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Pharmacology > Cardiovascular I > Flashcards

Cardiovascular I Flashcards

1
Q

How is angina characterized on the ECG?

A

By S-T segment depression or elevation

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2
Q

When does angina occur?

A

When oxygen supply to the myocardium is insufficient

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3
Q

What agents decrease oxygen demand?

A

Vasodilators, Ca++ entry blockers, organic nitrates

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4
Q

Typical Angina

  1. Result of?
  2. Induced by?
A
  1. Atherosclerotic coronary artery disease
  2. Excercise, eating, or emotional stress
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5
Q

Varient or Prinzmetals Angina:

  1. Result of?
  2. When can it occur?
A
  1. Coronary artery vasospasm possibly in conjunction with a coronary thrombosis
  2. at rest
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6
Q

What other things can cause myocardial ischemia?

A

Aortic valve disease, hypertrophic cardiomyopathy, stenosis of the coronary ostia, inflammation of the coronary arteries, and congenital anomalous origins of the coronary arteries arising from the pulmonary artery

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7
Q

Early reversible ischemia:

  1. Time period this occurs?
  2. What occurs with glycolysis?
  3. What occurs with phosphate?
A
  1. 15 minutes
  2. There is an increase in anaerobic glycolysis
  3. There is greater use than production
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8
Q

Early irreversible ischemia:

  1. Time period?
  2. What happens with high energy phosphates?
  3. What occurs to the mitochondria and plasmalemma?
  4. What ion influxes? Why is this important?
A
  1. 60 minutes
  2. Phosphate stores are depleted
  3. Mito swells and plasmalemmal defects
  4. Ca++ influx; stimulates lysozymes to destroy cells
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9
Q

Late irreversible Ischemia

  1. Time period?
  2. What occurs to the membrane? Result?
  3. What ion influxes? Why is this important?
A
  1. 24 hours
  2. It continues to pull apart and leak enzymes, co-factors and soluble cell components to the extracellular fluid
  3. Ca++ influx; stimulates lysozymes for cell destruction
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10
Q

The treatment of angina is targeted at imporvement of the balance between what?

What are the three classes of drugs traditionally used?

A

Balance between oxygen supply and demand in the heart

Beta blockers, Ca++ channel blockers, and organic nitrates

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11
Q

What do organic nitrates do?

Main example?

A

Cause direct, endothelium INDEPENDENT, relaxation of most sources of smooth muscle including that from arteries and veins

Nitroglycerin

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12
Q

Cellular mechanisms of action of nitrodilators:

Nitrodilators react with REDUCED _____ (example: ____) inside the cell to form unstable _____.

A

thiols; cysteine; nitrosothiols

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13
Q

Cellular mechanisms of action of nitrodilators:

Nitrosothiol is believed to release ____ which binds to the ___ moiety of ____ cyclase. This binding activates the enzyme resulting in the production of ____ and subsequent activation of the ____ elicits relaxation of the vascular smooth muscle.

A

NO; heme; guanylate; cGMP; G-kinase

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14
Q

Cellular mechanisms of action of nitrodilators:

No is not only a second messenger in vadodilation but it also has what other properties? (4)

What deactivates the conversion of GTP to cGMP?

A

Anti-thrombotic, anti-mitogenic, anti-atherogenic, and acts as an oxygen radical scavenger

Phosphodiesterases (PDEs)

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15
Q

Hemodynamic systemic effects of nitrovasodilators:

What does it dilate?

The systemic dilatory effects reduce ___ and ___ as well as?

Consequently the systemic effects improve ischemia by ___ ___ ___ by the heart.

A
  1. Veins and arteries with a preference for veins at low doses
  2. preload; afterload; ventricular chamber size
  3. reducing oxygen demand
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16
Q

What is the primary effect of nitrodilators upon stable exertional angina?

A

To reduce oxygen demand by the heart

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17
Q

Hemodynamic coronary effects of nitrovasodilators:

  1. What coronaries are most sensitive? (size)
  2. The dilating effect is of UNCERTAIN benefit but they may be important in what cases?
  3. There is some evidence that decreased ___ pressure brought about by nitrodilators may facilitate blood flow to the ____.
A
  1. Large are more sensitive than small
  2. Eccentric coronary stenosis or in classic variant angina where vasospasm may be the primary cause
  3. ventricular; endocardium
18
Q

Pharmacodynamics and Kinetics:

  1. Speed of absorption?
  2. Absorbed how?
  3. Speed of metabolism?
  4. Duration of action?
A
  1. Rapid
  2. Through mucous membranes
  3. Fast
  4. Short
19
Q

Nitroglycerin

  1. Peak effect in how much time?
  2. Duration of action?
  3. Good for what 2 things?
A
  1. 3 minutes
  2. 20/30 minutes
  3. Acute angina or prophylaxis before exertion
20
Q

Isosorbide dinitrate

  1. Onset in how much time?
  2. Peak effect time?
  3. Duration?
  4. Useful for?
A
  1. 20/45 minutes
  2. 45/120 minutes
  3. 2-6 hours
  4. Prevention of angina
21
Q

Side effects and limitations of nitrovasodilators:

The major drawback?

A

Tolerance

22
Q

What two ways is tolerance theorized to occur?

