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Pharmacology > Adrenergic Agonists and Antagonists > Flashcards

Adrenergic Agonists and Antagonists Flashcards

1
Q

Epinephrine’s dose dependent effect on different adrenoceptors

A

Functions as a hormone - acts on distant cells after release from adrenal medulla

Agonist at both a and b receptors

At low concentrations: epinephrine activates mainly b1 and b2 receptors

At higher concentrations, a1 effects become more pronounced

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2
Q

Effects of epinephrine at physiological doses

A

Increases heart rate and force of contradiction (b1). Cardiac output increases = oxygen demand of the myocardium increases

Increased renin release (b1)

Increased lipolysis (b1 and b2 effect)

Constricts arterioles in skin and viscera (a1)

Dilates blood vessels of skeletal muscle (b2)

Relaxes bronchial smooth muscle (b2)

Increases liver glycogenolysis

Increased glucagon release from a cells of pancreas (b2)

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3
Q

Effect of epinephrine on blood pressure when given IV in large doses vs low doses

A

Large dose: increase in MAP

  • Increased ventricular contraction (b1) –> increased systolic
  • Increased heart rate (b1) –> this may be opposed by the baroreceptor reflex
  • Vasoconstriction (a1) –> increased diastolic

Small dose: no change in MAP

  • Peripheral vascular resistance decreases due to vasodilation as b2 receptors are more sensitive to epinephrine than a1 –> fall in diastolic
  • Increased contractility due to b1 –> systolic increases
  • Heart rate increases (b1 effect) –> no change in blood pressure so baroreceptor reflex does not kick in
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4
Q

Uses of epinephrine

A

DOC for anaphylactic shock

Acute asthmatic attacks

Cardiac arrest

In local anesthetics: epinephrine increases duration of local anesthesia by producing vasoconstriction at teh site of injection

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5
Q

Norepinephrine specificity to adrenoceptors

A

Agonist at a1, a2 and b1 receptors

Little action on b2 receptors

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6
Q

Cardiovascular effects of IV infusion of norepinephrine

A

Peripheral vasoconstriction (a1)

Increases cardiac contractility (b1)

Increases PVR, systolic pressure and diastolic pressure –> increase in MAP –> triggers baroreceptor reflex –> reflex bradycardia

Cardiac output unchanged or decreases

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7
Q

Uses of norepinephrine

A

To treat shock because it increases vascular resistance and blood pressure

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8
Q

Baroreceptor reflex in response to increase in blood pressure

A

Baroreceptors in carotid sinus are mechanoreceptors that sense changes in blood pressure

1) Inhibits sympathetic activity at –> decrease force of contraction of heart (decreased activation of b1)
2) Stimulates parasympathetic activity –> Decreases heart rate (activation of m2 in atria)

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9
Q

Baroreceptor reflex in response to decrease in blood pressure

A

1) Stimulate sympathetic activity –> increase in force of contraction of heart
2) Inhibit parasympathetic activity –> increase in heart rate (inhibition of m2 receptors in atria)

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10
Q

Effect of atropine pre-treatment + norepinephrine on CVS

A

If atropine is given first, it will block the muscarinic receptors and block the baroreceptor reflex

So norepinephrine will cause increase in PVR, vasoconstriction and increased force of contraction which will increase MAP –> tachycardia

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11
Q

Dopamine selectivity for adrenoceptors

A

Dose dependent activation of a and b receptors. Physiologically activates D1 but in therapeutic doses can activate a1 and b1 too.

D1 > b1 > a1

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12
Q

Cardiovascular effects of low, intermediate and high rates of dopamine infusion

A 
Low rate infusion:
Activates D1 receptors in renal and other vascular beds leading to:
- Vasodilation 
- Increased GFR 
- Increase in renal blood flow 
- Increase in sodium excretion 
Intermediate rate of infusion 
Dopamine activates b1 receptors in heart and causes release of NE from nerve terminals which leads to:
- Increased cardiac output 
- Increased systolic BP
- Unchanged diastolic BP 
- Increased in MAP 
- PVR unchanged 
High rate of infusion:
Dopamine activates vascular a1 receptors:
- Vasoconstriction 
- Increased PVR 
- Increased MAP
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13
Q

Dopamine uses (2)

A

Treatment of severe CHF

Treatment of cariogenic and septic shock
–> Intermediate to high rates of infusion are used to activate b1 and a1 receptors

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14
Q

Fenoldopam MOA and uses

A

D1-receptor selective agonist –> peripheral vasodilation in some vascular beds.

