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PATHO/PHARM II > Conditions Effecting the Nervous System and PharmacotherapyPart Six: Neurodegenerative DX- Parkinson’s Disease PD > Flashcards

Conditions Effecting the Nervous System and PharmacotherapyPart Six: Neurodegenerative DX- Parkinson’s Disease PD Flashcards

Exam 4 (Final)

1
Q

Parkinson’s Disease (PD): What is it?

A

Chronic progressive neurodegenerative disorder

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2
Q

Parkinson’s Disease (PD): What is it a deficiency of?

A

Deficiency of NT dopamine (made by substania nigra in brain).

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3
Q

Parkinson’s Disease (PD):

Where is dopamine made?

A

(made by substania nigra in brain).

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4
Q

Parkinson’s Disease (PD):

When do symptoms appear?

A

Symptoms generally appear during middle age and progress

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5
Q

Parkinson’s Disease (PD):

Is there a cure for motor symptoms?

A

No cure for motor symptoms

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6
Q

Parkinson’s Disease (PD):

What can drug treatment do?

A

Drug tx can maintain functional mobility for years (ie, prolongs/improves QOL)

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7
Q

Parkinson’s Disease (PD):

What are cardinal motor symptoms of PD?

A

Cardinal motor sx:

tremor,

rigidity,

postural instability,

slowed movement (bradykinesia)

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8
Q

Parkinson’s Disease (PD):

What are nonmotor symptoms ?

A

Nonmotor sx:

sleep disturbances,

depression,

psychosis,

dementia,

autonomic disturbances

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9
Q

Parkinson’s Disease (PD):

When do early symptoms develop?

A

Early sx can develop years before function impairment (e.g. clumsiness, excessive salivation, worsening handwriting, tremors, slower gait, reduced voice volume)

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10
Q

Parkinson’s Disease (PD):

Secondary causes of Parkinson’s disease?

A

2° – caused by diagnosis other than PD (eg head trauma, infection, neoplasm, atherosclerosis, toxins, drug-induced EPS: neuroleptics, antiemetics, antihypertensives)

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11
Q

Patho of PD:

What is a probable cause?

A

Genetic-envi mutations probable cause

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12
Q

Patho of PD:

What is disrupted?

A

Neurotransmission is disrupted primarily in the brain’s striatum.

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13
Q

Patho of PD

What is misfolded?

A

Misfolded/dysfunctional alpha-synuclein

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14
Q

Patho of PD

Misfolded/dysfunctional alpha-synuclein:

What is it and what is it made by?

A

Toxic protein made by dopaminergic neurons accumulates

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15
Q

Patho of PD

Misfolded/dysfunctional alpha-synuclein:

What is it not broken down by?

A

Not broken down by 2 other proteins (parkin & ubiquitin)

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16
Q

Patho of PD

Misfolded/dysfunctional alpha-synuclein

What is defective?

A

Defective gene coding for all 3 proteins

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17
Q

Patho of PD

Misfolded/dysfunctional alpha-synuclein

What does it contribute to?

A

Contributes to neuron death/destruction of dopaminergic neurons

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18
Q

Patho of PD

Normally inhibitory actions of Dopamine are balanced by what?

A

Normally, inhibitory actions of Dopamine are balanced by excitatory actions of Ach –> controlled movement

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19
Q

Patho of PD

What is GABA?

A

GABA is an inhibitory NT blocking signals in nervous system

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20
Q

Patho of PD

Normally, inhibitory actions of Dopamine are balanced by excitatory actions of Ach –> controlled movement

In healthy people, what does GABA do?

A

In healthy individuals, GABA regulates movement by inhibiting certain brain signals.

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21
Q

Patho of PD
Normally,
Between do dopamine and GABA, what is needed?

A

Interplay between DA & GABA – need a balance

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22
Q

Patho of PD

Interplay between DA & GABA – need a balance

What does dopamine inhibit?

A

Dopamine inhibits the neurons that release GABA

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23
Q

Patho of PD

Interplay between DA & GABA – need a balance

What does acetylcholine excite?

A

Ach excites the neurons that release GABA

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24
Q

Patho of PD

In PD, what is there an imbalance between?

A

In PD – imbalance btwn DA & Ach

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25
Q

Patho of PD

What happens to neurons supplying DA

A

Neurons supplying DA to striatum degenerate

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26
Q

Patho of PD

Neurons supplying DA to striatum degenerate what does this lead to?

