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Pharm 2024 > Parkinsonism and Movement Disorders > Flashcards

Parkinsonism and Movement Disorders Flashcards

Exam 4

1
Q

The hallmark of Parkinsonism is ______

A

Tremor at rest

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2
Q

Tremor with intention or movement is usually associated with what?

A
  • Brain lesion
  • Alcohol or drug toxicity
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3
Q

______ is rhythmic movement around a joint

A

tremor

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4
Q

______ is muscle jerks in various areas that impair movement and coordination

A

Chorea

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5
Q

______ is a type of chorea that includes violent abnormal movements

A

Ballismus

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6
Q

______ - slow, writhing/twisting

A

Athetosis

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7
Q

______ – abnormal posture

A

Dystonia

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8
Q

____ – Single repetitive movements, especially of face

A

Tics

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9
Q

Choreathetosis combines which 3 involuntary movements?

A

Chorea, athetosis, and dystonia

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10
Q

The _____ relays signals to the motor cortex to guide movement

A

thalamus

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11
Q

Which neurotransmitter does the Substantia nigra release to control the thalamus?

A

Dopamine

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12
Q

What are the 4 parts of the basal ganglia?

A
  • Striatum
  • Substantia nigra
  • Globus pallidus
  • Subthalamic nucleus
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13
Q

Movement disorders are related to _________ dysfunction

A

basal ganglia

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14
Q

What are the symptoms of Parkinsons?

A

TRAP
- Tremor
- Rigidity
- Akinesia
- Postural instability

  • Cognitive decline
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15
Q

What is the pathogenesis of Parkinsons?

A

Dopaminergic neuron degradation
- Nigro-striatal pathway
- Decreased dopamine levels

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16
Q

What is the main gene associated with Parkinsons?

A

SNCA - α-Synuclein (neurotransmitter release)

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17
Q

What are the protective vs harmful environmental components of Parkinsons?

A

Protective – cigarette smoke, coffee, anti-inflammatories, uric acid
Harmful – lead, manganese exposure, Vit D deficiency

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18
Q

How does a mutation in the α-Synuclein gene predispose someone to Parkinsons?

A

Lewy bodies in the substantia nigra regions of the brain
- Misfolding associated with neurodegeneration

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19
Q

What are the 3 diseases associated with misfolding of proteins in neurons?

A
  • Parkinsonism
  • Alzheimer’s
  • MSA – Multiple System Atrophy
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20
Q

What are the 2 occupations that increase Parkinson’s risk?

A

Teaching and healthcare

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21
Q

What are the 3 main methods of treating Parkinsons?

A
  • Exercise – physical therapy
  • Restore dopamine levels – Levodopa
  • CNS Antimuscarinics – control dopaminergic release
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22
Q

What should be avoided in Parkinsons treatment?

A
  1. Dopamine receptor antagonists (antipsychotic agents)
  2. MPTP – destroys dopaminergic neurons - Impurity in some illicit drugs (synthetic opioids)
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23
Q

What is the difference between dopamine and L-DOPA?

A

Dopamine does not cross BBB, L-DOPA does

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24
Q

How does carbidopa increase the effectiveness of L-DOPA?

A

prevents COMT from breaking down L-dopa, increasing amount that can cross the BBB from 1-3% to 10%

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25
Q

What is the main adverse effect of L-DOPA? What is the treatment?

A

Hallucinations and delusions
Pimavanserin (Nuplazid) – antipsychotic

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26
Q

What is the MOA of Pimavanserin (Nuplazid)?

A

Antipsychotic - Inverse agonist at 5-HT2A – Visual cortex

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27
Q

What is the On-Off Phenomenon associated with the long-term use of L-DOPA?

A

Periods of increased mobility, followed by marked akinesia

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28
Q

What are the drug interactions of L-DOPA?

A

Vitamin B6, MAOIs

29
Q

What are the contraindications of L-DOPA?

A
  • Psychosis (enhanced dopamine signaling)
  • Glaucoma
  • Melanoma
30
Q

What is the medicaiton that can be given as an alternative to L-DOPA? What is its MOA?

A

Pramipexole - Early disease treatment
Dopamine Receptor Agonists

31
Q

What are the 2 types of MAO enzymes?

A
  • MAO-A – NE, 5-HT, Dopamine
  • MAO-B - Dopamine
32
Q

What is the MAOI used to treat Parkinsons? Which type of MAO does it target

A

Selegeline - MAO-B selective

33
Q

What is the MOA of Tolcapone? How does it treat Parkinson’s?

A

COMT Inhibitors – Increase circulating dopamine

34
Q

How is Apomorphine (Apokyn) used in the management of Parkinson’s?

A

Dopamine agonist – “off” periods, relief of akinesia

35
Q

What are the alternative treatments for Parkinson’s?

A
  • Lesional – ablation
  • Deep Brain Stimulation – electrode placement in basal ganglia
  • Stem Cell Therapy - Implantation of fetal substantia nigra
36
Q

Essential Tremor is associated with _____ dysfunction

A

B1 receptor dysfunction – beta-blockers

37
Q

What is the treatment for Benign Hereditary Chorea?

