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Pharm 1 Undergrad > Drugs for Regional Ischemia- CAD/ Angina > Flashcards

Drugs for Regional Ischemia- CAD/ Angina Flashcards

1
Q

What is Coronary Ischemia?

A
  • Inadequate supply of oxygen to to the heart which occurs due to narrowing of the coronary blood vessels.
  • CAD
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2
Q

What is angina pectoris?

A
  • The result of decreased blood supply to meet the increased metabolic demands on the heart.
  • ->Results in left side chest pain!
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3
Q

What are the 2 main goals to treating Angina?

A

1) Decrease oxygen demand to the heart (decrease workload on the heart)
2) Increase blood supply to the heart (promoting dilation)

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4
Q

What are Organic Nitrates, and what pathway do nitrates activate?

A
  • Prodrugs which act to release NO
  • ->NO activates soluble guanylyl cyclase (sGC) which leads to the increase in cGMP, causing dephosphorylation of the myosin light chain, resulting in a decrease in cytosolic Ca2+ and relaxation of both arteriolar and venous blood vessels.
  • Decreases myocardial wall tension/ O2 demand
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5
Q

What is Nitroglycerin most prevalent in treating?

A

Acute Angina

–>Increasing venous capacity, decreasing preload on the heart, venous return and heart rate.

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6
Q

What are the common Nitrate drugs?

A
  • Nitroglycerin
  • Isosorbide dinitrate
  • Sodium nitropruisside (SNP)
  • Minoxidil
  • Hydralazine (Mechanism not known- Ca2+ blocker)
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7
Q

What are some of the symptoms of using Nitrates?

A
  • TOLERANCE*
  • Flushing (due to subcutaneous dilatation)
  • Headaches
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8
Q

Why is SNP inappropriate for long term use of nitrates in controlling Angina?

A

-SNP can be used to temporarily bring down heart rate and blood pressure, but long term use can lead to cyanide poisoning.

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9
Q

True or False:

Nitrates dilate both arteriolar and venule blood vessels.

A

True.

*Mainly venodilation, but in high doses arteries/ arterioles also dilate!

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10
Q

Organic Nitrates :

A

(Mimics NO)
Acts directly on vascular smooth muscle cells (endothelial independent pathway) to increase NO which leads to activation of sGC, increased cGMP and decreased calcium (Vasorelaxation)

  • MAINLY act on venous capacitance vessels.
  • Rapidly deactivated by first pass metabolism.
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11
Q

What is problematic about administration of nitroglycerin?

A

-Can’t be administered orally.
Must be administered sublingually (transdermal patch)

-Fast onset and short half life!

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12
Q

Isosorbide dinitrate:

A

-After sublingual or oral administration, peak plasma concentration occur after 6 minutes!
(about twice the half life of nitroglycerin)

-Used for angina pectoris relief and as a prophylactic in situations likely to provoke angina. Short or Long term use

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13
Q

Isosorbide-2-mononitrate/ isosorbide-5-mononitrate:

A

-Active metabolites with a much longer half life than isosorbide dinitrate.
Approx. 3-6 hours.

–>isosorbide-5-dinitrate can be administered orally (excellent bioavailability)

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14
Q

What is the difference between true vascular tolerance and pseudotolerance using organic nitrates?

A

True vascular tolerance is due to reduced venous capacity, and a decreased ability to convert nitroglycerin into NO.

Psuedotolerance may be due to inactivation of mechanisms extraneous to the vessel wall.

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15
Q

Sodium Nitroprusside (SNP):

A
  • Nitrovasodilator used to increase levels of NO in vascular tissue.
  • NO activates sGC, cGMP, decrease in Ca2+ and vasodilation.
  • Mechanism not completely understood.
  • Dilates both arterioles and venules.
  • ->Can only be used during hypertensive emergency.
  • Especially used in patients with hypertension experiencing pulmonary edema.
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16
Q

Metoprolol:

A

Beta1 Blocker:

  • Used to reduce HR and BP in hypertension.
  • Competes with NE and Epi at B1 receptors.

