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Pharm > Anti-Anginal > Flashcards

Anti-Anginal Flashcards

1
Q

Classical angina

A
  1. occurs if the coronary artery is narrowed
  2. the reduced blood flow through narrowed arteries can’t meet the increased O2 demand–>
  3. Symptoms occur with increased emotional or physical exertion.
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2
Q

Variant Angina aka Prinzmetal’s angina

A
  1. results from a reversible spasm of large coronary arteries, usually at the site of atherosclerotic plaque
  2. can occur at rest or irrespective of the amount of physical or emotional exertion
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3
Q

acute coronary syndrome aka unstable angina

A
  1. characterized by increased frequency and severity as a result of combo of atherosclerotic plaques and vasospasm
  2. symptoms occur even at rest
  3. might signal an impending MI–>treat as medical emergency
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4
Q

2 strategies for treatment of angina

A
  1. increase O2 delivery: Nitrates & Ca Channel Blockers
  2. Reduce O2 requirement: beta blockers
  3. anti platelet drugs (i.e. low dose aspirin, abciximab) are also used
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5
Q

Which anti anginal meds work to increase Oxygen delivery to tissues?

A

Nitrates & Calcium Channel Blockers (CCB)

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6
Q

Which anti anginal meds work to reduce the oxygen requirement?

A

beta adrenergic blockers

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7
Q

Ranolazine

A

a newer drug that works to increase the efficiency of oxygen utilization by partial fatty acid oxidation inhibitors (pFOX inhibitors)

  1. a pFOX inhibitor (partial fatty acid oxidation inhibitor) in myocardium
  2. primary mechanism of action involves reduced contractility
  3. action results from blockade of a late sodium current that facilitates calcium entry via the sodium-calcium exchanger
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8
Q

Examples of Nitrates

A
  1. Nitroglycerine (GTN)
  2. Isosorbide dinitrate
  3. Isosorbide mononitrate
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9
Q

Nitrates

A
  1. powerful vasodilators
  2. act by releasing NO
  3. NO–> smooth muscle relaxation
  4. effectiveness due to action on capacitance vessels to reduce cardiac pre-load: Dilation of collateral coronary vessels
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10
Q

Nitrates MOA

A
  1. NO formation is triggered by Ach, Bradykinin, histamine & serotonin
  2. NO activates Guanylyl Cyclase (GC) to form cGMP–> smooth muscle relaxation
  3. Contraction of vascular smooth muscle is triggered by influx of calcium
  4. . Ca combines with calmodulin & converts enzyme myosin light chain kinase to its active form (MLCK)
  5. MLCK phosphorylates the myosin light chains–>initiates interaction btw myosin & actin
  6. Nitrates dephosphorylate Myosin light chains to prevent their interaction with actin
  7. phosphodiesterase breaks down cGMP. a phosphodiesterase inhibitor (i.e. Sildenafil) results in an increase in the amount of cGMP–>more dephospho rylation of MLC–>more muscle relaxation

Combining nitrates with sildenafil–>sudden severe hypotension

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11
Q

Sildenafil

A

phosphodiesterase inhibitor

phosphodiesterase breaks down cGMP. a phosphodiesterase inhibitor (i.e. Sildenafil) results in an increase in the amount of cGMP–>more dephospho rylation of MLC–>more muscle relaxation

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12
Q

Glyceryl trinitrate (GTN)

delivery?

A

aka nitroglycerine

  1. given sublingually to avoid 1st pass metab; also rapidly absorbed
  2. also available in transdermal patch & via IV
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13
Q

How do nitrates work?

Any other uses?

A

they decrease the cardiac preload by preferentially dilating veins

Other uses: cyanide poisoning (sodium nitrite, amyl nitrite with sodium thiosulfate)
NITRITE used in cyanide bc converts Hb to MetHb, which has higher affinity for cyanide.

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14
Q

Adverse effects of nitrates

A
  1. severe headache (from vasodilation of extracerebral bv)
  2. Tolerance occurs with long term use (need higher doses)
  3. Postural hypotension & reflex tachycardia
  4. Methemoglobinemia caused by NITRITES, not nitrates

“monday disease” in production of substances involving nitrates is an example of the tolerance (build it up over the week) & the symptoms (headache)

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15
Q

Nitrates have an interaction with? How?

A

Sildenafil (viagra)

  1. these agents inhibit a phosphodiesterase isoform (PDE5) that metabolizes cGMP in smooth muscle
  2. the increased cGMP in erectile smooth muscle relaxes it, allowing for greater inflow of blood & more effective & prolonged erection
  3. this effect also occurs in vascular sm. as a result the combo of nitrates (via increase in cGMP production) & a PDE5 inhibitor (through decreased breakdown of cGMP) –> synergistic relaxation of vascular sm with potentially dangerous HYPOTENSION & inadequate perfusion of critical organs
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16
Q

Calcium Channel Blockers block what type of channel? where is it located?

