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PATHO/PHARM II > Conditions Effecting the Nervous System and PharmacotherapyPart Four: Dementia & Alzheimer’s > Flashcards

Conditions Effecting the Nervous System and PharmacotherapyPart Four: Dementia & Alzheimer’s Flashcards

Exam 4 (Final)

1
Q

Dementia:

What occurs with this group of conditions? (What is there a decrease in?)

A

Decrease in cortical function and skills

Decrease in motor coordination

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2
Q

Dementia:

What commonly occurs?

A

Memory issues common

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3
Q

Dementia:

Memory issues common: What does this include?

A

Short-term losses
Confusion of historical events
Short attention span
Loss of word recall

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4
Q

Dementia:

What changes occur?

A

Behavioral & personality △

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5
Q

Dementia:

Behavioral & personality △: What does this include?

A

Effect relationships, work, QOL

Poor decision-making

Neuropsychiatric sx

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6
Q

Dementia:

Behavioral & personality △:

What Neuropsychiatric sx are included?

A

Hallucinations
Delusions

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7
Q

Dementia:

What are Causes

A

Vascular disease

Infections

Toxins

Genetics

Neuron degeneration

Compression of brain tissue

Atherosclerosis of cerebral vessels

Trauma

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7
Q

What is the most common form of dementia and leading cause of severe cognitive function in older persons?

A

Alzheimer’s Disease (AD)

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8
Q

What is included in Alzheimer’s Disease (AD)?

A

Progressive memory loss & impaired thinking

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9
Q

Alzheimer’s Disease (AD): Is it a normal part of aging?

A

⍉ part of normal aging

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10
Q

Alzheimer’s Disease (AD): What symptoms occur with this? How do they perform tasks?

A

Neuropsychiatric symptoms ~ hallucination delusions

Inability to perform routine tasks

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11
Q

Alzheimer’s Disease (AD):

Disease Process: What occurs before symptoms?

A

Irreversible neuronal damage develops years before sx

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12
Q

Alzheimer’s Disease (AD):

Disease Process: What happens to brain tissue? What happens to neurons? What else?

A

Degeneration of brain tissue

Cerebral atrophy

Degeneration of cholinergic neurons

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13
Q

Alzheimer’s Disease (AD)

Patho: What occurs?

A

Degeneration of neurons

Reduced cholinergic transmission

Beta-Amyloid & Neuritic plaques

Neurofibrillary tangles

Connections to other neurons lost

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14
Q

Alzheimer’s Disease (AD)

Patho: Degeneration of neurons

Where does it occur?

A

Occurs in hippocampus early in AD & subsequent degeneration of neurons in cerebral cortex

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15
Q

Alzheimer’s Disease (AD)

Patho: Reduced cholinergic transmission

What does this mean?

A

Levels of ACh 90% below normal

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16
Q

Alzheimer’s Disease (AD)

Patho: Reduced cholinergic transmission

Levels of ACh 90% below normal: What does this lead to?

A

Loss of Ach – memory decline & attention

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17
Q

Alzheimer’s Disease (AD)

Patho: Beta-Amyloid & Neuritic plaques

How does this happen?

A

In brain, outside neurons, accumulation of plaques containing beta-amyloid protein fragment

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18
Q

Alzheimer’s Disease (AD)

Patho: Beta-Amyloid & Neuritic plaques

In brain, outside neurons, accumulation of plaques containing beta-amyloid protein fragment

What do plaques do?

A

Plaques disrupt nerve impulse transmission –> death of neurons

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19
Q

Alzheimer’s Disease (AD)

Patho: Neurofibrillary tangles

Where do these form?

A

Form inside neurons

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20
Q

Alzheimer’s Disease (AD)

Patho: Neurofibrillary tangles

What do these do?

A

Disrupt arrangement of microtubules

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21
Q

Alzheimer’s Disease (AD)

Patho: Neurofibrillary tangles

What causes neurofibrillary tangles?

A

Caused by abnormal collections of tau protein

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22
Q

Comparison of Normal and Alzheimer Brain.

Volume and weight? Sulci? Gyri? Ventricles?

