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Drugs For Movement Disorders Flashcards

1
Q

What is a limitation of pharm tx of neurodegen disorders?

A

Limited mostly to symptomatic txs that do not alter the course of the underlying disease

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2
Q

Describe tremor

A

An involuntary trembling or quivering; rhythmic oscillatory movement around a joint; characterized by its relation to activity

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3
Q

What are different types of tremors?

A
  • postural: a tremor of a part during maintenance of sustained posture
  • essential: a tremor of a part during movement (intention tremor)
  • Parkinsonian tremor: slow, regular movements of the hands and sometimes the lower limbsm neck, face, or jaw; stops upon voluntary movement; intensified by stimuli such as cold fatigue and strong emotions (rest tremor)
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4
Q

Describe chorea

A

Occurrence of a variety of continual, rapid, highly complex, jerky, dyskinesia movements that look well coordinated but are involuntary
-hereditary (HD); or occur as complication of other disorders and drugs

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5
Q

Describe tics

A

Involuntary, compulsive, rapid, repetitive, movement or focalization

  • irresistible but can be suppressed for some length of time
  • stress, lack of sleep
  • psychogenic or neurogenic
  • Gilles de la Tourette => tics
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6
Q

What are the four Cardinal features of Parkinsonism?

A

(1) . Bradykinesia
(2) muscular rigidity
(3) resting tremor (abates during voluntary movement)
(4) impairment of postural balance leading to disturbances of gait and falling

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7
Q

Based on the pathophysiligy of PD, what can PD Pts be treated with?

A

Dopamine agonists and/or aanticholinergic agents
(PD= loss of dopaminergic neurons of SN; selective loss of dopaminergic neurons is Pts results in disinhibition of GABAergic neurons and disturbed movement)

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8
Q

Levodopa (L-Dopa) MOA

A

Agonist as mostly D2 Rc; rapidly absorbed from small intestine w/ peak plasma concentration btwn 1-2 hours after Na oral dose; only 1-3% of levodopa actually enters the brain unaltered (rest metabolized by decarboxylation to dopamine)

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9
Q

What is the benefit of administering levodopa with a DOPA carboxylate inhibitor that does not cross the BBB (carbidopa)?

A

Reduced peripheral metabolism, increased plasma levels, increased half-life, and increased levodopa available for entry into the brain
-may reduce the daily requirement of levodopa by 75%

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10
Q

What is the clinical use of Levodopa in the to of Parkinsonian syndrome?

A

Doesn’t stop progression of PD but does lower the mortality rate when initiated early on
-best results in the first few years of tx:

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11
Q

What is the wearing off phenomenon that occurs during long-term tx?

A

Each does of levodopa effectively improves mobility for a period of time (1-2 hours), but rigidity and akinesia return rapidly at the end of the dosing interval
-increasing the dose and frequency of admin can improve symptoms (limited by development of dyskinesias)

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12
Q

How do you mitigate the adverse GI effects of Levodopa?

-anorexia, nausea, vomiting (activation of chemoreceptor trigger zone in brainstem outside BBB)

A

A combination of levodopa/carbidopa causes less frequent and less troublesome GI SEs in 20% of Pts
-individual can require larger doses of carbidopa to minimize the GI SEs and administration of carbidopa alone can be beneficial

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13
Q

What can happen when taking large doses of levodopa or levodopa in combination with nonselective MOA inhibitors or sympathomimetics?

A

Hypertension

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14
Q

What are some adverse affects of levodopa (CV)?

A
  • postural hypotension
  • HTN
  • increases in cardiac arrhythmia (rare) due to increased peripheral catecholamines synthesis
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15
Q

What is the most common presentation of the adverse effect of dyskinesias (due to levodopa)?

A

Choreoathetosis (movement of intermediate speed ,btwn the quick, flitting movements of chorea and the slower, writhing movements of athetosis) Of the face and distal extremities
-development can be dose related

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16
Q

What are some of the mental effects associated with levodopa?

A

Depression, anxiety, agitation, insomnia, somnolence, confusion, delusions, hallucinations, nightmares, euphoria, changes in mood and personality

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17
Q

What are some atypical antipsychotic agents that can help counteract behavior complications?

A

Clozapine, olanzapine, quetiapine, risperidone

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18
Q

What causes fluctuations in response to levodopa?

A

Timing (wearing off phenomenon) of the dose or due to reasons unrelated to dose timing (on-off phenomenon)

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19
Q

What happens in the on-off phenomenon (levodopa)?

