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Pathophysiology Final > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What was parkinson’s disease first described as?

A

“shaking palsy”
1817
by British physician, James Parkinson

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2
Q

Parkinsonism

A
  • progressively deteriorating neurological disorder
  • hypokinetic or akinetic disease
  • the clinical syndrome that arises from the degeneration of the basal ganglia
  • the damage is to the substantial nigra (aka MAY NOT be b/c of loss of DA)
  • PD=IPD; secondary parkinsonism
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3
Q

Parkinson’s Disease

A
  • the most common cause of parkinsonism

- idiopathic neurodegenerative condition caused by loss of dopaminergic neutrons in the substantial nigra

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4
Q

What is PD characterized by

A
  • asymmetrical resting tremor
  • bradykinesia (brady means slow and kinesis means movement)
  • rigidity
  • postural instability (shuffling along, bent over)
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5
Q

secondary parkinsonism

A
  • secondary to a known cause
  • similar to Parkinson disease, but the symptoms are caused by certain medicines, a different nervous system disorder, or another illness
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6
Q

Akinesia

A
  • slowness or loss of normal motor function, resulting in impaired muscle movement
  • literally “without movement” or without much movement
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7
Q

Epidemiology

A
  • estimated 4 million people living world wide with PD
  • affects 1 in 100 over 65 (more than combined incidence of MS, muscular dystrophy and Lou Gehrig’s disease)
  • incidence increase as people age with average age of onset being around 60
  • affects males to females 2:1
  • development of IPD is inversely correlated with cigarette smoking and caffeine consumption
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8
Q

tyrosine

A
  • its an important aa that gets taken up from blood into surrounding fluids that our brain is exposed to (CNS)-> BRAIN
  • in this terminal, tyrosine gets taken up
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9
Q

what happens to tyrosine once it gets taken up by the substantial nigra neuron

A

-once taken up it is hydroxylated to L-dopa, then decarboxylated into DA

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10
Q

What happens to DA once it has been formed

A
  • it gets packed into vesicles
  • within the ion channels there is an influx of Ca/Na into the nerve channels-> inside becomes positive-> dumping of DA vesicles into the synaptic cleft
  • on the post synaptic side, it binds to the D1 and D2 receptors on the putamen neurons
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11
Q

What happens when DA binds to the D1/D2 receptor on the putamen neuron (general)

A
  • the pudamen neurons are located on the striatum
  • this ends up increasing the amount of GABA, which actually ends up reducing the putamen activity
  • this decrease in putamen activity ends up increasing activity of the ventrolateral thalamus, which controls movement
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12
Q

synaptic transmission (general)

A
  • APs are produced via depolarization of the neuronal membrane due to an influx of Na through Na voltage-gated channels
  • the produced AP propagates down the axon towards the pre–synaptic terminal
  • arrival of the AP at the pre-synaptic terminal opens Ca channels in the PM
  • the influx of Ca triggers the exocytosis of vesicles containing NT
  • the NT enters the synaptic cleft and binds to receptors on the post-synaptic membrane
  • following binding, the NT is cleaved and taken back up into the pre-synaptic terminal where it is recycled and stored in vesicles
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13
Q

DA synthesis

A
  • tyrosine is taken up form the blood to the brain’s ECF then into dopaminergic substantial nigra neurons via specific enzyme transporters
  • it becomes hydroxylated to form L-DOPA, the DA precursor
  • L-DOPA is then decarboxylated to make DA
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14
Q

Important anatomical structures involved

A

-basal ganglia
-substantia nigra
-striatum
-ventrolateral thalamus (VLT)
-motor cortex
(-subthalamic nucleus)

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15
Q

basal ganglia

A

-controls complex movement s and has a part in motor learning-located at the base of the forebrain and composed of substantia nigra, striatum, sub-thalamic nucleus (and palladum)

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16
Q

substantia nigra

A

located in the midbrain with an important role in reward, addiction and movement
-input form all over the bran relayed via dopaminergic neurons to striatum

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17
Q

striatum

A
  • composed of putamen and caudate nucleus and located below the cortex of the cerebrum
  • major input site of the basal ganglia system-putamen neurons have both D1 and D2 receptors
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18
Q

Ventrolateral thalamus

A
  • integration centre for basal-ganglionic and cerebellar impulses
  • brought to the corticospinal system
  • sends fibers to the percentile and supplementary motor cortices to initiate body movement
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19
Q

Motor cortex

A
  • input signals are changed to output which leads to movement
  • located in the frontal cortex of the brain
  • ultimate highest order that needs to be stimulated in order to move (but if the VLT is stimulated, so will the motor cortex)
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20
Q

what NT is overstimulated in any addiction?