A

The brain decreases in volume and weight,

the sulci widen, and the gyri thin, especially in the temporal and frontal lobes. The ventricles enlarge to fill the space.

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23
Q

Comparison of Normal and Alzheimer Brain.
Alzheimer’s Disease cont.

What does death of neurons result in?

A

Death of neurons results in extensive areas of the cerebral cortex unable to transmit impulses.

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24
Comparison of Normal and Alzheimer Brain. Alzheimer’s Disease cont. Why does the brain shrink dramatically in size and volume?
The brain shrinks dramatically in size and volume because of widespread cell death.
25
Comparison of Normal and Alzheimer Brain. Alzheimer’s Disease cont. The brain shrink dramatically in size and volume, what does this lead to?
Individuals lose the ability to communicate, recognize loved ones, and to care for themselves.
26
Patho of Alzheimer’s: What do amyloid proteins form? What do they do?
Amyloid proteins form plaques outside neurons, which disrupt neural conduction.
27
Patho of Alzheimer’s: How are plaque formations usually? How do they occur in a Alzheimer's brain?
Plaques are a normal formation in an aging brain, but these occur more frequently in Alzheimer’s in parts of the brain that affect cognitive function.
28
Patho of Alzheimer’s: What are the primary markers of Alzheimer's disease?
Neurofibrillary tangles are the primary markers of Alzheimer’s disease.
29
Patho of Alzheimer’s: What does tau do (in a normal healthy brain)?
Normal transport system in the brain is kept straight by a protein called tau. Tau maintains the transport system in orderly and parallel strands.
30
Patho of Alzheimer’s: What does tau do in Alzheimer's?
In AD, tau collapses into twisted strands, or neurofibrillary tangles.
31
Patho of Alzheimer’s: What happens to transport tracks in Alzheimer's?
The transport tracks no longer remain straight, and neurons begin to disintegrate.
32
Patho of Alzheimer’s: The transport tracks no longer remain straight, and neurons begin to disintegrate. What happens to cells?
Since oxygen and nutrients can no longer move through the cell, the cell dies.
33
Patho of Alzheimer’s: What is there a loss of connection with?
Loss of Connection Between Neurons
34
Patho of Alzheimer’s: When transport systems in neurons are tangled, what happens?
When transport systems in neurons are tangled, the ability of brain cells to transmit impulses from one to another is impaired.
35
Patho of Alzheimer’s: When there are many areas in the cerebral cortex with impaired transport ability, what is the result?
When there are many areas in the cerebral cortex with impaired transport ability, the result is an impairment of cognitive function.
36
Patho of Alzheimer’s: When there are many areas in the cerebral cortex with impaired transport ability, the result is an impairment of cognitive function. What does this result in?
This results in loss of memory and ability to perform activities of daily living.
37
Predisposing Factors & Underlying Conditions: Who does it occur more in?
More likely in women Lifestyle factors Lower SES/education level African/Native Americans and Hispanic
38
Predisposing Factors & Underlying Conditions: What are some factors?
Lifestyle factors Aging >65 & family hx* Combination of factors Head injury High AA homocysteine Production of apoE4 Genetic Link Cardiovascular Factors
39
Predisposing Factors & Underlying Conditions: Production of apoE4- What is apoE4
Cholesterol transport
40
Predisposing Factors & Underlying Conditions Genetic Link: What three forms?
Before 60 – early-onset familial AD Late onset Sporadic late onset
41
Predisposing Factors & Underlying Conditions Genetic Link: Before 60 – early-onset familial AD How is disease progression?
More rapid disease progression
42
Predisposing Factors & Underlying Conditions Genetic Link: Before 60 – early-onset familial AD Why does this occur?
3 genes (APP14, PSEN 1 &2) with mutations on chromosome 21 contribute to overproduction of amyloid proteins in brain
43
Predisposing Factors & Underlying Conditions Genetic Link: Late onset Why does this occur?
