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Neurodegenerative Diseases Flashcards

1
Q

Alzheimer’s Disease is a a form of _________ that is not related to a specific _________

A

dementia

cause

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2
Q

What 5 main things does alzheimers cause problems with?

A
  1. memory
  2. language
  3. judgement & thinking
  4. personality
  5. perception
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3
Q

What is the difference btw early and late onset of alzheimers? What is the prevalance?

A

Early: before 60 years old (genetic factors)
Late: after 60
Prevalence: 5% @ 65 years
>90% @ 95 years

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4
Q

In alzheimers there is shrinkage of the _________ and localized loss of ________________

A

brain

neurons

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5
Q

In alzheimers, the hippocampus and frontal cortex experience what?

A

decrease of cholinergic transmission

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6
Q

In alzheimers, there is also the development of _____________ and ____________

A

amyloid plaques

neurofibrillary tangles

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7
Q

What type of medication class is indicated for mild to moderate AD and show a slight improvement in cognitive function, but do not halt the disease?

A

Cholinesterase inhibitors

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8
Q

How do cholinesterase inhibitors work?

A

prevent breakdown of ACh

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9
Q

What are 3 examples of cholinesterase inhibitors?

A

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

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10
Q

How often are cholinesterase inhibitors taken? What route?

What are some s/e?

A

PO: 1-2x/day

s/e: nausea, diarrhea, dizziness, h/a, bronchoconstriction

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11
Q

What class of drug is indicated for moderate to severe AD? What kind of results do they have?

A

NMDA Receptor Antagonists

moderate

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12
Q

What is the main NMDA Receptor Antagonist?

A

Memantine (Namenda)

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13
Q

What are potential s/e of NMDA receptor antagonists? (10)

A 
dizziness
h/a
fatigue
sedation
HTN
rash
diarrhea
wt gain
urinary frequency
anemia
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14
Q

In what 2 ways is it supposed that Memantine is proposed to work?

A
  1. blocks “leaky” channels to help reduce Ca induced toxicity
  2. the action of #1 helps to reduce background noise, making signals relatively stronger
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15
Q

T/F: Neither therapy for AD is a cure for or halts progression of the disease

A

True

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16
Q

What are future treatments of AD looking to affect?

A

amyloid plaques and neurofibrillary tangles

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17
Q

In the normal physiological pathway, how is the Amyloid Precursor Protein (APP) cleaved?

A

APP cleaved by alpha-secretase & no AB is formed

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18
Q

In the amyloidogenic pathway (pathologic) how is the APP cleaved? What is formed?

A

APP is cleaved by Beta-secretase

AB40/42 aggregates forms plaques

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19
Q

Although AB aggregates form plaques, what do scientists believe to be the cause of cognitive disfunction in AD?

A

most likely the soluble AB derivatives from the plaques that cause the cognitive effects, rather than the plaques themselves

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20
Q

What are some genetic considerations of AD?

A

Early onset AD is heavily due to genetic factors!

Many mutations assoc w/ AD increase the amounts of AB

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21
Q

What does the ApoE gene code for?

A

a protein that facilitates the clearance of AB

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22
Q

T/F: Having a specific ApoE genotype is a significant risk factor for getting AD.

A

True!

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23
Q

What form of ApoE gene has a lower, normal, and increased risk for getting AD?

A

Lower: ApoE2
normal: ApoE3
Increased: ApoE4

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24
Q

If you have 1 copy of ApoE4 vs. 2 copies, what is the probability you will get AD?

