Pharmacology - Autonomic drugs Flashcards
Cholinomimetics (4)
- Bethane.chol
- Carba.chol
- Pilo.car.pine
- Metha.choline
GPCR’s
- list them, and which G-protein
Adrenergics: QISS Muscarinics: QIQ Dopamine: SI Histamine: QS Vasopressin: QS
actions of alpha-1
- vascular smooth muscle contraction
- pupillary dilator muscle contraction (mydriasis)
- intestinal and bladder sphincted muscle
Gq, so muscle contractions
actions of alpha-2
- decrease sympathetic outflow
- decrease insulin release
- decrease lipolysis
- decrease blood flood 2/2 plt aggregation
Gi, so decreases stuff
actions of beta-1
- increase HR and contractility
- increases renin
- increase lipolysis
Gs, so increase stuff
actions of beta-2
- increase HR and contractility
- increase blood flow (vasodilation)
- increase breathing (bronchodilation)
- increase lipolysis
- increase insulin release
- increase aqueous humor production
- increase intraocular pressure (relaxing ciliary muscle)
- decrease uterine tone
Gs, so increases stuff … beta-2, so more than beta-1
actions of M1
CNS and enteric NS
actions of M2
- decrease HR
- decrease atrial contractility
anti-beta-2
Gi, so decrease stuff
actions of M3
- exocrine gland muscle contraction –> secretions
- intestinal muscle contraction –> peristalsis
- bladder muscle contraction
- broncho muscle contraction (broncoconstriction)
- pupillary sphincter muscle contraction (miosis)
- ciliary muscle contration (accomodation and decreases IOP by allowing humor flow)
Gq, so contraction stuff
actions of D1
relaxes renal vascular smooth muscle
actions of D2
modulates NT release, esp brain
actions of H1
- nasal and bronchial mucus production
- increase vascular permeability
- bronchoconstriction
- pruritis
- pain
Gq, so contraction stuff
actions of H2
- increases gastric acid secretion by parietal cells
Gs, so increases stuff
actions of V1
increase vascular smooth muscle contraction
Gq, so muscle contraction
actions of V2
increase water permeability and reabsorption at collecting tubules
Gs, so increases stuff (v2, b/c 2 kidneys)
choline transporter inhibitor
Hemicholinium
Ach vescile loading inhibitor
Ves.ami.col
Ach release inhibitor
botilinum
Tyrosine hydroxylase inhibitor
Metyrosine
Dopamine vesicle loading inhibitor
Reserpine
vesicular NE release inhibitor
Bretylium
Guanethidine
vesicular NE release stimulator
amphetamine
Direct agonist Cholinomimetic agents (4)
- Bethane.chol
- Carb.a.chol
- Pilo.car.pine
- Metha.choline
Cholinomimetic agents (4)
- Bethane.chol
- Carb.a.chol
- Pilo.car.pine
- Metha.choline
Carb.a.chol
- action
- clinical application
- Carbon copy of Ach
- Glaucoma, pupillary constriction, relief of IOP
via M3
Pilocarpine
- action
- clinical application
- contracts ciliary muscle (allows flow of humor), contracts pupillary sphincter (miosis), stimulates glands (sweat, tears, saliva)
- open and close angle glaucoma; used to dx CF
via M3
Metha.choline
- action
- clinical application
- stimulates muscarinic receptors in airway when inhaled
- constricts bronchioles… used as the challenge test for asthma
Metha.choline
- action
- clinical application
- stimulates muscarinic receptors in airway when inhaled
- constricts bronchioles… used as the challenge test for asthma
Indirect agonist Cholinomimetic drugs (via AchE inhibition) (5 of them)
- Neo.stig.mine
- Pryido.stig.mine
- Physo.stig.mine
- Donepezil, Riva.stig.mine, Galantamine
- Edrophonium
Neo.stig.mine
- action
- clinical application
- increases endogenous Ach; NO cross BBB
- post-op and neurogenic ileus, urinary retention, myasthenia gravis, reversal or NMJ blockade (post-op)
Pyrido.stig.mine
- action
- clinical application
- increase endogenous Ach; NO cross BBB
- long acting Myasthenia Gravis relief of weakness
Physo.stig.mine
- action
- clinical application
- increases engodenous Ach; CAN cross BBB
- fixes anticholinergic toxicity b/c can cross BBB (e.g. atropine overdose)
Donepezil
- action
- clinical application
- increases endogenous Ach
- Alzheimers
Edrophonium
- action
- clinical application
- increases endogenous Ach
- extremely short-acting relief of Myasthenia Gravis (historically used to dx it)
Cholinesterase Inhibitor poisoning leads to:
DUMBBELSS
- Diarrhea/Diaphoresis, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of CNS and skeletal muscle/Emesis, Lacrimation, Sweating, Salivation
CNS excitation is by nAchR
Cholinesterase Inhibitor poisoning leads to:
DUMBBELSS
- Diarrhea/Diaphoresis, Urination, Miosis, Bronchospasm, Bradycardia, Emesis, Lacrimation, Sweating, Salivation
antidote for cholinesterase inhibitor poisoning?
