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Block 2: Pharmacology > Lecture 2 > Flashcards

Lecture 2 Flashcards

1
Q

(Adrenergic Receptors)
Adrenergic Receptors?

A

(Adrenoceptors)
-Class of G Protein-Coupled Receptors (GPCRs)
-Targets of catecholamines (norepinephrine and epinephrine)
-Stimulate sympathetic nervous system
-Activate different G protein

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2
Q

(Adrenergic Receptors)
Smooth Muscle Contraction?

A

A1 –> Gq –> Ca

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3
Q

(Adrenergic Receptors)
Inhibition of transmitter release?

A

A2 –> Gi –> Inhibit cAMP

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4
Q

(Adrenergic Receptors)
Heart Muscle Contraction Smooth Muscle Relaxation Glycogenolysis?

A

B –> Gs –> Increase cAMP

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5
Q

(Adrenergic Receptors)
50% of Drugs target?

A

GPCRs

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6
Q

(Adrenergic Receptors: Most Physiologically Relevant Effects)
a1?

A

-Tissue (most vascular smooth muscle, Heart, Prostate, Pupillary Dilator Muscle)
-G Protein (Gq)
-Effect (contraction, increased force, contraction, contraction (pupil dilation))

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7
Q

(Adrenergic Receptors: Most Physiologically Relevant Effects)
a2?

A

-Tissue (postsynaptic CNS, presynaptic ANS)
-G Protein (Gi)
-Effect (Multiple decreased SNS tone, decreased NT release)
(a2 = decreased sympathetic tone)

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8
Q

(Adrenergic Receptors: Most Physiologically Relevant Effects)
B1?

A

-Tissue (Heart, Juxtaglomerular cells)
-G Protein (Gs, Gi)
-Effect (increased force and rate, increased renin release) (retain fluid)

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9
Q

(Adrenergic Receptors: Most Physiologically Relevant Effects)
B2?

A

-Tissue (skeletal muscle blood vessels, bronchial smooth muscle, liver, uterus)
-G Protein (Gs, Gi)
-Effect (relaxation, relaxation (asthma), glycogenolysis and gluconeogenesis (increases blood glucose), relaxation)

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10
Q

(Adrenergic Receptors: Most Physiologically Relevant Effects)
B3?

A

-Tissue (adipose tissue (fat cells))
-G Protein (Gs)
-Effect (increased lipolysis)

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11
Q

Alpha 1 (Gq)?

A

(Smooth Muscle Contraction)
-Blood Vessels
-Pupils
-Pylorus
-Urinary Sphincter
-Prostate

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12
Q

Alpha 2 (Gi)?

A

(Inhibitory)
Presynaptic Nerve Terminals

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13
Q

Beta 1 (Gs)?

A

Gs coupled receptors, increase cAMP

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14
Q

Beta 2 (Gs)?

A

(Smooth Muscle Relaxation)
Gs coupled receptors, increase cAMP

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15
Q

Adrenergic Synapse Location?

A

-Dilate pupils
-Increase HR, contractility
-Increase respiratory rate (dilates bronchi)
-Inhibits digestion
-Diverts blood flow to muscles (by vasoconstriction/dilation)
-Inhibits urination

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16
Q

(Drugs to Know and Love #1: Agonists)
a1 Agonist?

A

Phenylephrine (vasoconstriction)

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17
Q

(Drugs to Know and Love #1: Agonists)
a2 Agonist?

A

-Clonidine (decrease sympathetic tone)
-Methyldopa (Gi = inhibitory)

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18
Q

(Drugs to Know and Love #1: Agonists)
Non-selective b Agonist (B1 + B2) ?

A

-Isoproterenol
-Dobutamine
(B1= increases HR)
(B2 = bronchodilator + smooth muscle dilation)

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19
Q

(Drugs to Know and Love #1: Agonists)
b2 Agonist ?

A

Albuterol (dilates bronchial SM)

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20
Q

(Drugs to Know and Love #2: Antagonists)
Non-selective a antagonist?

A

Phentolamine (vasodilation, increase HR)

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21
Q

(Drugs to Know and Love #2: Antagonists)
a1 antagonist?

A

Prazosin

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22
Q

(Drugs to Know and Love #2: Antagonists)
Non-selective b antagonist (b blockers) ?

A

Propranolol

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23
Q

(Drugs to Know and Love #2: Antagonists)
B = ?

A

-olol

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24
Q

(Drugs to Know and Love #2: Antagonists)
b1 antagonist (b blockers) ?

A

-Atenolol
-Metoprolol
(B1 antagonist = decrease HR)

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25
Q

(Drugs to Know and Love #2: Antagonists)
B1 antagonist ?

