Pharm Exam 4 (Adrenergic Receptor Antagonist)

Front 1

1. What categories are considered adrenergic receptor antagonist?

Back 1

a. Alpha Blockers
b. Beta Blockers

Front 2

1. What drugs are considered alpha-1 specific blockers?

Back 2

a. Doxazosin
b. Prazosin
c. Terazosin
d. Alfuzosin
e. Tamsulosin

Front 3

1. What drugs are considered Alpha 1 & 2 Blockers?

Back 3

a. Phenoxybenzamine
b. Pheontolamine

Front 4

1. What drugs are considered Beta 1 blockers?

Back 4

a. Acebutol
b. Atenolol
c. Esmolol
d. Metoprolol

Front 5

1. What drugs are considered Beta 1 & 2 Blockers?

Back 5

a. Nadolol
b. Pinadolol
c. Propanolol
d. Timolol

Front 6

1. What drugs are alpha and Beta blockers

Back 6

a. Carvedilol
b. Labetalol

Front 7

1. How do Alpha blockers decrease Bp?

Back 7

a. By decreasing peripheral resistance

Front 8

1. How do beta blockers decrease BP

Back 8

a. By decreasing Cardiac Output

Front 9

1. Of the alpha blockers which class affects the HR

Back 9

a. A2 receptors affect HR because they affect the Autoreceptors
b. Which causes increase in cAMP
c. Which causes increased release of NE
d. Which causes tachycardia

Front 10

1. What is the normal function of the autoreceptor

Back 10

a. The autoreceptor is the alpha 2 receptor
b. It is found on the presynaptic membrane
c. Normally NE would release from the synapse and some would stimulate the A2 receptor,
d. Stimulation of the A2 receptor leads to inhibition of the formation of cAMP
e. Inhibition of the formation of cAMP decreases the formation of NE

Front 11

1. MOA of Doxazosin

Back 11

a. Competitive Alpha -1 specific blocker

Front 12

1. Clinical use of Doxazosin

Back 12

a. Essential HTN
b. It is an A1 blocker so it does not affect HR like the A1 &2 blockers

Front 13

1. Adverse effects of Doxazosin

Back 13

a. First dose phenomenon – marked postural Hypotension and syncope 30-90 minutes after the first dose
b. Orthostatic HTN
c. Headache
d. Dizziness
e. Fainting
f. Reflex tachycardia
g. Edema

Front 14

1. DOA of Doxazosin

Back 14

a. 20 hours

Front 15

1. MOA of Prazosin

Back 15

a. Competitive Alpha -1 specific blocker

Front 16

1. Clinical use of Prazosin

Back 16

a. Essential HTN
b. It is an A1 blocker so it does not affect HR like the A1 &2 blockers

Front 17

1. Adverse effects of Prazosin

Back 17

a. First dose phenomenon – marked postural Hypotension and syncope 30-90 minutes after the first dose
b. Orthostatic HTN
c. Headache
d. Dizziness
e. Fainting
f. Reflex tachycardia
g. Edema

Front 18

1. DOA of Prazosin

Back 18

a. 12 hours
b. This is the shortest DOA of the A1 blockers

Front 19

1. MOA of terazosin

Back 19

a. Competitive Alpha -1 specific blocker

Front 20

1. Clinical use of terazosin

Back 20

a. Essential HTN
b. It is an A1 blocker so it does not affect HR like the A1 &2 blockers

Front 21

1. Adverse effects of terazosin

Back 21

a. First dose phenomenon – marked postural Hypotension and syncope 30-90 minutes after the first dose
b. Orthostatic HTN
c. Headache
d. Dizziness
e. Fainting
f. Reflex tachycardia
g. Edema

Front 22

1. DOA of terazosin

Back 22

a. 30 hours

Front 23

1. MOA of Alfuzosin

Back 23

a. Competitive AL blocker

Front 24

1. Clinical use of Alfuzosin

Back 24

a. Uteroselective specific (used to treat urinary symptoms)
b. Does not affect BP or HR

Front 25

1. DOA of Alfuzosin

Back 25

a. 48 hours

Front 26

1. MOA of Tamsulosin

Back 26

a. Competitive A1 selective antagonist

Front 27

1. Clinical use of Tamsulosin

Back 27

a. Uteroselective specific (used to treat urinary symptoms)
b. Does not affect BP or HR

