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🄼💊 M2 Adrenergic/Cholinergics > 8-19 Adrenergic Agonist / Antagonist > Flashcards

8-19 Adrenergic Agonist / Antagonist Flashcards

1
Q

ALPHA 1 RECEPTOR

Tissues - Actions (3)

A

(1) Most vascular smooth muscle- contracts (inc. vascular resistance)
(2) Pupillary Dilatormuscle- contracts (myDriasis)
(3) Internal Urethral Sphincter- contracts

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2
Q

ALPHA 2 RECEPTOR Tissues- Actions (3)

A

(1) Adrenergic and cholinergic nerve terminals- inhibits transmitter release (2) Platelets- stimulates aggregation (3) Some vascular smooth muscle- contracts

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3
Q

BETA 1 RECEPTOR

Actions (2)

A

(1) Heart- Stimulates rate and force
(2) Juxtaglomerular cells- Stimulates renin release

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4
Q

BETA 2 RECEPTOR

Tissues-Actions (4)

A

(1) Relaxes RUV - (Respiratory, Uterine and Vascular) smooth muscle
(2) Liver- stimulates glycogenolysis
(3) Pancreatic B cells- stimulates insulin release
(4) Somatic motor nerve terminals (voluntary muscle)- causes tremor

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5
Q

BETA 3 RECEPTOR Tissues-Actions

A

(B1 and B2 may also contribute) (1) Fat cells- stimulates lipolysis

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6
Q

DOPAMINE 1 RECEPTOR Tissues-Actions

A

(1) Renal and other splanchnic blood vessels- vasoDilates (reduces resistance)

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7
Q

DOPAMINE 2 RECEPTOR Tissues-Actions

A

(1) Nerve terminals- inhibits adenylyl cyclase

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8
Q

Timolol: Half-Life

A

4 hours

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9
Q

Timolol: Mechanism of Action

A

General B-blocker

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10
Q

Timolol: Indication

A

Glaucoma

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11
Q

Nadolol: Half-Life

A

20-24 hours

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12
Q

Nadolol: Mechanism of Action

A

General B-blocker

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13
Q

Nadolol: Indication (2)

A

Long term angina, hypertension

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14
Q

Atenolol: Mechanism of Action

A

B1-blocker

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15
Q

Atenolol: Indication (3)

A

Hypertension, angina, MI

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16
Q

Metoprolol: Mechanism of Action

A

B1-antagonist

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17
Q

Metoprolol: Indication (2)

A

Hypertension, long-term angina rx

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18
Q

Pindolol: A: Mechanism of Action B: Because of its MOA, it has less _______ effect on the heart.

A

A: B-antagonist with partial agonist activity at both B1 and B2 adrenergic R B: Since some B signal remains (partial agonist), partial agonist have less BRADYCARDIC effect, thus should be used when patients are less tolerant to bradycardic effects.

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19
Q

Pindolol: A: Indication B: Therapeutic benefit is good when (indication) is due to _________.

A

A: Hypertension B: Therapeutic benefit is good when HTN is due to HIGH SYMPATHETIC OUTPUT since blockade of endogenous agonist will predominate over partial agonist effect of drug.

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20
Q

Esmolol: Half-life

A

~9 minutes

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21
Q

Esmolol: Mechanism of Action

A

B1-blocker

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22
Q

Esmolol: A: Indication (3) B: Esmolol has a very ____ half life, so it is given ____(dosage form) in _______ crisis, _____ angina and _______

A

Esmolol: A: Indication: -HTN Crisis -Angina (unstable) -Supraventricular tachycardia B: Esmolol has a very SHORT half life (9 min), so it is given IV in hypertensive crisis, unstable angina, SVT