A

Excitatory effects of Ach go unopposed –> to excess stimulation of neurons that release GABA

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27
Q

Patho of PD

Excitatory effects of Ach go unopposed –> to excess stimulation of neurons that release GABA

What does this lead to?

A

Excess GABA interferes with motor function by blocking messages in movement centers

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28
Q

Patho of PD

Excess GABA interferes with motor function by blocking messages in movement centers

What is the result? (symptoms)

A

The result is difficulties with movement, such as stiffness, slowness, and tremors

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29
Q

Progression of Parkinson’s Disease:

What is it a degeneration of?

A

Degeneration of the dopamine-producing neurons in the substantia nigra of the midbrain

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30
Q

Progression of Parkinson’s Disease:

What balance is disrupted?

A

Disrupts the normal balance between dopamine and ACh in the basal ganglia

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31
Q

Progression of Parkinson’s Disease:

What dopamine normally essential for?

A

Dopamine is essential for normal functioning of the extrapyramidal motor system, including control of posture, support, and voluntary motion.

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32
Q

Progression of Parkinson’s Disease:

Manifestations of PD occur when how much of neurons are lost?

A

Manifestations of PD do not occur until 70-80% of neurons in the substantia nigra are lost.

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33
Q

Progression of Parkinson’s Disease:

WHen the amount og dopamine falls, how is acetylcholine?

A

When the amount of dopamine falls, ACh still functions. Its excitatory properties are responsible for the excess and exaggerated movements in PD.

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34
Q

Progression of Parkinson’s Disease

What is found in the brains of patients with PD?

A

Lewy bodies, abnormal accumulations of protein, are found in the brains of patients with PD.

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35
Q

Progression of Parkinson’s Disease

Lewy bodies, abnormal accumulations of protein, are found in the brains of patients with PD.

What causes these bodies to form? What does their presence indicate?

A

It is not known what causes these bodies to form, but their presence indicates abnormal functioning of the brain.

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36
Q

Progression of Parkinson’s Disease

How is onset?

How long does it take for loss of neurons to occur?

A

Onset insidious, loss of neurons takes place 5-20yrs, long before sx appear

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37
Q

Prevalence and Predisposing Factors of PD

Include what?

A

Genetic Link

Exposure to Chemicals and Drugs

Cellular Changes

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38
Q

Prevalence and Predisposing Factors of PD

Genetic Link: Approximately what % of patients with PD have a family history of PD?

A

Approximately 15% of patients with PD have a family history of PD.

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39
Q

Prevalence and Predisposing Factors of PD

Genetic Link: The most common genetic contributor to PD is what?

A

The most common genetic contributor to PD is the LRRK2 gene.

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40
Q

Prevalence and Predisposing Factors of PD

Genetic Link: Genes involved in familial PD are what?

What are mutations in these genes associated with?

A

Genes involved in familial PD are parkin (PARK2, PARK7), PINK1, and SNCA.

Mutations in these genes are often associated with a younger age of onset

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41
Q

Prevalence and Predisposing Factors of PD

Exposure to Chemicals and Drugs

A

Carbon monoxide

Metoclopramide (Reglan)

Antipsychotics

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42
Q

Prevalence and Predisposing Factors of PD

Exposure to Chemicals and Drugs:

Antipsychotics : What happens after stopping these drugs?

A

After stopping these drugs, symptoms of parkinsonism generally decrease or disappear

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43
Q

Prevalence and Predisposing Factors of PD

Cellular Changes

A

There are damaging effects of viruses or toxins on cells.

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44
Q

Prevalence and Predisposing Factors of PD

Cellular Changes: What does significant oxidative stress lead to?

A

Significant oxidative stress leads to the accumulation of free radicals within the cells in the brain.

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45
Q

Prevalence and Predisposing Factors of PD

Other causes of parkinsonism include?

A

Other causes of parkinsonism include infections, stroke, tumor, and trauma.

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46
Q

Clinical Presentation of PD

Motor Sx:

A

Resting tremors & Rigidity

Bradykinesia/akinesthesia

Postural disturbances

Dysarthria (difficulty with speech)

Dysphagia (difficulty swallowing)

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47
Q

Clinical Presentation of PD

How may symptoms develop?

