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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
Q

Phentolamine: Mechanism of Action

A

General alpha-blocker

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26
Q

Phentolamine: Indication

A

rx for pheochromocytoma before surgery

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27
Q

Prazosin: Mechanism of Action

A

[Alpha 1 BLOCKER]

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28
Q

What are the three cardioselective B1-blockers?

A

Metoprolol, Atenolol, Esmolol

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29
Q

What are the cardiovascular effects of the cardioselective B1-blockers…. -HR/Contractility? -Renin Release? -Vasoregulation?

A

Reduced heart rate and contractility, reduced renin release, reduced vasoconstriction (due to the reduced angio II) [same as non-selective B blockers]

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30
Q

Cardioselective B1 BLOCKERS: Therapeutic use (3)

A

Hypertension, angina, arrhythmia

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31
Q

Cardioselective B1-blockers: Toxicity (4)

A

Depression, insomnia, hypotension, bradycardia

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32
Q

Cardioselective B1-blockers: Contraindications (2)

A
  • Pt with 2nd/3rd degree heart block -Pt with cardiogenic shock
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33
Q

EPINEPHRINE Half-Life

A

Short

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34
Q

EPINEPHRINE MOA

A

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”

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35
Q

EPINEPHRINE ELIMINATION

A

COMT —> Urine

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36
Q

EPINEPHRINE INDICATION (4)

A

EPINEPHRINE Indication: •Anaphylaxis •Shock •Cardiac Arrest •Heart Block

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37
Q

EPINEPHRINE TOXICITY

A

Arrhythmias

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38
Q

NorEpi HALF-LIFE

A

short (just like EPi)

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39
Q

NorEpi

MOA (2)

A

[General alpha agonist] + [Beta 1 agonist]

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40
Q

NorEpi Elimination

A

MOA and COMT—> urine

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41
Q

NorEpi Indication

A

Acute hypOtension due to VASODILATORY shock

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42
Q

DOPAMINE TRADE NAME

A

DOPAMINE ;-)

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43
Q

DOPAMINE HALF-LIFE

A

2-3 MIN

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44
Q

DOPAMINE MOA

A

DOPAMINE MOA: [General Beta Agonist] + [SOME alpha agonist activity]

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45
Q

DOPAMINE ELIMINATION

A

MOA AND COMT

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46
Q

DOPAMINE INDICATION

A

Cardiogenic Shock

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47
Q

IsoProterenol Half-life

A

short

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48
Q

IsoProterenol

MOA

A

[General Beta Agonist]

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49
Q

IsoProterenol Elimination

A

COMT —> Urine

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50
Q

IsoProterenol INDICATIONS (2)

A

IsoProterenol 1) Transient Heart Block 2) Bronchospasm during Anesthesia

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51
Q

DoButamine HALF-LIFE

A

2-3 MIN

52
Q

DoButamine MOA

A

[MOSTLY Beta 1 AGONIST] ; some beta 2 activity

53
Q

DoButamine ELIMINATION

A

COMT—> Urine

54
Q

DoButamine INDICATION

A

Short term for INC cardiac contractility

55
Q

DoButamine TOXICITY

A

Hypotension (from vasoDilation;Beta 2 activity)

56
Q

IsoProterenol TOXICITY

A

Tachyarrhythmias

57
Q

DOPAMINE Toxicity (2)

A

-Low BP -Ischemia

58
Q

Norepi TOXICITY (2)

A
  • Ischemia - NE Extravasation (IV) –> Use [PhenTolamine as antidote]
59
Q

EPININEPHRINE TOXICITY

A

ARRHYTHMIAS

60
Q

NorEPINEPHRINE -CO? -TPR? -HR? -OVERALL MAP?

A

NorEPINEPHRINE Physiological effects: ºIncreased CO; ºincrease TPR; ºdecrease HR (baroreflex); ºoverall increased MAP

61
Q

DOPAMINE LOW DOSE: _____ TPR/ _______ CO; vs. HIGH DOSE: ______ TPR and _____ MAP

A

DOPAMINE LOW DOSE: decreased TPR/ increased CO; vs. HIGH DOSE: Increased MAP and TPR

62
Q

IsoProterenol Physiological effects -TPR? -CO? -MAP? -Broncho____(constricts/dilates)

A

IsoProterenol Physiological effects: Decreased TPR; Increased CO; Small decrease in MAP; bronchodilation

63
Q

DOBUTAMINE Physiological effects -CO? -inotropic vs. chronotropic?