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23
Q

Phenoxy-benzamine: Mechanism of Action

A

General alpha-blocker

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24
Q

Phenoxy-benzamine: Indication

A

Pheochromo-cytoma

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25
Phentolamine: Mechanism of Action
General alpha-blocker
26
Phentolamine: Indication
rx for pheochromocytoma before surgery
27
Prazosin: Mechanism of Action
[Alpha 1 BLOCKER]
28
What are the three cardioselective B1-blockers?
Metoprolol, Atenolol, Esmolol
29
What are the cardiovascular effects of the cardioselective B1-blockers.... -HR/Contractility? -Renin Release? -Vasoregulation?
Reduced heart rate and contractility, reduced renin release, reduced vasoconstriction (due to the reduced angio II) [same as non-selective B blockers]
30
Cardioselective B1 BLOCKERS: Therapeutic use (3)
Hypertension, angina, arrhythmia
31
Cardioselective B1-blockers: Toxicity (4)
Depression, insomnia, hypotension, bradycardia
32
Cardioselective B1-blockers: Contraindications (2)
- Pt with 2nd/3rd degree heart block -Pt with cardiogenic shock
33
EPINEPHRINE Half-Life
Short
34
EPINEPHRINE MOA
EPINEPHRINE MOA: [General alpha Agonist{HIGH CONCENTRATION} and [General Beta agonist{low concentration}] "with low effort you'll get a B....with HIGH EFFORT YOU'LL GET AN A"
35
EPINEPHRINE ELIMINATION
COMT ---\> Urine
36
EPINEPHRINE INDICATION (4)
EPINEPHRINE Indication: •Anaphylaxis •Shock •Cardiac Arrest •Heart Block
37
EPINEPHRINE TOXICITY
Arrhythmias
38
NorEpi HALF-LIFE
short (just like EPi)
39
NorEpi MOA (2)
[General alpha agonist] + [Beta 1 agonist]
40
NorEpi Elimination
MOA and COMT---\> urine
41
NorEpi Indication
Acute hypOtension due to VASODILATORY shock
42
DOPAMINE TRADE NAME
DOPAMINE ;-)
43
DOPAMINE HALF-LIFE
2-3 MIN
44
DOPAMINE MOA
DOPAMINE MOA: [General Beta Agonist] + [SOME alpha agonist activity]
45
DOPAMINE ELIMINATION
MOA AND COMT
46
DOPAMINE INDICATION
Cardiogenic Shock
47
IsoProterenol Half-life
short
48
IsoProterenol MOA
[General Beta Agonist]
49
IsoProterenol Elimination
COMT ---\> Urine
50
IsoProterenol INDICATIONS (2)
IsoProterenol 1) Transient Heart Block 2) Bronchospasm during Anesthesia
51
DoButamine HALF-LIFE
2-3 MIN
52
DoButamine MOA
[MOSTLY Beta 1 AGONIST] ; some beta 2 activity
53
DoButamine ELIMINATION
COMT---\> Urine
54
DoButamine INDICATION
Short term for INC cardiac contractility
55
DoButamine TOXICITY
Hypotension (from vasoDilation;Beta 2 activity)
56
IsoProterenol TOXICITY
Tachyarrhythmias
57
DOPAMINE Toxicity (2)
-Low BP -Ischemia
58
Norepi TOXICITY (2)
- Ischemia - NE Extravasation (IV) --\> Use [PhenTolamine as antidote]
59
EPININEPHRINE TOXICITY
ARRHYTHMIAS
60
NorEPINEPHRINE -CO? -TPR? -HR? -OVERALL MAP?
NorEPINEPHRINE Physiological effects: ºIncreased CO; ºincrease TPR; ºdecrease HR (baroreflex); ºoverall increased MAP
61
DOPAMINE LOW DOSE: _____ TPR/ _______ CO; vs. HIGH DOSE: ______ TPR and _____ MAP
