Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiology M2 > 11 11 2014 Vasodilatory drugs > Flashcards

11 11 2014 Vasodilatory drugs Flashcards

1
Q

Nitroglycerin (sublingual), Amyl nitrite, Isosorbide dinitrate

  1. mechanism:
  2. Effect on pulmonary vessel resistance at low and high doses:
  3. Adverse effects
  4. Overall effects:
A
  1. release NO in smooth muscle cells NO activates Guanylate Cyclase = increase in cGMP = dephospho rylation of myosin light chain and muscle relaxation Decreases internal Ca2+ release
  2. Low doses: decrease diastolic filling pressure; decrease pulmonary vessel resistance High doses: decrease in systemic peripheral resistance = reflex cardiac stimulation
  3. Adverse effects: - flushing, headache, orthostatic hypotension, coronary vasodilation * all are short acting!
  4. Decreased heart size and wall tension during systole. - reflex cardiac stimulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pharmodynamics of Nitroglycerin

A

– prodrugs First pass inactivation in liver by nitrate reductase more resistant to metabolism and are less potent. Tolerance, physical dependence

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

Why is nitroglycerin useful in angina?

A
  • acts primarily by lowering work of heart - extremely useful for suppressing acute attacks.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Nitroglycerin effects on perfusion? Effect on cardiac work?

A

no overall increase in coronary blood flow some redistribution from epicardial to endocardial ischemic regions Sublingual dose: 1. venodilation 2. arteriolar dilation 3. reflex cardiac stimulation of rate and contractility?

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

Sildenafil (Viagra), LEVITRA (Vardenafil HCl), Cialis (Tadalafil)

  1. mechanism
A

PDE5 is an important phosphodiester mediating cGMP breakdown in tissue ( NO = normal erectile function) Sildenafil blocks PDE5 and increase cGMP = enhancing erections in males whose innervation and NOs ynthesis ability is intact.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Mechanism of relaxing aerial smooth muscle:

A
  1. Hyperpolarization (open K+ channels) which
  2. blocks L-Type Ca2+ channels
  3. Increase cGMP = increase in NO
  4. increase cAMP = beta adrenergic agonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where are L-type calcium channels?

A

Resistance vessel smooth muscle cells Myocardial cells Role of L-channels are contraction. They are in many cell types and they have slow activation. usually activated around -45 mV

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

Muscle contraction and what mediates tone?

A

Tonic – not phasic tone is maintained by intracellular free Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Nifedipine 1. mechanism and binding? 2. therapeutic concentrations affect? 3. How good is it at vasodilation? 4. Reflex to cardiac activation? 5. Direct cardiac suppression? 6. overall

A

L-type calcium channel blocker - binds to closed L-channels and decrease frequency of opening

Therapeutic concentrations affect: 1. myocardial cells 2. vascular smooth muscle of resistance vessels

Strong vasodilation modest to strong cardiac activation modest to moderate direct cardiac suppression

Overall: vasodilation with modest cardiac stimulation

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

Administration/ pharmacokinetics of nifedipine?

A

orally large first pass metabolism Newer DHP are similar but more selective for L- ca+ channels (closed) in resistance vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Adverse effects of Nifedipine?

A

Flushing, headaches, hypotension, peripheral edema

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

Verapamil

  1. mechanism and binding?
  2. therapeutic concentrations affect?
  3. How good is it at vasodilation?
  4. Reflex to cardiac activation?
  5. Direct cardiac suppression? 6. overall
A

L-type calcium channel blocker - binds to open channels – thus frequency of opening determines extent of blockade T

herapeutic concentrations affect: 1. myocardial cells 2. vascular smooth muscle of resistance vessels

Moderate vasodialtion moderate cardiac activation moderate cardiac suppression

Overall: vasodialtion with moderate cardiac suppression

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

Pharmacology of Verapamil and adverse effects?

  1. what happens on clinical dosage
  2. Contraindicated?
  3. Does it hit any other receptors?
  4. Administration?
  5. metabolism?
  6. Adverse effects
A

Clinical dose causes: moderate vasodilation

Contraindicated in severe CHF b/c some alpha-adrenergic blockade

Oral administration

Large first pas metabolism

adverse effects: flushing, GI disturbances, LV dysfunction

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

Diltiazem 1. mechanism and binding? 2. therapeutic concentrations affect?

A

L-type calcium channel blocker - binds to refractory L-channels and decrease frequency of opening

Therapeutic concentrations affect: 1. myocardial cells 2. vascular smooth muscle of resistance vessels

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

Why are vasodilators useful in treating angina?

A

decrease vascular smooth muscle tone Decrease peripheral vascular resistance = decrease in after load = less myocardio work and decrease O2 consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Advantages to using calcium entry blockers?

A

No aggravation of diabetes, peripheral vascular disease, bronchospasm, blood profiles of lipids, glucose or potassium. Tolerance does not develop

17
Q

Effect of calcium entry blockers on perfusion? Effect on cardiac work?

A

increase coronary blood flow resistance vessel dilation reflex cardiac effects vary with agent work of heart is decreased

18
Q

Utility for typical angina in regards to calcium entry blockers?

A

-Reduce frequency of attacks -Reduce nitrate requirements -Increased exercise performance -no reducin in incidence of MI - Use when beta-blocekrs are not tolerated

19
Q

Beta adrenergic antagonists effect on cardiac work:

A
  • suppress cardiac activity - lower O2 consumption - prolongue diastole
20
Q

Utility of beta-blocerks in typical angina

A
  • most effective in reduction of cardiac ischemia
  • Reduces frequency and severity of attacks
  • useful for suppressing recurring myocardial infarcts

* not super effective in therapy for angian because they mostly affect the heart and not resistance.

21
Q

Adverse effects of beta blockers:

A
  • aggravation of peripheral insufficiency
  • increased airway resistance
  • produce rebound angina or MI on sudden withdrawal.
22
Q

Typical Angina? Atypical Angina? Unstable angina?

A

atherosclerotic narrowing of the coronary artery

coronary vasospasm

platelet aggregation secondary to plaque rupture

Cardiology M2 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions