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Applied Pathophysiology > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

Is Parkinson’s Disease (PD) a hypokinetic or hyperkinetic disease?

A

hypokinetic

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2
Q

what is PD?

A

idiopathic neurodegenerative condition caused by loss of dopaminergic neurons in the substantia nigra

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3
Q

what are 4 key characteristics of PD? briefly describe each characteristic

A

1) asymmetrical resting tremor (trying to grab something but hand is shaking)
2) bradykinesia (slow movements)
3) rigidity (stiff)
4) postural instability (don’t have unlocking mechanisms for muscles to relax)

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4
Q

what is parkinsonism?

A

the clinical syndrome that arises from the degeneration of the basal ganglia

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5
Q

what is the prevalence of PD in people over 65?

A

1 in 100

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6
Q

which gender is more affected by PD?

A

men 2: 1 women

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7
Q

what is the first step of synaptic transmission?

A

AP produced via depolarization of neuronal membrane due to Na influx through Na Vgated channels

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8
Q

what is the second step of synaptic transmission?

A

produced AP travels down axon towards pre-synaptic terminal

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9
Q

what is the 3rd step of synaptic transmission?

A

AP arrives at pre-synaptic terminal and causes Ca channels in plasma membrane to open

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10
Q

What is the 4th step of synaptic transmission?

A

influx of Ca triggers the exocytosis of vesicles containing neurotransmitter

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11
Q

what is the 5th step of synaptic transmission?

A

NT enters synaptic cleft and binds to receptors on post-synaptic membrane

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12
Q

what is the 6th step of synaptic transmission?

A

after binding, the NT is cleaved and taken back up by pre-synaptic terminal where it is recycled and stored in vesicles

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13
Q

What is the first step in dopamine synthesis?

A

tyrosine is taken up from the blood into the brain’s extracellular fluid then into dopaminergic substantia nigra neurons via specific enzyme transporters

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14
Q

what is the second step in dopamine synthesis?

A

tyr hydroxylated to form L-DOPA (dopamine precursor)

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15
Q

what is the 3rd step in dopamine synthesis?

A

L-DOPA is decarboxylated to form dopamine

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16
Q

what is the function of the basal ganglia?

A

controls complex movements and has a part in motor learning

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17
Q

where is the basal ganglia located?

A

base of the forebrain

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18
Q

what are 4 components of the basal ganglia?

A

substantia nigra
striatum
pallidum (not important)
subthalamic nucleus

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19
Q

what are 3 roles of the substantia nigra?

A

reward
addiction
movement

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20
Q

what is the striatum composed of?

A

putamen neurons

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21
Q

what kind of receptors are found on putamen neurons?

A

D1 and D2 receptors

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22
Q

what is the function of the striatum?

A

major input site of the basal ganglia system

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23
Q

what is the ventrolateral thalamus (VLT)?

A

integration centre for basal-ganglionic and cerebellar impulses

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24
Q

what is the function of the VLT?

A 
initiates body movements
sends impulses (received from putamen neurons) to the motor cortex to allow movement
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25
Q

What is the dopamine pathway responsible for? (5pts)

A 
reward (motivation)
pleasure, euphoria
motor function (fine tuning)
compulsion
perseveration
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26
Q

what is the serotonin pathway responsible for? (5pts)

A 
mood
memory
processing
sleep
cognition
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27
Q

what are the 3 major NTs involved in PD?

A

dopamine
Ach
GABA

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28
Q

is dopamine excitatory or inhibitory?

A

inhibitory

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29
Q

is Ach excitatory or inhibitory?

A

excitatory

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30
Q

what happens when there’s too much Ach?

A

over activity of cholinergic neurons and leads to muscle contraction and remain contracted (unable to repolarize)

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31
Q

what happens with Ach when dopaminergic cells are destroyed?

A

Ach runs unchecked because there is no DA released to compete with it

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32
Q

is GABA excitatory or inhibitory?

A

inhibitory

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33
Q

how are GABA and DA related?

A

GABA release is regulated by binding of DA to receptors

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34
Q

what happens to GABA in PD?

A

release of GABA increases and decreases in incorrect portions of the Nigro-Striatal pathway

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35
Q

what does a DA reduction mean in regards of GABA?

A

increased GABA leading to partial or full paralysis

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36
Q

what is the general procedure for normal movement?

A

1) info from different parts of the brain is sent to sub. nigra to stimulate DA synthesis
2) DA is released from sub. nigra where it binds to D1 and D2 receptors on putamen neurons in striatum
3) goes into direct pathway and indirect pathway to cause movement

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37
Q

what receptor is associated with the direct pathway? indirect pathway?

A

D1 - direct

D2 - indirect

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38
Q

What is the 1st step in the direct pathway?

A

DA binds to D1 receptor of substance P producing putamen neurons in the striatum

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39
Q

What is the 2nd step in the direct pathway?

A

DA binding causes an increase in Substance P which causes an increase in GABA levels

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40
Q

what is the third step of the direct pathway?

A

GABA inhibits the firing of D1 sub P containing putamen neurons

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41
Q

what is the 4th step of the direct pathway?

A

reduced firing of sub P containing putamen neurons causes a decrease in GABA release, resulting in an increase of activity of the VLT (VLT = less inhibited)

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42
Q

what is the 5th step of the direct pathway?

A

VLT stimulates motor cortex to initiate a movement

43
Q

what is the pathophysiology of PD in the direct pathway? (4 steps)

A

since DA is deficient (due to synaptic problems or neuron death):

1) DA doesn’t activate D1 receptors
2) no sub P released leading to decreased GABA
3) D1 neuron firing is increased in putamen since GABA is not inhibiting them
4) D1 neurons release GABA (therfore an increase in GABA) upon firing and inhibit VLT

44
Q

What is primary parkinsonism?

A

idiopathic parkinson’s disease (IPD)

degeneration of pigmented dopaminergic neurons in sub nigra leading to loss of DA

45
Q

what are Lewy bodies?

A

cytoplasmic, eosinophilic inclusions containing ubiquitin and alpha-synuclein
only present after death that confirm IPD diagnosis

46
Q

what are two possible factors to IPD?

A

genetics

oxidative stress

47
Q

what are the genetic factors for IPD?

A

alpha-synuclein

parkin genes

48
Q

how does oxidative stress affect IPD?

A

free radical (generated from dopamine metabolism) attack damages neurons because antioxidant defenses aren’t present

49
Q

what is excitotoxicity and what does it have to do with IPD?

A

pathological process where nerve cells are damaged or killed from excess Glu
IPD: inhibitory effects of DA not present, resulting in excessive glutaminergic stimulation

50
Q

what are 4 possible causes to secondary parkinsonism?

A

1) inability of DA to be produced
2) inability of DA to be secreted
3) inability of DA to bind to putamen neuron receptors
4) producing too many enzymes that degrade synaptic cleft?

51
Q

what are 5 causal factors of secondary parkinsonism?

A 
drugs
toxins
infections
head trauma
genetics
52
Q

what is drug induced secondary parkinsonism?

A

dopamine antagonists block DA receptors and output by sub nigra

53
Q

what does drug induced secondary parkinsonism look like?

A

rigid, hypokinesia, resting tremor
abrupt onset and symmetrical symptoms
symptoms go away when drug is discontinued

54
Q

what are two classes of drugs that could cause drug induced secondary parkinsonism?

A

antipsychotics

ca channel blockers

55
Q

How can toxins cause secondary parkinsonism?

A

environmental factors such as pesticides and exposures to heavy metals such as Fe and Mn irreversibly damage the dopaminergic neurons in sub nigra

56
Q

what infection could cause secondary parkinsonism?

A

post-encephalitic syndrome

57
Q

what is post-encephalitic syndrome?

A

viral illness which results in degeneration of nerve cells in the sub nigra

58
Q

what medical condition occurs before post-encephalitic syndrme?

A

encephalitis - inflammation of the brain

59
Q

what is the result of post-encephalitic syndrome?

A

pt is speechless and statue-like

60
Q

how can trauma cause secondary parkinsonism?

A

repeated head trauma can cause lesions to the sub nigra. this obstructs ventricular outflow leading to increased pressure on the brain. the lesions and pressure affect dopaminergic cells causing parkinsonian signs

61
Q

what is the normal rate of degeneration of sub nigra neurons?

A

0.5% per year

62
Q

what is the rate of degeneration of sub nigra neurons in someone with IPD?

A

1% per year

~45% lost in first 10 years

63
Q

at what percentage of lost dopaminergic neurons does PD become clinically detectable?

A

~70-80%

64
Q

what are primary symptoms of PD?

A

resting tremor
bradykinesia
cogwheel rigidity
postural instability

65
Q

what is the pill rolling phenomenon?

A

rubbing thumb in hand constantly, like rolling a pill in your hand

66
Q

where is the resting tremor most common in? least common?

A

common: hands
uncommon: jaw, legs, toes

67
Q

when is bradykinesia most prominent?

A

throughout an intended action

68
Q

what does a person with PD look like when they walk?

A

movements occur in a series of discontinuous steps rather than smooth motion
freeze in place near doorways and turning

69
Q

what is a shuffling gait?

A

difficulty changing strides

70
Q

what is cogwheel rigidity?

A

increased rigidity to passive movement of a limb

71
Q

what is postural instability?

A

stooped posture contributing to shuffling gait

increases risk of falling

72
Q

what is a pull test?