A

Sx may develop isolated or in combination

All are present as dx progresses

Sx bilateral but usually involve 1 side early in dx

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48
Q

Clinical Presentation of PD

As disease progresses –> ?

A

As disease progresses –> postural abnormalities, diff walking, weakness, shuffling gait

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49
Q

Clinical Presentation of PD

Nonmotor sx:

A

sleep disorders,

sensory disturbances (loss of smell, vision),

urinary urgency,

difficulty concentrating,

depression,

hallucinations

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50
Q

Clinical Presentation of PD

Autonomic sx:

A

diaphoresis,

orthostatic hypotension,

drooling,

gastric/urinary retention,

constipation

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51
Q

Motor Symptoms of PD

A

Tremor

Rigidity

Akinesia

Postural Instability

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52
Q

Motor Symptoms of PD:

What is the first sign?

A

Tremor- 1st sign & may be mild initially

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53
Q

Motor Symptoms of PD:

How are tremors in PD?

A

More prominent at rest and is aggravated by emotional stress or increased concentration.

Pill-rolling

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54
Q

Motor Symptoms of PD:

Akinesia- What is it?

A

absence or loss of control of voluntary muscle movements

loss of automatic (blinking, swallowing)

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55
Q

Motor Symptoms of PD:

Akinesia- What else is involved?

A

bradykinesia (slowness of movement)

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56
Q

Motor Symptoms of PD:

Postural Instability

A

Stooped posture

Shuffling gait

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57
Q

Parkinson’s Rigidity: What is it?

A

Muscle resistance to passive movement of rigid limb in both flexion & extension

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58
Q

Parkinson’s Rigidity:

What are the two types?

A

Plastic or lead-pipe rigidity:

Cogwheel rigidity:

59
Q

Parkinson’s Rigidity:

Plastic or lead-pipe rigidity: What is it?

A

Plastic or lead-pipe rigidity: increased muscle tone independent of force used in passive movement

60
Q

Parkinson’s Rigidity:

Cogwheel rigidity: What is it?

A

uniform resistance maybe interrupted by a series of brief jerks

61
Q

Parkinson’s Rigidity:

Complications

A

Dyskinesia (involuntary movements)

Weakness

Neuropsychiatric problems

Dysphagia

Infections

Skin breakdown

Orthostatic hypotension

62
Q

Diagnosis & Management Overview for PD

Diagnostics:

A

⍉ definitive test

PMH

PE

Testing to R/O other DX

63
Q

Diagnosis & Management Overview for PD

Diagnostics: PE includes?

A

Neuro assessment

64
Q

Diagnosis & Management Overview for PD

TX?

A

⍉ PX or cure

⍉ reverse damage

⍉ delay progression

Symptom control, relief only!!!

65
Q

Diagnosis & Management Overview for PD

Symptom control, relief only!!!- How do meds do this?

A

↑ DA & ↓ Ach to tx bradykinesia, gait disturbance, postural instability

66
Q

Diagnosis & Management Overview for PD

What are limitations of meds?

A

Diminished effects over time

Control lost @ max dosing

67
Q

Diagnosis & Management Overview for PD

SX options: What to do if unresponsive to drugs?

A

Deep brain stimulation - if unresponsive to drugs

68
Q

Diagnosis & Management Overview for PD

Maximizing function

A

PT & OT

Assistive devices ~ wheelchairs, walkers, handrails

69
Q

Diagnosis & Management Overview for PD

Overall health

A

Coping strategies & support

Proper nutrition

Adequate rest

Drug therapy!!!

70
Q

PD Agent Classification:

What is targeted?

A

Target problem: ↓↓ striatal DA

Target problem: ↑↑ ACh

71
Q

PD Agent Classification:

What drugs target ↓↓ striatal DA problem?

A

Dopaminergic meds

DA replacement

DA agonists

MAO-B inhibitors

DA releaser

COMT inhibitors??

72
Q

PD Agent Classification:

Dopaminergic meds:

How often are they used?
What do they do?

A

DA activation ~ direct & indirect

More widely used

73
Q

PD Agent Classification:

DA replacement includes?

A

Levodopa/Carbidopa

74
Q

PD Agent Classification

DA agonists: What are the two groups?