Indicated for in-hospital, short-term management of severe hypertension.

Fenoldopam should be administered by continuous intravenous infusion. A bolus dose should not be used.

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15
Q

Isoproterenol MOA and cardiovascular effects

A

Non-selective b-adrenergic agonist –> activates b1 and b2 receptors

Bronchodilation (b2)

Increases force of contraction and cardiac output (b1) –> systolic BP remains unchanged or rises

Dilates arterioles of skeletal muscle (b2) –> decrease in PVR –> diastolic BP falls

MAP typically falls –> increase in heart rate due to reflex tachycardia

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16
Q

Isoproterenol uses

A

Used in emergencies to stimulate heart rate in patients with bradycardia or heart block

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17
Q

Dobutamine MOA and cardiovascular effects

A

Predominantly b1 agonist

Increases force of contraction very well but has mild effect on heart rate.

Increases myocardial oxygen consumption therefore can be used for the dobutamine stress EKG

Causes mild vasodilation –> small decrease in PVR –> small increase in HR

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18
Q

Dobutamine uses (3)

A

Management of acute heart failure

Management of cardiogenic shock

Used in the dobutamine stress echocardiogram

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19
Q

Albuterol MOA and uses

A

Short acting b2 agonist –> bronchodilator

Management of acute asthma symptoms

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20
Q

Salmeterol and formoterol MOA and uses

A

Long acting b2 agonist –> bronchodilator

Prolonged duration of action (12 hours) due to very high lipid solubility –> slow onset of action

Used in asthma and COPD but cannot be used for prompt relief of acute symptoms

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21
Q

Albuterol, salmeterol and formoterol AE

A

b2 agonists

Tremor, restlessness, apprehension, anxiety

Yes are less likely with inhalation therapy than with parenteral or oral therapy

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22
Q

Phenylephrine MOA, cardiovascular effects

A

a1 agonist

Vasoconstriction –> large increase in PVR –> increased MAP –> reflex bradycardia

Decrease volume of nasal mucosa by decreasing resistance to airflow

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23
Q

Phenylephrine uses

A

a1 agonist

Nasal decongestant: given orally or topically

Mydriasis (but no cycloplegia)

Used to increase BP in hypotension resulting from vasodilation in septic shock or anaesthesia

Used to increase BP and terminate episodes of supra ventricular tachycardia

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24
Q

Clonidine MOA and cardiovascular effects of IV vs oral infusion, AE

A

Partial a2 agonist

Centrally acting antihypertensive

Activates central presynaptic a2 receptors –> reduces release of catecholamines –> reduces sympathetic outflow –> reduces blood pressure

IV infusion of clonidine causes an acute rise in blood pressure, because of activation of postsynaptic a2 adrenoceptors in vascular smooth muscle. This transient vasoconstriction is followed by a more prolonged hypotensive response which results from decreased sympathetic outflow from the CNS. The hypertensive response that follows IV administration is not seen when the drug is given orally.

AE: lethargy, sedation, xerostomia

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25
Q

Methyldopa MOA, effects, uses and AE

A

Taken up by noradrenergic neutrons –> converted to a-methynorepinephrine –> activates central a2 receptors

Decreases blood pressure

DOC for treatment of hypertension in pregnancy

AE: sedation, impaired mental concentration and xerostomia

26
Q

Brimonidine MOA and uses

A

Highly selective a2 agonist

Given ocularly to lower intraocular pressure in glaucoma

Reduces aqueous humour production and increases outflow

27
Q

Amphetemine MOA, effect and uses

A

Releasing agent –> displaces endogenous catecholamines from storage vesicles

Has central stimulatory action

Can increase blood pressure (a agonist action of vasculature) and b-stimulatory effects on heart

Marked behavioral effects including increased alertness, decreased fatigue, depressed appetite, and insomnia

Used to treat ADHD and narcolepsy

28
Q

Methyphenidate MOA, effect and uses

A

Structural analog of amphetamine

Releasing agent –> displaces endogenous catecholamines from storage vesicles

Has central stimulatory action

Used to treat ADHD in children

29
Q

Tyramine contraindications

A

Found in fermented foods such as ripe cheese and Chianti wine

Normally oxidised by MOA

If the patient is taking MAO inhibitors, it can precipitate serious vasopressor episodes.