A

Decrease HR

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26
Q

(Drugs to Know and Love #2: Antagonists)
B2 antagonist ?

A

Bronchoconstriction

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27
Q

(Drugs to Know and Love #2: Antagonists)
Mixed a1/B antagonists?

A

-Carvedilol
-Labetalol

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28
Q

(Drugs to Know and Love #2: Antagonists)
LOL = ?

A

Funny because it has both

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29
Q

Drugs to Know and Love #2: Antagonists?

A

Opposite Effect

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30
Q

(a1 Selective Agonists)
(Epinephrine vs. Phenylephrine)
Epinephrine?

A

-Oral usability: completely ineffective
-Duration of action: short
-CNS penetration: poor penetration

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31
Q

(a1 Selective Agonists)
(Epinephrine vs. Phenylephrine)
Phenylephrine?

A

-Phenylephrine is more stable, and does not get broken down so fast

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32
Q

(a1 Selective Agonists)
Epinephrine vs. Phenylephrine?

A

-Selectivity
-COMT Sensitivity (catechol-o-methyl transferase) (degrades catecholamines)

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33
Q

a1 Agonists: Mechanisms of Action and Pharmacology?

A

-Stimulation of a1
-Induce contraction of smooth muscle
-Primary effect- vasoconstriction of most vascular smooth muscle
-Decrease mucosal edema
(do not give if you have high BP)

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34
Q

a1 Selective Agonists: Clinical Use?

A

-Nasal Congestion (decreases inflammation markers reaching tissue)
-Hypotension (vasoconstriction increase BP)
-Hemorrhoids (vasoconstriction stop inflammation marker to swollen/inflamed vein)
-To dilate pupils

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35
Q

Phenylephrine?

A

-Type: A1 Agonist
-Effect: Vasoconstriction
-Tx: Nasal Congestion, Hypotension, Hemorrhoids
-SE: Angina, Bradycardia, HTN, Necrosis
-Contraindication: Fib, Tachy, HTN
-Interactions: MAOI

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36
Q

a1 Agonist (phenylephrine): Pharmacokinetics, Adverse Effects, Contraindications, Interactions?

A

-Longer duration of action than catecholamines. Metabolized by MAO (intestine, liver or plasma)
-Angina, anxiety, bradycardia, hypertension, tissue necrosis (similar to Epi)
-Ventricular fibrillation/tachycardia, hypertension (raises BP so think any heat issue don’t give)
-MAO inhibitors (breaks down NE

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37
Q

(a1 Agonist (phenylephrine): Pharmacokinetics, Adverse Effects, Contraindications, Interactions)
If you increase A1 agonists, you wouldn’t want to?

A

Inhibit NE via MAO inhibitors because then it would cause increased vasoconstriction

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38
Q

a2 Selective Agonists?

A

-Clonidine
-Methyldopa (SAFE WITH PREGNANCY)
(Postsynaptic CNS (Gi) Multiple (decreased SNS tone))
(Presynaptic ANS (Gi) Decreased NT release)

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39
Q

(a2 Selective Agonists)
Decrease SNS?

A

Parasympathetic Effects

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40
Q

a2 Agonists: Mechanisms of Action and Pharmacology?

A

-Stimulation of a2 receptors in medulla has sympathetic effects (no reflex tachycardia)
-Decrease overall NE release through stimulation of pre-synaptic receptors
-Net Effect (decreased BP, HR, CO)

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41
Q

(a2 Agonists: Mechanisms of Action and Pharmacology)
Still an Agonist?

A

Activated Gi that’s inhibitory (NOT an Antagonist)

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42
Q

a2 Agonists: Clinical Use?

A

-Hypertension (decreases SNS so less epilepsy = decreases BP) (Clonidine more potent and used more often than methyldopa but pregnancy category C (risk cannot be ruled out))
-Methyldopa first-line therapy for hypertension during pregnancy (“pro drug” that needs to be activated so safer)
-Clonidine: several CNS disorders including ADHD, mitigate drug withdrawal, severe pain

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43
Q

(a2 Agonists: Clinical Use)
Clonidine?

A

More potent but not used during pregnancy
(several CNS disorders including ADHD, mitigate drug withdrawal, severe pain)

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44
Q

(a2 Agonists: Clinical Use)
Methyldopa?

A

First-Line Therapy for hypertension during pregnancy
(“pro drug” that needs to be activated so safer)

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45
Q

(Clonidine vs. a-methyldopa)
Clonidine is effective both in?

A

Periphery and in Brain
(effect everywhere with does)

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46
Q

(Clonidine vs. a-methyldopa)
Alpha-methyldopa is effective ONLY in?

