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Step 1 USMLE Rx - Cardio > Cardio: Adrenergic / Cholinergics > Flashcards

Cardio: Adrenergic / Cholinergics Flashcards

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USMLE® Step 1 flashcards
1
Q

ALPHA 1 RECEPTOR

Tissues - Actions (3)

A

“Gimme an alpha 1 VID”

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

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2
Q

ALPHA 2 RECEPTOR

Tissues- Actions (4)

A

“You’ll find alpha 2 receptors on a PEAA”

(1) A**drenergic and cholinergic nerve terminals- inhibits NTS release–> [CNS-mediated BP DEC]
(2) *Platelets- stimulates aggregation
(3) *Adipocytes - DEC Lipolysis
(4) Eye - DEC Intraocular pressure

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3
Q

BETA 1 RECEPTOR

Actions (2)

A

(1) Heart- INC rate and force by [INC [Na+ I(f) channels] in phase 0 of AV node] –> shortens PR interval
(2) JGA 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

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

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7
Q

DOPAMINE 2 RECEPTORTissues-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

MOA

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 ActionB: 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: IndicationB: Therapeutic benefit is good when (indication) is due to _________.

A

A: HypertensionB: 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 tachycardiaB: 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

Phenoxybenzamine:

Mechanism of Action

A

Irreversible [General alpha-blocker]

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24
Q

Phenoxybenzamine:

Indication

A

Pheochromocytoma

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25
Q

Phentolamine:

Mechanism of Action

A

General alpha-blocker

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26
Q

Phentolamine

Indication (3)

A

Catecholamine-induced HTN Crisis

  1. rx for pheochromocytoma before surgery
  2. MAOI Crisis
  3. Cocaine OD

IS REVERSIBLE!

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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 (2)

A

[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

MOA (2)

A

[General alpha agonist] + [Beta 1 agonist]

a1 > a2 > B1

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39
Q

NorEpiElimination

A

MOA and COMT—> urine

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40
Q

NorEpiIndication

A

Acute hypOtension due to VASODILATORY shock

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41
Q

DOPAMINEHALF-LIFE

A

2-3 MIN

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42
Q

DOPAMINE

MOA (2)

A

[General Beta Agonist] + [SOME alpha agonist activity]

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43
Q

DOPAMINEELIMINATION

A

MOA AND COMT

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44
Q

DOPAMINEINDICATION

A

Cardiogenic Shock

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45
Q

IsoProterenolHalf-life

A

short

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46
Q

IsoProterenol

MOA

A

[General Beta Agonist]

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47
Q

IsoProterenolElimination

A

COMT —> Urine

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48
Q

IsoProterenolINDICATIONS (2)

A

IsoProterenol1) Transient Heart Block2) Bronchospasm during Anesthesia

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49
Q

DoButamineHALF-LIFE

A

2-3 MIN

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50
Q

DoButamine

MOA

A

[MOSTLY Beta 1 AGONIST] ; some beta 2 activity

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51
Q

DoButamineELIMINATION

A

COMT—> Urine

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52
Q

DoButamineINDICATION

A

Short term for INC cardiac contractility

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53
Q

DoButamineTOXICITY

A

Hypotension (from vasoDilation;Beta 2 activity)

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54
Q

IsoProterenol TOXICITY

A

Tachyarrhythmias

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55
Q

DOPAMINEToxicity (2)

A

-Low BP-Ischemia

56
Q

NorEpi

TOXICITY (2)

A
  • Ischemia
  • NE Extravasation (IV) –> Use [PhenTolamine as antidote]
57
Q

EPININEPHRINETOXICITY

A

ARRHYTHMIAS

58
Q

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

A

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

59
Q

DOPAMINE

A: LOW DOSE: _____ TPR/ _______ CO;

vs.

HIGH DOSE: ______ TPR and _____ MAP

A

LOW DOSE: decreased TPR/ increased CO;

vs.

