Brainscape's Knowledge GenomeTM

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


See full index

Cardio Block > Pharmacology of Sympathetic Agents > Flashcards

Pharmacology of Sympathetic Agents Flashcards

1
Q

Sympathetic pharmacologic agents act on which types of receptors?

A

Alpha and beta

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

What are the major neurotransmitters of the autonomic nervous system?

A

Acetylcholine and norepinephrine

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

What are the major neurotransmitters of the sympathetic nervous system and their associated targets? (3)

A
  1. Norepinephrine (cardiac muscle, smooth muscle, gland cells, nerve terminals)
  2. Acetylcholine (sweat glands)
  3. Dopamine (renal vascular smooth muscle)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathway of catecholamine synthesis (4 steps)

A

Tyrosine -> DOPA -> Dopamine -> Norepinephrine -> Epinephrine

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

Where is norepinephrine released and what is its mechanism of action?

A

Adrenergic postganglionic neurons; provides negative feedback on alpha-2 receptors on the presynaptic neuron

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

Where is epinephrine released?

A

Adrenal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do alpha-1 receptors do? (4)

A
  1. Increases contractility of vascular and GU smooth muscle
  2. Relaxes intestinal smooth muscle
    * 3. Increases contractility and excitability of cardiac muscle
  3. Promotes glycogenolysis and gluconeogenesis in the liver

*High-Yield Topic!

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

What do alpha-2 receptors do? (4)

A
  1. Decreases insulin secretion in pancreatic beta cells
  2. Promotes platelet aggregation
    * 3. Decreases norepinephrine release
  3. Increases vascular smooth muscle contraction

*High-Yield Topic!

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

What do beta-1 receptors do? (3)

A
    1. Increases rate and contractility of cardiac muscle
    1. Increases AV node conduction velocity
      1. Increases renin secretion in renal cells

*High-Yield Topic!

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

What do beta-2 receptors do? (3)

A
    1. Relaxes smooth muscle in the lungs
      1. Promotes glycogenolysis and gluconeogenesis in the liver
      2. Promotes glycogenolysis and K+ uptake in skeletal muscle

*High-Yield Topic!

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

What do beta-3 receptors do? (1)

A
  1. Promotes lipolysis in adipose tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Clinical applications for catecholamines (3)

A

Stimulates Sympathetic Nervous System:

  1. Cardiogenic shock (increase heart rate and contractility)
  2. Asthma (bronchodilator)
  3. Anaphylaxis (bronchodilator)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Norepinephrine selectivity and applications

A

Affects alpha-1 and alpha-2 equally
Affects beta-1 greater than beta-2
Potent vasoconstrictor (alpha-1) and cardiac stimulant (beta-1)
*Better for selective heart response without affecting the lungs

Can treat cardiogenic shock

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

Epinephrine selectivity and applications

A

Affects alpha-1 and alpha-2 equally
Affects beta-1 and beta-2 equally
Potent vasoconstrictor (alpha-1) and cardiac stimulant (beta-1)
Dilates bronchial smooth muscle and increases skeletal muscle blood flow (beta-2)

Can treat asthma and anaphylaxis

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

Dopamine selectivity and applications

A

Affects dopaminergic receptors greater than beta, and beta greater than alpha
Dilates renal vasculature to increase renal blood flow (D1)
Increased HR and contractility (B1)
Peripheral vasoconstriction (a1)

Can treat shock caused by low cardiac output (CO) and renal failure

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

In a patient with no history of a heart transplant, when drugs are used to increase BP, reflex ________ is seen.

A

Bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In a patient with no history of a heart transplant, when drugs are used to decrease BP, reflex ________ is seen.

A

Tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Sympathomimetics ________ the effects of ________ activation

A

Mimic; sympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Alpha-1 agonists are ________-acting sympathomimetics

A

Direct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Alpha-1 agonists effects (4)

A
  1. Increase peripheral vasoconstriction, which increases BP
  2. Result in baroreceptor-mediated reflex bradycardia
  3. Cardiac output stays relatively the same despite the drop in HR due to increased venous return, leading to increased stroke volume
  4. Modest positive inotropic effect
21
Q

Alpha-2 agonist effects (3)

A
  1. Activation of alpha-2 receptors in the CNS results in decreased sympathetic outflow
  2. Decreases heart rate by lowering NE release
  3. Prolonged hypotensive response
22
Q

Clinical applications for alpha-2 agonists (1)

A

Treatment of hypertension

23
Q

Alpha-methyldopa and clonidine MOA

A

Acts centrally to stimulate alpha-2 receptors.
Inhibits NE release.
Decreases sympathetic outflow and decreases BP.
Vasodilator = decreases venous tone/peripheral resistance.
Decreases heart rate.

24
Q

Alpha-methyldopa and clonidine ADRs (3 common/3 serious)

A

Common:

  1. Dizziness
  2. Headache
  3. Sedation

Serious:

  1. Hepatotoxicity (alpha-methyldopa)
  2. Hemolytic anemia (alpha-methyldopa)
  3. AV block (clonidine)
25
Q

Clinical applications for beta-1 agonists (1)

A

Treatment of heart failure

26
Q

Dobutamine MOA

A

Beta-1 selective agonist.
Direct-acting inotropic agent that stimulates the beta-receptors of the heart.
Positive inotropic effect is greater than chronotropic effect.
Results in increased contractility and cardiac output.