A

Brain
(readily enter Brain where it is metabolized to active compound a-methyl-norepinephrine (a2 agonist))
(needs to be activated in Brain)

47
Q

(a2 Agonists: Adverse Effects, Contraindications, Interaction)
Clonidine?

A

-Dry mouth, sedation, depression, orthostatic, hypotension
-Depression (caution: sudden withdrawal precipitates hypertensive crisis)
(decrease SNS, think depression, sedation, hypotension)

48
Q

(a2 Agonists: Adverse Effects, Contraindications, Interaction)
Methyldopa?

A

-Sedation, depression, tolerance
-Depression (MAO inhibitory therapy (would increase NE))

49
Q

(a2 Agonists: Adverse Effects, Contraindications, Interaction)
Do NOT give Clonidine if?

A

Depressed

50
Q

(a2 Agonists: Adverse Effects, Contraindications, Interaction)
If you decrease SNS?

A

Depression, Sedation and Hypotension

51
Q

(Non-Selective B Agonists)
Isoproterenol?

A

-MOA: agonist at both B1 and B2 receptors (potent vasodilator (B2), bronchodilator (B2), positive inotropic (B1) and chronotropic agent)
-Clinical Use: Cardiac arrest, AV block, bradycardia, tornado de pointes
-Pharmacokinetics: metabolized by COMT and MAO (like Epi)
-Adverse Effects: arrhythmias common

52
Q

(Non-Selective B Agonists)
What is NOT the first-line agent for use in bronchospasm during anesthesia or shock?

A

Isoproterenol

53
Q

(Cardiovascular Effects od Adrenergic Agonists)
Isoproterenol?

A

-Increase B1 = increase force and pulse rate
-Decrease resistance, B2

54
Q

(Other B Agonists)
Dobutamine (racemic mixture)?

A

-Formerly considered B1 selective
-Stimulates B1 receptors on Heart but produces greater inotropic than chronotropic effect
-There’s some B2 and a1 stimulation as well as a1 inhibition resulting in no net change in total peripheral resistance
-Inotrope

55
Q

B2 Selective Agonists?

A

-Albuterol (short-action-acute bronchospasm)
-Salmeterol (longer acting-maintenance)
-Metaproterenol (short-action-acute bronchospasm)
-Terbutaline (short-action)

56
Q

B2 Agonists: Mechanism of Action and Pharmacology?

A

-Relaxation of bronchial smooth muscle
-Relaxation of vascular smooth muscle (particularly in skeletal muscle vasculature)
(Decrease resistance to breathe in lung)
-Stimulation of glycogenolysis (may lead to hyperglycemia (DON’T GIVE TO DIABETES) (B2 in liver)
-Relaxation of uterine smooth muscle

57
Q

B2 Agonists: Clinical Use?

A

-Asthma
-Acute bronchospasm
-Bronchospasm prophylaxis
-Premature Labor

58
Q

B2 Agonists: Adverse Effects, Contraindication, Interactions?

A

-Tremors
-Stimulation (CNS)
-Palpitations
-Tachycardia (direct and reflex) (reflex = decrease in BP so response is increasing HR (Tachy))

59
Q

B2 Agonists: Adverse Effects, Contraindication, Interactions?

A

-Tremors
-Stimulation (CNS)
-Palpitations
-Tachycardia (direct and reflex) (reflex = decrease in BP so response is increasing HR (Tachy))

60
Q

(a-Adrenoceptors Antagonist)
Non-selective a antagonist?

A

Phentolamine

61
Q

(a-Adrenoceptors Antagonist)
a1-selective antagonist?

A

Prazosin

62
Q

a Antagonists: Mechanisms of Action and Pharmacology?

A

-Block a1 or both a1 and a2 receptors
-Decrease peripheral vascular resistance (dilation)
-Vasodilation triggers increased HR (reflex Tachy) (HR increase more pronounced with mixed a1/a2 (antagonists because of diminished a2 feedback in Heart))

63
Q

(a Antagonists: Mechanisms of Action and Pharmacology)
HR increase greater in Phentolamine than?

A

Prazosin

64
Q

(a Antagonist: Pharmacodynamics)
A1 Antagonist?

A

Vasodilation (decrease BP, increase HR)

65
Q

(a Antagonist: Pharmacodynamics)
A2 Antagonist?

A

Increase NE, Increase sympathetic

66
Q

(a Antagonists: Clinical Use)
Non-selective a antagonist?

A

-Drug Name: Phentolamine
-Clinical Use: Anesthesia reversal, Extravasation of a agonist, Pheochromocytoma (tumor at adrenal gland, high BP)

67
Q

(a Antagonists: Clinical Use)
a1 antagonist?