A

DA

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21
Q

What functions is DA involved in?

A
  • reward (motivation)
  • pleasure, euphoria
  • motor function (fine tuning)
  • compulsion
  • preservation
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22
Q

What functions is serotonin involved in?

A
  • mood
  • memory
  • processing
  • sleep
  • cognition
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23
Q

What are the 3 NT’s all involved in Parkinson’s disease?

A
  • DA
  • Ach
  • GABA
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24
Q

What do these 3 NT’s control?

A

movement

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25
Q

Dopamine

A
  • important in many brain fxns: motivation, cognition, learning, mood, attention, reward, sleep, & voluntary movement
  • works via the direct/indirect path within the basal ganglia to initiate movement
  • insufficient DA biosynthesis causes parkinson’s where a person loses the ability to execute smooth controlled movement
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26
Q

How much DA function must be lost before it manifests as Parkinson’s?

A

80%

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27
Q

Where are certain areas where problems could lead to DA loss and therefore Parkinson’s?

A
  • presynaptic production
  • postsynaptic effect (receptors)
  • synaptic cleft effect (destruction)

aka:

  • lack of DA (from an inability to be produced or inability to be secreted)
  • lack of receptors/ inability of DA to bind to receptors
  • over-producing amount of enzyme that chews up all the DA therefore isn’t allowed to work
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28
Q

What is the relationship between Ach and DA?

A

-antagonistic NTs (Ach excitatory, while DA is inhibitory)

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29
Q

What happens to Ach when there is less than normal DA

A

-if dopaminergic cells are destroyed, no DA released to compete and Ach runs out of check

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30
Q

What does too much Ach cause?

A
  • it causes over activity of cholinergic neurons

- leading muscles to contract but as there is excess Ach, muscles cant repolarize and will remain contracted

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31
Q

What is the main inhibitory NT?

A

GABA

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32
Q

In normal motor systems, what is GABA’s release regulated by?

A

-by binding of DA to receptors

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33
Q

What happens to the relationship between GABA and DA during Parkinsons

A
  • in Parkinson’s disease, release of GABA will increase and decrease in the incorrect portions of the Nigro-Striatal pathway
  • a reduction in DA causes an increase GABA resulting the individual to be partially or fully paralyzed
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34
Q

Normal movement

A
  • info from different parts of the brain is sent to the substantia nigra to stimulate DA synthesis
  • DA is released from the substantia nigra neurons where it binds to D1 and D2 receptors on the putamen neurons in the striatum
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35
Q

DA upon release binds to:

A
  • D1 DIRECT path

- D2 INDIRECT path (not required to know this path)

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36
Q

Direct path D1 receptors

A

-DA binds to the D1 receptor of Substance P producing putamen neurons in the striatum
-DA binding causes an increase in GABA levels which inhibits the firing of D1 putamen neurons
(increase in Sub P increases GABA)
-therefore they shut down (GABA shuts them down)
-by decreasing putamen activity, VLT activity increases
(TO MOVE YOU NEED THE PUTAMEN NEURONS TO BE SHUT DOWN)
-results in less inhibition to the VLT
-this allows VLT to send signal to the pre-motor and motor cortices of the brain which leads to bodily movement
(slide 19)

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37
Q

How do both the direct and indirect pathways produce movement?

A

-in normal movement they produce movement by decreasing inhibition of the VLT

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38
Q

control of GABA in normal movement

A

-GABA is either up or down regulated to facilitate necessary inhibition to propel the pathways

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39
Q

Pathophysiology of the direct path

A

-in PD, DA becomes deficient due to problems with synaptic transmission or death of neurons that produce it
-DA doesn’t activate D1 receptors (due to a complete or partial reduction in DA levels)
-no Sub P will be released, leading to decrease in GABA
-firing of D neurons will increase in the putamen as they are not inhibited by GABA that would normally be present
-D1 neurons release GABA upon firing to the VLT inhibiting the VLT from transmitting the signal to the motor cortex (VLT inhibited in both paths by an excess of GABA reaching it)
(slide 22)
net inhibition occurs in the system which stops the motor cortex from being activated resulting in no movement

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40
Q

idiopathic parkinson’s disease

A
  • aka primary parkinsonism
  • degeneration of pigmented Dopaminergic neurons in the substantia nigra-> results in loss of DA
  • remaining dopaminergic neurons contain Lewy bodies
  • this is what michael J fox has
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41
Q

Lewy bodies

A
  • abnormal aggregates of protein that develop inside nerve cells (DA neurons)
  • cytoplasmic inclusions
  • eosinophilic, contain ubiquitin and alpha-synuclein
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42
Q

is the true etiology of IPD known?

