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Pharm > Parkinson's Disease & Movement Disorders > Flashcards

Parkinson's Disease & Movement Disorders Flashcards

End Test 4

1
Q

What is a tremor?

A

Slow repetitive/rhythmic movement that a person doesn’t know they’re doing

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2
Q

What is a hallmark symptom of Parkinsons?

A

Tremor AT REST

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3
Q

What is likely the reason for a tremor with movement?

A

Brain lesion
Alcohol/drug toxicity

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4
Q

What is chorea?

A

Quick muscle jerks that can cause impaired movement/coordination

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5
Q

What is ballismus?

A

Wild, violent, abnormal movement

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6
Q

What is ballismus associated with?

A

This wild, violent, abnormal movement is associated with huntington’s disease

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7
Q

What is athetosis?

A

Slow, rotational/twisting movements (writhing)

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8
Q

What is Dystonia?

A

Abnormal posture

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9
Q

What is Tic?

A

Single repetitive movements, esp. in the face

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10
Q

What are tics normally associated with?

A

Antipsychotic drugs

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11
Q

What is Choreathetosis?

A

Combo of Chorea, Athetosis, Dystonia

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12
Q

What causes Choreathetosis?

A

Trauma
Chorea Gravidarum
Turmors
Cerebral Palsy
Huntingtons
Ataxia Telangectasia
Kernicterus

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13
Q

What are most movement issues associated with?

A

Problems with Basal Ganglia cells

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14
Q

Where are Basal Ganglia cells located? What do these areas do? What is the most important area when it comes to movement disorders?

A

Striatum
Substantia nigra
Globus pallidus
Subthalamic nucleus

Regulate motor activity

Substantia nigra

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15
Q

Why is the Substantia nigra the most important area of the Basal Ganglia?

A

it can inhibit the indirect pathway & stimulate the direct pathway.

Both pathways are important in fine muscle tuning & fine control in the thalamus

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16
Q

Movement disorders are related to dysfunction in the _______

A

Basal ganglia

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17
Q

What does the Basal ganglia cells in the substantial nigra secrete? To where?

A

Dopamine

To the striatum

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18
Q

What causes Parkinsons? What predisposes you to this? What decreases/increases symptoms?

A

Genetics: SNCA gene produces Alpha-synuclein
————————-
Environmental: Increases: cigarette smoke, coffee, antiinflammatories, uric acid
Decreases: lead, manganese, Vitamin D

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19
Q

What are symptoms of Parkinsons?

A

Idiopathic, progressive

Cognitive decline

TRAP:
Tremor
Rigidity
Akinesia (impairment in voluntary movement)
Posture

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20
Q

Describe Alpha-Synuclein’s role in movement disorders

A

Protein produced by the gene SNCA
Primary gene associated with parkinsons

Found in CNS neurons specifically in the substantia nigra in areas that can glomerate into Lewy Bodies

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21
Q

What are Lewy bodies?

A

Areas that show up as small white spots in the brain

small areas the brain that are concentrated with protein. Usualy seen in substantia nigra from alpha-synuclein

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22
Q

T/F: Alpha Synuclein should be diffused through the cell

A

T

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23
Q

What is Prion disease?

A

Mad cow disease

another cause of dementia

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24
Q

What neurodegeneration disorders are associated with proteins?

A

Parkinsons: Alpha-synuclein

Alzheimer’s: APP (Amyloid Precursor Protein)

MSA (Multiple system atrophy): Amyloid proteins

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25
Q

Patient’s with parkinson’s will have ______ upon an autopsy

A

Lewy bodies

26
Q

What is the only way to confirm parkinsons?

A

autopsy

27
Q

What is Dementia without parkinson’s symptoms, but with Lewy bodies upon autopsy?

A

Lewy Body disease

28
Q

What are Parkinson’s risk factors?

A
  • > 60 y/o
  • hereditary
    -Men:women 2:1
    -Occupation: teaching, healthcare, farming
    -toxin exposure
29
Q

What drugs do you want to avoid in parkinsons?

A

Dopamine-R antagonist (antipsychotics)
Street drugs

30
Q

What do you want to do to improve QOL with Parkinsons?

A

Exercise/PT
Increase/restore dopamine levels
CNS antimuscarinics

31
Q

Drugs: Levodopa/Carbidopa

A

1 Treatment for Parkinson

MOA: Levodopa: Prodrug crosses BBB –> Converts to dopamine
-L-isomer of dopamine

Carbipoa MOA: COMT inhibitor

Carbidopa prevents the breakdown of L-dopa by increasing reliance in COMT when combined with Levodopa

Racemic mixture

Decreased effectiveness with time

AE: Hallucinations, Delusions
-this is increased with carbidopa!!!
-Give Pimavanserin to combact this
-Dyskinesias- choreathethosis (mild)

Drug interactions: MAOIs, Vitamin B6

Contraindications: Psychosis, Glaucoma, Melanoma
-increase in dopamine
-dopanergic pathway produces melanin & produces needed for the eye

32
Q

What is the active form of Levodopa? Inactive?

A

Active: L-dopa

Inactive: D-dopa

33
Q

Drug: Pimavanserin

A

Class: Antipsychotic
MOA: 5-HT(2A) Inverse agonist
-visual cortex at thalamus substantia nigra

uses: assist with psychotic SE of Levodopa/Carbidopa

34
Q

What is the On-Off Phenomen?

