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Pharmacology test 2 > Alzheimers and Parkinsons > Flashcards

Alzheimers and Parkinsons Flashcards

1
Q

alzheimer disease

A

dementia
-not related to a distinct cause
causes problems: -memory, language, judgment/thinking -personality -perceptin

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2
Q

alzheimer patho

A
  • decrease in brain size from neuronal death
  • protein aggregation:
  • -neurofibrillary tangles: hyperphosephorylated tau (clumps together)
  • -amyloid plaque: amyloid beta
  • deficits in cholinergic signaling
  • -hippocampus (memory and learning)
  • -frontal cortex (executive function)
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3
Q

alzheimer decrease in 5 things

A 
choline acetyltransferase activity
ACh amount
AChsterase?
choline transport
Nicotinin ACh receptor expression
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4
Q

Alzheimer drug classes

A

cholinesterase inhibitors

NMDA receptor antagonist

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5
Q

Cholinesterase inhibitors MOA

A

preven action of AChsterase thereby increasing ACh [ ] in synapse

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6
Q

Cholinesterase inhibitors ex

A

Donepezil (Aricept)
Rivastigmine (Exelon)
Galantamine (Razadyne

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7
Q

Cholinesterase inhibitors: indication, route, side effects

A

mild to moderate AD, slight improvement in cognitive function, does not halt disease
-Oral 1-2/day
SE: N/D, dizziness, HA, bronchoconstriction

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8
Q

NMDA receptor antagonist MOA

A

signal to noise hypothesis/reduced excitotoxicity
2 different mechanisms:
1.Blocking “leaky” channels to help reduce calcium induced excitotoxicity
2.Blocking“leaky” channels helps reduce background noise, making signals relatively stronger
**Mg not blocking channel so too much Ca rushes in causing damage to neurons–chronic neruodegeneration
*these drugs act as Mg, block NMDA

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9
Q

NMDA receptor antagonist ex

A

Memantine (Namenda)

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10
Q

NMDA receptor antagonist indication, side effects

A

moderate to sever AD, very modest benefits
SE:Dizziness, Headache,
Fatigue, Sedation,
Hypertension, Rash,
Diarrhea, Weight Gain, Urinary Frequency, Anemia

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11
Q

AD future tx? Protein aggregates, 2 pathways

A

Amyloid plaques–amyloid beta AB
APP: amyloid precursor protein
Non-amyloidogenic pathway
-APP protein gets cleaved by a-secratase followed by gamma-secretase: NO AB formed
Amyloidogenic pathway
-APP protein gets cleaved by b-secretase followed by gamma-secretase: AB40/42 aggregates—forms plaques

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12
Q

effects of AB plaques

A

unclear

most likely the soluble AB derivates cause cognitive effects, rather than the plaques themselves

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13
Q

Genetic consideration

A

early onset AD–genetic factor

many mutations associated with AD increase amount of AB

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14
Q

ApoE genotype

A
  • encodes for a protein that facilitates the clearance of AB
  • significant risk factor…ones that are bad at facilitating the clearance of AB resulting in the build up
  • ApoE2: lower risk
  • ApoE3: normal risk
  • ApoE4: increased risk
  • –one copy: 3 fold increase risk
  • –2 copies: 12-15 fold increase risk
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15
Q

Tau Protein

A

in microtubules in normal neurons

  • hyperphosphorylated in AD–no longer support microtubules
  • proteins become tangled and form neurofibrillary tangles
  • correlates with neuronal death–neuron starts loosing shape
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16
Q

Potential new drug targets

A 
AB
-block synthesis
-promotes clearance
-block plaque formation 
Tau
-block aggregation
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17
Q

Parkinsons disease, definition, characterized

A 
a mvmt diaorder-occuring (mostly) in elderly
-no obvious cause
-some genetic risk factors
Characterized by
-Dyskinesia: difficulty of mvmt
-difficulty starting mvmt 
-difficulty stopping mvmt one started
-muscle rigidity
-tremor at rest
-cognitive impairments, depression
18
Q

Basal ganglia

A

striatum
Globus Pallidus
Subthalamic nuclei
Substantia nigra

19
Q

Basal ganglia function

A

start purposeful mvmt, suppresses unwanted mvmt
Normal: Dopamine (DA) and ACh are balanced–results in controlled mvmt
Parkinsons: decreased DA in striatum, creating a imbalance btwn DA and ACh -70% lose of DA neurons from substantial nigra to striatum BEFORE systems appear

20
Q

Pharm strategies (PD)