A

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
Q

TERBUTALINE Physiological effects -Broncho____(constricts/dilates) -Uterine contraction vs. relaxation?

A

TERBUTALINE Physiological effects: Bronchodilation; Uterine relaxation

65
Q

TERBUTALINE Toxicity (3)

A

TERBUTALINE Toxicity: Tachycardia; Muscle tremor; Tolerance

66
Q

TERBUTALINE MOA

A

TERBUTALINE [BETA TWO AGONIST]

67
Q

TERBUTALINE INDICATIONS

A

TERBUTALINE Prevent and Reverse Bronchospasm in [Asthma/Bronchitis/Emphysema] Pts

68
Q

ALBUTEROL MOA

A

[BETA TWO AGONIST]

69
Q

ALBUTEROL INDICATION

A

Bronchial Smooth Muscle Relaxation

70
Q

PHENYLEPHRINE Physiological effects: -TPR? -MAP? -HR? -PUPIL? -BRONCHIOLE SECRETION?

A

PHENYLEPHRINE Physiological effects: Increased TPR and MAP; decreased HR (baroreflex); Pupillary dilation; decrease bronchiole and sinus secretions.

71
Q

PHENYLEPHRINE HALF-LIFE

A

[less than 1 hour] - metabolizes slowly because it is NOT degraded by [Plasma COMT]

72
Q

PHENYLEPHRINE Mechanism of Action

A

[alpha 1 AGONIST]

73
Q

PHENYLEPHRINE ELIMINATION

A

MAO

74
Q

PHENYLEPHRINE Indication (4)

A

-PRESSOR during Anesthesia -Nasal Congestion -Dilate Pupils for Eye Exam (mydriatic agent) -SVT

75
Q

PHENYLEPHRINE Toxicity

A

HTN

76
Q

PHENYLEPHRINE: Can Cause ____[INC/DEC] in HR due to _____ ______

A

PHENYLEPHRINE: Can cause DEC in HR due to [Baroreceptor Reflex] when peripheral vasoconstriction is initiated

77
Q

CLONIDINE MOA

A

[alpha TWO AGONIST]

78
Q

CLONIDINE ELIMINATION

A

Urinated Out

79
Q

CLONIDINE INDICATION (2)

A

•HTN •Analgesia

80
Q

CLONIDINE TOXICITY

A

CLONIDINE Toxicity: (x) Dry Mouth (x) HTN Crisis if withdrawn after Chronic Usage

81
Q

CLONIDINE Works by _____[INC/DEC] Peripheral vasoconstriction CENTRALLY but will have some _____[INC/DEC] Peripheral vasoconstriction by acting directly in the ______

A

CLONIDINE Works by DECREASING Peripheral vasoconstriction CENTRALLY (inhibits sympathetics) but will have SOME INC peripheral vasoconstriction by acting directly in the PERIPHERY/ BODY

82
Q

AMPHETAMINE Physiological effects: -TPR? -Inotropic vs. Chronotropic? -MAP?

A

AMPHETAMINE Physiological effects: ºIncreased TPR/diastolic BP ºPositive inotropic and Positive chronotropic effects; º increased MAP pressure

83
Q

AMPHETAMINE MOA

A

AMPHETAMINE MOA: [Indirect sympathoMimetic] - Causes NorEpi Release

84
Q

AMPHETAMINE INDICATION (3)

A

ADHD / narcolepsy / [nasal congestion]

85
Q

AMPHETAMINE Toxicity (4)

A

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
Q

AMPHETAMINE is an _______ Agent

A

AMPHETAMINE is an Anorexic Agent

87
Q

PARTIAL BETA AGONIST Examples (1)

A

-Pindolol

88
Q

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]

A

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
Q

PARTIAL BETA AGONIST -HR? -Heart Contractility? -Renin Release?

