Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

Cardio: Adrenergic / Cholinergics 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

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

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

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

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

BETA 3 RECEPTOR Tissues-Actions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

DOPAMINE 1 RECEPTOR

Tissues-Actions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

DOPAMINE 2 RECEPTORTissues-Actions

A

(1) Nerve terminals- inhibits adenylyl cyclase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Timolol:Half-Life

A

4 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Timolol:Mechanism of Action

A

General B-blocker

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

Timolol:Indication

A

Glaucoma

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

Nadolol:Half-Life

A

20-24 hours

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

Nadolol:Mechanism of Action

A

General B-blocker

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

Nadolol:Indication (2)

A

Long term angina, hypertension

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

Atenolol

MOA

A

B1-blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Atenolol:Indication (3)

A

Hypertension, angina, MI

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

Metoprolol:Mechanism of Action

A

B1-antagonist

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

Metoprolol:Indication (2)

A

Hypertension, long-term angina rx

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

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

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

Esmolol:Half-life

A

~9 minutes

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

Esmolol:Mechanism of Action

A

B1-blocker

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

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

Phenoxybenzamine:

Mechanism of Action

A

Irreversible [General alpha-blocker]

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

Phenoxybenzamine:

Indication

A

Pheochromocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Phentolamine: Mechanism of Action
General alpha-blocker
26
Phentolamine Indication (3)
*Catecholamine-induced HTN Crisis* 1. rx for pheochromocytoma **before** surgery 2. MAOI Crisis 3. Cocaine OD ***IS REVERSIBLE!***
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 (2)
[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 MOA (2)
## Footnote **[General alpha agonist] + [Beta 1 agonist]** *a1 \> a2 \> B1*
39
NorEpiElimination
MOA and COMT---\> urine
40
NorEpiIndication
Acute hypOtension due to VASODILATORY shock
41
DOPAMINEHALF-LIFE
2-3 MIN
42
DOPAMINE MOA (2)
[General Beta Agonist] + [SOME alpha agonist activity]
43
DOPAMINEELIMINATION
MOA AND COMT
44
DOPAMINEINDICATION
Cardiogenic Shock
45
IsoProterenolHalf-life
short
46
IsoProterenol MOA
[General Beta **Agonist**]
47
IsoProterenolElimination
COMT ---\> Urine
48
IsoProterenolINDICATIONS (2)
IsoProterenol1) Transient Heart Block2) Bronchospasm during Anesthesia
49
DoButamineHALF-LIFE
2-3 MIN
50
DoButamine MOA
**[MOSTLY Beta 1 AGONIST]** ; some beta 2 activity
51
DoButamineELIMINATION
COMT---\> Urine
52
DoButamineINDICATION
Short term for INC cardiac contractility
53
DoButamineTOXICITY
Hypotension (from vasoDilation;Beta 2 activity)
54
IsoProterenol TOXICITY
Tachyarrhythmias
55
DOPAMINEToxicity (2)
-Low BP-Ischemia
56
NorEpi TOXICITY (2)
- Ischemia - NE Extravasation (IV) --\> Use [PhenTolamine as antidote]
57
EPININEPHRINETOXICITY
ARRHYTHMIAS
58
NorEPINEPHRINE -CO? -TPR? -HR? -OVERALL MAP?
NorEPINEPHRINE Physiological effects: ºIncreased CO; ºincrease TPR; ºdecrease HR (baroreflex); ºoverall increased MAP
59
