Cardio: Adrenergic / Cholinergics Flashcards
ALPHA 1 RECEPTOR
Tissues - Actions (3)
“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
ALPHA 2 RECEPTOR
Tissues- Actions (4)
“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
BETA 1 RECEPTOR
Actions (2)
(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
BETA 2 RECEPTOR
Tissues-Actions (4)
(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
BETA 3 RECEPTOR Tissues-Actions
(B1 and B2 may also contribute)(1) Fat cells- stimulates lipolysis
DOPAMINE 1 RECEPTOR
Tissues-Actions
Renal and other splanchnic blood vessels- vasoDilates (reduces resistance)
DOPAMINE 2 RECEPTORTissues-Actions
(1) Nerve terminals- inhibits adenylyl cyclase
Timolol:Half-Life
4 hours
Timolol:Mechanism of Action
General B-blocker
Timolol:Indication
Glaucoma
Nadolol:Half-Life
20-24 hours
Nadolol:Mechanism of Action
General B-blocker
Nadolol:Indication (2)
Long term angina, hypertension
Atenolol
MOA
B1-blocker
Atenolol:Indication (3)
Hypertension, angina, MI
Metoprolol:Mechanism of Action
B1-antagonist
Metoprolol:Indication (2)
Hypertension, long-term angina rx
Pindolol:A: Mechanism of ActionB: Because of its MOA, it has less _______ effect on the heart.
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.
Pindolol:A: IndicationB: Therapeutic benefit is good when (indication) is due to _________.
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.
Esmolol:Half-life
~9 minutes
Esmolol:Mechanism of Action
B1-blocker
Esmolol:A: Indication (3) B: Esmolol has a very ____ half life, so it is given ____(dosage form) in _______ crisis, _____ angina and _______
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
Phenoxybenzamine:
Mechanism of Action
Irreversible [General alpha-blocker]
Phenoxybenzamine:
Indication
Pheochromocytoma
Phentolamine:
Mechanism of Action
General alpha-blocker
Phentolamine
Indication (3)
Catecholamine-induced HTN Crisis
- rx for pheochromocytoma before surgery
- MAOI Crisis
- Cocaine OD
IS REVERSIBLE!
Prazosin:
Mechanism of Action
[Alpha 1 BLOCKER]
What are the three cardioselective B1-blockers?
Metoprolol, Atenolol, Esmolol
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]
Cardioselective B1 BLOCKERS:Therapeutic use (3)
Hypertension, angina, arrhythmia
Cardioselective B1-blockers:Toxicity (4)
Depression, insomnia, hypotension, bradycardia
Cardioselective B1-blockers:Contraindications (2)
- Pt with 2nd/3rd degree heart block -Pt with cardiogenic shock
EPINEPHRINE Half-Life
Short
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”
EPINEPHRINE ELIMINATION
COMT —> Urine
EPINEPHRINE INDICATION (4)
EPINEPHRINE Indication: •Anaphylaxis •Shock•Cardiac Arrest•Heart Block
EPINEPHRINE TOXICITY
Arrhythmias
NorEpi
MOA (2)
[General alpha agonist] + [Beta 1 agonist]
a1 > a2 > B1
NorEpiElimination
MOA and COMT—> urine
NorEpiIndication
Acute hypOtension due to VASODILATORY shock
DOPAMINEHALF-LIFE
2-3 MIN
DOPAMINE
MOA (2)
[General Beta Agonist] + [SOME alpha agonist activity]
DOPAMINEELIMINATION
MOA AND COMT
DOPAMINEINDICATION
Cardiogenic Shock
IsoProterenolHalf-life
short
IsoProterenol
MOA
[General Beta Agonist]
IsoProterenolElimination
COMT —> Urine
IsoProterenolINDICATIONS (2)
IsoProterenol1) Transient Heart Block2) Bronchospasm during Anesthesia
DoButamineHALF-LIFE
2-3 MIN
DoButamine
MOA
[MOSTLY Beta 1 AGONIST] ; some beta 2 activity
DoButamineELIMINATION
COMT—> Urine
DoButamineINDICATION
Short term for INC cardiac contractility
DoButamineTOXICITY
Hypotension (from vasoDilation;Beta 2 activity)
IsoProterenol TOXICITY
Tachyarrhythmias
DOPAMINEToxicity (2)
-Low BP-Ischemia
NorEpi
TOXICITY (2)
- Ischemia
- NE Extravasation (IV) –> Use [PhenTolamine as antidote]
EPININEPHRINETOXICITY
ARRHYTHMIAS
NorEPINEPHRINE -CO? -TPR? -HR? -OVERALL MAP?
