Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Block 2: Pharmacology > Lecture 2 > Flashcards

Lecture 2 Flashcards

(113 cards)

Start Studying
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

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

(Adrenergic Receptors)
Smooth Muscle Contraction?

A

A1 –> Gq –> Ca

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

(Adrenergic Receptors)
Inhibition of transmitter release?

A

A2 –> Gi –> Inhibit cAMP

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

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

A

B –> Gs –> Increase cAMP

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

(Adrenergic Receptors)
50% of Drugs target?

A

GPCRs

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

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

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

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

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

(Adrenergic Receptors: Most Physiologically Relevant Effects)
B3?

A

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

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

Alpha 1 (Gq)?

A

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

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

Alpha 2 (Gi)?

A

(Inhibitory)
Presynaptic Nerve Terminals

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

Beta 1 (Gs)?

A

Gs coupled receptors, increase cAMP

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

Beta 2 (Gs)?

A

(Smooth Muscle Relaxation)
Gs coupled receptors, increase cAMP

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

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

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

A

Phenylephrine (vasoconstriction)

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

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

A

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

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

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

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

A

Albuterol (dilates bronchial SM)

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

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

A

Phentolamine (vasodilation, increase HR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Prazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

Propranolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

-olol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

-Atenolol
-Metoprolol
(B1 antagonist = decrease HR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
(Drugs to Know and Love #2: Antagonists) B1 antagonist ?
Decrease HR
26
(Drugs to Know and Love #2: Antagonists) B2 antagonist ?
Bronchoconstriction
27
(Drugs to Know and Love #2: Antagonists) Mixed a1/B antagonists?
-Carvedilol -Labetalol
28
(Drugs to Know and Love #2: Antagonists) LOL = ?
Funny because it has both
29
Drugs to Know and Love #2: Antagonists?
Opposite Effect
30
(a1 Selective Agonists) (Epinephrine vs. Phenylephrine) Epinephrine?
-Oral usability: completely ineffective -Duration of action: short -CNS penetration: poor penetration
31
(a1 Selective Agonists) (Epinephrine vs. Phenylephrine) Phenylephrine?
-Phenylephrine is more stable, and does not get broken down so fast
32
(a1 Selective Agonists) Epinephrine vs. Phenylephrine?
-Selectivity -COMT Sensitivity (catechol-o-methyl transferase) (degrades catecholamines)
33
a1 Agonists: Mechanisms of Action and Pharmacology?
-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)
34
a1 Selective Agonists: Clinical Use?
-Nasal Congestion (decreases inflammation markers reaching tissue) -Hypotension (vasoconstriction increase BP) -Hemorrhoids (vasoconstriction stop inflammation marker to swollen/inflamed vein) -To dilate pupils
35
Phenylephrine?
-Type: A1 Agonist -Effect: Vasoconstriction -Tx: Nasal Congestion, Hypotension, Hemorrhoids -SE: Angina, Bradycardia, HTN, Necrosis -Contraindication: Fib, Tachy, HTN -Interactions: MAOI
36
a1 Agonist (phenylephrine): Pharmacokinetics, Adverse Effects, Contraindications, Interactions?
-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
37
(a1 Agonist (phenylephrine): Pharmacokinetics, Adverse Effects, Contraindications, Interactions) If you increase A1 agonists, you wouldn't want to?
Inhibit NE via MAO inhibitors because then it would cause increased vasoconstriction
38
a2 Selective Agonists?
-Clonidine -Methyldopa (SAFE WITH PREGNANCY) (Postsynaptic CNS (Gi) Multiple (decreased SNS tone)) (Presynaptic ANS (Gi) Decreased NT release)
39
(a2 Selective Agonists) Decrease SNS?
Parasympathetic Effects
40
