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Psych > Dementia Pharm > Flashcards

Dementia Pharm Flashcards

1
Q

ACHase inhibitors- agents approved for use in pts w dementia

A

-donepezil
-galantamine
-rivastigmine
-tacrine
(DGRT)

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2
Q

Other cholinesterase inhibitors

A
  • Ambenonium
  • Echothiophate
  • edrophonium
  • neostigmine
  • physostigmine
  • pyridostigmine
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3
Q

Antimuscarinic compounds

A

-atropine

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4
Q

Cholinesterase reactivators

A

-pralidoxime

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5
Q

ACHase inhibitors- subgroups

A
  • alcohols- edrophonium
  • carbamic esters- neostigmine, pyridostigmine, physostigmine, carbaryl
  • organophosphates (insecticides, n gases)
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6
Q

quaternary and charged ACHE inhibitors

A
  • parenteral admin is preferred
  • no CNS distribution
  • neostigmine, pyridostigmine, echothiophate, ambeonium
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7
Q

tertiary and uncharged ACHE inhibitors

A
  • well absorbed from all sites
  • CNS distribution
  • physostigmine, donepezil, galantamine, rivastigmine, tacrine (DGRT)
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8
Q

ACHE inhibitors- moa

A
  • inhibition of ACHE

- ACH accum thruout the body- act of nACHRs and mACHRs

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9
Q

ACHE inhibitors- duration of action

A
  • alcohols- short (2-10 min)
  • carbamic acid esters- 30 min to 6 hrs
  • organophosphates: aging (breaking 1 of oxygen-phosphorous bonds of inhibitor- strengthens the phosphorus-enzyme bond- stable)
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10
Q

ACHE inhibitors- organ system effects

A
  • quaternary- no CNS effects
  • organophosphates and tertiary- well abs after oral admin; CNS effects
  • stim mACHRs
  • stim nACHRs
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11
Q

ACHE inhibitors- CNS effects

A
  • low conc- diffuse act of electroencephalogram

- high conc- generalized convulsions due to neuronal hyperstimulation

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12
Q

ACHE inhibitors- eye, resp, GI, urinary tracts

A

-these organs innervated by mACHRs (parasymp)

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13
Q

ACHE inhibitors- CV system

A
  • inc activity of symp and parasymp ganglia (nACHRs and mACHRs) supplying the heart and mACHRs on cardiac cells
  • parasymp tone dominates- CO dec
  • net effects- modest bradycardia, dec in CO, inc in BP
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14
Q

ACHE inhibitors- NMJ

A
  • inc strength of contraction
  • fibrillation of m fibers and fasciculations- w high conc
  • continued inhibition- progression of depolarizing neuromuscular blockade to nondepolarizing blockade
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15
Q

therapeutic uses of ACHE inhibitors-

A
  • dementia
  • eye (glaucoma, accommodative esotropia)
  • GI and urinary tracts (postop atony, neurogenic bladder)
  • NMJ (MG, curare-induced paralysis)
  • heart (atrial arrhythmias)
  • Alzheimer dz
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16
Q

ACHE inhibitors- dementia

A

dementia of Alzheimer type- def of intact cholinergic neurons

  • Tacrine- high incidence of hepatotoxicity
  • newer agents (less SEs)- donepezil, rivastigmine, galantamine
  • also pts w dementia of Parkinson dz
17
Q

drug-drug interactions

A
  • nondepolarizing neuromuscular blocking agents: diminish NM blockade (Exception- mivacurium- blockade is prolonged)
  • succinylcholine- enhance phase 1 block, antagonize phase 2 block
  • cholinergic agonists
  • B-blockers- enhance bradycardia
  • systemic corticosteroids- enhance m weakness in MG
18
Q

Acute intoxication

A
  • signs- mACHR stimulation- miosis, salivation, sweating, bronchial constriction, vomiting, diarrhea
  • ingestion- GI sx’s first
  • percutaneous abs- sweating, m fasciculations in area
  • death- resp failure
19
Q

intoxication dx and tx

A
  • dx- exposure hx and characteristic signs
  • atropine (mACHR antagonist)- antidote for cholinergic poisoning!!!; decontamination (removal of clothing, washing of skin)
  • regenerate ACHE at NMJ- cholinesterase regenerators (atropine is ineffective against peripheral NM stim- nACHRs)
20
Q

Cholinesterase regenerators

A

(pralidoxime)

  • regenerates active enzyme from organophosphorus-cholinesterase complex via removal of phosphorous group from active site of enzyme
  • must be given before aging has occurred b/w organophosphate and cholinesterase!!!
  • antidote for organophosphate exposure!!
21
Q

Memantine- moa

A

[Glutamate (EAA of CNS)- contributes to Alzheimer’s dz by overstim glutamate Rs leading to excitotoxicity and neuronal cell death]

  • antagonist of NDMA type of glutamate Rs!!
  • under normal conditions, NMDA R ion channel is blocked by Mg ions
  • excessive R act prevents Mg from reentering and blocking the channel pore- results in chronically open state and excessive Ca influx
  • Memantine binds to intra-pore Mg state- R blocker only under conditions of excessive stim
22
Q

Memantine- SEs

A

-dizziness- most common

Psych (16 decks)

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