30
Q

Cocaine MOA

A

Blocks monoamine reuptake into presynaptic terminals. Most potent at blocking the dopamine transporter (DAT); higher concentrations block the serotonin transporter (SERT) and the norepinephrine transporter (NET).

This blockade leads to accumulation of the monoamines in the synaptic space resulting in potentiation and prolongation of their central and peripheral actions.

31
Q

Cocaine effects

A

The sympathetic effects of cocaine include tachycardia, hypertension, pupillary dilation and peripheral vasoconstriction.

The major action of cocaine in the CNS is the inhibition of dopamine reuptake into neurons of the pleasure centers (the limbic system) of the brain –> this produces the intense euphoria

32
Q

Atomoxetine MOA and use

A

Selective inhibitor of norepinephrine reuptake transporter

Used for treatment of ADHD

33
Q

Modafinil MOA and use

A

Psychostimulant –> inhibitors norepinephrine and dopamine transporters –> increases synaptic concentrations of NE, dopamine, serotonin and glutamate and decreases GABA levels

Used for treatment of narcolepsy

34
Q

Ephedrine MOA and PK

A

Mixed acting adrenergic agonists –> induce NE release and active adrenergic receptors

Not a catecholamine - poor substate for COMT and MOA –> long duration of action

Penetrates CNS and good oral absorption

35
Q

Ephedrine uses

A

Mixed acting adrenergic agonist

Uses are pressor agent –> especially during spinal anesthesia

Used as adjunct in myasthenia gravis

36
Q

Pseudoephredine MOA and uses

A

Mixed acting adrenergic agonists –> induce NE release and active adrenergic receptors

One of four ephedine enantiomers

Available OTC as a component of many decongestant mixtures

37
Q

Non-selective a antagonists

A

Phenoxybenzamine - irreversible

Phentolamine - reversible

38
Q

a1 selective antagonists

A

Prazosin
Terazosin
Doxazosin
Tamsulosin

39
Q

Non-selective b blockers

A

Propanolol
Nadolol
Timolol

40
Q

b1 selective antagonist

A

Atenolol
Metoprolol
Esmolol

41
Q

a1 and b-antagonists

A

Labetalol

Carvedilol

42
Q

Partial b-agonist

A

Pindolol

43
Q

Inhibitor of NE synthesis

A

Metyrosine - competitive inhibitor of tyrosine hydroxylase

44
Q

Inhibitors of NE storage

A

Reserpine –> Irreversibly blocks VMAT

Tetrabenazine –> Reversibly blocks VMAT

45
Q

Phenoxybenzamine MOA, uses

A

Irreversible non-selective a-agonist

Unsuccessful for HTN: Blocks a2 which are found pre-synaptically –> increases catecholamine release.

Prevent vasoconstriction –> decreased PVR –> reflex tachycardia

Used in pheochromocytoma

  • prior to surgical removal
  • for chronic management of inoperable tumors
46
Q

Phentolamine MOA and contraindications

A

Reversible non-selective a-agonist

Causes postural hypotension.

Phentolamine-induced reflex cardiac stimulation and tachycardia are mediated by the baroreceptor reflex and by blocking the a2-receptors of the cardiac sympathetic
nerves.

Contraindicated in patients with decreased coronary perfusion.