a2 Agonists: Mechanisms of Action and Pharmacology?
-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)
41
(a2 Agonists: Mechanisms of Action and Pharmacology) Still an Agonist?
Activated Gi that's inhibitory (NOT an Antagonist)
42
a2 Agonists: Clinical Use?
-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
43
(a2 Agonists: Clinical Use) Clonidine?
More potent but not used during pregnancy (several CNS disorders including ADHD, mitigate drug withdrawal, severe pain)
44
(a2 Agonists: Clinical Use) Methyldopa?
First-Line Therapy for hypertension during pregnancy ("pro drug" that needs to be activated so safer)
45
(Clonidine vs. a-methyldopa) Clonidine is effective both in?
Periphery and in Brain (effect everywhere with does)
46
(Clonidine vs. a-methyldopa) Alpha-methyldopa is effective ONLY in?
Brain (readily enter Brain where it is metabolized to active compound a-methyl-norepinephrine (a2 agonist)) (needs to be activated in Brain)
47
(a2 Agonists: Adverse Effects, Contraindications, Interaction) Clonidine?
-Dry mouth, sedation, depression, orthostatic, hypotension -Depression (caution: sudden withdrawal precipitates hypertensive crisis) (decrease SNS, think depression, sedation, hypotension)
48
(a2 Agonists: Adverse Effects, Contraindications, Interaction) Methyldopa?
-Sedation, depression, tolerance -Depression (MAO inhibitory therapy (would increase NE))
49
(a2 Agonists: Adverse Effects, Contraindications, Interaction) Do NOT give Clonidine if?
Depressed
50
(a2 Agonists: Adverse Effects, Contraindications, Interaction) If you decrease SNS?
Depression, Sedation and Hypotension
51
(Non-Selective B Agonists) Isoproterenol?
-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
(Non-Selective B Agonists) What is NOT the first-line agent for use in bronchospasm during anesthesia or shock?
Isoproterenol
53
(Cardiovascular Effects od Adrenergic Agonists) Isoproterenol?
-Increase B1 = increase force and pulse rate -Decrease resistance, B2
54
(Other B Agonists) Dobutamine (racemic mixture)?
-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
B2 Selective Agonists?
-Albuterol (short-action-acute bronchospasm) -Salmeterol (longer acting-maintenance) -Metaproterenol (short-action-acute bronchospasm) -Terbutaline (short-action)
56
B2 Agonists: Mechanism of Action and Pharmacology?
-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
B2 Agonists: Clinical Use?
-Asthma -Acute bronchospasm -Bronchospasm prophylaxis -Premature Labor
58
B2 Agonists: Adverse Effects, Contraindication, Interactions?
-Tremors -Stimulation (CNS) -Palpitations -Tachycardia (direct and reflex) (reflex = decrease in BP so response is increasing HR (Tachy))
59
B2 Agonists: Adverse Effects, Contraindication, Interactions?
-Tremors -Stimulation (CNS) -Palpitations -Tachycardia (direct and reflex) (reflex = decrease in BP so response is increasing HR (Tachy))
60
(a-Adrenoceptors Antagonist) Non-selective a antagonist?
Phentolamine
61
(a-Adrenoceptors Antagonist) a1-selective antagonist?
Prazosin
62
a Antagonists: Mechanisms of Action and Pharmacology?
-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
(a Antagonists: Mechanisms of Action and Pharmacology) HR increase greater in Phentolamine than?
Prazosin
64
(a Antagonist: Pharmacodynamics) A1 Antagonist?
Vasodilation (decrease BP, increase HR)
65
(a Antagonist: Pharmacodynamics) A2 Antagonist?
Increase NE, Increase sympathetic
66
(a Antagonists: Clinical Use) Non-selective a antagonist?
-Drug Name: Phentolamine -Clinical Use: Anesthesia reversal, Extravasation of a agonist, Pheochromocytoma (tumor at adrenal gland, high BP)
67
(a Antagonists: Clinical Use) a1 antagonist?
-Drug Name: Prazosin -Clinical Use: Hypertension, Benign prostatic hyperplasia (BPH)
68
(a Antagonists: Clinical Use) a1 antagonist?
-Drug Name: Prazosin -Clinical Use: Hypertension, Benign prostatic hyperplasia (BPH)
69
(a Antagonists: Adverse Effects Adverse Effects, Contraindications, Interactions) Phentolamine?
-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
(a Antagonists: Adverse Effects Adverse Effects, Contraindications, Interactions) Prazosin?
-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
(b-Adrenoceptor Antagonist) Non-selective b antagonist (1st generation) B1/B2?
Propranolol
72
(b-Adrenoceptor Antagonist) b1 antagonist (2nd generation)?
-Atenolol -Metoprolol
73
(b-Adrenoceptor Antagonist) Mixed a1/b antagonists (3rd generation)?
-Carvedilol -Labetalol (HTN EMERGENCY)
74
b Antagonists: Mechanisms of Action and Pharmacology?
-Block b, or both b and b2 receptors -Cardiovascular -CNS -Eye (opposite of SNS, so think Parasympathetic)
75
(b Antagonists: Mechanisms of Action and Pharmacology) Cardiovascular?