DOPAMINE LOW DOSE: decreased TPR/ increased CO; vs. HIGH DOSE: Increased MAP and TPR
62
IsoProterenol Physiological effects -TPR? -CO? -MAP? -Broncho\_\_\_\_(constricts/dilates)
IsoProterenol Physiological effects: Decreased TPR; Increased CO; Small decrease in MAP; bronchodilation
63
DOBUTAMINE Physiological effects -CO? -inotropic vs. chronotropic?
DOBUTAMINE Physiological effects: Increased CO -MORE INOTROPIC due to [LOW INVOLVEMENT OF baroreceptor reflex which would normally INC chronotropic effects from compensation to hypOtension]`
64
TERBUTALINE Physiological effects -Broncho\_\_\_\_(constricts/dilates) -Uterine contraction vs. relaxation?
TERBUTALINE Physiological effects: Bronchodilation; Uterine relaxation
65
TERBUTALINE Toxicity (3)
TERBUTALINE Toxicity: Tachycardia; Muscle tremor; Tolerance
66
TERBUTALINE MOA
TERBUTALINE [BETA TWO AGONIST]
67
TERBUTALINE INDICATIONS
TERBUTALINE Prevent and Reverse Bronchospasm in [Asthma/Bronchitis/Emphysema] Pts
68
ALBUTEROL MOA
[BETA TWO AGONIST]
69
ALBUTEROL INDICATION
Bronchial Smooth Muscle Relaxation
70
PHENYLEPHRINE Physiological effects: -TPR? -MAP? -HR? -PUPIL? -BRONCHIOLE SECRETION?
PHENYLEPHRINE Physiological effects: Increased TPR and MAP; decreased HR (baroreflex); Pupillary dilation; decrease bronchiole and sinus secretions.
71
PHENYLEPHRINE HALF-LIFE
[less than 1 hour] - metabolizes slowly because it is NOT degraded by [Plasma COMT]
72
PHENYLEPHRINE Mechanism of Action
[alpha 1 AGONIST]
73
PHENYLEPHRINE ELIMINATION
MAO
74
PHENYLEPHRINE Indication (4)
-PRESSOR during Anesthesia -Nasal Congestion -Dilate Pupils for Eye Exam (mydriatic agent) -SVT
75
PHENYLEPHRINE Toxicity
HTN
76
PHENYLEPHRINE: Can Cause \_\_\_\_[INC/DEC] in HR due to _____ \_\_\_\_\_\_
PHENYLEPHRINE: Can cause DEC in HR due to [Baroreceptor Reflex] when peripheral vasoconstriction is initiated
77
CLONIDINE MOA
[alpha TWO AGONIST]
78
CLONIDINE ELIMINATION
Urinated Out
79
CLONIDINE INDICATION (2)
•HTN •Analgesia
80
CLONIDINE TOXICITY
CLONIDINE Toxicity: (x) Dry Mouth (x) HTN Crisis if withdrawn after Chronic Usage
81
CLONIDINE Works by \_\_\_\_\_[INC/DEC] Peripheral vasoconstriction CENTRALLY but will have some \_\_\_\_\_[INC/DEC] Peripheral vasoconstriction by acting directly in the \_\_\_\_\_\_
CLONIDINE Works by DECREASING Peripheral vasoconstriction CENTRALLY (inhibits sympathetics) but will have SOME INC peripheral vasoconstriction by acting directly in the PERIPHERY/ BODY
82
AMPHETAMINE Physiological effects: -TPR? -Inotropic vs. Chronotropic? -MAP?
AMPHETAMINE Physiological effects: ºIncreased TPR/diastolic BP ºPositive inotropic and Positive chronotropic effects; º increased MAP pressure
83
AMPHETAMINE MOA
AMPHETAMINE MOA: [Indirect sympathoMimetic] - Causes NorEpi Release
84
AMPHETAMINE INDICATION (3)
ADHD / narcolepsy / [nasal congestion]
85
AMPHETAMINE Toxicity (4)
