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EXAM 5 PHARMACOLOGY > Parkinson's Disease & Movement Disorders (Exam V) > Flashcards

Parkinson's Disease & Movement Disorders (Exam V) Flashcards

1
Q

What symptom is the hallmark of Parkinson’s disease?

What are the TRAP symptoms with Parkinson’s disease? essay question

A

Tremor at rest (rhythmic movement around a joint)

Tremor
Rigidity
Akinesia - loss of ability to move muscle voluntarily
Postural instability.

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2
Q

What is Chorea?

What is Ballismus?

A
  • Muscle jerking in various areas
  • Violent abnormal movements (extreme version of chorea)
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3
Q

What is Athetosis?

Is this indicative of Parkinson’s disease?

A
  • Slow, writhing movement
  • Not typical of Parkinson’s
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4
Q

What is Dystonia?

What are Tics?

A
  • Abnormal posture w/ no movement, jointed locked, usually seen with cerebral palsy.
  • Single, repetitive movements (especially facial)
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5
Q

What collection of neurons regulates motor activities?

A
  • Basal Ganglia/Nuclei
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6
Q

Communication from the motor cortex to the thalamus goes through the _____ ______.

A

Basal Ganglia

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7
Q

What are two movement disorders related to basal ganglia dysfunction?

A

Parkinsons: Destruction of Dopaminergic Neurons
-Need Dopamine (L-Dopa)

Huntingtons: Destruction of GABAnergic Neurons
-Need to decrease dopamine (Tetrabenazine)

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8
Q

What is damaged in Parkinson’s.

A

The pars compacta in the substanstia nigra is damaged. No dopamine release to provide a negative feedback to the thalamus, this will lead to movement disorders.

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9
Q

What is the pathogenesis of Parkinsonism?

A

Decrease in Dopamine Levels in the Nigro-striatal pathway

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10
Q

What are protective environment factors for Parkinsonism?

What are harmful environment factors for Parkinsonism?

A

Protective factors: Cigarette smoking, Coffee, Anti-inflammatories, Uric Acid

Harmful: Lead, Manganese Exposure, Vit D Deficiency

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11
Q

What genetic component is often present in Parkinson’s patients?

What is the result of this mutation?

A
  • SNCA - α-Synuclein (NT release)

Misfolding produces Lewey Bodies

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12
Q

What drug is given as firstline treatment for Parkinson’s?
Why this drug?

A
  • Levo-dopa (dopamine precursor)
  • Able to cross BBB unlike dopamine
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13
Q

What are the treatments for Parkinson’s? Essay Question

A
  1. Exercise/ Physical Therapy
  2. Levo-Dopa- restore dopamine levels
    -Improve uptake with carbidopa- inhibits dopa decarboxylase
    -Improve uptake with COMT inhibitors (tolcapone)
    -Decrease toxicity (hallucinations) with pimavanserin (Nuplazid)
  3. CNS antimuscarinics- to reduce tremors
  4. Dopamine receptor agonist
  5. MAO-B Inhibitors (Selegeline)
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14
Q

What should be avoided when one has Parkinson’s Disease?

A

Dopamine receptor antagonist (antipsychotics, D2 antagonist, Haldol)

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15
Q

How much of L-Dopa crosses the BBB?
Can this be increased? With what? How much?

A
  • 1-3%
  • With Carbidopa (10% uptake of Levo-dopa)
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16
Q

How does carbadopa work?

A
  • Inhibits Dopa-Decarboxylase from forming dopamine peripherally (thus saving Levo-dopa for the CNS)
17
Q

Is Levo-dopa a treatment or a cure for Parkinson’s?

A
  • Treatment, effective for a period of time before more neurons degrade.
  • Over the next 10-15 years this will be less and less effective
18
Q

What adverse effects can be seen from levodopa?

How will you decrease the toxicity of levodopa?

A
  • Delusions and Hallucinations
    This is worse with carbidopa

Primavanserin (Nuplazid)

19
Q

What is the On-Off Phenomenon with Levo-dopa?

What can you take to decrease these symptoms?

Are drug holidays recommended?

A

Associated with long-term use (10 years+). Increased mobility followed by marked akinesia, very frustrating for patients.

Apomorphine

Drug holidays for 3 to 21 are not recommended, but patient’s will still self demedicate.

20
Q

What drug interactions exist for Levodopa?

What contraindications exist for Levodopa?

A

Vitamin B6 & MAOI’s

  • Psychosis (↑ dopamine signalling)
  • Glaucoma
  • Melanoma (L-dopa feeds these tumors)
21
Q

How is L-Dopa broken down peripherally?

What drug inhibits this?