A

CCB block voltage-gated L-type calcium channels in cardiac & smooth muscle

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17
Q

Examples of CCB

A

a) Dihydropyridines (DHP):
1. nifedipine, amlodipine, nicardipine, nimodipine
b) Verapamil, diltiazem

18
Q

Examples of Dihydropyridines (DHP)

A
  1. nifedipine
  2. amlodipine
  3. nicardipine
  4. nimodipine
19
Q

Important differences in vascular selectivity between CCB

A

in general, DHPs have a greater ratio of vascular smooth muscle effects compared to cardiac effects than either diltiazem or verapamil

20
Q

Nimodipine is particularly selective for

A

cerebral blood vessels–>used to treat subarachnoid hemorrhage

21
Q

Verapamil & Diltiazem function & use

A

block calcium-dependent conduction in the AV node & are used to treat AV nodal arrhythmias

22
Q

How do CCB work to treat angina?

A

They decrease both preload and after load–> decreasing workload on the heart!

23
Q

Nifedipine

  1. what is it?
  2. Effects?
  3. Use?
  4. ADR?
A
  1. mainly arteriolar vasodilator
  2. minimal effect on cardiac conduction or HR–>NOT USED FOR ARRHYTHMIAS
  3. useful to treat varying angina
  4. ADR:
  5. flushing
  6. headache
  7. hypotension
  8. peripheral edema

All the ADR are results of the vasodilation

24
Q

ADR of Nifedipine

A
  1. flushing
  2. headache
  3. hypotension
  4. peripheral edema

All the ADR are results of the vasodilation

25
Q

Verapamil

What? Use? Interactions/toxicities?

A

More selective for cardiac calcium channels (but will also affect bv)

  1. slows cardiac conduction
  2. decreases HR & O2 demand
  3. causes more negative inotropic effect than nifedipine
  4. Weaker vasodilator than nifedipine–DIP always more powerful
  5. Drug interaction: with digoxin (increases digoxin levels)
26
Q

Diltiazem

A

same as verapamil–More selective for cardiac calcium channels (but will also affect bv)

  1. has specific coronary vasodilating effect relieving coronary vasospasm
  2. particularly useful in variant angina
  3. ADR: low
27
Q

ADR of CCB (generally)

A
  1. cause hypotension due to vasodilation
  2. peripheral edema
  3. overdose leads to cardiac arrest (bc blocked channels–> decreased FOC), bradycardia, AV block & Heart Failure
28
Q

What condition is contraindicated against CCB?

A

Heart Failure! IN heart failure the cardiac output isn’t sufficient to meet the body’s demands. CCB will further decrease the heart’s FOC–> further decreasing it’s CO.

29
Q

How are Beta blockers used to treat angina?

A
  1. work by opposing the action of adrenaline on the heart
  2. block B1 receptors present in the heart–> results in unopposed alpha effects–>vasoconstriction
  3. results in a decrease in HR, BP & contractility
  4. this decreases the myocardial oxygen requirements at REST & DURING EXERCISE
  5. they do NOT HAVE ANY EFFECT ON MYOCARDIAL O2 SUPPLY!
  6. they are used in combo with other anti-anginal drugs
    ie beta blockers + nitrates bc nitrates –>vasodilation + reflex tachycardia but the beta blockers will help prevent the tachycardia
30
Q

When are beta blockers contraindicated in treating angina

A

in vasospastic angina, bc beta blockers will cause further vasoconstriction

block B1 receptors present in the heart–> results in unopposed alpha effects–>vasoconstriction

31
Q

DOC in acute relief of symptoms in all types of angina

A

Nitrates

32
Q

What is used as prophylactic therapy in vasospastic/variant/Prinzmetal’s angina?

A

Ca channel blockers

they’re also useful in angina of effort

33
Q

When should you use beta blockers to treat angina?

A

ONLY for prophylaxis of angina. They’re effective in preventing EXERCISE-INDUCED angina

34
Q

Nitrates have a preference for?

A

veins

35
Q

How do nitrates treat angina?

A

release NO–>sm relaxation through activation of cGMP–> ultimate reduction in preload

36
Q

How do you overcome the reflex tachycardia associated with nitrates?

A

Give them in conjunction with beta blockeres

37
Q

Nifedipine has a preference for?

A

arteries

38
Q

Nimodipine has a preference for

A

cerebral blood vessels

39
Q

decreases HR, BP & contractility

A

beta blockers

reducing these–>decreases myocardial oxygen requirements at rest & during exercise

40
Q

blocks AV nodal conduction

A

verapamil & diltiazem

41
Q

abciximab

A

anti platelet effect; used like aspirin in treatment of angina

42
Q

reduces contractility by blocking late sodium current that facilitates calcium entry via the sodium-calcium exchanger

A

Ranolazine

Pharm (32 decks)

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