AMPHETAMINE Toxicity: (x) Tachycardia (x) HTN (x) Anxiety (x) tyramine accumulation if patient has taken MAO inhibitor within the previous 2 weeks is why MAO inhibitors are CONTRAINDICATED w/Amphetamine ---------------------------------------------------------------------------------- "T.H.A.t Amphetamine is TOXIC"
86
AMPHETAMINE is an _______ Agent
AMPHETAMINE is an Anorexic Agent
87
PARTIAL BETA AGONIST Examples (1)
-Pindolol
88
PARTIAL BETA AGONIST Mechanism: Treats HTN effectively when HTN is secondary to\_\_\_\_\_\_\_\_. [Partial Beta Agonist] work by reducing _______ binding. They will still INC HR/Contractility BUT NOT AS MUCH AS _______ and since it prevents \_\_\_\_\_\_\_, the baseline HR/Contractility actually goes down from where it was initially \*\*Is used for pts who can't tolerate _______ very well with traditional [\_\_\_\_\_\_\_ _______ blockers]
PARTIAL BETA RECEPTOR AGONIST Mechanism: Treats HTN effectively when HTN is secondary to [HIGH Sympathetics]. [Partial Beta Agonist] work by reducing [NOrEPI/EPI] binding. Pindolol will still INC HR/Contractility BUT NOT AS MUCH AS NOrEPI/EPI and since it prevents NOREPI/EPI, the baseline HR/Contractility actually goes down from where it was initially \*\*Is used for pts who can't tolerate bradycardia very well with traditional [Cardioselective beta blockers]
89
PARTIAL BETA AGONIST -HR? -Heart Contractility? -Renin Release?
PARTIAL BETA RECEPTOR AGONIST CV Effects (These CV Effects are most manifested when Sympathetics is the original cause) \*DEC HR \*DEC Heart Contractility \*DEC Renin Release
90
PARTIAL BETA RECEPTOR AGONIST USES (1)
HTN (for pt less tolerant to bradycardia/reduced exercise capacity)
91
PARTIAL BETA RECEPTOR AGONIST TOXICITY (5)
Toxicity are the same as the [NON-SELECTIVE BETA BLOCKERS] (1) Bronchospasm (2) mask symptoms of hypoglycemia (3) CNS effects including insomnia and depression (4) can raise triglycerides (5) bradycardia
92
PARTIAL BETA RECEPTOR AGONIST Contraindications (2)
\*2nd/3rd Degree heart Block \*Cardiogenic Shock
93
ALPHA ADRENERGIC RECEPTOR BLOCKER EXAMPLES (2)
ALPHA ADRENERGIC RECEPTOR BLOCKER \*[iRReversible Phenoxybenazmine] \*[REVERSIBLE PHENTOLAMINE]
94
ALPHA ADRENERGIC RECEPTOR BLOCKER CV Effects (3)
ALPHA ADRENERGIC RECEPTOR BLOCKER 1. Prevents vasoconstriction--\> DEC BP---\>but will cause reflex INC in NorEpi release 2. INC inotropy and INC Chronotropy due to blocking the [a2 pre-synaptic receptor] --\> Release of NorEpi @ nerve terminals 3. will unmasks vasodilatory effect of Epi
95
ALPHA ADRENERGIC RECEPTOR BLOCKER USES (2)
\*perioperative tx of pheochromocytoma \*Dermal Necrosis
96
GENERAL ALPHA BLOCKER TOXICITY (3)
GENERAL ALPHA BLOCKER Toxicity: (x) Prolonged hypOtension (x) Reflex Tachycardia (x) Nasal Congestion "It's TOXIC to give ur pt [General Alpha Blocker's] PRN"
97
ALPHA ADRENERGIC RECEPTOR BLOCKER Contraindications (1)
ALPHA ADRENERGIC RECEPTOR BLOCKER Contraindications: Pt with Coronary Artery Dz
98
ALPHA 1 RECEPTOR BLOCKER EXAMPLES (3)
ALPHA 1 RECEPTOR BLOCKER Examples: -Prazosin -Doxazosin - Terazosin
99