Front 28

1. DOA of Tamsulosin

Back 28

a. 24 hours

Front 29

1. MOA of Phenoxybenzamine

Back 29

a. Noncompetitive Alpha 1&2 blocker
b. This is the only noncompetitive Alpha blocker

Front 30

1. Clinical use of Phenoxybenzamine

Back 30

a. HTN in pheochromocytoma (adrenergic secreting tumor)
b. Hypertensive emergencies

Front 31

1. Adverse effects of Phenoxybenzamine

Back 31

a. Postural HTN (accompanied with reflex tachacardia and cardiac arrhythmias)
b. Sexual dysfunction

Front 32

1. How does Phenoxybenzamine differ from other alpha blockers since it is a non competitive antagonist

Back 32

a. It will decrease the maximum effect an alpha agonist can achieve (decreases the agonists efficacy)
b. With competitive antagonist they can eventually be overcome if the agonists concentration is high enough

Front 33

1. DOA of Phenoxybenzamine

Back 33

a. 3-4 days

Front 34

1. MOA of Pheontolamine

Back 34

a. Competative Alpha 1&2 blocker

Front 35

1. Clinical use of Pheontolamine

Back 35

a. HTN in pheochromocytoma (adrenergic secreting tumor)
b. Hypertensive emergency
c. Necrosis and ischemia after injection of an alpha agonist

Front 36

1. Adverse effects of Pheontolamine

Back 36

a. Hypotension
b. Reflex tachacardia
c. Cardiac arrhythmi9a
d. Ischemic heart events (AMI)
e. GI stimulation may result in abdominal pain, nausea and exacerbation of peptic ulceras

Front 37

1. DOA of Pheontolamine

Back 37

a. IV = 15 min
b. IM = 3-7 hours

Front 38

1. What is an ISA

Back 38

a. Partial agonist

Front 39

1. Which drugs have ISA activity?

Back 39

a. Acebutol
b. Pinadolol

Front 40

1. What is a MSA

Back 40

a. Membrane stabilizing activity
b. Blocks Na+ channels in the heart…may have bad side effects if the pt has conduction problems already

Front 41

1. Which drugs have MSA activity

Back 41

a. Acebutol
b. Metoprolol
c. Pinadolol
d. Propanolol
e. Labetalol

Front 42

1. Clinical uses of BB

Back 42

a. Reduction in the frequency of migraine
b. Reduction in somatic manifestation of anxiety
c. Reduction in essential tremor
d. Glaucoma (reduce pressure)
e. Hyperthyroidism (decrease HR, BP, anxiety, tremors)
f. HTN (Often used with a diuretic and vasodilator)
g. Ischemic heart disease (Reduce frequency of angina episodes)
• Tx is prophylactically
• Reduces frequency not severity
h. Improves exercise intolerance
i. Increase stroke volume in some patients with obstructive cardiomyopathy
j. Useful in dissecting aortic aneurysms to decrease the rate of development (by decreasing systolic pressure)

Front 43

1. Adverse effects of BB

Back 43

a. Metabolism
• Blunt recognition of hypoglycemia (pt does not recognize symptoms that their glucose levels have dropped because the symptoms are blocked)(2/3 of the window time they would normally would have to get sugar in their system is gone by the time they have onset of symptoms)
b. Cardiovascular system
• May cause or exacerbate heart failure in patients with compensated heart failure, AMI, or cardiomegaly.
• Bradycardia
• in some pts with partial or complete AV conduction defects, life threatening bradyarrhythmias may occur
• a s a RULE: start with extremely low doses of BB when tx cardiac pts. Titrate up.
• Abrupt discontinuation after long term tx can exacerbate angina and may increase risk of sudden death

Front 44

1. MOA of acebutolol

Back 44

a. B1 blocker
b. ISA
c. MSA

Front 45

1. Pharmacological effects of acebutolol

Back 45

a. Decrease HR
b. Decrease cardiac O2 demand
c. Decrease BP

Front 46

1. Clinical use of acebutolol

Back 46

a. HTN
b. Not for migraines (b/c it is an ISA)