A

no

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43
Q

etiology of IPD; possible factors:

A
  • genetic factors (alpha-synuclein and parkin genes)-> if IPD develops before 50; over 12 gene mutations are implicated in parkinson’s; only constitute a small % of IPD cases
  • oxidative stress
  • excitotoxicity
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44
Q

explain the theory of oxidative stress behind the etiology of IPD

A

-substantia nigra is a region characterized by high levels of oxidative stress
-free radicals generated from DA metabolism
-healthy indivs have several anti-ox molecules in the SN to limit damage
IPD: free radical attack damages neurons b/c anti-ox defences not present

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45
Q

true or false: as a pharmacist it is important/ helpful to recommend antioxidants to people with IPD

A

true (i.e. Vitamin C or E)

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46
Q

explain the theory of excitotoxicity behind the etiology of IPD

A

-pathological process where nerve cells are damaged or killed from excess glutamate
IPD: inhibitory effects of DA not present, resulting in excessive glutaminergic stimulation
-> glutamate levels too high in comparison to DA

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47
Q

what is the main excitatory NT in the nigrostriatal pathway?

A

glutamine

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48
Q

Causes of secondary parkinsonism

A

Casual factors:

  • drugs
  • toxins
  • infections
  • head trauma
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49
Q

drug induced secondary parkinsonism

A
  • DA antagonists block DA receptors and output by the SN cells
  • cause parkinsonian signs such as rigidity, hypokinesia, and resting tremor
  • onset is abrupt, symptoms symmetrical
  • symptoms tend to disappear after use of the drug is discontinued
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50
Q

what are some drugs that causes drug induced secondary parkinsonism;
what are they doing to cause this?

A
  • antipsychotics
  • calcium channel blockers
  • in both of these you are preventing DA from being released into the synaptic cleft
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51
Q

secondary parkinsonism from toxins

A

-enviromental factors such as pesticides and exposure to heavy metals such as iron and manganese irreversibly damage the dopaminergic neurons in the SN

52
Q

what are some toxins that can cause these effects

A
  • MPTP

- carbon monoxide poisoning

53
Q

secondary parkinsonism from infections

A
  • post-encephalitic syndrome
  • due to a viral illness which results in degeneration of nerve cells in the SN
  • disease follows a condition called encephalitis lethargica which causes inflammation (encephalitis) of the brain
  • leaves patient speechless and statue-like
54
Q

secondary parkinsonism from trauma

A
  • repeated head trauma
  • 4 times more likely to develop Parkinson’s than individuals who have never experienced a head injury
  • lesions to the Sn, striatum cause hematoma
  • obstructs ventricular outflow resulting in pressure on the brain
  • lesions and pressure affect dopaminergic cells causing parkinsonian signs
55
Q

hematoma

A
  • collection of blood outside of the blood vessel

- usually a result of internal bleeding

56
Q

normal aging process of the SN neurons

A

-degenerate at rate of 0.5%/year

57
Q

aging of SN neurons in IPD

A

-rate of 1%/ year
-45% are lost in the first decade after their diagnosis
(remember the threshold for detectable PD is when 70-80% of the DA neurons have been lost)

58
Q

Before “reaching” threshold of IPD, and officially being diagnosed, what are a person’s symptoms like?