NorEPINEPHRINE Physiological effects: ºIncreased CO; ºincrease TPR; ºdecrease HR (baroreflex); ºoverall increased MAP
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
IsoProterenol Physiological effects-TPR? -CO? -MAP? -Broncho____(constricts/dilates)
IsoProterenol Physiological effects: Decreased TPR; Increased CO; Small decrease in MAP; bronchodilation
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]`
TERBUTALINE Physiological effects-Broncho____(constricts/dilates)-Uterine contraction vs. relaxation?
TERBUTALINE Physiological effects: Bronchodilation; Uterine relaxation
TERBUTALINEToxicity (3)
TERBUTALINEToxicity: Tachycardia; Muscle tremor; Tolerance
TERBUTALINEMOA
TERBUTALINE[BETA TWO AGONIST]
TERBUTALINEINDICATIONS
TERBUTALINEPrevent and Reverse Bronchospasm in [Asthma/Bronchitis/Emphysema] Pts
ALBUTEROLMOA
[BETA TWO AGONIST]
ALBUTEROLINDICATION
Bronchial Smooth Muscle Relaxation
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.
PHENYLEPHRINE
HALF-LIFE
metabolizes slowly (less than 1 hour) because it is NOT degraded by [Plasma COMT]
PHENYLEPHRINE
Mechanism of Action
[alpha 1 AGONIST]
PHENYLEPHRINEELIMINATION
MAO
PHENYLEPHRINE
Indication (4)
- PRESSOR during Anesthesia
- Nasal Congestion
- Dilate Pupils for Eye Exam (mydriatic agent)
- SVT
PHENYLEPHRINE:Can Cause ____[INC/DEC] in HR due to _____ ______
PHENYLEPHRINE: Can cause DEC in HR due to [Baroreceptor Reflex] when peripheral vasoconstriction is initiated
CLONIDINEMOA
[alpha TWO AGONIST]
CLONIDINEELIMINATION
Urinated Out
CLONIDINEINDICATION (2)
•HTN•Analgesia
CLONIDINETOXICITY
CLONIDINE Toxicity: (x) Dry Mouth(x) HTN Crisis if withdrawn after Chronic Usage
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
AMPHETAMINEPhysiological effects:-TPR?-Inotropic vs. Chronotropic? -MAP?
AMPHETAMINE Physiological effects: ºIncreased TPR/diastolic BP ºPositive inotropic and Positive chronotropic effects; º increased MAP pressure
AMPHETAMINEMOA
AMPHETAMINE MOA: [Indirect sympathoMimetic] - Causes NorEpi Release
AMPHETAMINEINDICATION (3)
ADHD / narcolepsy / [nasal congestion]
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”
AMPHETAMINE is an _______ Agent
AMPHETAMINE is an Anorexic Agent
PARTIAL BETA AGONISTExamples (1)
-Pindolol
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]
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
PARTIAL BETA RECEPTOR AGONISTUSES (1)
HTN (for pt less tolerant to bradycardia/reduced exercise capacity)
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
PARTIAL BETA RECEPTOR AGONISTContraindications (2)
*2nd/3rd Degree heart Block*Cardiogenic Shock
ALPHA ADRENERGIC RECEPTOR BLOCKEREXAMPLES (2)
ALPHA ADRENERGIC RECEPTOR BLOCKER*[iRReversible Phenoxybenazmine] *[REVERSIBLE PHENTOLAMINE]
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
ALPHA ADRENERGIC RECEPTOR BLOCKERUSES (2)
*perioperative tx of pheochromocytoma *Dermal Necrosis
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”
ALPHA ADRENERGIC RECEPTOR BLOCKERContraindications (1)
ALPHA ADRENERGIC RECEPTOR BLOCKERContraindications: Pt with Coronary Artery Dz
ALPHA 1 BLOCKER
EXAMPLES (3)
ALPHA 1 RECEPTOR BLOCKER
Examples: -Prazosin /Doxazosin /Terazosin
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
ALPHA 1 RECEPTOR BLOCKER
Indications (2)
ALPHA 1 RECEPTOR BLOCKER
ºHTN
ºBenign Prostatic Hyperplasia
ALPHA 1 RECEPTOR BLOCKERTOXICITY (2)
