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Pathopharm II Exam 1 > 2: RA/Gout/Movement (Part 3) > Flashcards

2: RA/Gout/Movement (Part 3) Flashcards

1
Q

What are the tremor characteristics for a pt with Parkinson’s?

A
  • Frequency: usually 4-to 6-Hz (4-6 cycles per second)
  • 7-8-Hz in about 10%-15% (resembling essential tremor)
  • Resting tremor (worsens with stress)
  • Initially rhythmic flexion-extension of fingers, hand, foot
  • May be associated with one limb or to limbs ipsilateral, initially, then becoming more widespread
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2
Q

Rigidity a/w Parkinson’s disease is defined as _____

A

increased resistance to passive movement
common feature (flexed posture)

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3
Q

What is the most disabling Parkinson’s disease manifestation?

A

Bradykinesia

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4
Q

What is the severest form of Bradykinesia?

A

akinesia

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5
Q

What is characteristic of bradykinesia?

A

voluntary movement: slowness

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6
Q

What kind of affect do Parkinson’s pts have?

A

flat
(flat facial expression)
Infrequent blinking

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7
Q

What is Blepharoclonus? What is it a/w?

A

closed eyelid fluttering; Parkinson’s

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8
Q

What is Blepharospasm? What is it a/w?

A

eyelid closure – involuntary; parkinsons

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9
Q

Parkinson’s pts drool T/F

A

TRUE

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10
Q

What happens to parkinson’s pts voice?

A

hypophonic/poorly modulated

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11
Q

How does parkinson’s pts handwriting change?

A

small, tremulous, perhaps illegible

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12
Q

How is Parkinson’s walking different than normal?

A

difficulty in initiation – patients may increasingly leaned forward to begin movement
small, shuffling steps
no arm-swing
stopping difficulty
festinating gait: walking with increasing speed to keep from falling (because of abnormal center of gravity)

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13
Q

How are reflexes different in parkinson’s?

A

Tendon: unaltered
Tapping over the glabella: sustained blink response (Myerson’s sign)

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14
Q

What are the mental changes a/w Parkinsons?

A

Depression
Impaired cognitive function
may reach dementia in advanced cases

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15
Q

Does Dopamine cross the BBB?

A

does not cross: blood-brain barrier
ineffective if administered peripherally

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16
Q

How is L-DOPA different than Dopamine?

A

crosses the blood-brain barrier
metabolic precursor dopamine
enters neuronal cells and is decarboxylated to dopamine

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17
Q

What are the differences between D1 and D2 receptors?

A

D1:
adenyl cyclase stimulation
increases cyclic AMP levels
located in high concentration in substantia nigra zona compacta
D2:
adenyl cyclase inhibition
decreases cyclic AMP levels
postsynaptic localization on striatal neurons

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18
Q

About ____%-____% of administered levodopa reaches the brain (the rest metabolized extracerebrally {mainly decarboxylation to dopamine}).

A

1-3

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19
Q

To achieve therapeutic brain levels of Levodopa, either:

A

give large quantities
or
give with a dopa decarboxylase inhibitor, such as carbidopa (does not penetrate the brain)

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20
Q

Levodopa With carbidopa (Lodosyn): What are the effects?

A

less peripheral decarboxylation of levodopa
levodopa plasma half-life: longer
more levodopa available for brain entry

Levodopa + Carbidopa = (Sinemet)
Rytary - extended release formulation

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21
Q

Levodopa with Entacapone (Comtan):

A

A COMT inhibitor
works similar to carbidopa in that it decreases metabolism of L-dopa which increases the amount that can cross the BBB

Levodopa + Carbidopa + Entacapone = (Stavelo)

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22
Q

Levodopa + Carbidopa + Entacapone =

A

(Stavelo)

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23
Q

use of a _______ allows 75% reduction in daily levodopa dose.

A

peripheral dopa decarboxylase inhibitor

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24
Q

How do the tolerable doses of Levodopa change over time?

A

Tolerable doses diminish with time, i.e. adverse effects develop to previously tolerated dosages

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25
Q

How does the efficacy to L-DOPA change over time?

A

Efficacy to L-DOPA diminishes with time (after approximately 3-4 years)

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26
Q

L-DOPA slows disease progression T/F

A

FALSE
L-DOPA: does not stop disease progression
early L-DOPA treatment may reduce Parkinson’s disease mortality rate

27
Q

Long-term levodopa therapy is a/w _____

A

difficulties in clinical management

28
Q

L-DOPA is most effective in diminishing what Parkinson’s symptom?

A

most effective in diminishing bradykinesia; improves all Parkinson’s disease symptoms

28
Q

L-DOPA should be used in combo with ______

A

dopa decarboxylase inhibitor
levodopa plus carbidopa

29
Q

What are the GI effects of Levodopa?

A
  • 20% frequency: if w/ carbidopa
  • 80% frequency: if monotherapy
  • vomiting: stimulate brain stem’s emetic center (tolerance often develops)
  • Phenothiazines: avoid – reduce efficacy of levodopa/disease exacerbation
30
Q

Why should Phenothiazines be avoided when on Levodopa?

A

reduce efficacy of levodopa/disease exacerbation

31
Q

What is the frequency of dyskinesia with long term treatment w/ levodopa

A

With long-term treatment – dyskinesia frequency = 80%
dose-related; more common with combination treatment (L-DOPA plus carbidopa)

32
Q

Dyskinesias include:

A

chorea, ballismus, athetosis, dystonia, myoclonus, takes, tremor
the particular dyskinesia in a patient tends to remain constant

33
Q

What is the most common dyskinesia?