A

tetrabenazine

38
Q

What is Benign Hereditary Chorea?

A

Chorea in childhood, no progression, no dementia

39
Q

What is Tardive Dyskinesia? What is the treatment?

A
  • Repetitive, involuntary movements
  • Antipsychotic drugs most common cause
40
Q

______ is the largest group of muscle disorders in childhood

A

Muscular Dystrophy (MD)

41
Q

How is Muscular Dystrophy (MD) characterized?

A

Characterized by progressive weakness and wasting of symmetric groups of skeletal muscle

42
Q

What is the most severe and common MD?

A

Duchenne Muscular Dystrophy

43
Q

What gene is absent in children with Duchenne Muscular Dystrophy?

A

Dystrophin

44
Q

What is the treatment for Duchenne Muscular Dystrophy?

A
  • No cure – gene therapy
  • Maximize quality of life
    • Corticosteroids
    • Beta-2 agonists – muscle strength
    • Orthopedic braces
  • Physical Therapy
  • Respiratory – Assisted ventilation
45
Q

______ sign is the hallmark sign for Duchenne Muscular Dystrophy

A

Gowers - using hands to push on legs to stand

46
Q

______ is a non-progressive motor disorder of the CNS resulting in alterations in movement and posture

A

Cerebral Palsy

47
Q

What are the signs of cerebral palsy?

A
  • Hyper- or hypo- tonia
  • Scissoring of legs
  • Absence of reflexes or reflexes extended beyond expected age
  • Failure to meet developmental norms
  • Seizures
48
Q

What are the therapies for cerebral palsy?

A

Surgery - Tendon release and Intrathecal pump
Medication - Botox and Baclofen

49
Q

What are the most common causes of CP?

A
  • Trauma
  • Hemorrhage
  • Anoxia
  • Infection
50
Q

What is the onset and symptoms of Huntington’s disease?

A
  • Onset – age 30-40
  • Progressive loss of muscle control, Chorea, Dementia, Death – 15-20 years after onset of symptoms
51
Q

What is the cause of Huntington’s disease?

A
  • Gene produces huntingtin protein – function unknown (neural health)
  • GABA reduced in basal ganglia
  • Reduction in Choline acetyltransferase (ChAT)
52
Q

What are the treatments for Huntington’s disease?

A
  • Tetrabenazine - Depletes dopamine
  • Dopamine Receptor Blockers - Haloperidol
  • Genetic counseling, speech therapy, PT/OT
53
Q

ALS is characterized by the loss of ________

A

motor neurons

54
Q

What is the other name for ALS?

A

“Lou Gehrig’s disease”

55
Q

What is the main treatment for ALS? What is the MOA?

A

Riluzole – sodium channel blocker (damaged neurons)
- extends QOL

56
Q

How is Alzheimer’s diagnosed?

A

autopsy

57
Q

What are the theories of causes of Alzheimer’s Disease?

A
  • Genetic predilection
  • Head injury
  • Dysregulated lipids
  • Low estrogen
58
Q

What are the 2 hallmark lesions of Alzheimer’s disease?

A

Neurofibrillary tangles: twisted fragments of protein within nerve cells
Senile plaques: products of dying nerve cells accumulate around protein (AB42)

59
Q

What are the clinical manifestations of Alzheimer’s?

A
  • Forgetfulness, emotional upset, disorientation, confusion, lack of concentration, decline in abstraction, problem solving, and judgment
  • Insidious onset
60
Q

How can Alzheimer’s be prevented?

A
  • Cardiovascular health
  • NSAIDs
  • Diet and Exercise
61
Q

What is the treatment for Alzheimer’s?

A

Palliative - Tacrine and Memantine

62
Q

What is the MOA of Tacrine?

A

CNS ACh esterase Inhibitor

63
Q

What is the MOA of Memantine?

A

NMDAr Antagonist

64
Q

What increases the likelihood of having restless leg syndrome?

A

Increased in pregnancy, diabetics

65
Q

What are the 4 treatments of restless leg syndrome?

A
  • Dopamine agonists
  • Gabapentin
  • Benzodiazepines
  • Opiates (clonazepam)
66
Q

________ is a sleep disorder that is characterized by a creeping discomfort in legs and the urge to move about

A

Restless Leg Syndrome

67
Q

Draw the pathway for levodopa metabolism and targets for dopamine receptor agonists, MAO-B antagonists, and COMT inhibitors.

A
68
Q

Explain the relationship between the basal ganglia, motor cortex, and thalamus; and describe the pathology in movement related disorders.

A

Thalamus - fine-tunes movements by relaying signals back to the cortex
Basal ganglia - regulates motor activity and thalamus
Substnatia nigra - controls dopamine release to either inhibit the indirect or stimulate the direct pathway
- dopamine neurons in substantia nigra degenerate in Parkinson’s

Pharm 2024 (32 decks)

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