A

COMT Enzyme will break down L-DOPA to 3-OMD
DOPA decarboxylase will break down L-DOPA to Dopamine (but its in the periphery, we need it in the brain)

Entacapone & Tolcapone will inhibit COMT Enzyme
Carbidopa will inhibit DOPA Decarboxylase

  • This will ensure there are more L-DOPAs in the periphery to cross the BBB.
22
Q

Once L-DOPA crosses the BBB, DOPA decarboxylase converts the compound to Dopamine. What breaks down dopamine in the brain?

What drug can prevent the breakdown of Dopamine in the CNS by inhibiting MAOB?

What drug can prevent the breakdown of Dopamine by inhibiting the COMT enzyme?

A

Monamine Oxidase B and COMT will break down Dopamine in the brain.

Selegiline, Rasagiline- these are given with L-DOPA

Tolcapone

23
Q

What is the most common movement disorder?

What is essential tremors indicative of?

What is the treatment?

A

Essential tremor (β1 receptor dysfunction) tremor with movement

Essential tremors are indicative of brain lesions or EtOH, not Parkinsons

  • βblockers
24
Q

What is benign hereditary chorea?

What is the treatment?

A

Chorea in childhood with no progression and no dementia.
Clear genetic predisposition: autosomal dominant 50% chance of passing this on to their offspring.

Tetrabenazine (↓ Dopamine)

25
Q

What is Tardive Dyskinesia?

What is the most common cause?

A

Repetitive, involuntary movements.

Anti-psychotic drugs, other drugs that will cause TD will include Levodopa, Phenytoin, other seizure drugs.

26
Q

What is the most common & severe muscular dystrophy disorder?

Who and how is it inherited?

A
  • Duchenne’s Muscular Dystrophy (most severe)
  • X-linked recessive (males) - passed by mother to sons
27
Q

What sign is seen with children who have Duchenne’s MD?

Where will muscle wasting occur in the body?

What is the life expectancy of someone with Duchenne Muscular Dystrophy?

Treatment?

A

Gower’s Sign - using hands to pushing on legs to stand.

Major Skeletal Muscle
Some Cardiac Muscle
Smooth Muscles

They don’t typically survive beyond their 20s.

Corticosteroids
Beta-2 agonist (muscle strength) - by increasing blood flow in the skeletal muscle.
Braces

28
Q

What characterizes Cerebral Palsy?

What is the usual cause?

Symptoms?

Treatment?

A

Non-progressive motor disorder of the CNS.

Birth Trauma, Hemorrhage, Anoxia

Wide spectrum of signs and symptoms can be hyper or hypotonia.

Surgery, Intrathecal Baclofen pump to the spinal column (muscle relaxant) to treat spasticity.

29
Q

When does Huntington’s disease normally occur?

Is this disease autosomal dominant or recessive?

Symptoms of Huntington disease?

When does death occur?

A

Age 30 - 40

Autosomal Dominant Disorder- Chromosome #4

Progressive loss of muscle control
Chorea
Dementia

Death 15-20 years after onset of symptoms. No cure.

30
Q

What characterizes the pathophysiology of Huntington’s disease?

A
  • GABA reduced in the basal ganglia
  • Reduction in ChAT (Choline Acetyltranferase)
  • Excess Dopamine
31
Q

What treatments are there for Huntington’s disease?

A
  • Tetrabenazine = ↓ excess dopamine
  • Dopamine Receptor blockers (ex. Haldol)
  • Genetic Counseling, Speech Therapy, PT/OT
32
Q

What is ALS/ Lou Gehrig’s Disease?

When does onset occur?

When does death occur?

A

A rare progressive neurological disorder characterized by loss of motor neurons

40-60 years old, more common in men.

2-6 years after diagnosis

33
Q

What are the treatments for Lou Gehrig’s disease?

A
  • Riluzole - Na⁺ channel blocker (specific for damaged neurons)
  • Edaravone - antioxidant.
34
Q

What are some theories involving Alzheimer’s Disease?

What two anatomical changes are seen in Alzheimer’s disease?

A

Genetic predilection/Nonhereditary
Head Injury
Dysregulated Lipids
Low Estrogen

  1. Neurofibrillary tangles inside the neuron (Tau proteins)
  2. Amyloid/Senile plaques outside the neuron
35
Q

What palliative treatments are available for Alzheimer’s disease?

Clinical Manifestations of Alzheimer Disease

How is diagnosis made?

A

CNS AChE inhibitors (Tacrine: ↑ACh at synapse)
NMDAr Antagonist (Memantine)- slow the effects of dementia.

Forgetfulness, emotional disturbance, disorientation, confusion, lack of concentration, decline in abstraction, problem solving, and judgement. Insidious onset.

Dx made by ruling out other causes of dementia.

36
Q

What are the treatment’s for restless leg syndrome?

A
  • Dopamine agonists
  • Opiates (Clonazepam)
  • Gabapentin
  • Benzodiazepines

EXAM 5 PHARMACOLOGY (8 decks)

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