14. Chronic ischemia Drugs Flashcards

1
Q

Nitrates IG are vasodialator but have most effect on:

A

venous blood vessels

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2
Q

Mech of action of nitrates

A

Become denitrated in Smooth muscle–> free nitrate converts to NO
NO–> activate GC which increases cGMP
cGMP–> activates cGMP protein kinase (PKG)
PKG phosphoylates stuff leading to decreased Ca and dephosphorylation of myosin

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3
Q

How do nitrates affect preload

A

Increase venous capacitance to DECREASE preload
this reduces diastolic wall tension thus Oxygen deman
Decreased preload has small increase in subendo blood flow

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4
Q

What effect do nitrates have on afterload?

A

SMALL REDUCTION to afterload or small reduciton in systemic atrial pressure
see reduction in systolic wall tension
slight reflex tachycardia

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5
Q

When are nitrates valuble as a coronary dialator?

A

if ischemia is dt vasospasm… not so much is pt has angina with maximal dilation d/t accumulation of local metabolites

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6
Q

How are nitrates activated?

A

by organic nitrate reductase in the liver: low bioavailability d/t 1st pass effect

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7
Q

What form of nitrate is biologically active?

A

Mononitrate: doesn’t need to be metabolized while isosorbide dinitrate gets metabolized in liver–> mono form

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8
Q

How can we acheive high conc of nitrates rapidly?

A

sublingual to avoid 1st pass affect; last 30 mins or so

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9
Q

Can we use nitrates for chronic angina?

A

yes, provides prophylaxsis against angina episodes

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10
Q

Nitrate with no first pass metabolism and 1/2 life of 5 hours

A

mononitrate

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11
Q

has 25% bioavailability with longer DOA (4-6hrs) and metabolized to be active

A

dinitrate

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12
Q

Nitrate that is orally controlled release tabs/capsules and available as patch and ointment/paste applied to skin

A

Nitroglycerin

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13
Q

Do pts devo tolerance to nitrates?

A

yes; if used constantly w/in in a few hours, but rapid reversal…. limits how effective slow release forms are so use small dose and schedule nitrate free period

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14
Q

Adverse effects of nitrates

A

headache, hypotension, reflex tachycardia, flushing

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15
Q

Why are beta blockers recommended for IHD?

A

have anti-anginal effect by reducing oxygen demand dt decrease force of ventricular cnx and HR; because blocks effects of catecholamines on B1 receptors

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16
Q

Propanolol and timolol are examples of

A

non-selective B blockers

17
Q

metoprolol and atenolol are examples of

A

selective B1 antagonists

18
Q

when are B blockers ineffecient at tx angina?

A

when its dt vasospasm (use nitroglycerin!)

19
Q

How do Beta blockers decrease oxygen demand in an ischemic heart?

A

Decreases HR, decreases contractility, decreases BP (afterload)

20
Q

Do Beta blockers help increase oxygen to ischemic areas?

A

a little– they slow the HR so that heart spends more time in diastole thus longer time in coronary perfusion

21
Q

When we have decreased CO we can have ______ prelaod that can lead to _______ wall tension

A

increased

increased

22
Q

Can we use B blockers in patients with COPD?

A

NOPE

23
Q

Pt comes in with IHD and you recommend he be treated with a Beta Blocker. Pt has:
elevated LDL
family hx of HTN
heart block
insulin-tx diabetes
Which of these prevents you from tx with beta blockers?

A

Insulin dependent diabetes and heart block (as well as bradycardia) are contraindicated for Beta Blocker

24
Q

Nifedipine and Amlodipine are examples of:

A

Dihydropyridine Ca+ channel blockers

25
Q

Verapamil and Diltiazem are examples of:

A

Non-dihydropyridine Ca+channel blockers

26
Q

Which are more potent vasoD; non-dihydropyridine or dihydropyridine

A

dihydropyridine: such as nifedipine and amlodipine

27
Q

How do dihydropyridine (nifedipine and amlodipine) relieve ischemia?

A

Decrease O demand via vasoD which will decrease Afterload thereby reducing wall stress

28
Q

What channel blockers are potent agents for relief of vasospasm?

A

Nifedipine or amlodipine

29
Q

Nondihydropyridine; verapamil or diltiazem relieve ischemia by:

A

decreasing O demand by reducing force of contraction and heart rate

30
Q

Which drug works by decreasing O demand by reducing force of contraction and heart rate

A

Nondihydropyridine; verapamil or diltiazem

31
Q

What negative effects are seen in all Ca+channel blockers?

A

headache and flushing

32
Q

Constipation is a side effect seen in which Ca+ blocker

A

Verapamil

33
Q

Which Ca+ blockers cause Edema the worse

A

Nifedipine and diltiazem

34
Q

Which Ca+ blocker cause bradycardia and decrease contractility?

A

verapamil and diltazem

35
Q

What benefits do we see from combinding a nitrate with a Beta Blocker?

A

Beta blocker prevents potential reflex increase in HR and contractility produced by nitrates
Nitrates prevent the potential increase in wall tension from beta blockers

36
Q

What do we need to be worried about when combinding a Beta blocker with Verapamil or Diltiazem Ca+ channel blocker?

A

additive negative inotropic effect can cause excessive cardiodepression

37
Q

How does RANOLAZINE work?

A

anti-ischemic tx; decreases frequency of anginal episodes and increases exercise capacity: but no effect on HR via vasodialation
Its works to inhibit late Na current in cardiac myocytes

38
Q

Which anti-ischemic tx works to inhibit late sodium current in cardiac myocytes

A

Ranolazine