Gene that codes for Apolipoprotein E4 (apoE4) ↑’d risk & chromosome 19
44
Predisposing Factors & Underlying Conditions Genetic Link: Sporadic late onset Why does this occur?
No genetic association, most common
45
Predisposing Factors & Underlying Conditions Cardiovascular Factors: What would interfere with the ability to breakdown amyloid?
Increased risk for atherosclerosis that occurs with DM & elevated blood glucose interfere with the ability to break down amyloid
45
Predisposing Factors & Underlying Conditions: Cardiovascular Factors: How can Homocysteine be lowered?
Homocysteine – can be lowered by eating foods with folic acid & VitB6 & B12
46
Predisposing Factors & Underlying Conditions Cardiovascular Factors
DM damage brain vessels, htn, smoking, obesity --> link to O2 to brain
47
Clinical Presentation of Alzheimer’s: How is onset? What age does it typically start? What occurs with it?
Insidious onset Typically start @ 65yo “Sundowning”
48
Clinical Presentation of Alzheimer’s: Typically starts at 65 but can start when?
May begin as early as 40yo
49
Clinical Presentation of Alzheimer’s: Life expectancy from onset? Progression representation?
Usually 4-8y For some, maybe ≥ 20y Progression does not represent final stages
50
Management of Alzheimer’s: how easy?
Often difficult
51
Management of Alzheimer’s: Diagnostics
PMH PE Head CT, MRI, PET
52
Management of Alzheimer’s: Treatment: What does treatment do?
RXs only modestly slow progression & prolong independent function
53
Management of Alzheimer’s: Treatment: What does treatment not do?
⍉ cure ⍉ reverse damage ⍉ stop progression
54
Management of Alzheimer’s Classes of drugs:
Cholinesterase inhibitors N-methyl-D-aspartate (NMDA) receptor antagonists
55
Management of Alzheimer’s Drug selection
⍉ superior efficacy of any agent Based on tolerability, ease of use, cost
56
Management of Alzheimer’s RXs: What is the optimal duration of treatment?
No optimal duration of TX
57
Management of Alzheimer’s RXs: How are improvements?
Modest improvements that last short time
58
Cholinesterase inhibitors: What are agents:
Donepezil (Aricept)
59
Cholinesterase inhibitors: What are uses? What may it do?
Mild to moderate Donepezil approved in severe May only slow disease progression
60
Cholinesterase inhibitors MOA
Prevent breakdown of ACh by acetylcholinesterase (AchE) in brain --> so more Ach is available at cholinergic synapse
61
Cholinesterase inhibitors Prevent breakdown of ACh by acetylcholinesterase (AchE) in brain --> so more Ach is available at cholinergic synapse. What is the result?
Result: enhanced transmission by cholinergic neurons that have not yet been destroyed
62
Cholinesterase inhibitors MOA What does it not do?
Do not stop AD progression nor cure AD – only may slow progression
63
Cholinesterase inhibitors Hepatic metabolism
CYP-450 pathway Protein-bound, 70hr ½ life, 15 days to achieve steady state
64
Cholinesterase inhibitors How is it primarily excreted?
Excretion primarily in urine, bile
65
Cholinesterase inhibitors How should doses be taken?
Stabilize on initial dose for 1-3 months before increase Take daily with & w/o food, swallow whole Adm @HS
66
Cholinesterase inhibitors ADEs from boosting Ach
Cholinergic ~ SLUD GI effects Dizziness, HA Bronchoconstriction – CVE uncommon
67
Cholinesterase inhibitors ADEs from boosting Ach Bronchoconstriction:
Bronchoconstriction – Ach at synapses in lungs Caution asthma & COPD
67
Cholinesterase inhibitors ADEs from boosting Ach: GI effects
N/V/D, dyspepsia
68
Cholinesterase inhibitors ADEs from boosting Ach What is an uncommon occurrance? What may it warrant?
CVE uncommon Potentially warrants D/C Symptomatic bradycardia --> falls & fractures, pacemaker placement
69
Cholinesterase inhibitors: What kind of drugs should be avoided with this? Why?
Avoid drugs blocking cholinergic receptors, will reduce therapeutic effects
70
Cholinesterase inhibitors: What kind of drugs should be avoided with this? (Name specifics)
↓ response of cholinesterase inhibitors Anticholinergics FG antihistamines TCAs Antipsychotics
71
NMDA Receptor Antagonist: Memantine (Namenda, Namenda XR): What are NMDA receptors for?