A

Associated with long term use of levodopa

Periods of increased mobility followed by marked akinesia

because of this, people woild do drug holidays and stop taking medication for a period of time to prevent this (Prevent the medication from having decreased effects)

35
Q

Drugs: Pramipexole

A

Class: Dopamine Receptor Agonist

Less effective than levadopa but good for early treatment

uses: parkinsons (early)

Less SE than levadopa

36
Q

Drugs: Selegeline

A

Class: MAOIs

MOA: MAO-B selective: specifically inhibits the dopamine transporter from reuptake
-slower breakdown of substantia nigra
-increase dopamine

ALL OF THESE FOOD, DRUG, HERB INTERACTIONS & SE!!!!!!!

37
Q

NE, Epi, and Dopamine are all _____

A

Catecholeamines

38
Q

F/T: You can take PO catecholamines. Why?

A

F

They are inactivated by COMT

39
Q

Drugs: Tolcapone

A

Class: COMT inhibitor
MOA: inhibits the enzyme that breakdown Dopamine
-increasing dopamine circulation

40
Q

What is COMT?

A

Enzyme that inactivates catecholamines….

Dopamine is a catecholamine

41
Q

Drugs: Apomorphine

A

Class: Dopamine agonist

uses: parkinsons during “drug vacation” or off period
-relief of akinesia

42
Q

What are Sx treatments for Parkinsons?

A

Lesion ablation
Deep brain stimulation of the basal ganglia
Implantation of fetal substantia nigra

43
Q

Describe Essential tremor

A

Causes: B1 receptor dysfunction

Tx: beta blockers that cross the BBB

44
Q

Describe Benign Hereditary Chorea

A

Jerky movments

Autosomal dominant-50% chance child will have it
-Chorea in childhood
-No progress, no dementia

Tx: Tetrabenazine

45
Q

Drugs: Tetrabenazine

A

Class: Dopamine Receptor blocker

Uses: Benign Hereditary Chorea

46
Q

Drugs: Baclofen

A

Muscle relaxant

Uses: Cerebral Palsy

47
Q

Describe Tardive Dyskinesia

A

Repetitive, involuntary movements in the face caused by antipsychotic drugs

48
Q

What are other drugs used to treat movement disorders?

A

Levodopa
Phenytoin
Seizures meds

49
Q

What is Muscular Dystrophy?

A

Genetic disorder

Progressive degenerstion of muscle fibers
Characterized by progressive muscle weakness/wasting

50
Q

Describe Duchenne’s MD

A

X-linked recessive: more common in males
-Results from gene that encodes Dystrophin
-Dystrophin absent in children with Duchenne

Muscle wasting (late: decrease muscle in diaphragm -> assisted ventilation)
Early onset in childhood
Usually do not survive beyond 20s

Tx: Improve QOL
Corticosteroids
Beta-2 agonist: increases blood flow to increase muscle strength

51
Q

Children with Duchenne’s _______ have Dystrophin

A

Dont

52
Q

What is a marked sign of muscle weakness in children?

A

Gowers Sign

When you ask them to stand up, they put their hands on their knees to assist them instead of standinf straight up

53
Q

Describe Cerebral Palsy

A

Non-progressive motor disorder of the CNS
-alterations in movement & posture

Caused by some something that happened at birth

SE: hyper/hypotonia or reflexes, scissoring of legs, failure to meet milestones seizures

Tx: No cure
Intrathecal pump -> botox or baclofen

54
Q

Describe Huntington

A

MOA: GABA reduced in basal ganglia

Includes Ballismus which is wild, violent, abnormal movement

Tx: Tetrabenazine, Haloperidol
Genetic counseling, ST/PT/OT

55
Q

Drugs: Tetrabenazine, Haloperidol

A

Class: Haloperidol: Dopamine Receptor Blocker/antagonist
-Tetrabenazine: Depletes dopamine

Uses: Huntington’s diseases
-decrease dopamine levels

56
Q

Describe Amyotropic Lateral Sclerosis (ALS)

A

“Lou Gehrig’s disease”

Loss of motor neurons
Death 2-6 years after diagnosis

More common in men than women

Tx: Extend QOL
Riluzole, Edaravone

57
Q

Drugs: Riluzole

A

Class: Na+ channel blocker

Uses: “Lou Gehrig’s disease”

58
Q

Describe Alzheimer’s

A

Has no definitive cause: hereditary or nonhereditary but more likely to develop if family history

Causes: Neurofibrillary tangles d/t hyperphosphorylation of tile-proteins within the cells
-Senile plaques caused by A-Beta 42 accumulation around protein

S/S: Forgetfulness, emotional, lack of concentration

Dx made by ruling out other causes of dementia

Death in 4-12 years

Prevention: CVS health, NSAIDs, diet/exercise

Tx: Palliative
-Tacrine, Rivastigmine, Memantine

59
Q

What is the #1 cause of dementia?

A

Alzheimer disease

60
Q

T/F: You get get Alzheimer’s at 30

A

T

61
Q

Drugs: Tacrine, Memantine

A

Class: CNS Ach esterase inhibitors
MOA: Prevents the breakdown of Ach which increase Ach circulation

62
Q

Describe Restless leg syndrom

A

Discomfort in legs causing an urge to move

Makes it hard to sleep
Increased risk of developing in pregnancy

Tx: dopamine, agonist, gabapentin, benzodiazepines, opiates (clonazepam)

Pharm (30 decks)

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