A
  • PD relatively asymptomatic until then (aka carrier for a disease or infection but experiences no symptoms)
  • patients prior to diagnosis, amy have subtle difficulty using one limb, asymmetrical tremor and slowing of movements
  • patients may associate signs with normal aging processes
59
Q

What are the main clinical features/ primary symptoms of IPD

A
  • resting tremor
  • bradykinesia
  • cogwheel rigidity
  • postural instability
60
Q

describe resting tremor

A
  • present in 2/3rds of patients with IPD
  • most common in the hands (accompanied by characteristic “pill rolling” motion)
  • less common in jaw, torso, and toes
  • begins unilaterally, but becomes bilateral as the disease progresses
  • tremor amplitude and severity increase under stress and in emotional situations
61
Q

when in resting tremor absent

A

in sleep

62
Q

describe bradykinesia

A
  • slowness of movement
  • movements often slow throughout an intended action
  • trouble initiating movements
  • unconscious associative movements occur in a series of discontinuous steps rather than in a smooth and coordinated manner
  • freeze in place; i.e. around doorways or in initiating turns
  • shuffling gait: difficulty changing strides
  • festing gait: involuntary quickening of gait
63
Q

describe cogwheel rigidity

A
  • increased rigidity to passive movement of a limb
  • ratchet like interruptions in tone that is seen when the limb is bent
  • thought of as a rigidity with a superimposed tremor
  • usually begins unilaterally, but becomes bilateral as PD progresses
64
Q

describe postural instability

A
  • stooped posture contributes to shuffling gait
  • most common in advanced stages of IPD
  • increases risk of falling (most people diagnosed with IPD are in the 6th decade of their life, or older, therefore have an increased risk of braking hip and other bones)
65
Q

how can you identify a patient’s risk of falling

A
  • execute a pull test

- when pulled back slightly at the shoulders, patient’s take several backwards steps in order to regain their balance

66
Q

what primary symptom if IPD is most disabling to the patient?

A

-postural instability

67
Q

what primary symptoms is the least amendable to pharmacotherapy?

A

-postural instability

68
Q

secondary symptoms of IPD

A
  • result of primary symptoms:
  • motor
  • autonomic
69
Q

what are the motor secondary symptoms of IPD

A
  • decrease in spontaneous blink rate (therefore dry out*)
  • hypomimia
  • monotonous voice
  • speech hurried and slurred
  • micrographia
  • drooling (b/c cannot swallow- could literally choke on own saliva- very difficult to feed them)
70
Q

hypomimia

A
  • no facial expression

- masked face

71
Q

micrographia

A

small writing as a result of decreased manual dexterity

72
Q

what are the autonomic secondary symptoms

A
  • uncontrolled sweating
  • excessive salivation (droolingg)*
  • lacrimation (secretion of tears)
  • impaired thermal regulation
  • constipation*
  • urinary incontinence*
  • impotence*
  • sexual dysfunction*

(those starred- key points and should be able to explain why they occur on an exam)

73
Q

psychological symptoms

A
  • dementia (20%)
  • anxiety
  • depression
  • psychosis
  • sleep disturbances
74
Q

what kind of psychosis can patients with IPD experience?

A
  • paranoia

- hallucinations

75
Q

What kind of depression can patients with IPD experience?

A
  • endogenous

- exogenous

76
Q

endogenous depression

A

due to biochemical changes in the basal ganglia

77
Q

exogenous depression

A

due to frustration with their condition

78
Q

Huntington’s disease

A
  • autosomal dominant neurodegenerative condition
  • HYPERkinetic movement disorder
  • progressive atrophy of the stratal neurons of the INDIRECT pathway and abnormalities in ALL 4 domains of the basal ganglia
  • usual age of onset between 30-50
79
Q

physical symptoms of Huntington’s disease

A
  • fidgety movements
  • tics
  • chorea (involuntary writhing movements)
80
Q

How can you treat Huntington’s disease?

A

-anti-dopaminergic agents

81
Q

True or false: diagnosing IPD in its early stages is easy

A

false

  • many of its symptoms may be interpreted as part of normal aging
  • there is nothing that we can find that will make us jump up and expect them to have IPD (just a slow process)
82
Q

Is there a current diagnostic test for IPD

A

no

  • genetic testing is not useful
  • medical imaging may be used to rule out other causes of parkinsonism (i.e. trauma induced)
83
Q

early in the progression of the disease, how are the primary symptoms exhibited?

A
  • unilaterally

- as it progresses, the symptoms become bilateral (although, one side may exhibit more severe symptoms than the other)

84
Q

How is diagnosis usually made

A
  • by way of clinical examination

- obtaining a medical history to rule out secondary parkinsonism

85
Q

when can clinically probable IPD be diagnosed?