A

Non-ergot

Ergot derivatives

75
Q

PD Agent Classification

DA agonists:
Non-ergot includes?

A

Apomorphine
Pramipexole
Ropinirole
Rotigotine

76
Q

PD Agent Classification

DA agonists:
Ergot derivatives includes?

A

Bromocriptine

Cabergoline (off-label)

77
Q

PD Agent Classification

COMT inhibitors: How do they work?

A

By inhibiting COMT, plasma half-life of levodopa prolonged

78
Q

PD Agent Classification

COMT inhibitors: What are the two?

A

Entacapone

Tolcapone

79
Q

PD Agent Classification

MAO-B inhibitors: What do they do?

A

MAO-B inactivates dopamine

80
Q

PD Agent Classification

MAO-B inhibitors: What are the two meds?

A

Selegiline
Rasagiline

81
Q

PD Agent Classification

DA releaser: What is the med?

A

Amantadine

82
Q

PD Agent Classification;

What meds Target problem: ↑↑ ACh?

A

Anticholinergic meds

83
Q

PD Agent Classification;’

‘Anticholinergic meds

A

ACh receptor blockade

Benztropine

Trihexyphenidyl

84
Q

Levodopa

MOA: How does it reduce symptoms?

A

Reduces symptoms by increasing dopamine synthesis in the striatum.

85
Q

Levodopa

MOA: How does this med enter brain?

A

Enters brain via active transport across BBB

86
Q

Levodopa

MOA: After entering brain, where does it go?

A

Taken up by nerve terminal in striatum

87
Q

Levodopa

MOA: After being taken up by nerve terminal in striatum

A

Get converted into active form & released into synapse

88
Q

Levodopa

MOA: Get converted into active form & released into synapse

What happens after this?

A

Binds to dopamine receptors on GABAergic neurons, causing them to fire at a slower rate

89
Q

Levodopa

MOA: Binds to dopamine receptors on GABAergic neurons, causing them to fire at a slower rate

What does this help with?

A

Helps restore balance btwn DA & ACh

90
Q

Levodopa

MOA:

What converts levodopa to dopamine? What is this enhanced by?

A

Decarboxylase (in brain, liver, intestine) converts levodopa to dopamine and is enhanced by Pyridoxine (vitamin B6)

91
Q

Levodopa

Why can’t we just give dopamine by itself?

A

Dopamine can’t cross BBB

Dopamine has very short half-life in the blood

92
Q

Levodopa:

What is the only way it is given?

A

Only given in combination with carbidopa or carbidopa/entacapone

93
Q

Levodopa:

How effective is it?

A

Highly effective, but benefits diminish over time

94
Q

Levodopa:

Highly effective, but benefits diminish over time

When do full effects develop?

A

Full effects take several months to develop, but it works

95
Q

Levodopa:

Highly effective, but benefits diminish over time

How are symptoms controlled? For how long? Why?

A

Symptoms well controlled for first 2 years

But….return to pretreatment state at end of 5 years probably because of disease progression, not tolerance

96
Q

Levodopa:

How is it administered?

A

Orally administered; rapidly absorbed from small intestine

97
Q

Levodopa:

How does food effect absorption? Why?

A

Food delays absorption by slowing gastric emptying

98
Q

Levodopa

Orally administered; rapidly absorbed from small intestine

What happens to levodopa (having to do with intestinal absorption)

A

Neutral amino acids compete with levodopa for intestinal absorption and for transport across blood-brain barrier

99
Q

Levodopa

Orally administered; rapidly absorbed from small intestine

What has an effect on therapeutic effects of the drug? How?

A

High-protein foods reduce therapeutic effects by competing for intestinal absorption

100
Q

What is Cornerstone of PD treatment!!!

A

Levodopa

101
Q

Levodopa

Acute loss of effect – returns of sx

What happens

A

Gradual loss (wearing off) – drug levels decline to subtherapeutic

102
Q

Levodopa

Gradual loss (wearing off) – drug levels decline to subtherapeutic

When does it develop?

A

Develops near the end of dosing interval

103
Q

Levodopa

Gradual loss (wearing off) – drug levels decline to subtherapeutic

How can it be minimized?

A

Can be minimized by shortening dosing interval

104
Q

Levodopa:

Gradual loss (wearing off) – drug levels decline to subtherapeutic

WHat do you do?

