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Neuropharm Concepts
All Concepts
| Question | Answer |
|---|---|
| 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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