HIGH DOSE: Increased MAP and TPR

60
Q

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

A

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

61
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]`

62
Q

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

A

TERBUTALINE Physiological effects: Bronchodilation; Uterine relaxation

63
Q

TERBUTALINEToxicity (3)

A

TERBUTALINEToxicity: Tachycardia; Muscle tremor; Tolerance

64
Q

TERBUTALINEMOA

A

TERBUTALINE[BETA TWO AGONIST]

65
Q

TERBUTALINEINDICATIONS

A

TERBUTALINEPrevent and Reverse Bronchospasm in [Asthma/Bronchitis/Emphysema] Pts

66
Q

ALBUTEROLMOA

A

[BETA TWO AGONIST]

67
Q

ALBUTEROLINDICATION

A

Bronchial Smooth Muscle Relaxation

68
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.
69
Q

PHENYLEPHRINE

HALF-LIFE

A

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

70
Q

PHENYLEPHRINE

Mechanism of Action

A

[alpha 1 AGONIST]

71
Q

PHENYLEPHRINEELIMINATION

A

MAO

72
Q

PHENYLEPHRINE

Indication (4)

A
  • PRESSOR during Anesthesia
  • Nasal Congestion
  • Dilate Pupils for Eye Exam (mydriatic agent)
  • SVT
73
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

74
Q

CLONIDINEMOA

A

[alpha TWO AGONIST]

75
Q

CLONIDINEELIMINATION

A

Urinated Out

76
Q

CLONIDINEINDICATION (2)

A

•HTN•Analgesia

77
Q

CLONIDINETOXICITY

A

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

78
Q

CLONIDINEWorks 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

79
Q

AMPHETAMINEPhysiological effects:-TPR?-Inotropic vs. Chronotropic? -MAP?

A

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

80
Q

AMPHETAMINEMOA

A

AMPHETAMINE MOA: [Indirect sympathoMimetic] - Causes NorEpi Release

81
Q

AMPHETAMINEINDICATION (3)

A

ADHD / narcolepsy / [nasal congestion]

82
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”

83
Q

AMPHETAMINE is an _______ Agent

A

AMPHETAMINE is an Anorexic Agent

84
Q

PARTIAL BETA AGONISTExamples (1)

A

-Pindolol

85
Q

PARTIAL BETA AGONISTMechanism: 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 AGONISTMechanism: 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]

86
Q

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

A

PARTIAL BETA RECEPTOR AGONISTCV Effects (These CV Effects are most manifested when Sympathetics is the original cause) *DEC HR*DEC Heart Contractility*DEC Renin Release

87
Q

PARTIAL BETA RECEPTOR AGONISTUSES (1)

A

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

88
Q

PARTIAL BETA RECEPTOR AGONISTTOXICITY (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

89
Q

PARTIAL BETA RECEPTOR AGONISTContraindications (2)

A

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

90
Q

ALPHA ADRENERGIC RECEPTOR BLOCKEREXAMPLES (2)

A

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

91
Q

ALPHA ADRENERGIC RECEPTOR BLOCKERCV Effects (3)

A

ALPHA ADRENERGIC RECEPTOR BLOCKER1. 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 terminals3. will unmasks vasodilatory effect of Epi

92
Q

ALPHA ADRENERGIC RECEPTOR BLOCKERUSES (2)

A

*perioperative tx of pheochromocytoma *Dermal Necrosis

93
Q

GENERAL ALPHA BLOCKERTOXICITY (3)

A

GENERAL ALPHA BLOCKERToxicity: (x) Prolonged hypOtension(x) Reflex Tachycardia (x) Nasal Congestion “It’s TOXIC to give ur pt [General Alpha Blocker’s] PRN”

94
Q

ALPHA ADRENERGIC RECEPTOR BLOCKERContraindications (1)

A

ALPHA ADRENERGIC RECEPTOR BLOCKERContraindications: Pt with Coronary Artery Dz

95
Q

ALPHA 1 BLOCKER

EXAMPLES (3)

A

ALPHA 1 RECEPTOR BLOCKER

Examples: -Prazosin /Doxazosin /Terazosin

96
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

97
Q

ALPHA 1 RECEPTOR BLOCKER

Indications (2)

A

ALPHA 1 RECEPTOR BLOCKER

ºHTN

ºBenign Prostatic Hyperplasia

98
Q

ALPHA 1 RECEPTOR BLOCKERTOXICITY (2)

A

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

99
Q

Methylphenidate:MOA

A

Indirect sympathomimetic (increases NE and dopamine)

100
Q

Methylphenidate:Indication

A

ADHD

101
Q

Ephedrine:MOA

A

Indirect sympathomimetic

102
Q

Ephedrine:Indication

A

Pressor agent with anesthesia

103
Q

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

A
  1. Amphetamine2. Methamphetamine3. Methylphenidate4. Ephedrine5. Pseudoephedrine 6. Tyramine
104
Q

