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ARCHIVED: Pharmacology for Nurse Anesthesia > Exam 2: Neurodegenerative Disease Therapies > Flashcards

Exam 2: Neurodegenerative Disease Therapies Flashcards

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1
Q

Early vs. late onset AD:

A

Early before age 60 (strong genetic implication); late after age 60

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2
Q

Two main pathologies of AD:

A

Brain atrophy

Protein aggregation

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3
Q

Parts of the brain that experience cholinergic neuron loss in AD:

A

Hippocampus

Frontal cortex

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4
Q

Five aspects of ACh signaling that are decreased in AD:

A
  1. Choline acetyltransferase activity (production of ACh)
  2. ACh amount
  3. ACh-ases
  4. Choline transport
  5. Nicotinic ACh receptor expression
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5
Q

Two types of protein aggregation in AD:

A

Amyloid plaques

Neurofibrillary tangles

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6
Q

Two classes of drug tx for AD:

A

Cholinesterase inhibitors

NMDA receptor antagonists

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7
Q

Three examples of cholinesterase inhibitors:

A

Donepezil (Aricept)
Rivastigmine (Exelon)
Galantamine (Razadyne)

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8
Q

MoA of cholinesterase inhibitors:

A

Prevents action of acetylcholinesterase, thus increasing ACh in the synapse

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9
Q

Indications for cholinesterase inhibitors:

A

Mild to moderate AD

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10
Q

Side effects of cholinesterase inhibitors:

A 
N/V
Diarrhea
Dizziness
Headache
Bronchoconstriction
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11
Q

Efficacy of cholinesterase inhibitors:

A

Slight improvements

Does not halt disease

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12
Q

Example of NMDA receptor antagonist:

A

Memantine (Namenda)

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13
Q

Indications for NMDA receptor antagonist:

A

Moderate to severe AD

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14
Q

Efficacy of NMDA receptor antagonist:

A

Very modest benefits

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15
Q

MoA of NMDA receptor antagonist:

A

Blocks “leaky” channels to reduce Ca2+ induced excitotoxicity

Intracellular Ca2+ reduction means less background noise, making nerve signals relatively stronger

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16
Q

Two types of amyloid precursor protein processing:

A

Amyloidogenic

Nonamyloidogenic

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17
Q

Non-amyloidogenic pathway:

A

APP protein gets cleaved by α-secretase then γ-secretase, no Aβ formed

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18
Q

Amyloidogenic pathway:

A

APP get cleaved by β-secretase then γ-secretase; Aβ40/42 formed

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19
Q

Effect of Aβ plaques on cognition:

A

Unclear; likely soluble derivatives that are problematic, not plaques themselves

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20
Q

Gene that encodes Aβ-clearing protein:

A

ApoE

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21
Q

ApoE genotype that increases AD risk:

A

ApoE4
One copy: 3-fold risk
Two copies: 12-15-fold risk

22
Q

State of tau proteins that causes their dysfunction:

A

Hyperphosphorylated

23
Q

Three ways Aβ can be targeted in future drug therapies:

A

Block Aβ synthesis
Promote Aβ clearance
Block plaque formation

24
Q

Four parts of the basal ganglia:

A 
GSSS
Globus pallidus
Striatum
Subthalamic nuclei
Substantia nigra
25
Q

Functions (2) of basal ganglia:

A

Start purposeful movement

Suppress unwanted movement

26
Q

Mechanism of PD:

A

Loss of dopaminergic neurons (70%+) from substantia nigra

27
Q

Two classes of drugs for PD:

A

Dopaminergic agents

Anticholinergic agents

28
Q

Efficacy of Levodopa:

A

80% show improvement, 20% regain near-normal motor function

Efficacy wears off after 2-3 years

29
Q

MoA of Levodopa:

A

Dopamine precursor

Converted to dopamine in both the periphery and brain - dopamine does not cross BBB though!

30
Q

Barrier to end-organ distribution of Levodopa and method of overcoming it:

A

Most is converted to dopamine in the periphery and will not cross BBB

Given along with carbidopa (1st) and entacapone (when carbidopa effectiveness wanes) to inhibit the enzymes that convert Levodopa to dopamine in the blood

31
Q

Side effects of Levodopa:

A

Acute: nausea, anorexia, hypotension, psychosis

Chronic: dyskinesias, on-off effect

Other: dysrhythmias, adrenergic stimulation

32
Q

Drug interactions with Levodopa:

A

Nonselective MAOIs (can cause overload of dopamine, norepi)

33
Q

MoA of carbidopa:

A

Peripheral decarboxylase inhibitor

34
Q

MoA of entacapone:

A

COMT inhibitor

35
Q

Examples of dopamine agonists:

A

Pramipexole

Ropinirole

36
Q

Receptors targeted by pramipexole/ropinirole:

A

D2/D3

37
Q

Efficacy of pramipexole/ropinirole:

A

Highly effective

38
Q

Side effects of pramipexole/ropinirole:

A

Hallucinations
Compulsive behaviors

(Think mania - dopamine overload)

39
Q

MoA of selegiline:

A

MAO-B inhibitor; decreases dopamine degradation

Not involved in norepi metabolism

40
Q

MoA of amantadine:

A

Enhances dopamine release into synapse

41
Q

Example of anticholinergic drug for PD:

A

Benztropine

42
Q

MoA of benztropine:

A

Blockage of muscarinic receptors, which relieves inhibition of dopaminergic neurons

43
Q

Side effects of benztropine:

A

Impaired vision
Urinary retention
Dry mouth
Constipation

44
Q

Lewy bodies are:

A

Alpha-syneuclein protein aggregates found in PD neurons; unclear if harmful or beneficial

45
Q

Anesthetic considerations for memantine:

A

Clearance reduced in alkaline urine

46
Q

Anesthetic considerations for cholinesterase inhibitors:

A

Prolongs succinylcholine; creates resistance to non-depolarizing NMBs

47
Q

Anesthetic considerations for anticholinergic drugs:

A

Side effects, especially HR

Avoid drugs that impact cholinergic tone (TCAs) or increase HR

48
Q

Anesthetic considerations for amantadine:

A

Rule-out CHF side effect

Identify anticholinergic-like side effects

49
Q

Anesthetic considerations for levodopa/carbidopa:

A

Must recieve q6-12 hours, even intra-op (via NG tube)

Assess for side effects: dysrhythmias, adrenergic stimulation, hypotension, GI

50
Q

Anesthetic considerations for synthetic dopamine agonists (pramipexole/ropinirole):

A

Assess for side effects: CV, hypotension, pleuropulmonary fibrosis

51
Q

Anesthetic considerations for selegiline:

A

Avoid ephedrine and meperidine! Extreme caution with vasoactive medications

Titrate NMBs, sedatives, diuretics, etc carefully

ARCHIVED: Pharmacology for Nurse Anesthesia (20 decks)

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