Front 47

1. Elimination half life of Acebutolol

Back 47

a. 10-12 hours

Front 48

1. MOA of Atenolol

Back 48

a. B1 blocker

Front 49

1. Pharmacological effects of Atenolol

Back 49

a. Decrease HR
b. Decrease cardiac O2 demand
c. Decrease BP

Front 50

1. Clinical use of Atenolol

Back 50

a. Hyperthyroidism
b. Essential tremor
c. HTN
d. Does not drop BP as bad as acebutolol so if you don’t want to drop the BP use this drug over acebutolol
e. CHF
f. Angina

Front 51

1. How does Atenolol affect patient with CHF

Back 51

a. Decreases cardiac contractility
b. Decreases HR (negative ionotropic)
c. May or may not decrease afterload
d. Increases Cardiac output and LV ejection fraction
e. Inhibits cardiac remodeling ***
a. BB do have a negative ionotreopic effect (which you wouldn’t think to be optimal in CHF) However, these drugs have been shown to reduce mortality in patients with class II and class III heart failure
f. Requires 2-3 months for improvement
g. Start with low dose and gradually work upward

Front 52

1. Elimination half life of Atenolol

Back 52

a. 6-7 hours

Front 53

1. MOA of Esmolol

Back 53

a. B1 blocker

Front 54

1. Route of administration of Esmolol

Back 54

a. IV Only

Front 55

1. Clinical use of Esmolol

Back 55

a. Acute supraventricular tachacardia (antiarrhythmic)
b. Hypertensive emergency

Front 56

1. Elimination half life of Esmolol

Back 56

a. 10 min

Front 57

1. Onset of action of Esmolol

Back 57

a. <5 min

Front 58

1. DOA of Esmolol

Back 58

a. 20-30 min

Front 59

1. How is Esmolol used as an antiarrhythmic drug?

Back 59

a. It is a Class II antiarrhythmic
b. Used to tx supraventricular and ventricular arrhythmias
c. Reduce sudden death in myocardial infarction
d. Class II drugs are the only drugs that reduce mortality in asymptomatic patients (or not increase mortality rate)
a. Class II and class Iv drugs slow phase 5 depolarization in the SA node and increase the PP interval. They also slow the AV node conduction velocity and increase the PR interval.

Front 60

1. MOA of Metoprolol

Back 60

a. B1 blocker
b. MSA

Front 61

1. Clinical use of Metoprolol

Back 61

a. HTN
b. Angina
c. AMI
d. Heart failure
e. Antiarrhythmic

Front 62

1. Elimination half life of Metoprolol

Back 62

a. 3-4 hours

Front 63

1. Onset of action of Metoprolol

Back 63

a. 1 hour

Front 64

1. Duration of action of Metoprolol

Back 64

a. 15 hours

Front 65

1. How is Metoprolol used in CHF

Back 65

a. Decreases cardiac contractility
b. Decreases HR (negative ionotropic)
c. May or may not decrease afterload
d. Increases Cardiac output and LV ejection fraction
e. Inhibits cardiac remodeling ***
a. BB do have a negative ionotreopic effect (which you wouldn’t think to be optimal in CHF) However, these drugs have been shown to reduce mortality in patients with class II and class III heart failure
f. Requires 2-3 months for improvement
g. Start with low dose and gradually work upward

Front 66

1. How is Metoprolol used as an antiarrhythmic

Back 66

a. It is a Class II antiarrhythmic
b. Used to tx supraventricular and ventricular arrhythmias
c. Reduce sudden death in myocardial infarction
d. Class II drugs are the only drugs that reduce mortality in asymptomatic patients (or not increase mortality rate)
a. Class II and class Iv drugs slow phase 5 depolarization in the SA node and increase the PP interval. They also slow the AV node conduction velocity and increase the PR interval.

