Pharm 28

Front 1

tremor

Back 1

rhythmic oscillatory movement around a joint; characterized by relation to activity

Front 2

tremor at rest

Back 2

characteristic of parkinsonism (along with rigidity and impairment of voluntary activity)

Front 3

conspicuous postural tremor is a cardinal feature of

Back 3

benign essential or familial tumor

Front 4

when does intention tremor occur

Back 4

lesions of brain stem or cerebellum, especially superior cerebellar peduncle involvement; manifestation of toxicity from alcohol or other drugs

Front 5

chorea

Back 5

irregular, unpredictable, involuntary muscle jerks that occur in different parts of the body and impair voluntary activity

Front 6

ballismus

Back 6

particularly violent chorea; occurs when proximal limbs involved

Front 7

athetosis

Back 7

abnormal movements that are slow and writhing

Front 8

dystonia

Back 8

abnormal postures

Front 9

when can athetosis and dystonia occur

Back 9

perinatal brain damage, focal or generalized cerebral lesions, or isolated phenomenon

Front 10

tics

Back 10

sudden coordinated abnormal movements that tend to occur repetatively, especially about face and head; can be suppressed voluntarily for short periods

Front 11

basal ganglia basic circuitry

Back 11

3 interacting neuronal loops that include cortex and thalamus as well as basal ganglia themselves

Front 12

what gene may cause autosomal dominant parkinson's

Back 12

alpha-synuclein; leucine-rich repeat kinase (LRRK2); UCHL1 gene

Front 13

normal role of dopaminergic neurons in substantia nigra

Back 13

inhibit output of GABAergic cells in the corpus striatum

Front 14

dopamine D1 receptor type location

Back 14

pars compacta of substantia nigra and presynaptically on striatal axons coming from cortical neurons and from dopaminergic cells in substantia nigra

Front 15

dopamine D2 receptor type location

Back 15

postsynaptically on striatal neurons and presynaptically an axons in the substantia nigra belonging to neurons in the basal ganglia

Front 16

benefits of dopaminergic antiparkinsonism drugs

Back 16

mostly on stimulation of D2 receptors

Front 17

dopamine agonists or partial agonist ergot derivatives like lergotrile and bromocriptine are powerful stimulators of

Back 17

D2 receptors

Front 18

dopa is an aa precursor to

Back 18

dopamine and norepinephrine; levodopa is the levorotary stereoisomer of dopa

Front 19

pharmacokinetics of levodopa

Back 19

rapidly absorbed in small intestine; aa's can compete with; peak plasma concentration 1-2 hours with half-life 1-3 hours; only 1-3% enters brain unaltered

Front 20

main metabolic product of levodopa

Back 20

homovannillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC)

Front 21

what can reduce peripheral metabolism of levodopa

Back 21

dopa decarboxylase inhibitor that doesn't penetrate blood-brain barrier like carbidopa

Front 22

Sinemet

Back 22

combination of levodopa and carbidopa

Front 23

GI effects of levodopa

Back 23

anorexia, nausea, vomiting in 80% without peripheral decarboxylase inhibitor; tolerance dvlps against these symtpoms

Front 24

what is cause of vomiting with levodopa

Back 24

stimulation of chemoreceptor trigger zone located in brain stem bit outside blood-brain barrier

Front 25

why should antemetics be avoided with parkinson's

Back 25

reduce antiparkinsonism effects of levodopa and may exacerbate the disease

Front 26

cardiovascular effects of levodopa

Back 26

tacycardia, ventricular extrasystoles, and rarely a fib; due to increased catecholamine formation peripherally; postural hypotension common, but asymptomatic; hypertensions when taken with MOAs

Front 27

dopa dyskinesia

Back 27

choreoathetosis of the face and distal extremities most common presentation

Front 28

on-off phenomenon of levodopa

Back 28

marked akinesia alternates over course of few hours with periods of improved mobility but often marked dyskinesia; unrelated to timing of doses

Front 29

drug holidays and levodopa

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may temporarily improve responsibeness and alleviate some adverse effects; not recommended

Front 30

pyridoxine (B6) and levodopa

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enhances extracerebral metabolism of levodopa and prevents therapeutic effect if not taken with decarboxylase inhibitor

Front 31

levodopa and MOAs

Back 31

don't take together or within 2 weeks of discontinuance due to hypertensive crisis possibility

Front 32

apomorphine primary use in parkinson's

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rescue drug for patients with disabling response fluctuations to levodopa

Front 33

bromocriptine

Back 33

D2 agonist; excreted in bile and feces; not commonly used now

Front 34

pergolide

Back 34

ergot derivative; directly stimulates D1 and D2 receptors; no longer available due to dvlpmnt of valvular heart disease