A

identify patient’s risk of falling

pull them back slightly at the shoulders, and see if they take several steps backwards to regain balance

73
Q

what are some secondary motor symptoms for PD? (6pts)

A

1) decrease in spontaneous blink rate (leads to dry eye)
2) hypomimia - masked face
3) monotonous voice
4) speech hurried, slurred
5) micrographia (small hand writing)
6) drooling (no muscles to swallow)

74
Q

what are some secondary autonomic symptoms for PD? (8pts)

A

1) uncontrolled sweating
2) excess salivation
3) lacrimation
4) impaired thermal regulation
5) constipation
6) urinary incontinence
7) impotence
8) sexual dysfunction

75
Q

what are some psychological symptoms for PD?

A

1) dementiia
2) anxiety
3) depression
4) psychosis (paranoia, hallucinations)
5) sleep disturbances

76
Q

what are two causes of depression with PD?

A

endogenous due to biochemical changes in basal ganglia

exogenous due to frustration with condition

77
Q

what is huntington’s disease?

A

autosomal dominant neurodegenerative condition

78
Q

is HD a hypokinetic or hyperkinetic disorder?

A

hyperkinetic

79
Q

what are 3 physical symptoms of HD?

A

fidgety movements
tics
chorea (involuntary writhing movements)

80
Q

what is the average age range of onset for HD?

A

30-50y.o

81
Q

what causes HD?

A

progressive atrophy of the striatal neurons of the indirect pathway and abnormalities in all 4 domains of the basal ganglia

82
Q

how is HD usually diagnosed?

A

clinical examination and obtaining a complete medical history to rule out secondary parkinsonism

83
Q

What are 6 classes of drugs that can help treat PD?

A

1) dopamine replacement
2) COMT inhibitor
3) MAO-B inhibitor
4) DA agonist
5) amantidine
6) anticholinergics

84
Q

How does dopamine replacement help treat PD?

A

administer L-dopa, which can cross the BBB (DA can’t) and be converted to DA and do it’s thang

85
Q

what is a problem with DA replacement?

A

conversion of L-dopa to DA occurs in both CNS and PNS, in the PNS it can cause severe side effects

86
Q

what is one way to prevent the problem with DA replacement?

A

Block conversion of L-dopa to DA and promote L-dopa absorption across BBB

87
Q

what are COMT and DDC and why are they important in PD treatment?

A

they are enzymes that convert L-dopa to other molecules
COMT converts to 3-OMD (want to block in PNS and CNS)
DDC converts to DA (want to block in PNS)

88
Q

what are some side effects to DA replacement?

A

dyskinesia
wearing off (desensitization)
on-off fluctuations
motor side effects

89
Q

how do MAO-B inhibitors help treat PD?

A 
monoamine oxidase (MAO-B) centrally catabolizes DA to DOPAC
inhibit MAO-B decreases the breakdown of DA (more DA recycled and stored in vesicles)
90
Q

how do COMT inhibitors help treat PD?

A

COMT breaks down L-dopa in PNS and CNS

inhibit COMT peripherally increases L-dopa available to cross BBB

91
Q

How do DA agonists help treat PD?

A

stimulates pathway by mimicking DA and interacting dopaminergic receptor

92
Q

what are some side effects to using a DA agonist?

A 
dyskinesia
motor fluctuations
confusion
hallucinations
sleep disorders
leg edema
postural hypotension
impulsive behaviors
93
Q

what is dyskinesia?

A

abnormal involuntary movement

94
Q

what is leg edema?

A

abnormal accumulation of fluid beneath skin

95
Q

what is postural hypotension?

A

sudden drop of blood pressure upon standing

96
Q

how do anticholinergics help treat PD?

A

decreases Ach and restores DA/Ach balance

97
Q

what are some side effects to anticholinergics?

A 
urinary retention
blurred vision
constipation
tachycardia
confusion
memory loss
restlessness
hallucinations
98
Q

how is amantidine helpful in treating PD?

A

anti-viral med
increases release of DA from presynaptic terminal, blocks reuptake by pre-synaptic terminal, and acts directly on receptors (up regulating D2 receptors)

99
Q

what is a general plan of approach for PD treatment?

A

begin with DA agonist or MAO-B inhibitor

introduce L-dopa/Carbidopa if symptoms not fully managed

100
Q

what are some non-pharm methods of PD treatment?

A

1) education
2) support groups
3) therapies (OT, physical)
4) diet and nutrition (antioxidants)
5) deep brain stimulation

101
Q

what is deep brain stimulation?

A

surgically implanted device to keep DA pathway running normally (only if you have anatomical functional steps working), targeting the thalamus, subthalamic nucleus and globus pallidus

102
Q

what are 3 components to DBS?

A

neurotransmitter
extension
lead (electrodes)

103
Q

how does DBS work to treat? (3 theories)

A

1) stimulates neurons that initiate movement
2) blocks inhibitory neurons, thereby allowing signals to resume
3) influences flow of information along axons

Applied Pathophysiology (11 decks)

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