A

Off periods of marked akinesia alternate over the course of a few hours with on-periods of improved mobility but often marked dyskinesia

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20
Q

What could provide temporary benefits to those pt with severe off-periods (levodopa)?

A

Subcutaneous injections of apomorphine may provide temporary benefit

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21
Q

What is the drug interaction between levodopa and MAO A inhibitors (or within 2 weeks of discontinuation)

A

HTN crisp when combined with levodopa

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22
Q

What are contraindications for levodopa?

A

Psychotic Pts; Pts with angle-closure glaucoma (ok for open angle), Pts w/ hx of melanoma or w/ undiagnosed skin lesions (precursor of skin melanin); active peptic ulcer (possible GI bleed)

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23
Q

Dopamine Receptor agonists

A

PD; lower incidence of the response fluctuations and dyskinesia so that occur with long-term therapy with levodopa

  • don’t response well to levodopa, don’t respond well dopamine Rc agonists
  • can be administered in addition to levodopa/carbidopa and in Pts who are taking levodopa and who have end-of -dose on-off phenomenon
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24
Q

Bromocriptine

A
  • ergot alkaloid derivative (D2 agonist)
  • used for tx of endocrine disorders
  • BA 28%; peak plasma concentration w/in 1-3 hours
  • t1/2: 15 hours
  • CYP3A4 (extensive first pass)
25
Pramipexole
- affinity for D3 - tx for mod-severe primary RLS - peak plasma reach in 2 hrs - t1/2 8 hrs - 90% excreted unchanged injuring (adjust dose in Pts w/ renal insufficiency)
26
Ropinirole
D2 Rc - RLS - metabolized by CYP450 (CYP1A2)=> coadmin w/ agents that are also metabolized with 1A2 at reduce the clearance - peak plasma: 1-2 hrs - T1/2: 6 hours
27
What are GI adverse effects of Dopamine Rc agonists?
Anorexia, nausea, vomiting (reduced if taken w/ meal) | -constipation, dyspepsia, reflux esophagitis
28
What are the adverse effects of dopamine Rc agonist on CV system?
- postural hypotension (at start of tx) - Bromocriptine may cause digital vasospasms (long term tx) - presence of peripheral edema and cardiac arrhythmia = DISCONTINUE THERAPY
29
What are adverse affects of dopamine Rc agonists (dyskinesia)?
Reduce total dose (like levodopa)
30
What are the mental disturbances assoc with dopamine Rc agonists?
Confusion, hallucinations, delusions, etc | Clear with withdrawal of meds
31
What are the contraindications to using dopamine receptor agonists?
Pts w/ hx of psychotic illness, recent MI, active peptic ulcer -Bromocriptine: Pts w/ peripheral vascular disease (vasoconstriction effects)
32
What are the MAO inhibitors?
Selegiline and Rasagiline
33
What are the two forms of monos mine oxidase?
A: metabolizes NE and serotonin B: metabolizes phenylethylamine and benzoyl amine Dopamine and tryptamine are metabolized equally by and A and M
34
Selegine
- irreversible B inhibitor (A at high doses) - slows breakdown of dopamine and prolongs antiparkinsonian effects of levodopa (may reduce on-off or wearing) - adjunctive therapy in Pts w/ declining or fluctuating response to levodopa - 10% BA ; peak plasma 1 hour - CI: Pts taking meperidine, tricyclic antidepressants, or serotonin reuptake inhibitors (serotonin syndrome)
35
Rasagiline
- irreversible inhibitor of MAO-B; more potent | - neuroprotective agent and early symptomatic tx of PD
36
Why must combined administration of levodopa and nonselective MAO inhibitor?
Lead to hypertensive crisis (peripheral accumulation of NE)
37
COMT inhibitors
- MOA of COMT: metabolizes levodopa to 3-O-methyl dopa=> competes with levodopa for transport across the intestinal mucosa and BBB - inhibitors: tolcapone and entacaponse=> prolong activity of levodopa (inhibit peripheral metab--increase BA) - Pts w/ response fluctuations
38
What type of effects do tolcapone and entacapone have?
Tolcapone: central and peripheral Entacapone: peripheral
39
What are the side effects of COMT inhibitors?
- Tolcapone: increase in liver enzyme levels and has been associated with death from acute hepatic failure - SE due to levodopa: orange discoloration of urine, diarrhea, abdominal pain, and sleep disturbances
40
Apomorphine
MOA: dopamine agonist; stimulating D2 Rc in the caudate-put amen - injected subcutaneously for quick, temp, relief for off-periods of akinesia (pt on domaminergic therapy) - adverse effects: nausea (pretreat with trimethobenzamminde), dyskinesias, drowsiness, sweating, hypothension, and injection site bruising