DOPAMINE A: LOW DOSE: _____ TPR/ _______ CO; vs. HIGH DOSE: ______ TPR and _____ MAP
LOW DOSE: decreased TPR/ increased CO; vs. HIGH DOSE: Increased MAP and TPR
60
IsoProterenol Physiological effects-TPR? -CO? -MAP? -Broncho\_\_\_\_(constricts/dilates)
IsoProterenol Physiological effects: Decreased TPR; Increased CO; Small decrease in MAP; bronchodilation
61
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]`
62
TERBUTALINE Physiological effects-Broncho\_\_\_\_(constricts/dilates)-Uterine contraction vs. relaxation?
TERBUTALINE Physiological effects: Bronchodilation; Uterine relaxation
63
TERBUTALINEToxicity (3)
TERBUTALINEToxicity: Tachycardia; Muscle tremor; Tolerance
64
TERBUTALINEMOA
TERBUTALINE[BETA TWO AGONIST]
65
TERBUTALINEINDICATIONS
TERBUTALINEPrevent and Reverse Bronchospasm in [Asthma/Bronchitis/Emphysema] Pts
66
ALBUTEROLMOA
[BETA TWO AGONIST]
67
ALBUTEROLINDICATION
Bronchial Smooth Muscle Relaxation
68
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.
69
PHENYLEPHRINE HALF-LIFE
**metabolizes slowly** (*less than 1 hour*) because it is NOT degraded by [Plasma COMT]
70
PHENYLEPHRINE Mechanism of Action
[alpha 1 AGONIST]
71
PHENYLEPHRINEELIMINATION
MAO
72
PHENYLEPHRINE Indication (4)
- PRESSOR during Anesthesia - Nasal Congestion - Dilate Pupils for Eye Exam (mydriatic agent) - SVT
73
PHENYLEPHRINE:Can Cause \_\_\_\_[INC/DEC] in HR due to _____ \_\_\_\_\_\_
PHENYLEPHRINE: Can cause DEC in HR due to [Baroreceptor Reflex] when peripheral vasoconstriction is initiated
74
CLONIDINEMOA
[alpha TWO AGONIST]
75
CLONIDINEELIMINATION
Urinated Out
76
CLONIDINEINDICATION (2)
•HTN•Analgesia
77
CLONIDINETOXICITY
CLONIDINE Toxicity: (x) Dry Mouth(x) HTN Crisis if withdrawn after Chronic Usage
78
CLONIDINEWorks 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
79
AMPHETAMINEPhysiological effects:-TPR?-Inotropic vs. Chronotropic? -MAP?
AMPHETAMINE Physiological effects: ºIncreased TPR/diastolic BP ºPositive inotropic and Positive chronotropic effects; º increased MAP pressure
80
AMPHETAMINEMOA
AMPHETAMINE MOA: [Indirect sympathoMimetic] - Causes NorEpi Release
81
AMPHETAMINEINDICATION (3)
ADHD / narcolepsy / [nasal congestion]
82
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"
83
AMPHETAMINE is an _______ Agent
AMPHETAMINE is an Anorexic Agent
84
PARTIAL BETA AGONISTExamples (1)
-Pindolol
85
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]
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
PARTIAL BETA AGONIST-HR? -Heart Contractility? -Renin Release?
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
PARTIAL BETA RECEPTOR AGONISTUSES (1)
HTN (for pt less tolerant to bradycardia/reduced exercise capacity)
88
PARTIAL BETA RECEPTOR AGONISTTOXICITY (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
89
PARTIAL BETA RECEPTOR AGONISTContraindications (2)
\*2nd/3rd Degree heart Block\*Cardiogenic Shock
90
ALPHA ADRENERGIC RECEPTOR BLOCKEREXAMPLES (2)
ALPHA ADRENERGIC RECEPTOR BLOCKER\*[iRReversible Phenoxybenazmine] \*[REVERSIBLE PHENTOLAMINE]
91
ALPHA ADRENERGIC RECEPTOR BLOCKERCV Effects (3)
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
ALPHA ADRENERGIC RECEPTOR BLOCKERUSES (2)
\*perioperative tx of pheochromocytoma \*Dermal Necrosis
93
GENERAL ALPHA BLOCKERTOXICITY (3)
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
ALPHA ADRENERGIC RECEPTOR BLOCKERContraindications (1)
ALPHA ADRENERGIC RECEPTOR BLOCKERContraindications: Pt with Coronary Artery Dz
95
ALPHA 1 BLOCKER EXAMPLES (3)
ALPHA 1 RECEPTOR BLOCKER Examples: -Prazosin /Doxazosin /Terazosin
96
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
97
ALPHA 1 RECEPTOR BLOCKER Indications (2)
ALPHA 1 RECEPTOR BLOCKER ºHTN ºBenign Prostatic Hyperplasia
98
ALPHA 1 RECEPTOR BLOCKERTOXICITY (2)
ALPHA 1 RECEPTOR BLOCKER TOXICITY: (x) Syncope (x) Orthostatic hypOtension
99
Methylphenidate:MOA