A

Give another PD (e.g entacapone) drug to prolong levodopa ½-life

Give direct acting dopamine agonist (e.g. pramipexole, ropinirole)

105
Q

Levodopa:

Abrupt loss of effect (“on-off”) - sudden and unpredictable fluctuations in motor response, rapid transition between periods of improved mobility (“on” state) and worsened symptoms (“off” state).

When does this occur?

A

Occurs anytime during dosing interval, even if drug levels are high

106
Q

Levodopa

This drug may go “on-off” What does this mean?

A

Abrupt loss of effect (“on-off”) - sudden and unpredictable fluctuations in motor response, rapid transition between periods of improved mobility (“on” state) and worsened symptoms (“off” state).

107
Q

Levodopa:

Abrupt loss of effect (“on-off”) - sudden and unpredictable fluctuations in motor response, rapid transition between periods of improved mobility (“on” state) and worsened symptoms (“off” state).

How long is “off” time?

A

Off times may last minutes to hours

108
Q

Levodopa:

Abrupt loss of effect (“on-off”) - sudden and unpredictable fluctuations in motor response, rapid transition between periods of improved mobility (“on” state) and worsened symptoms (“off” state).

Over course of treatment, what is likely to happen to off periods?

A

Over course of tx, off periods likely to increase, so many need add’l drugs (e.g COMT-I, MAO-I)

109
Q

What is a precursor to dopamine?

A

Levodopa is a precursor of dopamine.

110
Q

PD Pharmacology: Carbidopa

After oral administration, how is levodopa metabolized? Where? What is it converted to?

A

After oral administration, levodopa undergoes significant metabolism by decarboxylase in the GUT & blood vessels –> converted dopamine.

111
Q

PD Pharmacology: Carbidopa

What happens to large amounts of levodopa before it reaches the brain?

A

Large amounts of levodopa are decarboxylated in the periphery before reaching brain & converted to dopamine

112
Q

PD Pharmacology: Carbidopa

What does carbidopa enhance?

A

Carbidopa enhances effects of levodopa

113
Q

PD Pharmacology: Carbidopa

What kind of effect does carbadopa have on its own?

What does it do to levodopa?

A

Carbidopa has no effect on it’s own but inhibits conversion of levodopa to dopamine by decarboxylase in the periphery, so it can reach the brain

114
Q

PD Pharmacology: Carbidopa

Why does carbidopa not affect the levodopa’s conversion to dopamine in the brain?

A

Carbidopa does NOT cross BBB so it does not affect the levodopa ’s conversion to dopamine in the brain

115
Q

PD Pharmacology: Carbidopa

Levodopa/Carbidopa (Sinemet)

How is it available? How is dosing?

A

Immediate or Continuous Release

Dose gradually increased from 1 tab daily –> 8 tabs daily

116
Q

Levodopa ADRs

A

Nausea and vomiting

Dyskinesias

Cardiovascular

Psychosis from dopamine activation

Central nervous system (CNS) effects

Others

117
Q

Levodopa ADRs

Nausea and vomiting: How can this be dealt with?

A

Low initial doses and administration with food….but food can reduce therapeutic effects by decreasing absorption, avoid if possible

Giving additional carbidopa (without levodopa) can help reduce nausea and vomiting

117
Q

Levodopa ADRs

Nausea and vomiting: Why does this occur?

A

Activation of dopamine receptors in the chemoreceptor trigger zone of the medulla

118
Q

Levodopa ADRs

Nausea and vomiting

A

By minimizing peripheral conversion, less levodopa is converted into dopamine outside the brain

119
Q

Levodopa ADRs

What are the most troubling adverse effects?

A

Dyskinesias

120
Q

Levodopa ADRs

Dyskinesias: Levodopa given to help with movement disorders it can cause What?

A

Although levodopa given to help with movement disorders it can cause movement disorders

121
Q

Levodopa ADRs

Dyskinesias: What can be done about this

A

Reduce dose (but PD sx may emerge) or give Amantadine (dopamine releaser)

122
Q

Levodopa ADRs

Dyskinesias: Reduce dose (but PD sx may emerge) or give Amantadine (dopamine releaser)

What does this do?

A

Regulates glutamate neurotransmission & NMDA receptors

123
Q

Levodopa ADRs

Cardiovascular

What issues?