A

choreoathetosis

34
Q

Management of dyskinesias:

A

dosage reduction (reduced antiparkinsonism effect)
drug holidays may be helpful

35
Q

Selegiline (Eldepryl)

A

selective monoamine oxidase B inhibitor
prolongs levodopa effect (inhibits metabolism)

36
Q

What are the Anticholinergics used in tx of Parkinson’s? What do they improve?

A

Benztropine (Cogentin), Biperiden (Akineton), Orphenadrine (Norflex), Trihexyphenidyl HCl

Improvement: rigidity/tremor
Minor effect: bradykinesia
Not used as much now

36
Q

Amantadine

A

Antiviral drug
Mechanism of action: unclear; may influence dopamine release /reuptake/synthesis
- may also be in part due to its anticholinergic activity

37
Q

Physiologic postural tremor (normal) is increased by:

A

thyrotoxicosis
isoproterenol (Isuprel)/epinephrine (IV)
anxiety
fatigue

38
Q

Drug induced tremors - increasing normal physiologic tremor: What drugs cause this?

A

bronchodilators
tricyclic antidepressants
lithium

39
Q

Tremors induced/enhanced by sympathomimetics: blocked by propranolol (sometimes not blocked by metoprolol – ß1 antagonist), suggesting tremor may be due to _________.

A

ß2 receptor activation

40
Q

What is an essential tremor?

A

Postural tremor, similar to normal physiologic tremor; maybe familial
ß1 antagonists effective in reducing tremor indicative of possible ß1 receptor mediation

41
Q

Drugs/Drug Classes useful in management of the essential tremor:

A

Beta adrenergic receptor blockers
Primidone (Mysoline)
Alprazolam (Xanax) (occasionally useful)

benzodiazepines/anti-parkinsonian agents not useful

42
Q

What causes/alleviates symptoms associated with Intentional Tremor?

A

May be caused by toxic reactions to alcohol and other drugs (e.g. phenytoin)
Withdrawal of causative agents alleviates symptoms

43
Q

What is Huntington’s DIsease?

A

Dominant, inherited
Progressive chorea in dementia (typically adult onset)
Chorea: dopamine/acetylcholine/GABA basal ganglia imbalance (too much dopamine?)

44
Q

What is the mechanism of chorea?

A

Dopaminergic nigrostriatal pathway overactivity

Possibilities:
postsynaptic dopamine receptor hypersensitivity
reduction in dopamine antagonizing neurotransmitter concentration

45
Q

What kind of agents are used to reduce chorea a/w Huntington’s disease?

A

Anti-dopaminergic agents
reserpine
phenothiazines and butyrophenones (haloperidol)

46
Q

What drugs increase chorea?

A

Dopaminergic drugs (e.g. levodopa): increase chorea

47
Q

Chorea as a complication of non-neurological disorder could be caused by:

A

Thyrotoxicosis, hypocalcemia, lupus erythematosus, hepatic cirrhosis, polycythemia vera rubra
treat the underlying disease

48
Q

Drug induced chorea could be caused by:

A

levodopa, antimuscarinics, lithium, phenytoin, oral contraceptives, amphetamine, etc.

treatment: withdraw the drug antipsychotics: acute or tardive dyskinesia – more difficult to manage

49
Q

Ballismus treatment

A

dopamine-blocking drugs, e.g., perphenazine, haloperidol

50
Q

Athetosis & Dystonia Treatment

A

Pharmacological treatments – not usually satisfactory

Try:

  • diazepam
  • high-dose antimuscarinic agents
  • levodopa
  • baclofen
  • phenothiazines
  • amantadine
51
Q

Chronic, multiple tics is characteristic of _____

A

Tourette’s syndrome

52
Q

How should you treat tics?

A

haloperidol (most effective available)

if haloperidol is not effective:

  • temazepam (Restoril)
  • carbamazepine (Tegretol)
  • clonidine (Catapres)
  • fluphenazine (Prolixin)
53
Q

What can cause drug induced dyskinesia?

A

Phenothiazines: acute dyskinesia/dystonia

54
Q

What can be used to treat drug induced dyskinesia?

A

Treatment: antimuscarinic agents primarily:
benztropine (Cogentin)(IV)
diphenhydramine (Benadryl) (IV)
biperiden (Akineton) (IV / IM)
diazepam (Valium) (IV)

55
Q

Tardive dyskinesia are the consequence of ________

A

long-term antipsychotic drug treatment

56
Q

How does changing the antipsychotic drug dosage affect the tardive dyskinesia symtpoms?

A

Dosage reduction: worsens symptoms
Dosage increase: suppresses symptoms

57
Q

Is it hard to treat tardive dyskinesia?

A

Difficult to treat; in adults may well be irreversible

58
Q

_________ do not appear to cause tardive dyskinesia, thus avoiding the problem

A

Newer antipsychotic agents, e.g. olanzapine and risperidone

59
Q

What is WIlson’s disease? What causes it?

A
  • Recessive, inherited copper metabolism error
  • Reduced serum copper/ceruloplasmin
  • Increased copper concentration: brain, viscera
60
Q

What are the clinical manifestations of Wilson’s disease?

A

hepatic dysfunction
neurologic dysfunction
Dystonias, spasticity, seizures

61
Q

What are the treatments for Wilson’s disease?

A
  • Penicillamine (dimethylcysteine) – copper chelating agent
  • Trientine (Syprine) chelating agent – for patients not tolerating penicillamine
  • Zinc acetate: increases copper excretion
  • Zinc sulfate: decreases copper absorption

Pathopharm II Exam 1 (11 decks)

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