Indirect sympathomimetic (increases NE and dopamine)
100
Methylphenidate:Indication
ADHD
101
Ephedrine:MOA
Indirect sympathomimetic
102
Ephedrine:Indication
Pressor agent with anesthesia
103
What main drugs make up the Amphetamine family ? (6)
1. Amphetamine2. Methamphetamine3. Methylphenidate4. Ephedrine5. Pseudoephedrine 6. Tyramine
104
Pseudo-ephedrine:MOA
Indirect sympathomimetic
105
Pseudo-ephedrine:Indication
Nasal decongestion
106
Tyramine:MOA
Displaces NE
107
Tyramine:Half-life
Normally very short
108
Tyramine:Indications
Not therapeutic
109
Tyramine:Elimination
MAO
110
Propanolol:MOA
General (non-selective) Beta Blocker
111
Propanolol:Indications (3)
1. Hypertension2. Angina due to atherosclerosis3. MI
112
Timolol:MOA
General (non-selective) Beta Blocker
113
Timolol: Indications
Glaucoma
114
Nadolol:Half-life
20-24 hrs
115
Nadolol:MOA
General (non-selective) Beta-blocker
116
Nadolol:Indications (2)
1. Long-term angina2. Hypertension
117
What are the Non-selective Beta-blockers? (3)
Propanolol, nadolol, timolol
118
Cardiovascular effects of Non-selective Beta-blockers? (3)
1. Reduced heart rate2. Reduced contractility3. Reduced vasoconstriction (as a result of reduced RENIN release)
119
Effect of Non-selective Beta-blockers on bronchioles? (1)
Can cause bronchiole constriction in those with asthma or COPD.
120
Non-selective Beta-blockers:Toxicity (5)
1. Bronchospasm2. Bradycardia3. CNS effects (insomnia/depression)4. MASK sx of hypOglycemia 5. Triglyceride INC----------------------------------------------------------------------------------"(General) B Blockers Can Modulate Triglycerides "
121
Non-selective Beta-blockers:Contraindications (4)
1. Heart Block2. Sinus bradycardia3. Bronchial Asthma4. Cardiogenic shock"[He Should Be Careful] w/General Beta Blockers"
122
LIST THE 5 Drugs Eliminated by COMT
"COMT d.i.N.e.D on 5 Drugs"1. doButamine2. isoProterenol 3. NOREPI [MAO and COMT]4 epi5. DOPAMINE [MAO and COMT]
123
Name the 4 Medications that **Prevent LV Remodeling** in HF pts
"**BANA** helps HF pts live Loonger" 1. **B**eta Blockers (Metoprolol / Carvedilol) 2. [**A**CEk2 inhibitors _AND_ ARBs] 3. **A**ldosterone Blockers (Spironolactone / Eplerenone) 4. [**N**itrates + Hydralazine]
124
A: Tx for [**Stable** Angina] B: MOA
A: Sublingual NTG B: Systemic VasoDilation (**venodilation**) --\> [DEC LV Preload] ---\> [DEC myocardial O2 demand]
125
Bethanechol MOA
Muscarinic Cholinergic Agonist
126
A: Bethanechol Indication (2) B: What *situation* is this indication most commonly seen
A: 1. [PostOp Urinary **Retention** from Atonic bladder] 2. [Stimulates peristalsis in PostOp ileus] B: After Operations, post usually have Urinary Retention in non-moving ileus --\> Use Bethanechol
127
Oxybutynin MOA
Antimuscarinic
128
What target organ does the **M1 Receptor** work
Brain
129
What target organ does the **M2 Receptor** work
Heart
130
What target organ does the **M3 Receptor** work (6)
"M3's **BEGS** for **P**rivate **L**ounges" ## Footnote **B**ladder / **E**yes / **G**I / **S**kin / **P**eripheral Vasculature / **L**ungs
131
M1 receptor Effect
Memory Function & Congnition
132
M2 receptor Effect
**DECREASES** HR & atrial contraction
133
Which condition are [AntiCholinergics (such as Atropine)] contraindicated in?
GLAUCOMA! It causes MyDriasis --\> DEC outflow of aqueous humor --\> worsens [Closed angle Glaucoma]
134
Which Rx is commonly used to treat Bradycardia
Atropine (Anticholinergic) | (DEC vagal influence on SA & AV nodes)
135
Which 2 drugs lower intraocular pressure in Glaucoma? How?
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
[Muscarinic Cholinergic agonist] SE (5)
[GI: NVD / Abd pain] (INC GI smooth m. tone) INC Secretions (sweating/lacrimation/salivation) Dyspnea Bradycardia hypOtension

Step 1 USMLE Rx - Cardio (5 decks)

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