Atropine (comp inhibitor) + Pralidoxine (releases AchE is given early)
antidote for cholinesterase inhibitor poisoning?
Atropine (comp inhibitor) + Pralidoxine (releases AchE is given early)
Muscarinic antagonists used on eye (3)
- what action
- Atropine
- Homatropine
- Tropicamide
- mydriasis and cyclopegia
Muscarinic antagonist used for CNS (2)
- Benz.tropine for PD and EPS
2. Scopolamine for motion sickness
Muscarinic antagonist used for respiratory (2)
- Ipra.tropium
- Tio.tropium
for COPD and asthma
Muscarinic antagonist used for GU (3)
- Oxy.buty.nin
- Dari.fenacin
- Soli.fenacin
- Reduce urgency in mild cystitis and reduce bladder spasms
Muscarinic antagonist used for GI and respiratory
Glyco.pyrro.late
IV: pre-op use to reduce airway secretions
PO: drooling, peptic ulcer
Atropine toxicity results in?
“Hot as a hare, Dry as a bone, Red as a beet, Blind as a bat, Mad as a hatter”
- Hot b/c can’t sweat and tachycardic
- Dry mouth and skin
- Red skin
- Blind b/c cyclopegia and acute angle glaucoma (2/2 mydriasis)
- Mad b/c disorientation
Atropine toxicity results in?
“Hot as a hare, Dry as a bone, Red as a beet, Blind as a bat, Mad as a hatter”
- Hot b/c can’t sweat and tachycardic
- Dry mouth and skin
- Red skin
- Blind b/c cyclopegia and acute angle glaucoma (2/2 mydriasis)
- Mad b/c disorientation
What garden plant leads to mydriasis
Jimson weed (Datura) 2/2 plant alklaloids
Direct Sympathomimetics (8)
- Epi
- NE
- Iso.pro.terenol
- Dopamine
- Dobutamine
- Phenylephrine
- Albuterol, Salmetrol
- Terbutaline
Epi
- what receptors (at high doses which one more)
- applications
- beta > alpha (but at high doses, alpha more)
- anaphylaxis, open-angle glaucoma (not closed angle) w/alpha, asthma, hypotension
NE
- what receptors
- applications
- alpha-1 > alpha-2 > beta- 1
- treats hypotension by contraction of vascular smooth muscle, but causes decrease in renal perfusion
Iso.pro.terenol
- what receptors
- applications
- beta-1 = beta-2
- used in electrophysiological evaluation of tachyarrhythmias, but can worsen ischemia
Dopamine
- what receptors
- applications
- D1 = D2 > beta > alpha
- unstable bradycardia, HF, shock; inotropic and chronotropic alpha effects predominante ate higher doses
Dobutamine
- what receptors
- applications
- beta-1 > beta-2
- HF (inotropic > chronotropic); cardiac stress testing
Phenylephrine
- what receptors
- applications
- alpha-1 > alpha-2
- hypotension (by vasoconstriction); ocular procedures (b/c mydriatic); rhinitis (decongestant)
terbutaline
- what receptors
- applications
- beta-2 > beta-1
- reduce premature uterine contractions
terbutaline
- what receptors
- applications
- beta-2 > beta-1
- reduce premature uterine contractions
Indirect Sympathomimetics (3)
- Amphetamine
- Ephedrine
- Cocaine
Amphetamine
- effect
- applications
- indirect general agonist, reuptake inhibitor, release of stored catecholamines
- Narcolepsy, obesity, ADD
Ephedrine
- effect
- applications
- indirect general agonist releases stored catecholamines
- Nasal decongestant, urinary incontinence, hypotension
what should you never give suspected cocaine intoxication? and why?