A

1 copy: 3x increased risk

2 copies: 12-15x increased risk

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25
Where is a Tau protein found?
in microtubules in normal neurons
26
What happens to tau proteins in AD?
they become hyperphosphorylated and can no longer support microtubules Then the proteins become tangled & form neurfibrillary tangles
27
What do neurofibrillary tangles correlate with?
neuronal death
28
What are potential new drug therapies in AD trying to do?
in AB: block synthesis, promote clearance, block plaque formation in Tau: block aggregation
29
What is Parkinson's Disease? What causes it?
a movement disorder occuring (mostly) in the elderly | Caused mostly by env factors w/ some genetic risk factors
30
What is PD characterized by?
``` dyskinesias: difficulty of movement muscle rigidity tremor at rest difficulty starting movement, difficulty stopping movement once started cognitive impairments, depression ```
31
What are 3 common and obvious s/s that would make you think a pt had PD?
repetitive "pill rolling" movement Persistent tremors shuffling gait, taking small steps
32
What does the basal ganglia include? What is its fx?
striatum, globus pallidus, subthalamic nuclei, substantia nigra Fx: starts purposeful movement, suppresses unwanted movement
33
When the neurotransmitters _______ & __________ are balanced, there is controlled movement.
dopamine (DA) & ACh
34
In PD there is reduced ____________ in the ______ of the basal ganglia
DA | Striatum
35
How much DA must be lost from the substantia nigra to the striatum before PD s/s appear
~70%
36
What are 2 broad startegies to fight PD?
increase dopamine | or anticholinergic agents
37
How do dopaminergic agents work?
increase amount of dopamine in striatum: increased delivery or decreased degradation -mimic effects of dopamine (DA agonists
38
How do anticholinergic agents for PD work?
prevent cholinergic inhibition of DA release
39
What is the first line treatment for PD?
Levodopa
40
W/ levodopa, how many patients show improvement and how many regain normal motor fx? Does this level of effectiveness last forever?
80% show improvement 20% regain near normal motor fx No: effectiveness lasts ~2-3 years (prob d/t advancing disease)
41
What kind of drug is levodopa? Where does it take its effect?
DA precursor: converted to DA which is provided to the striatum Occurs in the periphery and brain
42
What is the problem with the fact that levodopa is converted to DA in both the brain and periphery?
DA does not cross BBB; t/f even w/ large doses, very little of the DA reaches the brain Also: a lot DA in the periphery can cause problems
43
What is the solution to the fact that levodopa converts to DA in the periphery?
give it w/ Carbidopa (peripheral decarboxylase inhibitor) & entacapone (COMT inhibitor) -allow the same amount of levodopa to reach the brain w/ a smaller dose
44
When is entacapone given w/ the levodopa//carbidopa combo?
when the levodopa/carbidopa effectiveness wanes
45
What are 2 main s/e of levodopa?
``` involunary movements (dyskinesias) on-off effect: fluctuations btw hypokinesia and improvements ```
46
What are some acute s/e of levodopa that disappear after a few weeks?
Nausea anorexia hypotension psychosis: schizophrenia like s/s from excess DA
47
What class of medications does levodopa interact with and cause really bad s/s? What can occur and why?
non-selective MAO inhibitors= overload of DA and epi | possible HTN
48
What 2 meds cause an increase in DA in the synapse?
Selegiline | Amantadine
49
What kind of med is Selegiline? How does it work? What is a benefit of using it?
it is a MAO-B inhibitor: it decreases DA degredation | It does not have unwanted effects of non-selective MAOIs
50
How does Amantadine work?
enhances DA release into synapse
51
How do DA agonists work? What are 2 examples
mimic DA in striatum; selective for D2/D3 receptors | Pramipexole & ropinirole
52
Are DA agonists effective? What kind of s/e do they cause?
highly effective | may cause hallucinations, compulsive behaviors (eating, gambling, etc)
53
T/F: newer DA agonists that act at D2/D3 receptors cause fewer s/e (i.e. n/v) than the old DA agonists that hit D1/D2 receptors.
True
54
What kind of drugs are muscarinic receptor antagonists? What is an example?
anticholinergic drugs | ie. Benztropine
55
How does Benztropine work?
blocks muscarinic recepotrs that inhibit DA release from DA neurons in the striatum = more DA release
56
What are some s/e of Benztropine?
dry mouth, constipation, impaired vision, urinary retention
57
T/F: None of the therapies for PD cure or stop the progression of the disease.
True
58
What is the primary pathology of PD?
Lewey bodies: protein aggregates composed of alpha-synuclein protein may function at synpases or ER-golgi trafficking
59
What are anesthetic considerations of memantine?
clearance can be reduced by increasing urine pH | -be careful w/ bicarb, etc
60
What type of drug can cause a prolongation of succs and cause relative resistance to non depolarizing NMBs?
cholinesterase inhibitors
61
What are some anesthetic consdierations of anticholinergic drugs?
- assess for anticholinergic s/e (esp. HR) | - avoid drugs that impact cholinergic tone (TCAs) or increase s/e if possible
62
What drug should you eval for anti-cholinergic like s/e and rule out CHF s/e?
Amantadine
63
What drug must be given every 6-12 hours?
levodopa + decarboxylase inhibitors
64
How should you give levdopa cocktail pre and intra op? Why?
admin 20 min preop and intraop per NG tube | avoid sudden loss of effect and NM/resp failuer
65
What should you assess for w/ levo cocktail during surgery?
s/e: cardiac dysrhythmias, adrenergic stimulation, orthostatic hypotension, GI
66
What should you assess for w/ synthetic DA agonists?
s/e: CV, hypotension, pleuopulmonary fibrosis
67
With what type of drug whould you avoid using ephedrine and meperdine, and use extreme caution w/ using vasoactive drugs?
Selegiline (MAO type B)
68
What type of med has a prolonged effect w/ NMB, sedatives, diuretics
Selegiline (MAO type B)

550 Pharm (6 decks)

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