41
Amantadine
Antiviral agent; MOA in Parkinsonism is unknown; - t1/2 2-4 hours; peak plasma concentrations: 1-4 hours (excreted mostly unchanged in the urine) - short-lived benefits - adverse effects: restlessness, depression, irritability, insomnia, agitations, excitement, hallucinations, and confusions; HA, HF, postural hypotension, urinary retention, GI disturbances
42
What are some of the adverse effects of Amantadine?
Livedo reticularis. (Vascular condition: purplish mottled dis colorations of skin (legs)) -caution in Pts w/ hx of seizures or HF!
43
Anticholinergic drugs
Centrally acting - mAChR antagonists may improve tremor or rigidity (little effect on bradykinesia) - benzotrpine, bike ridden, orphaned rinse, procyclindine, trihexyphenidyl - low dose--> titrated upwards until benefit - adverse effects: common peripheral anticholinergic effects (sedation, mental confusion, constipation, urinary retention, blurred vision)
44
Tremor
beta-1 Rc implicated in some tremors; tremors respond well to metoprolol and propranolol - symptomatic tremor: antiepileptic drug primed one in smaller doses - Topirimate (serotonin receptor agonist) - alprazolam (BZD) and intramuscular injections of botulinum toxin A
45
What is HD?
Autosomal dominant disorder caused by an abn in chromosome 4 and is characterized by progressive chorea and dementia that usually begin in childhood
46
What causes the development of chorea in HD?
Imbalance of dopamine, ACh, and GABA in the basal ganglia that results in over activity of domaminergic nigrostriatal pathways
47
HD therapy
- no current therapy slows disease progression - drugs that impair domaminergic neurotransmission alleviates chorea (reserpine, tetrabenazine, olanzapine,..etc); drugs that activate domaminergic signaling exacerbate it
48
What is reduced in HD?
GABA, glutamic acid decarboxylase , and choline acetlytransferase are reduced in basal ganglia
49
What are the effects of reserpine (irreversible) and tetrabenazine (reversible)
Block the vesicular monoamine transporter and deplete cerebral dopamine stores -the effects of tetrabenazine resemble respective but with less peripheral activity and a shorter duration of action
50
Most therapy is for Pts who are depressed, irritable, parnoid, anxious, or psychotic
(1) antidepressants w/ anticholinergic profiles can exacerbate chorea (2) fluoxetine is effective for depression and irritability; carbamazepine is effective for depression
51
Tics
Neuroleptic antipsychotics: tetrabenazine, haloperidol, priority) - tendency to cause extra pyramidal syndromes, weight gain sedation irritibilty, phobias (so not first choice) - alpha-adernergic agents (clonidine, guanfacine) are effective and cause fewer long-tern adverse effects - injection of botulinum toxin A at site of tic beneficial
52
RLS
Cause unknown - correction of coexisting fe-deficiency anemia (if present) and respond to domamine agonists, levodopa, diazepam, clonazepam, or opiates - non-ergot dopamine agonists pramiplexole and Ropinirole are only drugs approved by FDA for RLS and considered first-line tx
53
ALS
- riluzole is the only drug to have impact on survival in ALS - MOA: inhibits glutamate release and blocks post-synaptic NMDA and Kainite-type glutamate receptors and inhibits voltage-dependent Na channels - nausea and weakness
54
Wilson disease
Recessive discover of copper metabolism (1) reduced ceruloplasin (2) increase [Cu] in brain and viscera (3) signs of hepatic and neurological dysfunction (tremor, chore form movements, rigidity, hypokinesia, dysarthria, and dysphasia
55
Wilson dz treatment
Agents that reduce serum Cu levels and low-Cu diet | -penicillamine, potassium sulfide, trientine, zinc acetate, zinc sulfate
56
Penicillamine
MOA: cheating agent that forms a stable complex with copper and is readily excreted by the kidney - adverse affects: nausea, vomiting, nephritic syndrome, myasthenia, blood disorders - Maintance dose after remission
57
Postassium disulfide
Reduces intestinal absorption of copper and can be prescribed in addition to penicillamine
58
Other agents for wilsons
Trientine (cheating agent) | Zinc acetate and zinc sulfate (increase fecal excretion of copper by decreasing GI absorption)
59
What are some examples of neuro degenerative disorders that manifest as abns in the control of movement?
PD and HD | -AD and ALS are also neurodegen disorders but result in impaired memory and cognitive ability and muscular weakness

Neuro Drugs (3 decks)

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