Autonomicdrugs Format

7/29/2019 Autonomicdrugs Format

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Drug Site of Action Effect Use Adverse Effects

Epinephrine 1, 2, 1 & 2-agonist

> effect bronchodilator, blocksmast cells, used with LAs

Norepinephrine 1, 2, 1 agonist > effect shock

All A1-sympathomimetics

Pupil dilation =MyadriasisVasoconstriction:use with LocalanestheticsNasalDecongestion[avoid prolonged useb/c reboundcongestion]

Phenylephrine. 1-agonist constricts vessels and

contracts Sm. Muscle.[inc. peripheral resistance,inc. bp]-inc. IP3 and DAG1> 2

1.Hypotensive state

2.mydriatic (topical);3. nasal decongestant(topical);4. used w/LocalAnesthesia

Clonidine Central 2-agonist Acts at brain to decreasesympathetic outflow andat NE terminals to cAMP= decreas e NE release

1.2nd or 3rd line drug inHTN; 2.opioid withdrawal

Abrupt withdrawalhypertensive crisis

Brimonidine

Peripheral 2-agonist Inhibits ciliary bodysecretions Open angle Glaucoma


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B 1 Receptors

Increase campRenin releaseIncrease rate & forceof heart, CO &HR

-Sinus Tachycardia

B2 ReceptorsIncrease campRELAX: Brocho

dilator, Vasodilator,Uterine relaxation,GI smooth muscleNerve Terminals:TremorLiver: inc/glycogenolysis

-Skeletal musculTremor

Isoproterenol B1 = B2 HR

Dobutamine 1-agonist CO, HRB1> B2

-short term management ofheart failure after surgery-post MI-Cardiogenic shock

Albuterol 2>1 agonist bronchodilation acute asthma, chronicasthma

Terbutaline

Ritodrine 2 agonist uterine relaxant arrest premature labor maternal mortali

Indirect Acting

Amine

Displaces NE fromvesicles = Increase NE

release

Neuronal uptakeTachyphylaxis: Rapiddesensitization to a drug

Cont..

Cont effect

Displaced NE:deaminated by MAO, re-uptake by pumps


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Levodopa Pro-drug; DOPAdecarboxylase

Dopamine synthesis Enters CNS,Parkinsonism

Methyldopa False substrate;DOPAdecarboxylase

Production of false NT HTN in pregnant women

Reserpine Vesicular NEtransporter

Irreversible inhibition ofvesicular transporter- eventually NE isdegraded by MAO = lessNE, 5HT, Dopamineavailable,

For HTN b/c causes fallBP

-PNS dominance Vasodilation = nasstuffiness, diarrh-Parkinsonism &Galactorrhea b/cdopamine deplet amines = depres

Cocaine Reuptake channelblocker

NE is not pumped backinto nerve terminal

-w/ LA forvasoconstriction -Potentiates SNS and NE-BP & HR-impairs IAAs b/c can'tenter cell

OD: myocardialischemia, HA, CNbleeding

Imipramine Reuptake channelblocker

NE is not pumped backinto nerve terminal

Antidepressant

Duloxetine


Alpha Blockers

Phentolamine non-selective -

competitiveantagonist

Vasodilation but strong

reflex leading to angina orMI

Pheochromocytoma-

controls BP surge duringsurgical removal;- give -blocker after the-blocker[A receptor =vasodilate= bad]


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Phenoxybenzamine non-selective -irreversibleantagonist

Vasodilation-reduces maximal effectof NE, dose/ responsewill progressivelydecrease

Increase CO = carischemia

Prazosin

selective(A-1)reversible

1 reversibleselectiveantagonist ( all endin osin)

vasodilation Hypertension Postruralhypotens ion wi th

dose!! [give 1st at

Fai lure to ejacula

sympathetic tone inprostate

BPHImprove Urinary flow inBPH


B blockers -up regulation of Breceptors-dec. HDL levels

Can make CF wo-Inc. asthma, CO- Worsen Raynau- WorsenHypoglycemic

Diabet ic episode

of change insulinresponsiveness toreceptors-Claudication: anpain in muscles

PropranololTimolol- Non intransicactivity

Non-selective -blocker

Both B1: HR & CO:good for CFAV conduction: good forarrhythmias, 1 yearPost

MI

renin: anti-HTN B1and B2 Blocker af fects:

cont.

Lipophilic = enter brainCont effects.

Decreased

Bronchodi la t ion= badasthmatics, COPD

vasodilation: WorsenRaynaulds gluconeogenesis &glycog enolysis: Worsen

Diabetes


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Open angledGlaucoma

longest t1/2

Pindolol - partial

antagonist -competitiveantagonist

ISA(sympathomimeticaffect)

Carvedilol andLabetolol

Non-selective -blocker and 1-blocker

Class Three anti-arrhythmic

Metoprolol Cardio-selective1-blockerAtenolol water sol.Metoprolol is lipidsol.

Used in CongestedCardiac failure

Atenolol HTN emergency

Esmolol B1 Blocker withVasodilator action

Blocker affects only:HR & CO: good for CFAV conduction: good forarrhythmias, 1 yearPostMI

renin: anti-HTN B1

Can act on B2Receptors:contraindicated inasthmatics and Cb/cbronchoconstrict

Nevibolol

Glucagon VERY short t1/2-good for acute MI-Test pt susceptibilityto B blocker


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CHOLINERGICDRUGS

Heartincreases Nitric Oxideformation

MuscarinicReceptors

Increases HR and CO Used in -blockeroverdose, physiologiccompetition

In severeBradycardia,Glucagon can cau

Tachycardia by aon a diff receptor

ACh-esteraseactivity

MuscarineM2 CNS, IP3, DAG

M3 Heart, inhibitory

M4 Heart, Inhibitory, Kchannels = NOrelease=vasodilation

ESTER hydrolysis,usually fast

Smooth muscle,Glands, IP3

Pilocarpine M-receptor agonist

Methacholine M receptor agonist HR & CO-Vasodilation-Broncoconstriction,-Contracts bladderdetrusors

-Exocrine gland secretion-Git inc. motility-CNS excitation

Mushroom can causepoisonings (containmuscarine), treat withAtropine [ Blocks ACh]

-Not broken down byAchE

HypotensionAsthma attacksUrinary incontineUrgencyExcessive Salvat

sweatingDiarrheaTremors

Neostigmine M-receptor agonist miosis & ciliary secretion Closed angle Glaucoma-Not broken down by AchE

Affects accommod


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Carbachol AChE antagonist(false-substrate)

Bronchoconstriction Diagnostic tool for asthma-Is broken down by AchE

Organophosphate M and N receptor increases Ach in synapse,won't enter CNS

-reversal of compet i t iveNeuromusc ular blockers

-prevents breakdown ofAch

Pralidoxime[2-PAM]

AChE irreversibleantagonist(Phosphorylates it)

-Not broken down byAchE

Physostigmine Reactivates AChE Bronchoconstrx,bronchial secretions-paralyses diaphragm,vasodilation, HR,incontinence, diarrhea

Pesticide PoisoningsTreat w/high doseAtropine andPralidoxime

Terrorist attacks

Pyridostigmine AChE Inhibitor breaks bond btw OPP &AChE

Antidote (fororganophosphatepoisoning)

Edrophonium poisoning:belladonna plants orTricyclicantidepressants:

Red: Vasodilation Hot: hyperthermia,vasodilation

Cont..

Cont site of act

Dry: reducedsweating, decreasedsecretions,decreased sweatingand salivaMad: deliriumBlind: cyclopegia

and mydriasis

Long acting increase inAch

Tx: alzheimers, increasefxn., acts in CNS [not 4structure]


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ANticholinergicsPoisoning

Long acting increasein Ach

Tx: Myasthenia Gravisby increasing strength-Does not enter CNS[good b/c want to stay inperiphery]

s/s of muscarine over-stimulation:Excessive Salvation/sweatingDiarrheaWheezing

Atropine Short acting

increase in Ach

DIAGNOSIS of

Myasthenia Gravis if seetransientImprovement infunction-OR to measure correctACh dose [too much=impaired fxn still]

Scopolamine MUSCARINIC-Antagonist

Oxybutynin

Muscarinicantagonists

Treating Muscarine Over-

stimulation/ Poisoning

-eyes dilate =

Mydriasis, makesglaucoma worstcycloplegia= cantaccommodate,-tachycardia,-bronchi relaxed,-decreased secretdry mouth,Constipation: baGI distresses-decreased sweabad for HOT clim

decreased GI mot-urinary retention(avoid if BPH pre


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TolterodineMotion sickness, topicalpatch

Darifenacine bladder retention Overactive Bladder

Ipratropium

Benztropine bladder retention Overactive Bladder/URGENCY

Homatropine/Tropicamide

Bronchodilator COPD - inhaled

Propantheline non ionized; excitesCNS

Parkinson Disease -enters CNS

Antihistamine Mydriatic Uveitis

Neuroleptic Anticholinergic

Antispasmatic Reduce GIT contractility

TCAN2 NICOTINIC NMJbinds toDecamethonium >Hexamethonium [10 > 7 ]

Side Effects ofAnticholinergics


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NICOTINICANTAGONISTS

CURARE:Tubocurarine, end: a/curonium

Atracurium/Vecuronium

N-Ach 1 receptorcompetitive antagonist

Mivacurium Small muscles Largemuscles diaphragmskeletal muscle paralysis

Muscle relaxant-reversed byneostigmine,Prridostigmine-histamine release-TX: Botulinium poison

no CNS = still feel

Pancuronium Muscle relaxantHoffman hydrolysis inplasma, good for renalfailure

Succinylcholine Muscle Relaxant-SHORTEST durationbesides Succinycholine

Nm receptor agonist Longest duration

Effect

Causes continuousendplatedepolarization/Fasiculations

paralysis, noelectrical activity[Phase I I block]

Use.

-Not degraded by AChEbut bypseudocholinesterase -Muscle Relaxant

Cont adverse..

Tx: Dantrolene b/cprevents Ca release-Myalgias; Apnea

- Intra Ocular Pressure-Hyperkalemia [b/cprolonged depolarizations,seen in traumas, burns etc.]

-fasciculations (wpost op pain)-MalignantHyperthermia [ADgene],


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