47
Q

Phentolamine Uses (4)

A

Pheochromocytoma - control of hypertension during prep preparation and surgical excision

Diagnosis of pheochromocytoma - phentolamine blocking test

Prevention of dermal necrosis after extravasation of NE

Hypertensive crisis due to stimulant drug overdose (Cocaine, methamphetamines, MOA inhibitors + tyramine ingestion)

48
Q

CVS effects of prazosin, terazosin, doxazaosin, tamsulosin

A

a1 selective blockers

Lower arterial BP by relaxing both arterial and venous smooth muscle

First dose produces an exaggerated hypotensive response that can result in syncope

First dose must be 1/3 or 1/4 of normal dose

49
Q

a1 blockers uses

A

Hypertension –> but not DOC

DOC for symptom relief from BPH –> relaxation of smooth muscle in bladder neck, prostate capsule and prostatic urethra –> improved urinary flow

50
Q

Tamsulosin MOA

A

Selective antagonist of a1A receptors that predominate in GU smooth muscle

Approved for BPH

Little effect on BP and less likely to cause orthostatic hypertension

51
Q

Uses of b-adrenergic antagonists

A

Hypertension - lower BP by decreasing cardiac output

Glaucoma - Decrease aqueous humor secretion. Decreased IOP (Timolol)

Migraine - effective for prophylaxis of migraine

Hyperthyroidism

Angina Pectoris - decrease the O2 requirement of the heart muscle –> reduce chest main on exertion. Contraindicated in variant angina

Atrial Fibrillation - control ventricular rate

MI - protective effect on myocardium

Performance Anxiety

Essential tremor

52
Q

Non-selective b-blockers effects on CVS, lungs and metabolism

A

Propanolol
Nadolol
Timolol

CVS:

  • Slow heart rate and decrease myocardial contractility
  • Reduction in cardiac output
  • Reduction of renin release from the juxtaglomerular cells of the kidney
  • A central action, reducing sympathetic activity
  • b-blockers don’t induce postural hypotension because a1-adrenoceptors remain unblocked, therefore, normal sympathetic control of the vasculature is maintained

Lungs: blocking b2 can precipitate respiratory crisis in patients with COPD or asthma (causes bronchoconstriction)

Metabolic effects:

  • Decreased glycogenolysis
  • Decreased glucagon secretion
53
Q

Contraindication of non-selective b-blockers

A

Asthma patients

If an insulin-dependent diabetic is to be given propranolol, very careful monitoring of glucose is essential, since pronounced hypoglycemia may occur after insulin injection and if it occurs, the symptoms of hypoglycemia will be masked

54
Q

b1 selective antagonists uses

A

Atenolol
Metoprolol

  • useful in hypertensive patients with impaired pulmonary function
  • useful in diabetic hypertensive patients who are receiving insulin or oral hypoglycemic agents

Esmolol

  • ultra-short acting
  • given IV for rapid control of ventricular rate in patients with atrial fibrillation or atrial flutter
55
Q

Labetalol and carvedilol MOA and uses

A

Competitive a1 and b antagonists (more potent as a b-antagonist)

Labetalol - used in HTN
Carvedilol - used in HTN and CHF, has antioxidant properties

56
Q

Pindolol MOA and uses

A

Partial b-agonist

B-blockers with partial agonist activity may produce smaller reductions in resting heart rate and blood pressure.

May be preferred as antihypertensive agents in individuals with diminished cardiac reserve or a propensity to bradycardia

57
Q

b-blockers AE

A

Non-selective b-blockers:

  • Bronchoconstriction
  • Hypoglycemia

Lipid metabolism:

  • Inhibits release of free FAs from adipose tissue
  • Increase TG and reduce HDL

CNS effects:

  • Sedation
  • Dizziness
  • Lethargy
  • Fatigue
58
Q

Precautions when giving b-blockers

A

Should not be withdrawn abruptly (especially in patients with CAD)

Gradually tapered to avoid acute tachycardia, hypertension and/or schema

AE are due to up regulation of b-receptors

59
Q

a-methyltyrosine MOA and uses

A

Competitive inhibitor of tyrosine hydroxylase –> inhibitor of NE synthesis

Used for management of malignant pheochromocytoma

Used pre-op before resection of pheochromocytoma

60
Q

Reserpine MOA and uses

A

Irreversible blocks VMAT –> vesicles cannot store NE or dopamine –> depletion of NE

Gradual decrease in blood pressure and decreased HR –> slow onset but long duration of action

Used in the past to treat HTN

61
Q

Tetrabenazine MOA and use

A

Reversible inhibitor of VMAT –> vesicles cannot store NE or dopamine

Treatment of chorea associated with Huntington’s Disease

Pharmacology (20 decks)

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