-Have negative inotropic, dromotropic (conduction speed) and chronotropic effects -Decrease renin release -Block of b2 may increase peripheral resistance (mild)
76
(b Antagonists: Mechanisms of Action and Pharmacology) CNS?
-Anxiolytic -CNS effects may contribute to decrease HTN
77
(b Antagonists: Mechanisms of Action and Pharmacology) Eye?
-Decrease aqueous humor production -Decrease intraocular pressure
78
(b Antagonists: Mechanisms of Action and Pharmacology) Lungs?
Bronchoconstriction- "spasm" (more prominent in b1,b2 than b1-selective)
79
(b Antagonists: Mechanisms of Action and Pharmacology) Metabolic?
-Lipolysis and glycogenolysis are inhibited -Inhibit recovery from hypoglycemia (more prominent in b1/b2 than b1-selective)
80
b2 Antagonist?
(skeletal muscle only) In skeletal muscle BV and broncho constriction
81
b1 Antagonist?
Decrease HR, Renin release
82
(Non-Selective b Antagonists: Clinical Use) Non-selective b antagonist?
-Drug Name: Propranolol -Clinical Use: angina, cardiac arrhythmias, hypertension, migraine prophylaxis, myocardial infarction prophylaxis, pheochromocytoma, post-myocardial infarction, thyrotoxicosis, essential tremor
83
When are b blockers first-line therapy for hypertension?
-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
(Non-selective b Antagonists: Adverse Effects Adverse Effects, Contraindications, Interactions) (Propranolol) Adverse Effects?
Dizziness, fatigue, lethargy, sinus bradycardia and hypotension, exacerbation of asthma, dyspnea, or bronchospasm, diabetes mellitus, hypertriglyceridemia and decrease plasma HDL
85
(Non-selective b Antagonists: Adverse Effects Adverse Effects, Contraindications, Interactions) (Propranolol) Precautions/Contraindications?
-Diabetes mellitus, hyperthryoidism -Pregnancy category C -Asthma, AV block, bradycardia, cariogenic shock, sick sinus syndrome
86
(Non-selective b Antagonists: Adverse Effects Adverse Effects, Contraindications, Interactions) (Propranolol) Interactions?
Drugs that depress AV conduction or have negative inotropic actions, clonidine withdrawal
87
Withdrawal Syndrome?
Rebound hypertension, MI, cardiac arrhythmias and panic attacks can result from sudden withdrawal
88
B Receptor get sensitive so a sudden withdrawal from medications can be?
Dangerous (beta receptors get sensitive so you increase NE)
89
(b1 Antagonists) b1 antagonist?
-Atenolol -Metoprolol (Heart, Juxtaglomerular cells) (Gs, Gi) (increased force and rate, increase renin release)
90
b1 Antagonists: Mechanisms of Action and Pharmacology?
-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
(b1 Antagonists: Mechanisms of Action and Pharmacology) History of Diabetes and Asthma?
Beta
92
(b1 Antagonists: Clinical Use) (b1 Antagonist) Atenolol?
-Acute MI -angina -Hypertension
93
(b1 Antagonists: Clinical Use) (b1 Antagonist) Metoprolol?
-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
(b1 Antagonists: Clinical Use) (b1 Antagonist) Not safe for?
Pregnancy
95
b1 Antagonists: Adverse Effects, Contraindications, Interactions?
-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
(Mixed a1/b-Adrenoceptor Antagonist) Mixed a1/b antagonists?
-Carvedilol -Labetalol
97
A1?
Vasodilation
98
B1?
Decrease HR
99
B2?
Bronchoconstriction
100
(Mixed a1/b-Adrenoceptor Antagonist: Clinical Use) (Mixed a1/b Antagonist) Carvedilol?
-angina -cardiomyopathy -heart failure (1 of 3 recommended) -hypertension -myocardial infarction (acute and post-MI)
101
(Mixed a1/b-Adrenoceptor Antagonist: Clinical Use) (Mixed a1/b Antagonist) Labetalol?
-hypertension -hypertensive emergency (IV) -HTN emergency in pregnancy -#1 is still methyldopa
102
Mixed a1/b-Adrenoceptor Antagonist: Adverse Effects, Contraindications, Interactions?
-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
(Drugs to Know and Love #1: Agonists) a1 agonist?
Phenylephrine
104
(Drugs to Know and Love #1: Agonists) a2 agonist?
-Clonidine -Methyldopa
105
(Drugs to Know and Love #1: Agonists) Non-selective b agonist?
-Isoproterenol -Dobutamine
106
(Drugs to Know and Love #1: Agonists) b2 agonist?
Albuterol
107
Drugs to Know and Love #1: Agonists?
-Phenylephrine -Clonidine -Methyldopa -Isoproterenol -Dobutamine -Albuterol
108
(Drugs to Know and Love #2: Antagonists) Non-selective a antagonist?
Phentolamine
109
(Drugs to Know and Love #2: Antagonists) a1 antagonist?
Prazosin
110
(Drugs to Know and Love #2: Antagonists) Non-selective b antagonist (b-blockers)?
Propranolol
111
(Drugs to Know and Love #2: Antagonists) b1 antagonist (b-blockers)
-Atenolol -Metoprolol
112
(Drugs to Know and Love #2: Antagonists) Mixed a1/b antagonists?
-Carvedilol -Labetalol
113
In a patient with _____ would propranolol be contraindicated?
Asthma

Block 2: Pharmacology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions