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231 Pharmacology > 2 Autonomic Drugs > Flashcards

2 Autonomic Drugs Flashcards

1
Q

parasympathetic outflow

  • preganglionic axon type?
  • preganglionic NT released?
  • postganglionic axon type?
  • postganglionic NT released?
A
  • cholinergic
  • ACh
  • cholinergic
  • ACh
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2
Q

sympathetic outflow

  • preganglionic axon type?
  • preganglionic NT released?
  • postganglionic axon type?
  • postganglionic NT released?
A
  • cholinergic
  • ACh
  • adrenergic
  • NE
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3
Q

what’s the organization of parasympathomimetic drugs?

A
  • cholinergic receptor agonists
    • direct-acting
    • indirect-acting
  • – anticholinesterases (reversible)
  • – anticholinesterases (irreversible)
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4
Q

what’s the organization of direct-acting cholinergic receptor agonists?

A
  • muscarinic receptor agonists
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5
Q

what’s the organization of indirect-acting cholinomimetic receptor agonists?

A
  • reversible inhibitors
    • quaternary alcohols
    • carbamate esters
  • irreversible inhibitors
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6
Q
  • (direct-acting cholinomimetic drug) muscarinic receptor agonist MOA
  • 2 drug examples
A
  • mimics ACh at junctions of PNS
  • eg. bethanechol - resistant to cholinesterases = persistent
  • eg. pilocarpine - resistant to cholinesterases, CNS disturbances, sweating, salivation
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7
Q
  • indirect-acting cholinomimetic drug characteristics and MOA?
A
  • anticholinesterase drugs - inhibit ACh metabolism

- MOA - blocks hydrolysis of ACh, increases ACh in synpase = muscarinic or nicotinic effects

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8
Q
  • (indirect-acting cholinomimetic drug) - reversible inhibitor - quaternary alcohol MOA
  • 1 drug example
A
  • binds reversibly to active site of cholinesterase
  • prevents access by ACh - 10-20 min
  • eg. edrophnium
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9
Q
  • (indirect-acting cholinomimetic drug) - reversible inhibitor - carbamate esters MOA
  • 2 drug examples
A
  • bind to carbamylate active site of cholinesterase
  • more resistant to hydration - 30-120 min
  • eg. neostigmine - blurred vision, headache, bradycardia
  • eg. physostigmine - lipid soluble, enters CNS = convulsions
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10
Q
  • irreversible inhibitors MOA

- 1 drug example

A
  • phosphorylates cholinesterase, enzyme inactivated
  • resynthesis of enzyme needed for recovery
  • miotic agent for glaucoma
  • causes intense, prolonged miosis
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11
Q

primary target organs of parasympathomimetic drugs

A
  • eye
  • NM junctions
  • GI and urinary tracts
  • respiratory tract
  • heart
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12
Q

major uses of parasympathomimetic drugs

A
  • glaucoma
  • myasthenia gravis
  • increase GI and GU motility
  • reversal of NM blockade
  • atropine poisoning
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13
Q

what’re 3 objectives of treating glaucoma?

A
  • decrease IOP
  • increase AH outflow
  • decrease AH production
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14
Q

how do you treat glaucoma?

A
  • muscarinic cholinomimetics contracts ciliary m. and opens drainage angle
    • direct-acting: pilocarpine
    • indirect-acting: physostigmine, isofluorophate
  • a adrenoceptor agonists (eg. epinephrine)
    • dilates iris
    • increases AH outflow
    • decreases AH secretion (ciliary epithelium)
  • b adrenoceptor blockers (eg. timolol)
    • decreases AH production (ciliary epithelium)
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15
Q

how are reversible inhibitors used in

  • myasthenia gravis
  • reversal of NM blockade
  • GI and GU
  • cardiovascular
A
  • neostigmine increases strength of contraction
  • cholinesterase inhibitors increase amount of ACh, competes with NM blocker for nicotinic receptors
  • stimulates peristalsis and bladder contraction
  • decreases HR, contractility, CO
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16
Q

where are 3 places that cholinergic receptor antagonists block actions of ACh?

A
  • central and peripheral muscarinic receptors
  • nicotinic receptors at NM junction
  • nicotinic receptors in ganglia
17
Q

2 drugs that are muscarinic blockers

A

atropine

tropicamide

18
Q

1 drug that’s a neuromuscular blocker (antinicotinic)

A

curare

19
Q

MOA of muscarinic blocking drugs

A
  • reversible blockade of ACh at M receptors by competitive binding
  • reverse by increasing ACh or agonist to decrease blockade
20
Q

atropine (M blocking prototype) characteristics

A
  • lipid soluble, enters CNS
  • effect lasts longer than tropicamide
  • blocks all parasympathetic functions
    • decreased sweating, decreased salivation
    • rapid heart rate, dilation, blurred vision
    • hallucination delirium, coma
    • toxicity tx: physostigmine
21
Q

ophthalmic uses of antimuscarinics (eg. atropine, tropicamide)?

A
  • mydriasis and
    cycloplegia
    – measure ref errors without accommodation
    – retinal exam
22
Q

describe adrenergic receptor agonists

A
  • they’re sympathomimetic drugs
  • mimic actions of NE and EP
  • profound effects on heart and peripheral circulation
  • undesirable side effects
23
Q

cardiovascular action of adrenergic agonists?

A
  • alter rate and force of heart contractions
  • alter tone of bvs
  • influences BP since BP = CO x PVR
24
Q

organization of adrenergic receptor agonists - drugs increase sympathetic activity

A
  • direct acting
    • a agonists
  • – non-selective
  • – selective a1
    • b agonists
  • – non-selective
  • – selective b1 or b2
  • indirect-acting
    • releasers
    • reuptake inhibitors
25
Q

4 effects of direct-acting, non-selective adrenergic receptor agonists (eg. epinephrine)

A
  • cardiac - b1 activation –> increases CO and increases force/rate of contraction
  • vascular smooth muscle - a1 stimulation –> vasoconstriction in skin/kidneys –> increases PVR
  • smooth muscle
    • a1 stimulation –> contraction of spleen, bladder sphincter, dilator
    • b2 stimulation –> bronchodilation, decreases GI contractions, decreases tone/contraction of pregnant uterus, relaxes urinary bladder
  • metabolic - increases circulating glucose, lactic acid, free fatty acids
26
Q

effects of direct-acting, selective adrenergic receptor a agonists for phenylephrine and clonidine

A
  • phenylephrine - a1 agonist, vasoconstriction, increases BP, pupillary dilation
  • clonidine - a2 adrenoceptor agonist in brain stem, decreases sympathetic outflow, decreases BP
27
Q

effects of direct-acting, selective adrenergic receptor b agonists for dopamine/dobutamine and albuterol

A
  • dopamine/dobutamine - b1 receptor agonist, increases contractility, stimulates hearts, dilates renal vasculature, increases GFR (used in renal failure)
  • albuterol - b2 agonist, dilator (used in asthma), no stimulation of heart, short duration
28
Q

effects of indirect-acting, selective adrenergic receptor b agonists for pseudephedrine and amphetamine

A
  • pseudephedrine (Benadryl-D, Sudafed) - stimulates NE release, hay fever release
  • amphetaine - facilitates release and blocks reuptake of NE and dopamine (cocaine only block reuptake), central and peripheral sympathomimetic effects
29
Q

cardiovascular system applications of adrenergic agonists

A
  • hypotension/shock - tx: fluids, a1 agonists eg. phenylephrine
  • cardiac insufficiency - b agonist eg. epinephrine, dobutamine, dopamine
  • ## local vasoconstriction - lidocaine HCl with epinephrine
30
Q

respiratory applications of adrenergic agonists

A
  • asthma - b2 activation for bronchodilation eg. albuterol
31
Q

mucous membrane congestion applications of adrenergic agonists

A
  • hay fever/colds - a receptor activation for decongestion eg. phenylephrine, pseudephedrine
32
Q

anaphylaxis applications of adrenergic agonists

A

tx: epinehphrine

33
Q

ophthalmology applications of adrenergic agonists

A
  • a1 activation, mydriasis, decrease synechiae
34
Q

organization of adrenergic receptor antagonists - drugs decrease sympathetic activity

A
  • direct acting
    • a blockers
  • – non-selective
  • – selective a1 or a2
    • b blockers
  • – non-selective
  • – selective b1 or b2
35
Q

a receptor blocking drugs MOA

A
  • a1 blockade –> vasodilation –> decreases peripheral resistance and BP
  • non-selective (eg. phentolamine) - competitive reversible non-selective a1&2 blocker for pheochromocytoma
  • selective (eg. prazosin) - a1 blockage –> dilation of arterial and venous smooth muscle for chronic hypertension –> dizziness/headache
36
Q

b receptor blocking drugs MOA

A
  • drugs with higher affinity for b1 are more important clinically
  • low bioavailability
  • for cardiovascular and ophthalmic applications
  • AE - decreased drug elimination with liver disease, decreased blood flow to liver, inhibition of liver enzymes
37
Q

2 non-selective b adrenergic blockers

A
  • propranolol - reversible b1&2 R antagonist, -ve chronotrope (decrease heart rate) and inotrope (decrease force of muscular contractions)
    • for cardiovascular diseases
    • AE due to b2 blockade
  • – worsens asthma by increasing airway resistance
  • – worsens HF by decreasing cardiac contractility
  • – hypoglycemia after insulin in diabetics
  • timolol - decreases IOP in glaucoma
    decreases AH production
38
Q

1 selective b1 adrenergic blocker

A
  • metoprolol - -ve chronotrope and inotrope, used in hypertension, safe for asthmatics
39
Q

3 therapeutic applications of b blockers

A
  • hypertension - decreases BP due to effects on heart (-ve inotrope and chronotrope)
  • ischemic heart disease - decreases angina, increases exercise tolerance, decreases HR, decreases oxygen demand
  • cardiac arrhythmias due to b1 blockade - decreases rate of SA discharge, decreases AV conduction, decreases ventricular response to atrial arrhythmias

231 Pharmacology (10 decks)

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