ischemia3 Flashcards

1
Q

what is the half life of nitroglycerin

A

1-3 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the two active metabolites of nitroglycerin

A

glyceryl 1, 2-dinitrate

glyceryl 1, 3-dinitrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

isosorbide-5-mononitrate (ISMN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

why is isosorbide 5-mononitrate preferred

A

4 hour half life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what nitrates are used for angina prevention

A

ISDN and ISMN

not NTG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

transdermal NTG

drug free in afternoon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is preferred ISMN or ISDN?

why (4 reasons)?

A
ISMN
longer half life
almost completely absorbed
less rebound angina
greater efficacy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

phosphorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what has an inhibitory effect in cardiac cells

A

troponin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what stops troponin’s effect in cardiac cells

A

calcium binding (stops inhibition)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what effect do CCBs have on cardiac cells

A

negative inotropic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

the negative ionotropic effect of dihydropyridines is caused by what?

A

peripheral dilation leading to baroreceptor reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
arrange these drugs in order of ability to increase blood supply (coronary blood flow): diltiazem, verapamil, dihydropyridines
dihydropyridines> verapamil > Diltiazem
26
what CCBs increase coronary blood flow the most
dihydropyridines
27
what are dihydropyridines effects on BP? what does this lead to?
decrease BP leading to:sympathetic reflexes | SNS reflexes cause increased HR and FOC
28
what CCBs have most potent inotropic effects
verapamil
29
CCB's have little effect on what related to blood flow
venous tone (so A > V)
30
what are some adverse effects of CCBs
1. edema 2. GERD 3. Urine retention 4. Rash 5. increased LFT's
31
what causes edema with CCB's
precapillary dilation and postcapillary constriction
32
what are 3 adverse effects common with verapamil
1. constipation 2. bradycardia 3. HF exacerbation
33
why is urinary retention common with CCBs?
detrusor muscle can't contract as well (can't squeeze pee out)
34
why is GERD common with CCBs?
esophageal sphincter doesn't fully contract
35
why is IR nifedipine not used much
extreme tachycardia can cause MI (too abrupt vasodilation)
36
nifedipine has what unique adverse effect
gingival hyperplasia
37
why do verapamil and diltiazem cause bradycardia?
decreases FOC