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Neuropharm Concepts

All Concepts

CNS Target for Analgesia Spinal Cord Cortex
CNS Target for Amnesia Hippocampus Cortex
CNS Target for Loss of Consciousness RAS brainstem Cortex Hypothalamus
CNS Target for Loss of Reflex Spinal Cord
CNS Target for Muscle Relaxation Spinal Cord
What is Meyer-Overton Equation? for general anesthetic drugs, the partition coefficient is inversely proportional to anesthetic power
What is Minimum Alveolar Concentration? concentration of gas you need in alveoli you need to have an anesthetic effect. as partition coefficient increases, the onset of effects and recovery are both slower
What is the MAO of Inhaled Anesthetics? Specific and Non-specific actions on neuronal activity effects ion channels - AP opens the pore, but drug molecules do not allow for conduction, inhibit -> anesthetized
What is the adverse effects of Inhaled Anesthetics? respiratory and cardiac depression hypotension increase in skeletal muscle tone Diabetes Insipidus - methoxyfluxane Hepatotoxicity - halothane
What is the MAO of Intravenous Anesthetics? GABA NT (inhibitor) and glutamate NT (excitatory)
What is the most common drug classes in Intravenous Aneesthetics? Barbiturates Benzodiazepines
What are other uses of IV Anesthetics? insomnia treatment, anxiety, epilepsy
Sedative Hypnotic Effects shared with alcohol and can be potentially deadly when mixed
What is the mechanism of Barbiturates? directly open GABA-A receptor without GABA increase length of interval for Cl- IN opening
What is the mechanism of Benzodiazepines? needs GABA GABA-A receptor agonist binds to benzodiazepine receptor a binding site on GABA-A receptor Cl- IN -> hyperpolarization (inhibit firing)
What is the mechanism of Atypical Benzodiazepines? binds to subpopulation of GABA receptors
Types of drugs for Anticonvulsant long half-life, rapidly into brain
Types of drugs for Hypnotic short half-life to pretty groggy after taking drug, abuse liability, can induce withdrawal seizures
Types of drugs for Anti-anxiety long half-life (want protection all the time)
Types of drugs for pre-anesthetic Rapid onset, short half-life
What is the Therapeutic Effects of Benzodiazepines? sedation, hypnosis, decreased anxiety, muscle relaxation, anterograde amnesia
What is the Adverse Effects of Benzodiazepines? lightheadedness, dizziness, vertigo, weakness, blurred vision, headache, increase reaction time and decrease coordiation, confusion, disorientation, day time tiredness, GI, highly abusive + withdrawal -> seizures, depression
What is the adverse effects of Barbiturates? dizziness, weakness, fatigue, vertigo, visual disturbance, hypothermia, respiratory and cardiac depression, coma
What are the conditions associated with Anxiety? Depression, panic disorder, PTSD, phobias, OCD, eating disorders
What is the structure of GABA-A receptor? Heterologous Pentamers. 5 subunits, 7 families an active pentamer has at least 1 alpha and 1 beta Most common orientation = 2 alpha, 2 beta, 1 gamma
Binding of Benzodiazepines requires? Gamma subunit in receptor complex
Where are Benzodiazepine receptors found most commonly in? emotional center of the brain frontal cortex, cerebellum, amygdala, hippocampus, hypothalamus
Difference between Benzodiazepine and Barbiturates? does not require gamma subunit does not require GABA
What is Manic-Depression? bipolar affective disorder. extreme sadness and happiness Type I and II
What are the symptoms of Manic Depression? Bipolar Symptoms Mania Symptoms - excessive happiness, excitement, irritability Depression symptoms
What is the Treatment of Manic Depression? Lithium - lots of adverse effects
What is Monoamines? Major Neurotransmitter Systems: norepinephrine, dopamine, seratonin (catecholamine)
What is the cause of depression? low activity of Monoamine - mostly involving serotonin and norepinephrine
What is the cause of mania? over-activity of Monoamine
Where are monoamine stored? synaptic vesicles
Where are monoamine synthesize? nerve terminal
WHere is the reuptake of monoamine occur? pre-synaptic nerve terminal
What is the mechanism of action of antidepressant MAO? degradation via monoamine oxidase inhibit Ne, DA, 5HT degradation increase synaptic monoamine levels enhance synaptic neurotransmission Therapeutic effects wont occur for several weeks
WHat is the mechanisms for Tricylic Anti-Depressant (TCA) block reuptake of noepinephrine (NE)
What is the precursor to seratonin Tryptophan (pineal hormone)
Which monoamines has the least role in antidepressant effects? dopamine - no current drug hany any action of blocking the reuptake of dopamine
Which drug is the only one that has effects on all 3 monoamines? Venlafaxine
What happens when H1 Histamine receptors are inhibited? hypertension, sedation, weight gain
What happens when cholinergic receptors are inhibitied? muscarinic? memory dysfunction, blurred vision, dry mouth, sinus tachycardia, urinary retention, constipation, ANS
What is serotonin syndrome?