A
  • when the patient shows 2 of the following primary symptoms (muscle rigidity, bradykinesia, resting tremor, postural instability)
  • and have ruled secondary parkinsonism (infections, toxins, drug-induced, trauma-induced)
86
Q

What happens if a causation is unable to be determined

A
  • assumed to be IPD
  • test to see if patient responds to L-DOPA treatment as
    • IPD responds positively to L-DOPA
    • other forms of parkinsonism do not
87
Q

what is the one way you can confirm IPD

A
  • there is a diagnosis that can be used to confirm after death
  • autopsy reveals presence of Lewy bodies in the SN
88
Q

Pharmacological Management

A
  • dopamine replacement (levodopa and dopa decarboxylase inhibitor- this ensures that the it gets to the brain to convert to DA there)
  • COMT inhibitors- b/c COMT tries to break down LDOPA (which we need)
  • MAO-B inhibitors- MAOB is the enzyme in the brain that degrades DA
  • DA agonists- isn’t DA, but is similar enough to still bind D1, D2
  • amantidine- shown to increase release of pre-synaptic DA release from the SN neurons
  • anticholinergics blocks Ach
89
Q

The physiology of dopamine replacement

A

-symptoms of PD are due to a DA deficiency related to the degeneration of dopaminergic neurons

90
Q

treatment strategy of DA replacement

A
  • administer L-dopa to replace depleted DA
  • levodopa (L-DOPA; precursor to DA) is administered as it may cross the BBB, while DA can’t
  • L-DOPA converted to DA via dopa decarboxylase (DDC) in the PNS and CNS
  • once converted to DA in the SN of the brain, binds with D1, D2 on putamen neurons in the striatum to exert movement via the direct and indirect pathways
91
Q

what happens if L-DOPA is converted to DA outside of the CNS

A

-conversion of L-DOPA to DA in the periphery is associated with severe side effects-> nausea, vomiting

92
Q

Physiology behind the prevention of L-DOPA to DA conversion in the peripheral blood

A

-DDC converts L-DOPA to DA in the CNS and PNS

93
Q

treatment strategy behind the prevention of L-DOPA to DA conversion in the peripheral blood

A
  • mitigate (block) the catabolism of L-DOPA to DA in the periphery to promote L-DOPA absorption across the BBB
  • administer L-DOPA with a DDC inhibitor (Carbidopa)
  • reduces conversion of L-DOPA to DA outside CNS; thus, increasing bioavailability, decreasing dose amounts (70%) and reducing side effects related to DA in the periphery
  • carbidopa doesn’t cross BBB
94
Q

what is the most potent therapy for controlling symptoms/ gold standard for therapy?

A

DA replacement via LDOPA delivery across the BBB

95
Q

what are the main side effects from DA replacement via LDOPA delivery

A

dyskinesia- abnormal involuntary movement

  • wearing off- presentation of PD symptoms between doses; becomes longer as desensitization occurs
  • on/off fluctuations- sporadic fluctuation of motor states
  • motor side effects may be due to periodic L-DOPA administration, erratic absorption, and a short half life producing a pulsatile stimulation of dopaminergic receptors
96
Q

when do side effects of DA replacement start to be seen?

A

-within 5 years of treatment

97
Q

Physiology behind the MAO-B inhibitors

A

-found within the mitochondria of dopaminergic neurons, Monoamine Oxidase (MAO-B) centrally catabolizes DA to 3,4-dihidrophenylacetic acid (DOPAC)

98
Q

treatment strategy of MAO-B inhibitors

A
  • inhibitions of MAO-B increases amount of DA that is recycled and stored within protective vesicles
  • increases “on” time and decreases “off” time of motor fluctuations
  • increased precedence of dyskinesia
  • rasagiline, selegiline
99
Q

physiology behind COMT inhibitors

A

-catechol-O-methyltransferase (COMT) breaks down L-DOPA into 3-O-methyldopa (3-OMD) in PNS and CNS

100
Q

treatment strategy behind COMT inhibitors

A
  • inhibiting COMT peripherally increases the L-DOPA available to cross the BBB
  • inhibiting COMT centrally increases amount of DA available to bind to D1/D2
  • increases “on” time and decreases “off” time
  • increased incidence of dyskinesia
  • tolcanpone (high liver toxicity), Entacapone
101
Q

what other treatment is commonly used with COMT inhibitors?

