, systemic BP.
    • secondary vasc smooth muscle relaxation.
  5. the clinical fx of CCB's include peripheral ___________ (which decreases afterload), depression of ________ _____________, improving myocardial _______,electrophys conduction (fx= ______________).
    • vasodilation
    • myocardial contractility
    • ischemia
    • anti-arrythmic
  6. Clincal Uses of CCB's. 
    CSCH
    • coronary artery spasm
    • stable angina
    • cerebral vasospasm
    • HTN
  7. Verapamil is a derivative of __________.  It is in the class _______________, and also works on ____ __ ________ potentiating the fx of _____ __________.
    • papavarine
    • phenylalkylamine
    • fast Na channels
    • Local anesthetics
    • ****Can be injected locally
  8. Verapmil causes depression of what node? is also a negative __________ and ________ and causes vasodilation.
    • AV, SA
    • chronotrope, inotrope
  9. Verapamil is good for tx of arrythmias _____ the SA node.
    above
  10. What are the clinical uses of verapamil?
    SSEMI
    • SVT tx
    • Stable angina
    • essential HTN
    • maternal and fetal tachydyrhthmias
    • intra-arterial injection for cerebral vasospasm
  11. Nifedipine causes ___________, no _____ depression, reflex __________ and myocardial __________.
    • VASODILATION
    • nodes
    • tachycardia
    • depression
  12. What are the clinical uses of Nifedipine?
    Angina and HTN emergencies
  13. Why is nifedipine not often used? what are some other facts about it?
    • LIGHT SENSitive
    • severe hypotension and reflex tachy
    • causes edema

    no myocardial depression, no conduction fx
  14. Nicardipine causes arterial and venous ___________.  It is used for perioperative ___, to improve __ _______ during ischemia, and coronary spasm.
    • VASODILATION
    • HTN
    • LV function
  15. Nicardipine dose, half life, infusion rate:
    • 1-2ml's (100mcg/ml)
    • 14 min
    • 5 mg/hr
  16. NIMODIPINE is the ____ ________ analogue of __________.  It crosses the ___
    • lipid solube
    • nifedipine
    • BBB
  17. what is the clinical use of NIMODIPINE?
    to treat cerebral vasospasm
  18. Diltiazem (cardizem) is a _______________.  it effects __ node function and can be used for SVT's including _ ___ and _______.  It has minimal myocardial __________ and causes coronary ____________.  Can be used to treat _________ HTN.
    • Benzothiazepine
    • AV
    • a fib, flutter
    • depression
    • vasodilation
    • essential
  19. What drugs can interact with CCB's?
    • anesthetics
    • NMBs
    • local anest
    • K+ containing solutions
    • Dantrolene
    • plt function
    • Digoxin (increased plasma concentration)
  20. CCBs can cause increased plasma concentrations of with anti - dysrhythmic?
    digoxin
  21. the "PINES" do what?
    dilate
  22. CLEVIDIPINE is a 3rd generation _______________ that causes ________ vasodilation, has a ____ onset, a half-life of _ minute, and is cleared by ______ ____________.  It looks like what drug?
    • dihydropyridine
    • arterial
    • fast
    • 1
    • plasma cholinesterase
    • PROPOFOL
  23. What are 2 reasons why SNP is not often used?
    methemoglobinemia and cyanide poisoning

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