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USMLE - Pharm

Kaplan Section 4 Chapter 1 CNS Pharm - Dopaminergic Drugs

QuestionAnswer
what makes up the striatum? caudate, putamen, nucleus accumbens
what do the pathways through the basal ganglia control? general motor, eye movements, cognitive functions, emotional functions
what is the most important part of the striatum for motor control pathways? putamen
Give the path of the Direct Dopaminergic Nigrostriatal Pathway. striatum (caudate/putamen/nucleus accumbens) --> internal segment of globus pallidus OR substantia nigra pars reticulata
Give the path of the Indirect Dopaminergic Nigrostriatal Pathway. striatum (caudate/putamen/nucleus accumbens) --> external segment of the globus pallidus --> subthalamic nucleus --> internal segment of globus pallidus OR substantia nigra pars reticulata
What is the problem in Parkinson's? Is it hypo or hyperkinetic? Degeneration of substantia nigra pars compacta --> decrease release of dopamine --> decrease stimulation of direct pathway (dec movement) and decrease inhibition of indirect pathway (dec movement). HYPOkinetic disorder.
What is the problem in hemiballismus? Is it hypo or hyperkinetic? Lesion in subthalamic nucleus --> decrease inhib of indirect pathway --> increase movement. HYPERkinetic.
What is the problem in early Huntington's disease? Is it hypo or hyperkinetic? degeneration of caudate and putamen cells. Early phase-->dec in cells making enkephalins-->dec inhib of ext glob pall-->inc inhib of subthal nuc (like lesion of subthal nuc in hemiballismus)-->dec inhib of indirect pathway-->inc movement. HYPERkinetic.
What is the problem in advanced Huntington's disease? Is it hypo or hyperkinetic? degeneration of caudate and putamen cells. Later phase, both direct and indirect pathways are affected --> rigid HYPOkinetic parkingsonian state.
How does Ach relate to Parkinson's? Degeneration of substantia nigra pars compacta --> decrease release of dopamine --> dec movement and inc Ach activity (Ach inhibits movement); decreased DA in relation to Ach
What is the effect of giving dopamine receptor antagonists? Cause reversible pseudo-parkinsonism
What is the effect of giving dopamine receptor agonists? Cause dyskinesias (hyperkinetic involuntary movement; can present in Parkinson's pts on long term l-dopa therapy)
The nigrostriatal pathway starts where and goes to where? Starts in the substantia nigra pars compacta and goes to striatum (putamen and caudate)
The mesolimbic pathway starts where and goes to where? Starts in the ventral tegmental area and goes to the limbic structures (cingulate cortex nucleus accumbens, amygdala, etc)
The mesocortical pathway starts where and goes to where? Starts in the ventral tegmental area and parts of substantia nigra and goes to the prefrontal cortex
What are the positive signs of schizophrenia (i.e. hallucinations) attributed to? overactivity of the mesolimbic tract
What are the negative signs of schizophrenia attributed to? damage to the mesocortical tract
What are the cognitive defects and dyskinesia of Parkinson's attributed to? damage to the mesocortical tract
In the mesolimbic and mesocortical tracts, what happens with increased dopamine? increased psychomotor activity (high doses can cause psychoses)
In the mesolimbic and mesocortical tracts, what do dopamine antagonists do? decreases psychomotor activity
what is psychomotor activity? pertaining to motor effects of cerebral or psychic activity (e.g. incoherent conversation expansive gesturing pacing and hair twirling)
What is the tubero-Infundibular tract? hypothalamus --> anterior pituitary --> release dopamine --> inhibit release of prolactin
What category of drugs would you use to treat hyperprolactinemia? Dopamine agonists
What are the effects of dopamine antagonists? hyperprolactinemia, gynecomastia, and amenorrhea-galactorrhea
What is amenorrhea-galactorrhea? rare endocrine disorder characterized by the abnormal production of breast milk (lactation), lack of ovulation (anovulation), and the absence of regular menstrual periods (amenorrhea).
what is the chemoreceptor trigger zone? communicates with the vomit center.
What happens when you activate dopamine receptors in the chemoreceptor trigger zone? increased emesis.
What is the effect of dopamine agonists like apomorphine on the chemoreceptor trigger zone? promotes emesis
What is the effect of dopamine antagonists on the chemoreceptor trigger zone? antiemetic
What is the effect of increased dopamine:Ach ratio in the nigrostriatal pathway (less Ach relative to dopamine)? HYPERkinetic states: Huntington's chorea, Tourette syndrome; tardive dyskinesia
What is the effect of decreased dopamine:Ach ratio in the nigrostriatal pathway (more Ach relative to dopamine)? HYPOkinetic states: Parkinson disease, acute EPS, dystonias
What is the effect of increased dopamine:Ach ratio in the mesolimbic and mesocortical pathway (less Ach relative to dopamine)? Euphoria, paranoia, psychoses, and schizophrenia
