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N929 Pharmacology > Psychopharmacologic Therapy- Neurodegenerative Disease > Flashcards

Psychopharmacologic Therapy- Neurodegenerative Disease Flashcards

1
Q

Define Parkinson’s Disease

A

movement disorder occuring mostly age >60
chronic progression
some genetic risk factors

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2
Q

Parkinson’s Disease is characterized by:

A

dyskinesia
muscle rigidity
tremor at rest
cognitive impairments, depression

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3
Q

Pathology of Parkinson’s Disease

A

neurodegenerative disease resulting from a loss of dopaminergic neurons in the substantia nigra of the basal ganglia
degeneration of the nitrostriatal pathway leads to depletion of the inhibitory neurotransmitter dopamine

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4
Q

In PD, what is imbalanced?

A

reduced dopamine in the striatum

imbalance between Ach and Dopamine

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5
Q

Goal of Antiparkinson’s drugs

A

enhance the inhibitory effect of dopamine
increases amount of dopamine
drug therapy that mimics dopamine
decrease excitatory effect of ach with the administeration of centrally acting drugs

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6
Q

Parkinson’s Drug Therapy Treatments

A

treats motor symptoms
treats other adverse effects of disease (depression, autonomic disturbances, cognitive impairment, side effects of drug therapy)
deep brain stimulation

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7
Q

Levodopa

A

crosses BBB and is converted to dopamine, replenishes stores in the basal ganglia

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8
Q

Side Effects of Levodopa

A

N/V
cardiovascular
abnormal involuntary movements
psychatric disturbances

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9
Q

Why does N/V occur with levodopa?

A

due to dopamine induced stimulation of the chemoreceptor trigger zone

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10
Q

Why can you have cardiovascular s/e with levodopa?

A

alpha and beta responses evoked by higher plasma levels of dopamine result in transient flushing of skim, sinus tachycardia, PACs, PVCs and orthostatic hypotension

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11
Q

Lab measurements of Levodopa

A

urinary metabolites can cause false positive tests for ketoacidosis
transient increase in BUN
increase in liver enzymes

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12
Q

Levodopa Drug Interactions

A 
butyrophenones and phenothiazines
antagonize effect of dopamine (avoid!)
metoclopramide 
droperidol
MAO inhibitors
anticholinergics
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13
Q

Levodopa is administered with

A

peripheral decarboxylase inhibitor
as it enables levodopa to enter CNS and decreases s/e of systemic dopamine
decreases incidence of N/V and cardiac dysrhymia

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14
Q

Examples of peripheral decarboxylase inhibitors

A

carbidopa (sinemet)-levodopa and cardidopa

benserazide (madopar) levodopa and benserazide

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15
Q

Levodopa can also be administered with

A

catachol-O-methytransferase inhibitors (COMT)
responsible for the peripheral breakdown of Levodopa
block COMT enzyme-> augments the action of levodopa by slowing elimination time

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16
Q

Examples of COMT

A

tolcapone (tasmar)

entacapone (comtan)

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17
Q

Synethetic dopamine agonist

A

act directly on post synaptic dopamine receptors
no enzymatic conversion required
longer 1/2 life then levodopa

18
Q

Examples of dopamine agonist

A

bromocriptine (parlodel) ergot derivative
pramipexole (mirapex) non ergot
ropinirole (requip) non ergot
rotigotine- non ergot

19
Q

Side effects of Synthetic dopamine agonist

A

sedation, vivid dreams, hallucinations

non-ergots: less nausea and orthostatic hypotension then ergot derivatives

20
Q

Anticholinergics

A

trihexyphenidyl (artane) and benztropine (cogentin)

21
Q

trihexyphenidyl (artane) and benztropine (cogentin)

A

blunt effects of excitatory neurotransmitter ach correcting balance between dopamine and ach

22
Q

side effects of trihexyphenidyl (artane) and benztropine (cogentin)

A

confusion, hallucinations, confusion, urinary retention

23
Q

Amantadine (symmetrel)

A

symptomatic improvement of parkinsonian symptoms

enhance dopamine release into the synapse and delay re-uptake into the nerve ending

24
Q

Selegiline (eldepryl)

A

highly selective irreversible inhibitor of MAOB

used as adjunct to carbidopa-levodopa

25
Q

Nonpharmacologic Rx for parkinson’s

A

deep brain stimulation
controls symptoms if resistant to drug therapy and/or allows reduced doses
stem cell transplantation and other therapeutic mechanisms are under investigation

26
Q

Alzheimer’s Disease

A

dementia

27
Q

Alzheimer’s causes problems with

A 
memory
language
judgement and thinking
personality
perception
28
Q

Who gets alzheimer’s disease?

A

5% at 65 years of age

>90% at 95 years of age

29
Q

Early onset

A

symptoms before age 60

genetic factors

30
Q

Late onset

A

symptoms appear after age 60

31
Q

Pathology of alzheimer’s

A 
deficits in cholinergic signaling
cholinergic neuron loss 
-hippocampus (memory and learning) and frontal cortex (executive function)
Protein aggregates: amyloid plaques
neurofibrillary tangles
32
Q

Alzheimer’s have decreases in

A 
choline acetyltransferase activity
acetylcholine amount
acetylcholinersterases
choline transport
nicotinic acetylcholine receptor expression
33
Q

Current drug treatments:

A

cholinersterase inhibitors

NMDA receptor antagonist

34
Q

Cholinesterase Inhibitors MOA

A

prevents action of acetylcholinesterase thereby increasing acetylcholine concentrations in the synapse

35
Q

Examples of Cholinesterase inhibitors

A

donepezil (aricept)
rivastigmine (exelon)
galantamine (razadyne)

36
Q

Cholinesterase Inhibitors

A

indicated for mild to moderate AD

oral administration 1-2x/day

37
Q

S/E of Cholinesterase Inhibitors

A

nausea, diarrhea, dizziness, headache, bronchoconstriction
slight improvement in cognitive function
does not halter disease

38
Q

NMDA Receptor Antagonist: Memantine (Namenda)

A

indicated for moderate to severe AD

very modest benefits

39
Q

Potential side effects of Memantine (Namenda)

A

anemia, dizziness, diarrhea, fatigue, headache, HTN, rash, sedation, urinary frequency, weight gain

40
Q

memantine is proposed to work by two diferent mechanism

A

Signal To noise hypothesis/reduced excitotoxicity
blocking leaky channels to help reduce calcium induced excitotoxicity
blocking leaky channels helps reduce background noise, making signals relatively stronger

N929 Pharmacology (16 decks)

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