27
Q

Dobutamine pharmacokinetics

A

Dosed by IV

Half-life: 2 minutes

28
Q

Dobutamine ADRs (Common: 3/Serious: 2)

A

Common:

  1. Hypertension
  2. Tachyarrhythmia
  3. Headache

Serious:

  1. Cardiac dysrhythmia
  2. Dyspnea
29
Q

Clinical applications for beta-2 agonists (2)

A
  1. Asthma

2. COPD

30
Q

Albuterol MOA

A

Beta-2 selective agonist.

Bronchodilation without cardiac effects.

31
Q

Clinical applications for nonselective beta agonists (5)

A
  1. Bradycardia
  2. Heart block
  3. Cardiac arrest
  4. COPD
  5. Asthma
32
Q

Isoproterenol MOA

A

Potent nonselective beta-adrenergic agonist.
Positive inotropic and chronotropic effects (B1).
Results in increased contractility and cardiac output (B1).
Vasodilation of some vascular beds and bronchodilation (B2).

33
Q

Isopropterenol ADRs (Common: 3/Serious: 1)

A

Common:

  1. Tachyarrhythmia
  2. Headache
  3. Tremor

Serious:
1. Cardiac dysrhythmia

34
Q

Antagonist vs partial agonist

A

Antagonists inhibit the release of a particular neurotransmitter.
Partial agonists do not fully promote the release of that neurotransmitter (slows down release).

35
Q

General effects of beta receptor antagonists (7)

A
  1. Negative chronotropic and inotropic effects
  2. Lowers BP in hypertensive patients (lower CO and blocks renin release)
  3. Acutely increases BP if B2 is blocked and a1 vasoconstriction is unopposed
  4. Bronchoconstriction due to B2 blockade (caution in patients with asthma and COPD)
  5. Inhibits lipolysis
  6. Partially inhibits glycogenolysis (caution in diabetic patients as hypoglycemic events may be blunted)
  7. Increases VLDL and decreases HDL
36
Q

Clinical applications for beta antagonists (4)

A
  1. Hypertension (B1 blockade): decreases cardiac output and suppresses renin release
  2. Ischemic heart disease (B1 blockade): negative inotropic and chronotropic effect, decreases cardiac work-load and oxygen demand; reduces the frequency of angina, improves exercise tolerance, and prolongs survival post-MI
  3. Cardiac Arrhythmias (B1 blockade): slows and regulates heart rate
  4. Heart failure (B2 blockade): reduces mortality in patients with CHF, but beneficial effects on myocardial remodeling are unknown
37
Q

Carvedilol and labetalol MOA

A

Nonselective beta antagonists and alpha-1 antagonists.
Hypotensive effects due to alpha-1 blockade and less reflexive tachycardia due to beta blockade.
Decreases systemic vascular resistance.

38
Q

Carvedilol and labetalol ADRs (Common: 3/Serious: 1)

A

Common:

  1. Orthostatic hypotension
  2. Dizziness (labetalol)
  3. Fatigue (labetalol)

Serious:
1. Liver damage (labetalol)

39
Q

Propranolol, nadolol, and timolol MOA

A

Nonselective beta antagonists.
Lowers HR and BP
Reduces renin activity

40
Q

Propranolol, nadolol, and timolol ADRs (Common: 4)

A

Common:

  1. Bradycardia
  2. Fatigue
  3. Dizziness
  4. Sleep disorder
41
Q

Metoprolol, atenolol, betaxolol, and nevivolol MOA

A

Nonselective beta antagonists. Affects B1 > B2.
Lowers HR and BP
Reduces renin activity
May be safer in asthmatics

42
Q

Metoprolol, atenolol, betaxolol, and nevivolol ADRs (Common: 3)

A
  1. Bradycardia
  2. Fatigue
  3. Hypotension
43
Q

Esmolol MOA

A

Nonselective beta antagonist. Affects B1 > B2.
Very brief cardiac beta blockade
Rapid control of BP and arrhythmias
Also treatment for thyroid storm

44
Q

Esmolol ADRs (Common: 2)

A
  1. Bradycardia

2. Hypotension

45
Q

Pindolol, acebutolol, carteolol, and penbutolol MOA

A

Partial agonists of both beta receptors.
Acebutolol affects B1 > B2.
Lowers BP
Modestly lowers HR

46
Q

Pindolol, acebutolol, carteolol, and penbutolol ADRs (Common:2)

A
  1. Fatigue

2. Edema

47
Q

General effects of alpha receptor antagonists (3)

A
  1. Hypotension: decreased a-1 activity-mediated vasoconstriction in arteries and veins
  2. Orthostatic hypotension: decreased BP upon standing
  3. Reflex tachycardia: compensatory increase in heart rate, indirect chronotropic effect (most prominent during a-2 blockade where ultimately the result is increased NE release and increased b-1 activation)
48
Q

Prazosin, terazosin, and doxazosin MOA

A

Selective a-1 blockers.
Blocks the binding of endogenous catecholamines to a-1. Results in vasodilation, decreased BP, and decreased peripheral resistance.

49
Q

Prazosin, terazosin, and doxazosin ADRs (Common: 6/Serious: 1)

A

Common:

  1. Orthostatic hypotension
  2. Dizziness
  3. Headache
  4. Sedation
  5. Palpitations
  6. Nasal congestion

Serious:
1. Pancreatitis

*Marked first-dose often results in postural hypotension

Cardio Block (9 decks)

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