What is the effect of increased dopamine:Ach ratio in the tubero-infundibular pathway (less Ach relative to dopamine)? HYPOprolactinemia (dopamine inhibits the release of prolactin)
What is the effect of decreased dopamine:Ach ratio in the tubero-infundibular pathway (more Ach relative to dopamine)? HYPERprolactinemia
Dopamine receptor type D1a increased cAMP; micromolar DA sensitivity; similar to peripheral DA receptors
Dopamine receptor type D1b increased cAMP
Dopamine receptor type D2a decreased cAMP; nanomolar DA sensitivity; main type in striatum; associated with Parkinsonian effects of older antipsychotic drugs (blcoks these receptors)
Dopamine receptor type D2b decreased cAMP
Dopamine receptor type D2c decreased cAMP; antagonized by clozapine
Signs and sx's of parkinson disease (PD) restine tremor, bradykinesia, muscle rigidity, postural instability, flat facies
what is pathologic basis of parkinson disease? degeneration of the nigrostriatal tract so that chemical balance shifts toward a decreased DA and increased Ach balance
what is the pharmacologic strategy for treating Parkinson's disease? restore normal balance by increasing DA activity and/or decreasing Ach activity at M receptors in the striatum
How does levo-dopa work? converted to DOPA by AAAD (dopa-decarboxylase) --> increases synthesis of DA
What is carbidopa? drug that inhibits peripheral AAAD (decreases peripheral conversion of L-dopa to dopa) and increases availability of L-dopa for the CNS (carbidopa doesn't cross the BBB)
what are the adverse effects of Levodopa? dyskinesias, hypoTN, on-off effects, hallucinations, psychoses
What is the effect of increased AAAD inhibition in the periphery? more L-dopa available --> more L-dopa is converted by COMT to 3-0-methyldopa --> 3-0-methyldopa competes with L-dopa for uptake into the CNS --> on-off effects of levodopa
What is tolcapone? inhibits peripheral COMT --> decreases conversion of L-dopa into 3-0-methyldopa --> more L-dopa uptake into CNS --> decrease on-off effects of Levodopa
What is entacapone? inhibits peripheral COMT --> decreases conversion of L-dopa into 3-0-methyldopa --> more L-dopa uptake into CNS --> decrease on-off effects of Levodopa
what is adverse effect of tolcapone? hepatotoxic
what is bromocriptine? prototype DA receptor agonist
what is adverse effect of bromocriptine? marked dyskinesias and CNS dysfunctions (hallucinations, confusion, and psychosis)
what has replaced bromocriptine? pramipexole and ropinirole (DA receptor agonists) -- less toxic than bromocriptine
adverse effects of pramipexole and ropinirole? sedation, including abrupt onset of sleep
What is selegiline? selective MAO type B inhibitor --> increases dopamine availability in CNS
when is selegiline used? initial drug in Parkinson's as sole drug or in conjunction with L-dopa
what is the secondary effect of selegiline? metabolized to amphetamine --> releases NE from the mobile pool --> increased NE availability/release --> CNS stimulation
For Parkinson's, which 2 drugs would you want to use to decrease Ach function? For what reasons are they preferable to other similar drugs? benztropine and trihexyphenidyl -- M receptor blockers and more lipid-soluble than atropine --> greater CNS access.
What are the effects of drugs that decrease Ach function to treat Parkinson's? 1. Reduce tremor and rigidity. Little effect on bradykinesia. 2. reduce extrapyramidal dysfunction (pseudo-Parkinsonism, dystonias) caused by DA receptor antagonists
What is "extrapyramidal"? Physical symptoms, including tremor, slurred speech, akathisia, dystonia, anxiety, distress, paranoia, and bradyphrenia
What is "dystonia"? state of abnormal (either excessive or inadequate) muscle tone; involuntary movements and prolonged muscle contraction, resulting in twisting body motions, tremor, and abnormal posture
what drug is especially useful in acute dystonias? Diphenhydramine
What are the adverse effects of drugs that decrease Ach function (M receptor antagonists) in Parkinson's? exacerbates tardive dyskinesia; cause typical atropine-like adverse effects
what is tardive dyskinesia? Symptom caused by the long-term or high-dose use of dopamine antagonists; Dyskinesia refers to an involuntary movement (like tics); effect of these drugs can be tardive, meaning the dyskinesia continues even after the drugs are no longer taken
Features of tardive dyskinesia Tardive dyskinesia is characterized by repetitive, involuntary, purposeless movements. Features of the disorder may include grimacing, tongue protrusion, lip smacking, puckering and pursing of the lips, and rapid eye blinking. Rapid movements of the arms,
What is amantadine? probably M receptor block --> mild and temporary anti-PD actions
Adverse effects of amantadine? atropine-like side effects (M block) and livedo reticularis (edema and skin mottling)
Created by: Missy Kratz Missy Kratz on 2008-03-14



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