beta blockers
this would lead to unopposed alpha-1 activation and extreme hypertension b/c of loss of beta-2 which vasodilates and counteracts it
what should you never give suspected cocaine intoxication? and why?
beta blockers
this would lead to unopposed alpha-1 activation and extreme hypertension b/c of loss of beta-2 which vasodilates and counteracts it
NE vs. Isoproterenol
- BP and HR effects
NE is more alpha and Isoproterenol is beta
NE: alpha-1 –> increases BP –> reflex bradycardia
Isoproterenol: beta -2 –> decrease BP –> reflex tacycardia + beta-1 tachycardia
Sympatholytics (alpha-2 agonists) (2)
- clonidine
2. alpha-methyldopa
Clonidine
- what receptors
- applications
- toxicity
- alpha-2 agonist (decrease sympathetic outflow)
- HTN emergency (doesn’t decrease renal flow); ADHD, severe pain, ethanol/opioid withdrawal
- toxic: CNS depression, bradycardia, hypotension, respiratory distress, miosis
alpha-methyldopa
- what receptors
- application
- toxicity
- alpha 2 agonist
- HTN in pregnancy b/c safe in pregnancy
- Direct Coombs + hemolytic anemia; SLE-like syndrome
Non-selective alpha blockers (2)
- Phenoxybenzamine (irreversible)
2. Phentolamine (reversible)
Alpha-1 selective alpha blocker (4)
- Praz.osin
- Teraz.osin
- Doxaz.osin
- Tamsul.osin`
Alpha-2 selective alpha blockers (1)
Mirtazapine
Phen.oxy.benz.amine
- what receptors
- applications
- toxicity
- nonselective irreversible alpha blockade
- pheochromocytoma (used pre-op) to prevent catecholamine crisis
- orthostatic hypotension, reflex tachycardia
Phen.tol.amine
- what receptors
- applications
- toxicity
- nonselective reversible alpha blockade
- give to pts on MAO-I’s who eat tyramine containing foods
Mirtazapine (Remeron)
- what receptors
- applications
- toxicity
- selective alpha-2 antagonism
- depression
- sedation, increase serum cholesterol and increase appetite
Epinephrine vs. Phenylephrine on BP
- before and after alpha-blockade
Epi at high doses acts more on alphas, so acts as a pressor… however, if administered after alpha-blockade, will have beta response of vasodilation and decrease in BP
Phenylephrine is a pure alpha-agonist, so acts as a pressor… so after alpha-blockade, will have no effect on BP
Beta-1 selective Beta Blocker (5)
- Ace.but.olol
- A.ten.olol
- Bet.ax.olol
- Esm.olol
- Metopr.olol
beta-1 .. first 1st half of alphabet
Non-selective Beta blocker (4)
- Nad.olol
- Pind.olol
- Propran.olol
- Tim.olol
both beta 1- and 2 … second half of alphabet
non-selective alpha AND beta antagonism (2)
- Carvedi.lol
- Labeta.lol
these are not -olol’s, but just -lol’s
Special beta blocker that blocks beta-1 and activates beta-3
what does it lead to?
Nebiv.olol
cardiac selective beta-1 blockade with beta-3 agonism
- beta-3 stimualtes activation of NO synthase in vasculature
How does BB work to treat: angina pectoris
decreases HR and contractility, resulting in decrease O2 consumption
How does BB work to treat: MI
- which ones
metoprolol, carvedilol, bisoprolol
decreases mortality
How does BB work to treat: SVT
- which ones
metoprolol and esmolol - class II antiarrhythmics that decrease AV conduction velocity
How does BB work to treat: HTN
- which ones
- decreases CO by decreasing HR and contractility
- decreases renin secretion by blocking beta-1 on JGA cells
How does BB work to treat: CHF
- slows progression of chronic failure
How does BB work to treat: glaucoma
- which one
Timolol
decreases secretion of aqueous humor (beta-2 blockade)
Toxicity of beta blockers (5)
- impotence
- CV ADRs (brady, AV block, CHF)
- CNS ADRs (sz, sedation, sleep alteration)
- Dyslipidemia (w/metoprolol)
- Exacerbation of COPD and asthma