A

L-DOPA/ Carbidopa therapy

102
Q

physiology behind DA agonists

A

-stimulated pathway by mimicking DA and interacting directly with the dopaminergic receptor

103
Q

treatment strategy of DA agonists

A
  • drug bypasses presynaptic neutron and acts directly on the dopaminergic receptors
  • crosses BBB
  • longer half life provides more continuous stimulation of the dopaminergic receptors
  • pramipexole, ropinirole
104
Q

physiology behind anticholinergics

A

-in PD, Ach and DA levels are unbalanced (reduced DA, and too much Ach)

105
Q

treatment strategy of anticholinergics

A
  • decrease Ach levels to restore DA/Ach balance
  • effective in treating involuntary resting tremors
  • good efficacy, not often reserved for resting tremors
  • mech not understood, but may reduce NT mediated by Ach at muscarinic receptors
106
Q

true or false: anticholinergics are well tolerated in the elderly

A

false

107
Q

side effects of anticholinergics

A
  • urinary retention
  • blurred vision- loss of accommodation
  • constipation
  • tachycardia
  • confusion*
  • memory loss *
  • restlessness*
  • hallucinations*
  • -problematic in elderly with increased risk of dementia
108
Q

physiology behind amantidine

A
  • originally an antiviral

- shown to relieve symptoms associated with PD

109
Q

treatment strategy of PD

A

-mech of action unknown
-improves motor fluctuations and tremors
Presynaptically:
-increase release of DA from presynaptic terminal
-blocks reuptake of FA into presynaptic terminal
Postsynaptically:
-acts directly on receptors, up regulating D2 receptors

110
Q

How do we choose which pharmacological management to use?

A
  • currently, treat PD symptomatically based on response to medications
  • typically, begin with a DA agonist or MAO-B inhibitor until a more potent regimen, such as L-DOPA/Carbidopa is required to manage symptoms
111
Q

what is L-DOPA/carbidopa commonly supplemented with

A

-COMT and/or MAO-B inhibitor

112
Q

What may be used to supplement L-DOPA/Carbidopa when a tolerance starts to develop

A

-a DA agonist or anticholinergic (uncommon)

113
Q

true or false: we now have a rubric to follow for the pharmacological treatment of PD

A

false: treatment is individualized

114
Q

Non-Pharmacological management

A
  • education
  • support groups
  • OT/PT
  • diet and nutrition
  • deep brain stimulation * (more significance)
115
Q

When can DBS only be used?

A

-used only to treat patients whose symptoms cannot be adequately controlled by meds to stimulate release of Da from SN neurons

116
Q

DBS

A
  • surgical procedure used to treat debilitating symptoms of PD such as tremor, rigidity, and bradykinesia
  • neurostimulator delivers electrical stimulation to targeted area’s of the brain that control movement
  • the neurostimulator is a battery operated device similar to a pacemaker
  • stimulates DA from the pre-synaptic SN neurons
117
Q

what are the main areas of the brain that control movement and are thus targeted by DBS

A
  • thalamus
  • SN
  • globus pallidus
118
Q

What are the DBS symptoms 3 components:

A

1) neurotransmitter
2) extension
3) lead (electrodes)

119
Q

describe the neurotransmitter of the DBS

A

-implanted under the skin either near the collarbone, lower in the chest or under the skin over the abdomen

120
Q

describe the extension portion of the DBS

A
  • insulated wire

- passes under the skin of the head, neck and shoulder

121
Q

describe the lead (electrodes)

A

-tip of the lead inserted into the targeted brain area

122
Q

were are the electrical impulses passed from and to?

A

-passed from the neurostimulator, up the extension, and released from the leads into the targeted brain areas

123
Q

How does DBS treat the debilitating symptoms of PD?

A

three theories:

1) DBS stimulates neurons that initiate movement
2) DBS blocks inhibitory neurons, thereby allowing brain signals to resume
3) DBS influences the flow of info along axons- fibres that connect neurons to each other

124
Q

What does DBS work specifically on, according to a recent study

A

-DBS works on axons, specifically those that feed into the sub thalamic nucleus, rather than on the neurons in the structure

125
Q

side effects of DA antagonists

A

-dyskinesia
-motor functions
confusion
-hallucinations
-sleep disorders- sleep attacks
-leg edema- abnormal accumulation of fluid beneath skin
-postural hypotension- sudden drop in bp upon standing
-impulsive behavious- gambling, sex, shopping
-side effects are reversible
(the risk of dyskinesia and motor fluctuations are lower here than in LDOPA therapy)

Pathophysiology Final (10 decks)

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