A

goal to increased DA

  • Dopaminergic agent: increase amt of DA in striatum, increase delivery or decrease degradation
  • mimics effects of DA (dopamine agonists)
  • Alternative: ACH agents
  • -prevent Cholinergic inhibition of DA release
21
Q

Levodopa: dopamine precursor

A
  • Levodopa is converted to Dopamine, providing dopamine to the striatum
  • This happens in periphery AND brain
  • *Dosing problem……
  • Levodopa can be degraded by decarboxylases and also by catecholamine O-methyl transferase (COMT), but dopamine does not cross the blood-brain barrier
  • Despite large doses of Levodopa, only a small amount of will reach the brain.
  • Large amounts of dopamine cause problems in the periphery.
22
Q

Solution to Levodopa dosing problem

A
  • Dose Levodopa with:
  • Carbidopa (peripheral decarboxylase inhibitor)
  • entacapone (COMT inhibitor)
  • means the same amount of Levodopa can reach the brain with a smaller dose.
  • *Entacapone is added when effectiveness of Levodopa/Carbidopa wanes.
23
Q

Levodopa side effects

A

-Involuntary movements (Dyskinesias)
-‘on-off’ effect: fluctuations between hypokinesia and improvements
-Acute (disappear after a few weeks)
Nausea
Anorexia
Hypotension
Psychosis: schizophrenia like symptoms with excess dopamine

24
Q

Levodopa drug interactions

A

In patients taking Non-selective MAO Inhibitors: an overload of dopamine and norepinephrine can occur.
-May cause peripheral side effects.

25
Q

Dopamine agonists

A

Pramipexole

Ropinirole

26
Q

Dopamine agonists MOA

A

mimic DA in stiatum
selective for D2/D3 receptor
-highly effective

27
Q

Dopamine agonists side effects

A

Fewer side effects (nausea/vomiting) than old dopamine agonists that hit D1/D2 receptors
– May cause hallucinations, compulsive behaviors (eating, gambling, etc.)

28
Q

Drugs that increasing DA in synapse

A

Selegiline

Amantadine

29
Q

Drugs that increasing DA in synapse class

A

MOA-B inhibitor

  • MAO-B is not involved in NE metabolism
  • decreased DA degradation
  • does not have unwanted effects of non-select MAOIs
30
Q

Selegiline

A

MOA-B inhibitor

  • MAO-B is not involved in NE metabolism
  • decreased DA degradation
  • does not have unwanted effects of non-select MAOIs
31
Q

Amantadine

A

enhances DA release into synapse

32
Q

Benztropine

A

anticholinergic drug

  • muscarinic receptor antagonist
  • Muscarinic receptors are present in striatum they inhibit dopamine release from dopamine neurons
  • Blockade of Muscarinic Receptors relieves the inhibition of Dopaminergic Neurons
  • – end result, more Dopamine Release
33
Q

Benztropine side effects

A

Dry mouth, constipation, impaired vision, urinary retention

34
Q

Parkinsons patho

A
  • Lewy bodies: may be harmful or beneficial
  • Protein aggregates composed of alpha-synuclein protein.
  • –Alpha-synuclein function is unclear.
  • –May function at synapses or ER-golgi trafficking
35
Q

Memantine: Anesthetic Considerations (AC)

A

-Clearance can be reduced by increasing urinary pH be careful with bicarbonate, etc.

36
Q

Cholinesterase Inhibitors AC

A

-Prolongation of succinylcholine
-Relative resistance to non-
depolarizing muscle relaxants

37
Q

Anticholinergic drugs AC

A
  • Assess for anticholinergic side effects ( especially HR).

- Avoid drugs that impact cholinergic tone (TCAs) or increase side effects (i.e. HR) if possible.

38
Q

Amantadine

A

-Evaluate for anti-cholinergic like side effects, rule-out congestive heart failure side effect

39
Q

Levadopa and decarboxylase inhibitors AC

A
  • Must receive q 6-12 hours. Administer 20 min pre-op and intra- op per NG tube to avoid sudden loss of effect and neuromuscular/respiratory failure
  • Assess for side effects: cardiac dysrhythmias, adrenergic stimulation, orthostatic hypotension, GI
40
Q

Synthetic Dopamine agonists AC

A

-Assess for side effects: CV, hypotension, pleuropulmonary fibrosis.

41
Q

Selegiline

A
  • Avoid ephedrine, meperidine. Use extreme caution with vasoactive medications
  • Pronounced effect with neuromuscular blockers, sedative agents, diuretics, etc. (titrate carefully)

Pharmacology test 2 (6 decks)

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