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550 Pharm > Neurodegenerative Diseases > Flashcards

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
Q

Where is a Tau protein found?

A

in microtubules in normal neurons

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26
Q

What happens to tau proteins in AD?

A

they become hyperphosphorylated and can no longer support microtubules
Then the proteins become tangled & form neurfibrillary tangles

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27
Q

What do neurofibrillary tangles correlate with?

A

neuronal death

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28
Q

What are potential new drug therapies in AD trying to do?

A

in AB: block synthesis, promote clearance, block plaque formation
in Tau: block aggregation

29
Q

What is Parkinson’s Disease? What causes it?

A

a movement disorder occuring (mostly) in the elderly

Caused mostly by env factors w/ some genetic risk factors

30
Q

What is PD characterized by?

A 
dyskinesias: difficulty of movement
muscle rigidity
tremor at rest
difficulty starting movement, difficulty stopping movement once started
cognitive impairments, depression
31
Q

What are 3 common and obvious s/s that would make you think a pt had PD?

A

repetitive “pill rolling” movement
Persistent tremors
shuffling gait, taking small steps

32
Q

What does the basal ganglia include? What is its fx?

A

striatum, globus pallidus, subthalamic nuclei, substantia nigra
Fx: starts purposeful movement, suppresses unwanted movement

33
Q

When the neurotransmitters _______ & __________ are balanced, there is controlled movement.

A

dopamine (DA) & ACh

34
Q

In PD there is reduced ____________ in the ______ of the basal ganglia

A

DA

Striatum

35
Q

How much DA must be lost from the substantia nigra to the striatum before PD s/s appear

A

~70%

36
Q

What are 2 broad startegies to fight PD?

A

increase dopamine

or anticholinergic agents

37
Q

How do dopaminergic agents work?

A

increase amount of dopamine in striatum: increased delivery or decreased degradation
-mimic effects of dopamine (DA agonists

38
Q

How do anticholinergic agents for PD work?

A

prevent cholinergic inhibition of DA release

39
Q

What is the first line treatment for PD?

A

Levodopa

40
Q

W/ levodopa, how many patients show improvement and how many regain normal motor fx? Does this level of effectiveness last forever?

A

80% show improvement
20% regain near normal motor fx
No: effectiveness lasts ~2-3 years (prob d/t advancing disease)

41
Q

What kind of drug is levodopa? Where does it take its effect?

A

DA precursor: converted to DA which is provided to the striatum
Occurs in the periphery and brain

42
Q

What is the problem with the fact that levodopa is converted to DA in both the brain and periphery?

A

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
Q

What is the solution to the fact that levodopa converts to DA in the periphery?

A

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
Q

When is entacapone given w/ the levodopa//carbidopa combo?

A

when the levodopa/carbidopa effectiveness wanes

45
Q

What are 2 main s/e of levodopa?

A 
involunary movements (dyskinesias)
on-off effect: fluctuations btw hypokinesia and improvements
46
Q

What are some acute s/e of levodopa that disappear after a few weeks?

A

Nausea
anorexia
hypotension
psychosis: schizophrenia like s/s from excess DA

47
Q

What class of medications does levodopa interact with and cause really bad s/s? What can occur and why?

A

non-selective MAO inhibitors= overload of DA and epi

possible HTN

48
Q

What 2 meds cause an increase in DA in the synapse?

A

Selegiline

Amantadine

49
Q

What kind of med is Selegiline? How does it work? What is a benefit of using it?

A

it is a MAO-B inhibitor: it decreases DA degredation

It does not have unwanted effects of non-selective MAOIs

50
Q

How does Amantadine work?

A

enhances DA release into synapse

51
Q

How do DA agonists work? What are 2 examples

A

mimic DA in striatum; selective for D2/D3 receptors

Pramipexole & ropinirole

52
Q

Are DA agonists effective? What kind of s/e do they cause?

A

highly effective

may cause hallucinations, compulsive behaviors (eating, gambling, etc)

53
Q

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.

A

True

54
Q

What kind of drugs are muscarinic receptor antagonists? What is an example?

A

anticholinergic drugs

ie. Benztropine

55
Q

How does Benztropine work?

A

blocks muscarinic recepotrs that inhibit DA release from DA neurons in the striatum
= more DA release

56
Q

What are some s/e of Benztropine?

A

dry mouth, constipation, impaired vision, urinary retention

57
Q

T/F: None of the therapies for PD cure or stop the progression of the disease.

A

True

58
Q

What is the primary pathology of PD?

A

Lewey bodies: protein aggregates composed of alpha-synuclein protein
may function at synpases or ER-golgi trafficking

59
Q

What are anesthetic considerations of memantine?

A

clearance can be reduced by increasing urine pH

-be careful w/ bicarb, etc

60
Q

What type of drug can cause a prolongation of succs and cause relative resistance to non depolarizing NMBs?

A

cholinesterase inhibitors

61
Q

What are some anesthetic consdierations of anticholinergic drugs?

A
  • assess for anticholinergic s/e (esp. HR)

- avoid drugs that impact cholinergic tone (TCAs) or increase s/e if possible

62
Q

What drug should you eval for anti-cholinergic like s/e and rule out CHF s/e?

A

Amantadine

63
Q

What drug must be given every 6-12 hours?

A

levodopa + decarboxylase inhibitors

64
Q

How should you give levdopa cocktail pre and intra op? Why?

A

admin 20 min preop and intraop per NG tube

avoid sudden loss of effect and NM/resp failuer

65
Q

What should you assess for w/ levo cocktail during surgery?

A

s/e: cardiac dysrhythmias, adrenergic stimulation, orthostatic hypotension, GI

66
Q

What should you assess for w/ synthetic DA agonists?

A

s/e: CV, hypotension, pleuopulmonary fibrosis

67
Q

With what type of drug whould you avoid using ephedrine and meperdine, and use extreme caution w/ using vasoactive drugs?

A

Selegiline (MAO type B)

68
Q

What type of med has a prolonged effect w/ NMB, sedatives, diuretics

A

Selegiline (MAO type B)

550 Pharm (6 decks)

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