Pseudo-ephedrine:MOA

A

Indirect sympathomimetic

105
Q

Pseudo-ephedrine:Indication

A

Nasal decongestion

106
Q

Tyramine:MOA

A

Displaces NE

107
Q

Tyramine:Half-life

A

Normally very short

108
Q

Tyramine:Indications

A

Not therapeutic

109
Q

Tyramine:Elimination

A

MAO

110
Q

Propanolol:MOA

A

General (non-selective) Beta Blocker

111
Q

Propanolol:Indications (3)

A
  1. Hypertension2. Angina due to atherosclerosis3. MI
112
Q

Timolol:MOA

A

General (non-selective) Beta Blocker

113
Q

Timolol: Indications

A

Glaucoma

114
Q

Nadolol:Half-life

A

20-24 hrs

115
Q

Nadolol:MOA

A

General (non-selective) Beta-blocker

116
Q

Nadolol:Indications (2)

A
  1. Long-term angina2. Hypertension
117
Q

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

A

Propanolol, nadolol, timolol

118
Q

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

A
  1. Reduced heart rate2. Reduced contractility3. Reduced vasoconstriction (as a result of reduced RENIN release)
119
Q

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

A

Can cause bronchiole constriction in those with asthma or COPD.

120
Q

Non-selective Beta-blockers:Toxicity (5)

A
  1. Bronchospasm2. Bradycardia3. CNS effects (insomnia/depression)4. MASK sx of hypOglycemia 5. Triglyceride INC———————————————————————————-“(General) B Blockers Can Modulate Triglycerides “
121
Q

Non-selective Beta-blockers:Contraindications (4)

A
  1. Heart Block2. Sinus bradycardia3. Bronchial Asthma4. Cardiogenic shock”[He Should Be Careful] w/General Beta Blockers”
122
Q

LIST THE 5 Drugs Eliminated by COMT

A

“COMT d.i.N.e.D on 5 Drugs”1. doButamine2. isoProterenol 3. NOREPI [MAO and COMT]4 epi5. DOPAMINE [MAO and COMT]

123
Q

Name the 4 Medications that Prevent LV Remodeling in HF pts

A

“BANA helps HF pts live Loonger”

  1. Beta Blockers (Metoprolol / Carvedilol)
  2. [ACEk2 inhibitors AND ARBs]
  3. Aldosterone Blockers (Spironolactone / Eplerenone)
  4. [Nitrates + Hydralazine]
124
Q

A: Tx for [Stable Angina]

B: MOA

A

A: Sublingual NTG

B: Systemic VasoDilation (venodilation) –> [DEC LV Preload] —> [DEC myocardial O2 demand]

125
Q

Bethanechol MOA

A

Muscarinic Cholinergic Agonist

126
Q

A: Bethanechol Indication (2)

B: What situation is this indication most commonly seen

A

A: 1. [PostOp Urinary Retention from Atonic bladder]

  1. [Stimulates peristalsis in PostOp ileus]

B: After Operations, post usually have Urinary Retention in non-moving ileus –> Use Bethanechol

127
Q

Oxybutynin MOA

A

Antimuscarinic

128
Q

What target organ does the M1 Receptor work

A

Brain

129
Q

What target organ does the M2 Receptor work

A

Heart

130
Q

What target organ does the M3 Receptor work (6)

A

“M3’s BEGS for Private Lounges”

Bladder / Eyes / GI / Skin / Peripheral Vasculature / Lungs

131
Q

M1 receptor

Effect

A

Memory Function & Congnition

132
Q

M2 receptor

Effect

A

DECREASES HR & atrial contraction

133
Q

Which condition are [AntiCholinergics (such as Atropine)] contraindicated in?

A

GLAUCOMA!

It causes MyDriasis –> DEC outflow of aqueous humor –> worsens [Closed angle Glaucoma]

134
Q

Which Rx is commonly used to treat Bradycardia

A

Atropine (Anticholinergic)

(DEC vagal influence on SA & AV nodes)

135
Q

Which 2 drugs lower intraocular pressure in Glaucoma? How?

A

Carbachol & Pilocarpine

These [Muscarinic Cholinergic agnoist] cause miosis which moves iris further from the cornea and widens [ANT chamber angle] to allow outflow of aqueous humor

136
Q

[Muscarinic Cholinergic agonist] SE (5)

A

[GI: NVD / Abd pain] (INC GI smooth m. tone)

INC Secretions (sweating/lacrimation/salivation)

Dyspnea

Bradycardia

hypOtension

Step 1 USMLE Rx - Cardio (5 decks)

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