Front 67

1. MOA of Nadolol

Back 67

a. B1 and B2 blocker

Front 68

1. Pharmicological effects of Nadolol

Back 68

a. Decrease HR
b. Decrease cardiac O2 demand
c. Decrease BP

Front 69

1. Clinical use of Nadolol

Back 69

a. HTN
b. Angina
c. Migraine Headaches

Front 70

1. Elimination half life of Nadolol

Back 70

a. 15-20 hours

Front 71

1. MOA of Pinadolol

Back 71

a. B1 and B2 blocker
b. ISA
c. MSA

Front 72

1. Pharmacological effects of Pinadolol

Back 72

a. Decrease HR
b. Decrease cardiac O2 demand
c. Decrease BP

Front 73

1. Clinical use of Pinadolol

Back 73

a. HTN

Front 74

1. Contraindication of Pinadolol

Back 74

a. Asthma

Front 75

1. Elimination Half life of pinball

Back 75

a. 3-4 hours

Front 76

1. MOA of Propanolol

Back 76

a. B1 and B2 blocker
b. MSA

Front 77

1. Pharmacological effects of Propanolol

Back 77

a. Decrease HR
b. Decrease cardiac O2 demand
c. Decrease BP

Front 78

1. ROA for Propanolol

Back 78

a. IV
b. Oral

Front 79

1. Clinical use for Propanolol

Back 79

a. Hyperthyroidism
b. HTN
c. Angina pectoris
d. Cardiac arrhythmias
e. Hypertrophic subaortic stenosis
f. Essential tremors
g. Migraines
h. Acute thyrotoxicosis
i. AMI
j. Phechrommocytoma

Front 80

1. Elimination half life of Propanolola.

Back 80

4-6 hours

Front 81

1. DOA of Propanolol

Back 81

a. 4 hours

Front 82

1. If a BB is needed during pregnancy use

Back 82

a. Propanolol
b. Has to do with fetal development

Front 83

1. How is Propanolol used as an antiarrhythmic?

Back 83

a. It is a Class II antiarrhythmic
b. Used to tx supraventricular and ventricular arrhythmias
c. Reduce sudden death in myocardial infarction
d. Class II drugs are the only drugs that reduce mortality in asymptomatic patients (or not increase mortality rate)
a. Class II and class Iv drugs slow phase 5 depolarization in the SA node and increase the PP interval. They also slow the AV node conduction velocity and increase the PR interval.

Front 84

1. MOA of Timolol

Back 84

a. B and B2 blocker

Front 85

1. Pharmacological effects of Timolol

Back 85

a. Decrease HR
b. Decrease cardiac O2 demand
c. Decrease BP
d. ***Unlike other BB it also decreases intraocular pressure

Front 86

1. Clinical use of Timolol

Back 86

a. HTN
b. Migraines
c. Glaucoma (reduces secretion of aqueous humor)

Front 87

1. Elimination half life of Timolol

Back 87

a. 4—6 hours

Front 88

1. MOA of Carvedilol

Back 88

a. B1, B2 and A1 blocker

Front 89

1. Pharmacological effects of Carvedilol

Back 89

a. Vasodilation
b. Decrease HR
c. Decrease BP
d. Increase cardiac output

Front 90

1. Clinical use of Carvedilol

Back 90

a. HTN
b. Heart failure (cardioprotective properties)
c. Antiarrhythmic drug

Front 91

1. How us cardedilol used to tx CHF

Back 91

a. ***No effect on cardiac contractility
b. ***May or may not decrease HR
c. ***Decreases afterload
d. Increases cardiac output and LV ejection fraction
e. BB do have a negative ionotreopic effect (which you wouldn’t think to be optimal in CHF) However, these drugs have been shown to reduce mortality in patients with class II and class III heart failure
a. Requires 2-3 months for improvement
b. Start with low dose and gradually work upward
c. Inhibits cardiac remodeling
d. ***Carvedilol has been shown to decrease mortality rate and improve ejection fraction

Front 92

1. Elimination half life of Carvedilol

Back 92

a. 6-8 hours

Front 93

1. How is Carvedilol used as an antiarrhythmic drug?

Back 93

a. It is a Class II antiarrhythmic
b. Used to tx supraventricular and ventricular arrhythmias
c. Reduce sudden death in myocardial infarction
d. Class II drugs are the only drugs that reduce mortality in asymptomatic patients (or not increase mortality rate)
a. Class II and class Iv drugs slow phase 5 depolarization in the SA node and increase the PP interval. They also slow the AV node conduction velocity and increase the PR interval.

Front 94

1. MOA of Labetalol

Back 94

a. B1,B2, and A1 blocker
b. MSA

Front 95

1. Pharmacological effects of Labetalol

Back 95

a. Vasodilation
b. Decrease HR
c. Decrease BP

Front 96

1. Clinical use of Labetalol

Back 96

a. HTN
b. Is is a MSA so it wont be used in CHF

Front 97

1. Elimination half life of Labetalol

Back 97

a. 6-8 hours