A

Postural hypotension – dopamine can cause vasodilation in periphery

124
Q

Levodopa ADRs

Cardiovascular: Postural hypotension – dopamine can cause vasodilation in periphery

What should be done?

A

Increase intake of salt and water

Alpha-adrenergic agonist

125
Q

Levodopa ADRs

Cardiovascular: Why do dysrhythmias occur?

A

Dysrhythmias from dopamine conversion in periphery – activation of beta1 receptors

126
Q

Levodopa ADRs:

Psychosis from dopamine activation: WHat does this include?

A

Visual hallucinations

Vivid dreams or nightmares

Paranoid ideation

127
Q

Levodopa ADRs:

Psychosis from dopamine activation: WHat is this caused by?

A

Caused by activation of dopamine receptors

128
Q

Levodopa ADRs:

Central nervous system (CNS) effects

What does this include?

A

Anxiety and agitation

Memory and cognitive impairment

Insomnia and nightmares are common

Problems with impulse control

Behavioral changes associated with promiscuity, gambling, binge eating, and alcohol abuse

129
Q

Levodopa ADRs

Others

A

Darken sweat/urine (harmless)

130
Q

Drug interactions cont’d & Food interactions

A

Anti-psychotics that block receptors for dopamine in the striatum

MAO-Inhibitors

Anticholinergics

Pyridoxine (vitamin B6)

High-protein meals can reduce absorption

131
Q

Drug interactions cont’d & Food interactions

Anti-psychotics that block receptors for dopamine in the striatum: What do they cause?

A

Anti-psychotics that block receptors for dopamine in the striatum

132
Q

Drug interactions cont’d & Food interactions

MAO-Inhibitors: What do they cause?

A

Can cause hypertensive crisis from vasoconstrictive effects

133
Q

Drug interactions cont’d & Food interactions

Anticholinergics: What do they cause?

A

By blocking cholinergic receptors, these agents enhance responses to levodopa

134
Q

Drug interactions cont’d & Food interactions

Pyridoxine (vitamin B6): What do they cause?

A

Altho Vitamin B6 accelerates decarboxylation (conversion) of levodopa in periphery, no need to limit it since levodopa is taken with carbidopa

Carbidopa inhibits decarboxylase, so this eliminates concern about decreasing effects of levodopa by taking Vitamin B6

135
Q

Drug interactions cont’d & Food interactions

High-protein meals can reduce absorption

Why does this happen?

A

Amino acids compete with levodopa for intestinal absorption & transport across BBB

136
Q

Drug interactions cont’d & Food interactions

High-protein meals can reduce absorption

So what are patients advised to do?

A

Advise pts to spread protein consumption evenly throughout the day

136
Q

Drug interactions cont’d & Food interactions

High-protein meals can reduce absorption

What does this do?

A

Could trigger an abrupt loss of effect

137
Q

Levodopa/Carbidopa [Sinemet and Parcopa]

Advantages

A

Most effective therapy for PD

138
Q

Levodopa/Carbidopa [Sinemet and Parcopa]

Mechanism of action

A

Carbidopa is used to enhance the effects of levodopa

Carbidopa has no therapeutic effects of its own

Carbidopa inhibits the decarboxylation (conversion) of levodopa in the intestine and the peripheral tissues

More levodopa is available to the CNS

Carbidopa is unable to cross the blood-brain barrier

139
Q

Levodopa/Carbidopa [Sinemet] (Cont.)
Advantages:
By increasing the fraction of levodopa available for action in the CNS, what does carbidopa allow for?

A

By increasing the fraction of levodopa available for action in the CNS, carbidopa allows the dosage of levodopa to be reduced by about 75%

140
Q

Levodopa/Carbidopa [Sinemet] (Cont.)
Advantages:

By causing the direct inhibition of decarboxylase, carbidopa does what?

A

By causing the direct inhibition of decarboxylase, carbidopa eliminates concerns about decreasing the effects of levodopa by taking a vitamin preparation that contains pyridoxine

140
Q

Levodopa/Carbidopa [Sinemet] (Cont.)
Advantages:
By reducing the production of dopamine in the periphery, carbidopa does what?

A

By reducing the production of dopamine in the periphery, carbidopa reduces cardiovascular responses to levodopa as well as nausea and vomiting

PATHO/PHARM II (27 decks)

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