Front 35

pramipexole

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preferential affinity for D3 receptors; effective as monotherapy for mild parkinson's; mostly excreted unchanged into urine

Front 36

neuroprotective MOA of pramipexole

Back 36

scavenge hydrogen peroxide and enhance neurotrophic activity in mesencephalic dopaminergic cell cultures

Front 37

ropinirole

Back 37

relatively pure D2 agonist; metabolized by CYP1A2

Front 38

Rotigotine

Back 38

dopamine agonist; early Parkinson's-more continuous dopaminergic stimulation via skin patch; recalled 2008

Front 39

GI effects and dopamine agonists

Back 39

anorexia and nausea and vomiting-minimized by taking with meals; constipation, dyspepsia, and symptoms of reflux esophagitis, bleeding peptic ulceration

Front 40

cardiovacular effects and dopamine agonists

Back 40

postural hypotension; painless digital vasospasm; peripheral edema; cardiac valvulopathy with pergolide

Front 41

erythromelalgia

Back 41

red, tender, painful, swollen feet and occasionally hands, at times associated with arthralgia; reported adverse effect of dopamine agonists

Front 42

contraindications of dopamine agonists

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history of psychotic illness or recent MI or active peptic ulceration; peripheral vascular disease with ergot-derived agonists

Front 43

Monoamine oxidase A (MOA)

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metabolizes norepi, serotonin, and dopamine

Front 44

Monoamine oxidase B

Back 44

metabolized dopamine selectively

Front 45

selegiline

Back 45

selective MOB inhibitor

Front 46

rasagiline

Back 46

MOB inhibitor; more potent

Front 47

catechol-O-methyltransferase (COMT) inhibitors

Back 47

talcapone and entacapone=prolong action of levodopa by diminishing its peripheral metabolism

Front 48

talcapone and entacapone specs

Back 48

rapidly absorbed; bound to plasma proteins; metabolized b4 excretion; half lives ~2 hours

Front 49

adverse effects of talcapone and entacapone

Back 49

diarrhea, abdominal pain, orthostatic hypotension, sleep disturbances, orange discoloration of urine; talcapone may increase liver enzymes

Front 50

antiemetic used before apomorphine treatment

Back 50

trimethobenzamide

Front 51

amatadine

Back 51

antiviral agent with antiparkinsonism properties; MOA uncertain; benefits may be short lived

Front 52

undesirable CNS effects of amantadine

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restlessness, depression, irritability, insomnia, agitation, excitement, hallucinations, and confusion; OD can produce acute toxic psychosis

Front 53

withdrawal of ancetylcholine-blocking drugs

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gradually rather than abruptly to prevent acute exacerbation of parkinsonism

Front 54

reserpine and tetrabenazine

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deplete biogenic monoamines from storage sites

Front 55

haloperidol, metochlopramide, and phenothiazines

Back 55

block dopamine receptors

Front 56

treatment of drug induced parkinsonism

Back 56

antimuscarinic agents; levodopa if of no help and may exacerbate antipsychotics

Front 57

dvlpmnt of chorea in huntington's related to

Back 57

imbalance of dopamine, acetylcholine, GABA, and perhaps other neurotransmitters of the basal ganglia

Front 58

overactivity of dopaminergic nigrostriatal pathways causes

Back 58

increased responsiveness of postsynaptic dopamine receptors or deficiency of neurotransmitter that normally antagonizes dopamine

Front 59

drugs that imapir dopaminergic neurotransmission by depleting central monoamines

Back 59

reserpine, tetrabenazine

Front 60

drugs that imapir dopaminergic neurotransmission by blocking dopamine receptors

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phenothiazines, butyrophenones

Front 61

most effective pharmacologic approach to Tourett's

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haloperidol

Front 62

clonidine

Back 62

reduces motor or vocal tics in ~50% children; reduce activity in noradrenergic neurons in locus coeruleus-possible MOA

Front 63

drug induced chorea

Back 63

phenytoin, carbazepine, amphetamines, lithium, oral contraceptives

Front 64

drug induced dystonia

Back 64

dopaminergic agents, lithium, SSRI, carbamazepine, and metoclopramide

Front 65

drug induced postural tremor

Back 65

theophylline, caffeine, lithium, valproic acid, TH, tricyclic antidepressants, and isoproterenol

Front 66

Tardive dyskinesia causes

Back 66

long-term neuroleptic or metoclopramide treatment

Front 67

Rabbit syndrome

Back 67

neuroleptic-induced disorder; rhythmic movements about the mouth; may respond to anticholinergics

Front 68

neuroleptic malignant syndrome

Back 68

rare complication of treatment with neuroleptics; rigidity, fever, changes in mental status, and sutonomic dysfunction; dvlps over 1-3 days; occurs at anytime during treatment; 20% mortality