A

Counter-regulatory mechanism

Tissue metabolic mechanisms

23
Q

Counter-regulatory mechanisms of tolerance:

  1. Decreased BP results in reflex activation of?
  2. ____ ___ in response to these reflexes counteracts the ____ effect of the nitrodilator.
A
  1. SNS as well as the Renin-angiotensin system
  2. Volume retention; unloading
24
Q

Tissue metabolic mechanisms of tolerance:

  1. Where does tolerance develop? What does this suggest?
  2. Current research indicates a role for ___ in the development of tolerance
  3. Sustained exposure to NO results in excessive production of what? This production then does that?
A
  1. In isolated arteries suggesting that tolerance originates at the cellular level
  2. ROS
  3. ROS; Radicals inactivate NO, convert NO Synthase to a superoxide ion producing enzyme, and stimulate other superoxide enzymes
25
Q

Other side effects of nitrodilators? (extensions of their normal physiological effects) Why?

A

Postural hypotension (from preferred venodilation)

Syncope (from too severe of a decrease in arterial pressure)

Headache (from cerebral arterial vasodilation)

26
Q

What in conjunction with nitrodilators can result in severe hypotension and exacerbation of angina?

What is this used as treatment for?

A

PDE5 inhibitors

Erectile dysfunction

27
Q

Factors associated with ED parallel those of ___ ___ __. What are these factors?

A

coronary artery disease; hypertension, diabetes, and hypercholesterolemia

28
Q

3 PDE5 inhibitors used for the treatment of ED?

A

Sildenafil (short), Vardenafil (short), and Tadafil (long)

29
Q

PDE5 inhibitors mechanism of action:

What specific PDE do PDE5 inhibitors inhibit?

Consequently what is increased? This is stimulated by?

A

They inhibit the cyclic GMP-specific PDE5 family of phosphodiesterases

Intracellular concentrations of cGMP stimulated by cellular agonists, such as NO, that activate guanylate cyclase

30
Q

PDE5 inhibitors mechanism of action:

Because they increase intracelullar concentrations of cGMP, they amplify the actions of?

A

NO

31
Q

PDE5 mechanism of action:

  1. What is associated with excess oxygen radical formation? Excess ROS chemically reduces ___ concentration at target tissues.
  2. What does diabetes do specifically?
A
  1. Hypertension, diabetes, and hypercholesterolemia; NO
  2. Damages nerves, including the NANC nerves, that release NO in the corpus cavernosum to induce penile erection.
32
Q

PDE5 inhibitors mechanism of action:

PDE5 inhibitors counteract the effect of decreased NO bioavailabilty by enhancing the amount of ___ produced in the ___ ____ and ____ arteries.

A

cGMP; corpus cavernosum; penile

33
Q

Minor adverse events of PDE5 inhibitors?

A

Headache, flushing, rhinitis, possible dyspepsia (due to relaxation of the LES), weak inhibition of PDE6 (mediator of photoreceptor signal transduction)

34
Q

Major adverse effects of PDE5 inhibitors:

  1. Taken alone?
  2. Interaction with organic nitrates?
A
  1. Only minimally decrease BP
  2. Together they produce extreme reductions in BP
35
Q

PDE5 inhibitors are contraindicated in what patients?

A

Patients taking any form of nitrate or alpha adrenergic receptor ANtagonists

36
Q

Review Nitrodilator therapeutic mechanisms:

  1. Venodilations –> reduce ___ __ –> reduce ventricular size, volume, and ____ –> decreased wall stress. Overall decreased ___ ____.
  2. Arterial dilation –> decreased ventricular ____
  3. Dilate ____ free wall
  4. Improve endocardial ___ __
A
  1. ventricular preload; pressure; oxygen demand
  2. afterload
  3. coronary
  4. blood flow
37
Q

Review nitrodilator limitations:

  1. What two things stimulate the SNS and cause reflex tachycardia and +inotropic effect?
  2. Development of ___
  3. Complications associated with concurrent use of ___ ___.
A
  1. Hypotension and decreased stroke volume
  2. tolerance
  3. PDE5 inhibitors
38
Q

Review Nitrodilator adverse reactions?

Name 7.

A

Headache, dizziness, postural hypotension, syncope, palpitations, weakness, and Angina

39
Q

Why is angina an adverse reaction of nitrodilators if its used for the treatment of angina?

A

In coronary artery disease, if too much is taken, there can be exacerbation of the current angina and will drop BP/blood flow too low. It occurs when people take another one too soon

40
Q

Review - Beta adrenergic antagonist therapeutic mechanisms:

  1. Limit catecholamine induced ___ __
  2. Decrease ventricular ____ by decreasing ___.
  3. Inhibit ___ aggregation
  4. ___ stabilizing effect (although not all)
A
  1. Increased HR
  2. afterload; BP
  3. platelet
  4. membrane
41
Q

Review beta adrenergic antagonist limitations:

  1. Potential for constriction of?
  2. What occurs with withdrawl?
  3. What occurs with sudden withdrawl?
A
  1. vasculature and bronchi
  2. Decompensation in borderline heart failure
  3. Angina and possible MI
42
Q

Review - beta adrenergic antagonist adverse rxns:

Name 8.

A

Bradycardia, heart block, hypotension, heart failure, bronchoconstriction, unrecognized hypoglycemia (in diabetes), cold extremities, claudication (too little blood flow during exercise)

Pharmacology (24 decks)

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