-Adverse Effects: Reduced max. exercise tolerance, asthma, cold hands/ feet, bad dreams, depression, erectile dysfunction, altered plasma/ glucose levels

17
Q

Verapamil:

A

-Phenylalkylamines:
L- type Calcium Channel Blocker
-Reduces automaticity and AV conduction.

18
Q

Diltiazem:

A

-Benzothiazepine:
L- type Calcium Channel Blocker
-Reduces cardiac contractility, automaticity and AV conduction.

19
Q

Amlodipine, Nifedipine:

A

Dihydropyrimidines (DHPs)
–>L- type Calcium Channel Blockers:

-Have a higher affinity for smooth muscle than cardiac muscle.

Adverse Effects: Constipation, Urinary Retention and headaches.

20
Q

Which two calcium channel blockers inhibit one another’s binding?

A

Nifedipine and Verapamil

21
Q

Nifedipine:

A
  • Short half life (approx. 4 hours) - frequent dosing
  • Significant first pass metabolism
  • Rapid onset and fall in BP leads to reflex tachycardia, which can worsen myocardial ischemia)
22
Q

Amlodipine:

A
  • Better for treating hypertension
  • -High bioavailable (longer half life- approx. 40 hours)
  • Slower onset

-Significantly less tachycardia

23
Q

Toxicity/ Contraindications of Calcium Channel Blockers:

A
  • Flushing
  • Constipation
  • Bradycardia, AV Block and Heart Failure
24
Q

What is the main drug used to treat angina?

A

-Diltiazem (preferentially acts on coronary vessels)

25
Q

What is/ are the main drugs used to treat hypertension?

A

-AMLODIPINE (DHP), Nifedipine (DHP)

26
Q

What is/ are the main drugs used to treat Atrial Flutter, Atrial Fibrillation, Arrhythmia and Supraventricular Tachycardia?

A

-Verapamil

27
Q

Are DHP’s useful in the treatment of angina?

A

-NO! Amlodipine and Nifedipine decrease blood pressure quickly and can cause reflex tachycardia.

28
Q

Non Selective Beta Blockers in the treatment of angina?

A
  • Effective in stable angina as they reduce myocardial O2 demand by decreasing HR and contractility.
  • Used for long term chronic prophylactic treatment of stable angina.
29
Q

B1 Blockers in the treatment of angina?

A
  • Decrease heart contractility but are used with caution in variant/ vasospastic angina due to in-opposed alpha- mediated coronary vasoconstriction could be further augmented.
  • B1 blockers have a much longer duration of action compared to nitroglycerin (non-selective)
30
Q

Nitrates MAIN treatment:

A

Immediate relief of angina

*Tolerance develops

31
Q

Beta Blockers MAIN treatment:

A

Effective in stable angina to decrease myocardial O2 demand

32
Q

Beta 1 Blockers MAIN treatment:

A

Longer duration of action in comparison to non selective beta blockers

  • tolerance is less common
  • Chronic Prophylaxis of angina*
33
Q

CCB’s MAIN treatment:

A

Diltiazem and verapamil are preferred for the treatment of stable and variant angina.

  • Amlodipine (DHPs) not used for angina
  • Used to treat essential hypertension due to selective decrease of workload on vasculature over heart.
34
Q

Drugs which decrease heart rate?

35
Q

Drugs which decrease preload?

A

Nitrates (NTG)

36
Q

Drugs which decrease afterload?

A

CCB’s, Nitrates, Beta Blockers

37
Q

Drugs which decrease contractility?

A

Beta Blockers, CCB’s

38
Q

Pentoxifylline:

A
  • Methylated xanthine derivative
  • Useful to treat peripheral vascular disease symptoms of vasospasm
  • PDE inhibitor, TNF inhibitor and adenosine antagonist.
  • ->Vasodilator

Pharm 1 Undergrad (9 decks)

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