A

-Drug Name: Prazosin
-Clinical Use: Hypertension, Benign prostatic hyperplasia (BPH)

68
Q

(a Antagonists: Clinical Use)
a1 antagonist?

A

-Drug Name: Prazosin
-Clinical Use: Hypertension, Benign prostatic hyperplasia (BPH)

69
Q

(a Antagonists: Adverse Effects Adverse Effects, Contraindications, Interactions)
Phentolamine?

A

-Adverse Effects: tolerance, Na/H2O retention when used alone for HTN, dizziness, hypotension, postural hypotension, reflex tachycardia, mitosis, nasal stuffiness, inhibitor of ejaculation
-Precautions/Contraindications: angina, myocardia infarction
-Interactions: None

70
Q

(a Antagonists: Adverse Effects Adverse Effects, Contraindications, Interactions)
Prazosin?

A

-Adverse Effects: tolerance, Na/H2O retention when used alone for HTN, dizziness, hypotension, postural hypotension, reflex tachycardia, mitosis, nasal stuffiness, inhibitor of ejaculation
-Interactions: Beta-blocker withdrawal

71
Q

(b-Adrenoceptor Antagonist)
Non-selective b antagonist (1st generation) B1/B2?

A

Propranolol

72
Q

(b-Adrenoceptor Antagonist)
b1 antagonist (2nd generation)?

A

-Atenolol
-Metoprolol

73
Q

(b-Adrenoceptor Antagonist)
Mixed a1/b antagonists (3rd generation)?

A

-Carvedilol
-Labetalol (HTN EMERGENCY)

74
Q

b Antagonists: Mechanisms of Action and Pharmacology?

A

-Block b, or both b and b2 receptors
-Cardiovascular
-CNS
-Eye
(opposite of SNS, so think Parasympathetic)

75
Q

(b Antagonists: Mechanisms of Action and Pharmacology)
Cardiovascular?

A

-Have negative inotropic, dromotropic (conduction speed) and chronotropic effects
-Decrease renin release
-Block of b2 may increase peripheral resistance (mild)

76
Q

(b Antagonists: Mechanisms of Action and Pharmacology)
CNS?

A

-Anxiolytic
-CNS effects may contribute to decrease HTN

77
Q

(b Antagonists: Mechanisms of Action and Pharmacology)
Eye?

A

-Decrease aqueous humor production
-Decrease intraocular pressure

78
Q

(b Antagonists: Mechanisms of Action and Pharmacology)
Lungs?

A

Bronchoconstriction- “spasm” (more prominent in b1,b2 than b1-selective)

79
Q

(b Antagonists: Mechanisms of Action and Pharmacology)
Metabolic?

A

-Lipolysis and glycogenolysis are inhibited
-Inhibit recovery from hypoglycemia (more prominent in b1/b2 than b1-selective)

80
Q

b2 Antagonist?

A

(skeletal muscle only)
In skeletal muscle BV and broncho constriction

81
Q

b1 Antagonist?

A

Decrease HR, Renin release

82
Q

(Non-Selective b Antagonists: Clinical Use)
Non-selective b antagonist?

A

-Drug Name: Propranolol
-Clinical Use: angina, cardiac arrhythmias, hypertension, migraine prophylaxis, myocardial infarction prophylaxis, pheochromocytoma, post-myocardial infarction, thyrotoxicosis, essential tremor

83
Q

When are b blockers first-line therapy for hypertension?

A

-Ischemic Heart Disease
-Recent STEMI or non-STEMI (ST-Elevation Myocardial Infarction)
-Left Ventricular Systolic Dysfunction
-Some Arrhythmias
(if there’s a history of these THEN use beta blockers as first-line use)

84
Q

(Non-selective b Antagonists: Adverse Effects Adverse Effects, Contraindications, Interactions)
(Propranolol)
Adverse Effects?

A

Dizziness, fatigue, lethargy, sinus bradycardia and hypotension, exacerbation of asthma, dyspnea, or bronchospasm, diabetes mellitus, hypertriglyceridemia and decrease plasma HDL

85
Q

(Non-selective b Antagonists: Adverse Effects Adverse Effects, Contraindications, Interactions)
(Propranolol)
Precautions/Contraindications?

A

-Diabetes mellitus, hyperthryoidism
-Pregnancy category C
-Asthma, AV block, bradycardia, cariogenic shock, sick sinus syndrome

86
Q

(Non-selective b Antagonists: Adverse Effects Adverse Effects, Contraindications, Interactions)
(Propranolol)
Interactions?