What is a hypertensive crisis? When tyramine pretend to be a NT and MAO metabolize tyramine when it attaches to adrenergic receptor no fish, cheese, red wine with MAO
Mechanism of lithium treatment? alteration of phosphatidyl inositol metabolism
What is positive symptom? bizzare delusios, auditory hallucination, unusual behaviors. treatable with drugs
What is negative symptom? social isolation, poverty of speech, flat affect, lack of motivation. untreatable with drugs. true for 1st gen drug. may be treatable with newer drugs
Which drugs produce the same symptoms as schizophrenia? cocaine, amphetamine. LSD contains both inhibit dopamine reuptake.
What is the cause of psychosis? Too much dopamine in the specific brain areas
What are the main strategies for treatment of psychosis and schizophrenia? decrease dopamine NT Dopamine Receptor Antagonist
Where is dopamine effected in the brain? Substantia Nigra Ventral Tegmental Area - mesolimbic and mesocortical pathway (tubular infundibular tract) - pleasure center of brain
What is the principle of antipsychotic drugs? reduce activity of dopamine neurons from VTA to accumbens and frontal cortex
Antipsychotic drugs antagonist of what other receptors? muscarinic, alpha-adrenergic, H1 histaminic, 5HT2 serotonergic, dopaminergic
What cell are neurogenesis? pluripotent cells in hippocampus
What is the dopamine receptor affinity for Phenothiazines? binds D2 and D1 strongly Chlorpromazine Thioridazine Fluphenazine
What is the dopamine receptor affinity for Typical Non-phenothiazine? binds D2 and D1 strongly Chloprothixine Haloperidol
What is the dopamine receptor affinity for Atypical Non-phenothiazine? Binds D3 and D4 strongly Clozapine Sertindole Risperidone
Where are the Dopamine receptor D1 and D2 localized? Caudate and Putamen
Where are the Dopamine receptor D3 and D4 localized? accumbens amygdala cortex
Which drugs has the greatest anti-muscurinic potency? Thioridizine
Wgich drugs has the least anti-muscurinic potency? Haloperidole
What are the advantages of atypical non-phenothiazines? no extrapyramidal morot side effects no tardive dyskinesia lack of action in motor function - unique receptor binding
What is tardive dyskinesia? abnormal involuntary movements of face and head. 50% irreversible.
What is the adverse effect of Anti-psychotic drugs in chronic treatment? endocrine imbalance - blockage of dopamine ->increase prolactin extrapyramidal motor side effects - parkinson akathesia-hyperactivity tardive dyskinesia
What is the adverse effect of Anti-psychotic drugs in acute treatment? anti-muscarinic effects anti-adrenergic effect anti-histamine effect neuroleptic malignant syndrome
What are the anti-muscarinic effects? dry eyes, mouth, skin blurred vision tachycardia urinary retention and constipation
What are the anti-adrenergic effects? orthostatic hypotension
What drug resembles serotonin structurally? Indolealkylamines = LSD = Psilocybin = DMT = DET
What drug resembles norepinephrine structurally? Phenylethylamines = mescaline (natural, peyote cactus) = dimethoxymethylamphetamine (synthetic DOM, STP)
What is the primary mechanism of LSD? stimulation of serotonin 5HT2a receptors (raphe nuclei)-> hyperpolarization
What is the result of stimulating 5HT2a receptors? binding of G protein cascade increase PI turnover -> activation of protein kinase C and activate K+ channels -> K+ OUT = hyperpolarization
What are the somatic effects? sympathetic nervous system pupillary dilation tachycardia, hypertension hyperreflexia and tremor nausea. GI cramping hyperthermia, piloerection
What is the adverse effects of LSD? bad trip flashbacks
What is the adverse effects of MDMA (ecstacy)? serotonin neurotoxicity maybe dopamine
What is the adverse effects of GHB? vomiting, seizures, unconcsciousness, coma, dependency and withdrawal
Created by: prinny916
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