A

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
Q

PARTIAL BETA RECEPTOR AGONIST USES (1)

A

HTN (for pt less tolerant to bradycardia/reduced exercise capacity)

91
Q

PARTIAL BETA RECEPTOR AGONIST TOXICITY (5)

A

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
Q

PARTIAL BETA RECEPTOR AGONIST Contraindications (2)

A

*2nd/3rd Degree heart Block *Cardiogenic Shock

93
Q

ALPHA ADRENERGIC RECEPTOR BLOCKER EXAMPLES (2)

A

ALPHA ADRENERGIC RECEPTOR BLOCKER *[iRReversible Phenoxybenazmine] *[REVERSIBLE PHENTOLAMINE]

94
Q

ALPHA ADRENERGIC RECEPTOR BLOCKER CV Effects (3)

A

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
Q

ALPHA ADRENERGIC RECEPTOR BLOCKER USES (2)

A

*perioperative tx of pheochromocytoma *Dermal Necrosis

96
Q

GENERAL ALPHA BLOCKER TOXICITY (3)

A

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
Q

ALPHA ADRENERGIC RECEPTOR BLOCKER Contraindications (1)

A

ALPHA ADRENERGIC RECEPTOR BLOCKER Contraindications: Pt with Coronary Artery Dz

98
Q

ALPHA 1 RECEPTOR BLOCKER EXAMPLES (3)

A

ALPHA 1 RECEPTOR BLOCKER Examples: -Prazosin -Doxazosin - Terazosin

99
Q

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

A

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
Q

ALPHA 1 RECEPTOR BLOCKER USES (2)

A

ALPHA 1 RECEPTOR BLOCKER ºHTN ºBenign Prostatic Hyperplasia

101
Q

ALPHA 1 RECEPTOR BLOCKER TOXICITY (2)

A

ALPHA 1 RECEPTOR BLOCKER TOXICITY: (x) Syncope (x) Orthostatic hypOtension

102
Q

Methylphenidate: MOA

A

Indirect sympathomimetic (increases NE and dopamine)

103
Q

Methylphenidate: Indication

A

ADHD

104
Q

Ephedrine: MOA

A

Indirect sympathomimetic

105
Q

Ephedrine: Indication

A

Pressor agent with anesthesia

106
Q

What main drugs make up the Amphetamine family ? (6)

A
  1. Amphetamine 2. Methamphetamine 3. Methylphenidate 4. Ephedrine 5. Pseudoephedrine 6. Tyramine
107
Q

Pseudo-ephedrine: MOA

A

Indirect sympathomimetic

108
Q

Pseudo-ephedrine: Indication

A

Nasal decongestion

109
Q

Tyramine: MOA

A

Displaces NE

110
Q

Tyramine: Half-life

A

Normally very short

111
Q

Tyramine: Indications

A

Not therapeutic

112
Q

Tyramine: Elimination

A

MAO

113
Q

Propanolol: MOA

A

General (non-selective) Beta Blocker

114
Q

Propanolol: Indications (3)

A
  1. Hypertension 2. Angina due to atherosclerosis 3. MI
115
Q

Timolol: MOA

A

General (non-selective) Beta Blocker

116
Q

Timolol: Indications

A

Glaucoma

117
Q

Nadolol: Half-life

A

20-24 hrs

118
Q

Nadolol: MOA

A

General (non-selective) Beta-blocker

119
Q

Nadolol: Indications (2)

A
  1. Long-term angina 2. Hypertension
120
Q

What are the Non-selective Beta-blockers? (3)

A

Propanolol, nadolol, timolol

121
Q

Cardiovascular effects of Non-selective Beta-blockers? (3)

A
  1. Reduced heart rate 2. Reduced contractility 3. Reduced vasoconstriction (as a result of reduced RENIN release)
122
Q

Effect of Non-selective Beta-blockers on bronchioles? (1)

A

Can cause bronchiole constriction in those with asthma or COPD.

123
Q

Non-selective Beta-blockers: Toxicity (5)

A
  1. Bronchospasm 2. Bradycardia 3. CNS effects (insomnia/depression) 4. MASK sx of hypOglycemia 5. Triglyceride INC ———————————————————————————- “(General) B Blockers Can Modulate Triglycerides “
124
Q

Non-selective Beta-blockers: Contraindications (4)

A
  1. Heart Block 2. Sinus bradycardia 3. Bronchial Asthma 4. Cardiogenic shock “[He Should Be Careful] w/General Beta Blockers”
125
Q

LIST THE 5 Drugs Eliminated by COMT

A

“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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