A

Drugs that depress AV conduction or have negative inotropic actions, clonidine withdrawal

87
Q

Withdrawal Syndrome?

A

Rebound hypertension, MI, cardiac arrhythmias and panic attacks can result from sudden withdrawal

88
Q

B Receptor get sensitive so a sudden withdrawal from medications can be?

A

Dangerous
(beta receptors get sensitive so you increase NE)

89
Q

(b1 Antagonists)
b1 antagonist?

A

-Atenolol
-Metoprolol
(Heart, Juxtaglomerular cells) (Gs, Gi) (increased force and rate, increase renin release)

90
Q

b1 Antagonists: Mechanisms of Action and Pharmacology?

A

-Similar cardiovascular actions as non-selective antagonists
-Since they have no b2 activity, they’re preferred in patients with bronchospasm, diabetes and peripheral vascular disease

91
Q

(b1 Antagonists: Mechanisms of Action and Pharmacology)
History of Diabetes and Asthma?

A

Beta

92
Q

(b1 Antagonists: Clinical Use)
(b1 Antagonist)
Atenolol?

A

-Acute MI
-angina
-Hypertension

93
Q

(b1 Antagonists: Clinical Use)
(b1 Antagonist)
Metoprolol?

A

-Same as atenolol
-heart failure (1 of 3 recommended) (long-acting form: succinate for SUCCESS)
-Longer Half Life, MI usually in morning due to catecholamine surge. Can give to patient at night and they will wake up before next dose

94
Q

(b1 Antagonists: Clinical Use)
(b1 Antagonist)
Not safe for?

A

Pregnancy

95
Q

b1 Antagonists: Adverse Effects, Contraindications, Interactions?

A

-Similar to non-selective b antagonists
-Less effect on glucose levels
-Asthma and bronchospasm are no longer absolute contraindication, but b1 antagonists should be used with great caution in these individuals
-Atenolol-Pregnancy category D (intrauterine growth restriction) NO PREGNANCY

96
Q

(Mixed a1/b-Adrenoceptor Antagonist)
Mixed a1/b antagonists?

A

-Carvedilol
-Labetalol

97
Q

A1?

A

Vasodilation

98
Q

B1?

A

Decrease HR

99
Q

B2?

A

Bronchoconstriction

100
Q

(Mixed a1/b-Adrenoceptor Antagonist: Clinical Use)
(Mixed a1/b Antagonist)
Carvedilol?

A

-angina
-cardiomyopathy
-heart failure (1 of 3 recommended)
-hypertension
-myocardial infarction (acute and post-MI)

101
Q

(Mixed a1/b-Adrenoceptor Antagonist: Clinical Use)
(Mixed a1/b Antagonist)
Labetalol?

A

-hypertension
-hypertensive emergency (IV)
-HTN emergency in pregnancy
-#1 is still methyldopa

102
Q

Mixed a1/b-Adrenoceptor Antagonist: Adverse Effects, Contraindications, Interactions?

A

-Similar to non-selective b-blockers (ex. bronchospasms) and a1 antagonists (postural hypotension)
-Less reflex tachycardia than a1 antagonists (because of B2), less peripheral vasoconstriction than with b-blockers (because A1)

103
Q

(Drugs to Know and Love #1: Agonists)
a1 agonist?

A

Phenylephrine

104
Q

(Drugs to Know and Love #1: Agonists)
a2 agonist?

A

-Clonidine
-Methyldopa

105
Q

(Drugs to Know and Love #1: Agonists)
Non-selective b agonist?

A

-Isoproterenol
-Dobutamine

106
Q

(Drugs to Know and Love #1: Agonists)
b2 agonist?

A

Albuterol

107
Q

Drugs to Know and Love #1: Agonists?

A

-Phenylephrine
-Clonidine
-Methyldopa
-Isoproterenol
-Dobutamine
-Albuterol

108
Q

(Drugs to Know and Love #2: Antagonists)
Non-selective a antagonist?

A

Phentolamine

109
Q

(Drugs to Know and Love #2: Antagonists)
a1 antagonist?

A

Prazosin

110
Q

(Drugs to Know and Love #2: Antagonists)
Non-selective b antagonist (b-blockers)?

A

Propranolol

111
Q

(Drugs to Know and Love #2: Antagonists)
b1 antagonist (b-blockers)

A

-Atenolol
-Metoprolol

112
Q

(Drugs to Know and Love #2: Antagonists)
Mixed a1/b antagonists?

A

-Carvedilol
-Labetalol

113
Q

In a patient with _____ would propranolol be contraindicated?

A

Asthma

Block 2: Pharmacology (5 decks)

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