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Pharm Exam 3 > Neurodegenerative Disorders > Flashcards

Neurodegenerative Disorders Flashcards

1
Q

What happens to the CNS in alzheimers disease (AL)?

A

loss of hippocampal and cortical neurons results in impaired memory formation and cognitive deficits

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2
Q

Alzheimers disease - main characteristics:

A
  • progressive and irreversible loss of neurons from hippocampus and cortical areas
  • genetic and environmental factors
  • aggregation of Beta-amyloid plaques and intracytoplasmic neurofibrillary tangles
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3
Q

Aggregation of what proteins in alzheimers?

A

Beta-amyloid plaques and intracytoplasmic neurofibrillary tangles

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4
Q

Onset of alzheimers is when?

A

usually after age 65 in neurologically normal people

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5
Q

**Two types of AD symptoms:

A
  • 1) cognitive
  • loss of short term memory (poor recall and losing items)
  • aphasia (difficulty remembering works to being completely unable to speak, read, or write)
  • apraxia (cant carry out motor activities despite intact motor system)
  • agnosia (inability to recognize objects, persons, sounds, shapes, or smells despite intact sensory system)
  • disorientation (impaired perception of time; impaired executive function)
    2) Non-cognitive:
  • depression
  • psychotic symptoms (hallucinations/delusions)
  • behavioral disturbances (aggression, motor hyperactivity, repetitive mannerisms, uncooperativeness)
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6
Q

Which AD symptoms appear initially?

A

cognitive symptoms

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7
Q

Main way to Dx AD?

Can also use?

A
  • clinical assessment - need presence of dementia –> cognitive impairments beyond normal aging process
  • also can use Neuroimaging - CT or MRI
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8
Q

initial manifestation of degenerative dementia is called? Relationship to AD?

A
  • Mild cognitive impairment (MCI)

- some of these patients get AD and some dont

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9
Q

*death due to demensia how long?

A

6-12 years of AD onset

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10
Q

Gross pathology of AD?

A

massive tissue damage and decrease in brain volume

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11
Q

micro-pathology of AD?

A

1) neuronal degeneration and cortical atrophy
2) Neuritic plaques (amyloid or senile)
3) neurofibriallary tangles

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12
Q

Brain areas affected?

A
  • hippocampus - memory
  • frontal lobe - cognitive
  • patietal and centers for language etc..
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13
Q

Cholinergic Hypothesis - how does it relate to alzheimers?

A

degeneration of subcortical cholinergic neurons = Deficiency of ACh ==> memory formation areas affected (hippocampus)

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14
Q

Early neuronal-finding of AD?

A

cholinergic deficit

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15
Q

severity of AD is directly correlated to…

A

loss of Ach activity

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16
Q

Amyloid hypothesis - how does it relate to alzheimers ?

A
  • extracellular accumulations of Beta-amyloid peptides (betaA) that are toxic to neurons)
  • deposition of betaA does not correlate well with neuronal loss
17
Q

Where does Beta-amyloid come from?

A

betaA is cleaved from amyloid precursor protein (APP) on the cell membrane

18
Q

**Early onset AD - amyloid hypothesis

A
  • rare-
  • related to mutations in:
  • ->APP (amyloid beta precursor proteins) - more protein
  • ->PSEN1 & PSEN2 (presenilin 1&2 membrane proteins involved in cleaving APP) = increased cleavage of APP
  • ->mutations cause over production of betaA
19
Q

**Late onset AD - amyloid hypothesis:

A
  • common-
  • ApoE enhanced proteolytic breakdown and clearance of betaA within and between cells
  • mutation in ApoE=epsilon4 allele of APOE (apolipoprotein E) = not effective at degrading betaA
20
Q

*Tau hypothesis - how does it related to AD?

A
  • microtubule associated protein Tau
  • tau provides support to microtubules and neuronal cytoskeleton
  • -hyperphosphorylation of tau = forms aggregates and neurofibrillary tangles
  • -microtubular disintegration and instability
  • -collapse of neuronal transport system
  • -altered NT release and synaptic function
  • -cell death
21
Q

***Two main cholinesterase enzymes that are blocked?

A
  • acetylcholinesterase

- butyrylcholinesterase

22
Q

Cholinesterase inhibitors MOA?

A

-reduce breakdown of endoenously released ACH, resulting in greater activation of postsynaptic Ach receptors
==>reduced phosphorylation of Tau
==>secretion of soluble APP returned toward normal
==>reduced betaA production
==>glutaminergic neurotransmission returns toward normal

23
Q

Cholinesterase inhibitors for AD - list drugs?

A

Donepezil
Rivastigmine
Galantamine

24
Q

NMDA (Glutamate) receptor inhibitors - list drugs:

A

Memantine

25
Q

Donepezil

  • what type of drug/MOA?
  • benefit to using this drug over others?
A
  • Acetylcholinesterase Inhibitor
  • less severe side effects and longer half-life = easier once-a-day dosing

-additional side effect of bradycardia

26
Q

Rivastigmine

  • what type of drug/MOA?
  • what is benefit to taking this drug over others?
A
  • inhibits BOTH acetylcholinesterase (ACHE) and butyrylcholinesterase enzymes
  • available as a patch = improved GI effect
  • dosing is 2x per day - half life isnt as long as donezepil
27
Q

Galantamine

-what type of drug/MOA?

A
  • AchE inhibitor

- nicotinic receptors?

28
Q

**Main cholinesterase inhibitor side effects?

A
  • *nausea
  • *vomiting
  • *diarrhea

**Basically cholinergic side effects: DUMBBELLS
+emesis
+GI cramps

29
Q

Memantine

  • *-type of Drug/MOA?
  • *-why use this drug over others?
A
  • *-glutamate antagonist/ blocks NMDA receptors

* -provides neuroprotection by reducing intracellular Ca influx and glutamate induced excitotoxicity

30
Q

What may help older females over age 75 with cognitive issues?

A

Estrogen replacement therapy
= somehow enhances neuronal growth and repair
= somehow decreases formation of betaA formation

No real clinical evidence here

31
Q

What is another strategy that can be used for cognitive issues?

A

1) ANTIOXIDANTS - prevent formation of free radicals in AD
- Vitamin E (alpha tocopherol): combo with MAO-B
- Ginkgo biloba
2) NSAIDS- decrease inflammatory process with cyclooxygenase1 and 2 (COX1&2)

32
Q

Best treatment for non-cognitive symptom of psychosis (agitation, hallucinations.. etc) that develops later in AD:

A

Give ATYPICAL antipsychotics - Risperidone, olanapine, quetiapine

33
Q

Best treatment for non-cognitive symptom of depression/anxiety that develops later in AD?

WHAT NOT TO GIVE?

A

-SSRI= sertraline and citalopram = better side effects

  • NO NOT GIVE TRICYCLICS-TCAs!!! ==> sedation, anticholinergic effects, and confusion (ORTHOSTATIC HYPOTENSION NOT GOOD FOR OLD PATIENTS
  • MOOD STABILIZERS are high risk - some trials showed benefit but little evidence

Pharm Exam 3 (11 decks)

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