Method of action for Dopamine precursors
Levodopa-carbidopa
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⢠Levodopa ā CNS ā converted to dopamine
⢠Carbidopa: inhibits metabolism of levodopa, ā availability
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MOA: muscarinic antagonist
benztropine
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blocks CNS muscarinic receptors from Ach ā improve tremors
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What is the mechanism of action of Entacapone?
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inhibit COMT ā reduce metabolism of Ldopa
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What is the mechanism of action of Selegiline?
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MAO-B inhibitor ā decrease dopamine metabolism
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What is the therapeutic goal of antipsychotic drugs in the treatment of schizophrenia?
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block dopamine and/or serotonin receptors
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What is the dopamine hypothesis?
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attributes schizophrenia symptoms to the hyperactivity of central dopamine pathways
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What are the two main categories of antipsychotics?
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First-generation antipsychotics and Second-generation antipsychotics
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What are the typical side effects of first-generation antipsychotics?
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Higher incidence of extrapyramidal symptoms (EPS)
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What are the typical side effects of second generation anti psychotics
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lower incidence of EPS but higher risks of metabolic side effects
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First gen psych meds
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Chlorpromazine
Fluphenazine
Haloperidol
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What is the mechanism of action of first-generation antipsychotics?
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Competitive blocker of D2 receptors in the mesolimbic pathway
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second-generation antipsychotics?
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Clozapine
Risperidone
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What is the Extrapyramidal syndrome?
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A group of motor symptoms including Parkinson-like movements, muscle rigidity, and spasms of the neck and facial muscles.
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What is tardive dyskinesia?
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irreversible motor disorder
⢠involuntary facial jaw movements
⢠sticking-out the tongue
⢠lip smacking
⢠uncontrollable movements in the arm, leg, and torso
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What oral health issues might patients with schizophrenia face?
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Poor oral hygiene and self-harming behaviors such as tongue, lip, and/or cheek biting
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What is the therapeutic goal of drugs for dementia disorders?
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mostly palliative to help with decreasing symptoms or stabilizing patient condition
What is the primary characteristic of Amyotrophic Lateral Sclerosis (ALS)?
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Degeneration of motor neurons leading to the inability to control muscle movement.
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Drug and MOA for ALS treatment
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Riluzole
Inhibits glutamate release and inactivate sodium channels
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What is the main storage location for serotonin?
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Enterochromaffin cells of the small intestine
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What enzyme degrades serotonin?
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Monoamine oxidase (MAO)
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How is serotonin transported to storage vesicles?
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Via vesicular monoamine transporter
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What is 5-HT1-receptor coupled with?
Controls?
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Gi coupled
Mood regulation, anxiety, and pain perception.
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What is 5-HT2-receptor coupled with?
Controls?
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Gq coupled
CNS and mediate hallucinogenic effects
Platelet and lead to platelet aggregation
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What is 5-HT3-receptors coupled with?
Controls?
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sodium and potassium ion channels
nausea and vomiting response and pain perception in PNS
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What is 5-HT4-receptors coupled with?
Controls?
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Gs coupled
GI tract
Increase in secretion & peristalsis
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What are the pharmacological effects of serotonin in the CNS?
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mood, appetite, body temperature regulation, and sleep cycle
vasoconstriction, inhibition of gastric secretion, GI motility and stimulation of smooth muscle contraction.
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What is the monoamine hypothesis of depression?
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depression is caused by the lack of monoamine transmitters in the brain, particularly serotonin and norepinephrine
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What role does dopamine deficiency play in depression?
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role in the lack of interest (anhedonia) symptom commonly seen in depression
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What is the time frame for the clinical response to antidepressant drugs?
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Weeks
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What is the Neuroplasticity Hypothesis?
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suggests lowered levels of brain-derived neurotrophic factor (BDNF) or dysfunction of its receptor, TrkB, plays a significant role in depression development