Role in learning & memory Regulates Ca entry into neurons
72
NMDA Receptor Antagonist: Memantine (Namenda, Namenda XR): NMDA receptors: What promotes Ca influx into neurons?
Binding of Glutamate (Glu) promotes Ca influx --> neuron
73
NMDA Receptor Antagonist: Memantine (Namenda, Namenda XR): In AD how is glutamate release and what does this lead to?
In AD there is excessive glutamate release, leading to overactivation of NMDA receptors.
74
NMDA Receptor Antagonist: Memantine (Namenda, Namenda XR): In AD what does overactivation of NMDA receptors this lead to?
Overactivation of NMDA receptors causes excessive Ca influx --> excitotoxicity—neurons damaged and killed due to overstimulation.
75
NMDA Receptor Antagonist: Memantine (Namenda, Namenda XR): MOA: What does Memantine do?
Memantine binds to NMDA receptors and blocks excessive glutamate activity, reducing the influx of calcium ions.
76
NMDA Receptor Antagonist: Memantine (Namenda, Namenda XR): MOA: Memantine binds to NMDA receptors and blocks excessive glutamate activity, reducing the influx of calcium ions.
Protects neurons from further damage and death, which may slow the progression of symptoms
77
NMDA Receptor Antagonist: Memantine cont. Use? What does it not benefit?
only for moderate or severe AD ⍉ benefit in mild AD
78
NMDA Receptor Antagonist: Memantine cont. Use: Study of memantine + donepezil?
Less decline with combo > mono-TX ? Synergistic effect
79
NMDA Receptor Antagonist: Memantine cont. Pharmacokinetics Absorption? Metabolism? Excretion?
Good oral absorption +/- food Little metabolism Excreted largely unchanged in urine
80
NMDA Receptor Antagonist: Memantine cont. Pharmacokinetics When do plasma levels peak? How long is half life?
Plasma levels peak in 3-7 hrs Long ½ life 60-80 hrs
81
NMDA Receptor Antagonist: Memantine cont. ADE?
Well tolerated Common: dizziness, HA, confusion, constipation
82
NMDA Receptor Antagonist: Memantine cont. Admin
Dosage titrated Severe renal impairment ~ reduce dose
83
NMDA Receptor Antagonist: Memantine cont. Drug interaction
Sodium bicarbonate & drugs alkalinizing urine
84
NMDA Receptor Antagonist: Memantine cont. ADE: Sodium bicarbonate & drugs alkalinizing urine What does it lead to?
↓ renal excretion of memantine Drug accumulation & toxicity
85
Nursing Implications of Alz Drugs What must be assessed?
Assess swallowing because patients may develop difficulty as the disease progresses and be at risk for aspiration. Reassess the patient’s cognitive function often.
86
Nursing Implications of Alz Drugs Assess swallowing because patients may develop difficulty as the disease progresses and be at risk for aspiration. So how should drugs be given?
Drugs may need to be crushed or given in liquid form.
87
Nursing Implications of Alz Drugs What should not be done with time released or open time released capsules?
Do not crush time-released pills or open time-released capsule
88
Nursing Implications of Alz Drugs: What should the nurse watch for?
Watch for changes in memory, attention, reasoning, language, and ability to perform simple tasks.
89
Nursing Implications of Alz Drugs: What is a long term task completed by nurses? Why is it long term?
Cognitive assessment is a long-term task because changes may take time to appear.
90
Nursing Implications of Alz Drugs: What else should be monitored in general?
Recheck and monitor the patient’s heart rate and rhythm, and blood pressure. Monitor intake and output and daily weights. Watch for potential seizure activity.
91
Nursing Implications of Alz Drugs: What should patients be instructed about with drugs?
Because these drugs may cause dizziness and fatigue, instruct any in-patient to call for help when getting out of bed and ensure that the call light is within easy reach. Instruct patients at home to also call for help getting up. Suggest the use of a bell or other call device for help.
92
Nursing Implications of Alz Drugs: What things should you be asking the patient?
Ask the patient about nausea, vomiting, and GI discomfort. Notify the prescriber if side effects occur.

PATHO/PHARM II (27 decks)

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