ALPHA 1 RECEPTOR BLOCKER CV Effects (2) \*Prevents _______ \*[Less HR INC / Contractility INC] than [NON-selctive alpha receptor blockers] because \_\_\_\_\_\_\_\_\_\_\_\_. This ultimately DEC _______ release in the synaptic cleft and SA Node is not stimulated any further
ALPHA 1 RECEPTOR BLOCKER CV Effects: \*Prevents Vasoconstriction \*[Less HR INC / Contractility INC] than [NON-selctive alpha receptor blockers] since [alpha 2 receptor] on [pre-synpatic nerve terminal] IS STILL FUNCTIONAL and can still negatively feedback when NorEpi is released---\> ultimately DEC NorEpi release in the synaptic cleft and SA Node is not stimulated no further
100
ALPHA 1 RECEPTOR BLOCKER USES (2)
ALPHA 1 RECEPTOR BLOCKER ºHTN ºBenign Prostatic Hyperplasia
101
ALPHA 1 RECEPTOR BLOCKER TOXICITY (2)
ALPHA 1 RECEPTOR BLOCKER TOXICITY: (x) Syncope (x) Orthostatic hypOtension
102
Methylphenidate: MOA
Indirect sympathomimetic (increases NE and dopamine)
103
Methylphenidate: Indication
ADHD
104
Ephedrine: MOA
Indirect sympathomimetic
105
Ephedrine: Indication
Pressor agent with anesthesia
106
What main drugs make up the Amphetamine family ? (6)
1. Amphetamine 2. Methamphetamine 3. Methylphenidate 4. Ephedrine 5. Pseudoephedrine 6. Tyramine
107
Pseudo-ephedrine: MOA
Indirect sympathomimetic
108
Pseudo-ephedrine: Indication
Nasal decongestion
109
Tyramine: MOA
Displaces NE
110
Tyramine: Half-life
Normally very short
111
Tyramine: Indications
Not therapeutic
112
Tyramine: Elimination
MAO
113
Propanolol: MOA
General (non-selective) Beta Blocker
114
Propanolol: Indications (3)
1. Hypertension 2. Angina due to atherosclerosis 3. MI
115
Timolol: MOA
General (non-selective) Beta Blocker
116
Timolol: Indications
Glaucoma
117
Nadolol: Half-life
20-24 hrs
118
Nadolol: MOA
General (non-selective) Beta-blocker
119
Nadolol: Indications (2)
1. Long-term angina 2. Hypertension
120
What are the Non-selective Beta-blockers? (3)
Propanolol, nadolol, timolol
121
Cardiovascular effects of Non-selective Beta-blockers? (3)
1. Reduced heart rate 2. Reduced contractility 3. Reduced vasoconstriction (as a result of reduced RENIN release)
122
Effect of Non-selective Beta-blockers on bronchioles? (1)
Can cause bronchiole constriction in those with asthma or COPD.
123
Non-selective Beta-blockers: Toxicity (5)
1. Bronchospasm 2. Bradycardia 3. CNS effects (insomnia/depression) 4. MASK sx of hypOglycemia 5. Triglyceride INC ---------------------------------------------------------------------------------- "(General) B Blockers Can Modulate Triglycerides "
124
Non-selective Beta-blockers: Contraindications (4)
1. Heart Block 2. Sinus bradycardia 3. Bronchial Asthma 4. Cardiogenic shock "[He Should Be Careful] w/General Beta Blockers"
125
LIST THE 5 Drugs Eliminated by COMT
"COMT d.i.N.e.D on 5 Drugs" 1. doButamine 2. isoProterenol 3. NOREPI [MAO and COMT] 4 epi 5. DOPAMINE [MAO and COMT]

🄼💊 M2 Adrenergic/Cholinergics (5 decks)

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