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Pharmacology II > ischemia3 > Flashcards

ischemia3 Flashcards

1
Q

what is the half life of nitroglycerin

A

1-3 minutes

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2
Q

what are the two active metabolites of nitroglycerin

A

glyceryl 1, 2-dinitrate

glyceryl 1, 3-dinitrate

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3
Q

what is the active metabolite of isosorbide dinitrate (ISDN)?

A

isosorbide-5-mononitrate (ISMN)

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4
Q

why is isosorbide 5-mononitrate preferred

A

4 hour half life

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5
Q

what nitrates are used for angina prevention

A

ISDN and ISMN

not NTG

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6
Q

how would you counsel a patient taking both NTG and sildinafil

A

48 hours before taking nitrates with Cialis

others 24 hours before taking nitrate

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7
Q

what dosing form is best for a patient with chest pain at night

A

transdermal NTG

drug free in afternoon

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8
Q

what is preferred ISMN or ISDN?

why (4 reasons)?

A 
ISMN
longer half life
almost completely absorbed
less rebound angina
greater efficacy
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9
Q

what type of Ca channel is in vascular smooth muscle?

what is it’s rate like?

A

voltage gated L-type Ca channels

slow rate

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10
Q

what is calcium entering a vascular smooth muscle’s effect on MLCK

A

phosphorylation

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11
Q

what are the 3 main mechanisms of contraction of vascular tissue?
which is the main one CCB’s inhibit?

A
  1. voltage sensitive Ca channels open in response to depolarization
  2. agonist induced release of calcium from SR
  3. receptor mediated entry of calcium
    #1=CCBs
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12
Q

what has an inhibitory effect in cardiac cells

A

troponin

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13
Q

what stops troponin’s effect in cardiac cells

A

calcium binding (stops inhibition)

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14
Q

what effect do CCBs have on cardiac cells

A

negative inotropic effect

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15
Q

the negative ionotropic effect of dihydropyridines is caused by what?

A

peripheral dilation leading to baroreceptor reflex

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16
Q

what is CCB’s effect on force of contration

A

decrease it

17
Q

what is another term for inotropic effect on the heart

A

force of contraction

18
Q

dihyropyridines peripheral dilation causes an increase in what?
what can this effect overcome?

A

increase SNS tone

can overcome negative inotropic effects on heart (why non-dihydro are better for myocardial ischemia)

19
Q

what is significantly effected by nondihydropyridines

A

SA and AV nodes

20
Q

what rate is not changed from dihydropyridines

A

does not change rate of recovery from Ca inhibition

21
Q

what decreases rate of recovery from inhibition in cardiac cells

A

nondihydropyridines

22
Q

what CCBs show use/ frequency dependance

A

nondihydropyridines

23
Q

list the two nondihydropyridines

A

verapamil

diltiazem

24
Q

all CCB’s have what effect

A

vasodilation

25
Q

arrange these drugs in order of ability to increase blood supply (coronary blood flow):
diltiazem, verapamil, dihydropyridines

A

dihydropyridines> verapamil > Diltiazem

26
Q

what CCBs increase coronary blood flow the most

A

dihydropyridines

27
Q

what are dihydropyridines effects on BP? what does this lead to?

A

decrease BP leading to:sympathetic reflexes

SNS reflexes cause increased HR and FOC

28
Q

what CCBs have most potent inotropic effects

A

verapamil

29
Q

CCB’s have little effect on what related to blood flow

A

venous tone (so A > V)

30
Q

what are some adverse effects of CCBs

A
  1. edema
  2. GERD
  3. Urine retention
  4. Rash
  5. increased LFT’s
31
Q

what causes edema with CCB’s

A

precapillary dilation and postcapillary constriction

32
Q

what are 3 adverse effects common with verapamil

A
  1. constipation
  2. bradycardia
  3. HF exacerbation
33
Q

why is urinary retention common with CCBs?

A

detrusor muscle can’t contract as well (can’t squeeze pee out)

34
Q

why is GERD common with CCBs?

A

esophageal sphincter doesn’t fully contract

35
Q

why is IR nifedipine not used much

A

extreme tachycardia
can cause MI
(too abrupt vasodilation)

36
Q

nifedipine has what unique adverse effect

A

gingival hyperplasia

37
Q

why do verapamil and diltiazem cause bradycardia?

A

decreases FOC

Pharmacology II (15 decks)

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