ALPHA 1 RECEPTOR BLOCKER TOXICITY: (x) Syncope (x) Orthostatic hypOtension
Methylphenidate:MOA
Indirect sympathomimetic (increases NE and dopamine)
Methylphenidate:Indication
ADHD
Ephedrine:MOA
Indirect sympathomimetic
Ephedrine:Indication
Pressor agent with anesthesia
What main drugs make up the Amphetamine family ? (6)
- Amphetamine2. Methamphetamine3. Methylphenidate4. Ephedrine5. Pseudoephedrine 6. Tyramine
Pseudo-ephedrine:MOA
Indirect sympathomimetic
Pseudo-ephedrine:Indication
Nasal decongestion
Tyramine:MOA
Displaces NE
Tyramine:Half-life
Normally very short
Tyramine:Indications
Not therapeutic
Tyramine:Elimination
MAO
Propanolol:MOA
General (non-selective) Beta Blocker
Propanolol:Indications (3)
- Hypertension2. Angina due to atherosclerosis3. MI
Timolol:MOA
General (non-selective) Beta Blocker
Timolol: Indications
Glaucoma
Nadolol:Half-life
20-24 hrs
Nadolol:MOA
General (non-selective) Beta-blocker
Nadolol:Indications (2)
- Long-term angina2. Hypertension
What are the Non-selective Beta-blockers? (3)
Propanolol, nadolol, timolol
Cardiovascular effects of Non-selective Beta-blockers? (3)
- Reduced heart rate2. Reduced contractility3. Reduced vasoconstriction (as a result of reduced RENIN release)
Effect of Non-selective Beta-blockers on bronchioles? (1)
Can cause bronchiole constriction in those with asthma or COPD.
Non-selective Beta-blockers:Toxicity (5)
- Bronchospasm2. Bradycardia3. CNS effects (insomnia/depression)4. MASK sx of hypOglycemia 5. Triglyceride INC———————————————————————————-“(General) B Blockers Can Modulate Triglycerides “
Non-selective Beta-blockers:Contraindications (4)
- Heart Block2. Sinus bradycardia3. Bronchial Asthma4. Cardiogenic shock”[He Should Be Careful] w/General Beta Blockers”
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]
Name the 4 Medications that Prevent LV Remodeling in HF pts
“BANA helps HF pts live Loonger”
- Beta Blockers (Metoprolol / Carvedilol)
- [ACEk2 inhibitors AND ARBs]
- Aldosterone Blockers (Spironolactone / Eplerenone)
- [Nitrates + Hydralazine]
A: Tx for [Stable Angina]
B: MOA
A: Sublingual NTG
B: Systemic VasoDilation (venodilation) –> [DEC LV Preload] —> [DEC myocardial O2 demand]
Bethanechol MOA
Muscarinic Cholinergic Agonist
A: Bethanechol Indication (2)
B: What situation is this indication most commonly seen
A: 1. [PostOp Urinary Retention from Atonic bladder]
- [Stimulates peristalsis in PostOp ileus]
B: After Operations, post usually have Urinary Retention in non-moving ileus –> Use Bethanechol
Oxybutynin MOA
Antimuscarinic
What target organ does the M1 Receptor work
Brain
What target organ does the M2 Receptor work
Heart
What target organ does the M3 Receptor work (6)
“M3’s BEGS for Private Lounges”
Bladder / Eyes / GI / Skin / Peripheral Vasculature / Lungs
M1 receptor
Effect
Memory Function & Congnition
M2 receptor
Effect
DECREASES HR & atrial contraction
Which condition are [AntiCholinergics (such as Atropine)] contraindicated in?
GLAUCOMA!
It causes MyDriasis –> DEC outflow of aqueous humor –> worsens [Closed angle Glaucoma]
Which Rx is commonly used to treat Bradycardia
Atropine (Anticholinergic)
(DEC vagal influence on SA & AV nodes)
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
[Muscarinic Cholinergic agonist] SE (5)
[GI: NVD / Abd pain] (INC GI smooth m. tone)
INC Secretions (sweating/lacrimation/salivation)
Dyspnea
Bradycardia
hypOtension