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Pharm Exam #2
Concepts and Definitions
| Question | Answer |
|---|---|
| LSD | Hallucinations, Psychedelic |
| Morphine | Euphoria, Relaxation |
| Amphetamines | "Upper", excitement |
| Inhalants | General high, unknown mechanism |
| GHB | Enhanced sensory perception, social closeness |
| What sites do we target in using anti-seizure medications? What are we trying to accomplish? | Anti-seizure medication targets ion channels and neurotransmitters to restore balance between excitation and inhibition in the brain |
| How does a general anesthetic work? Discuss. | General anesthetics act by depressing the CNS to produce a reversible loss of consciousness, sensation, and reflexes. They reduce neuronal excitability throughout the brain |
| What is the mechanism of action for local anesthetics? Why might active tissue be anesthetized before inactive tissue? | Local anesthetics block Na+ channels to stop nerve signals. They work faster in active tissue because those nerves have more open channels for the drug to bind to. |
| What is considered the "standard treatment" for Parkinson's? How does it work? Why does this seem to work? | Standard treatment is Levodopa + Carbidopa. It restores dopamine levels in the brain to help reduce tremors and stiffness caused by dopamine loss due to Parkinson's. |
| What is the role of Ropinirole in changing a patients behavior of addiction and potentially why a switch to Selegiline helped to get rid of both motor symptoms and addictions? | Ropinirole stimulates dopamine receptors in the mesolimbic pathway relieving symptoms but activating addiction drive. Selegiline works at MAO-B enzyme site in substantia nigra to increase dopamine to restore movement and reduce addictive behaviors. |
| Devise a potential site in the brain, three types of receptors you might focus on, and how these would possibly be able to stop his addiction (think about the nucleus accumbens and VTA in your answer). | Targeting D2 receptors balances dopamine reward signals , GABA-B strengthens natural inhibition of dopamine firing , NMDA helps to weaken drug-related memory . All together they help to break the addiction in the VTA-nucleus accumbens. |
| What are extrapyramidal side effects? What drugs cause them? Why? | Involuntary movements caused by Dopamine D2 receptor blockers in the nigrostriatal pathway , often from antipsychotics. |
| What are 5 things you studied for but were not asked about on the exam? | - Anti-Epileptics Drugs - The stages of General Anesthesia - Neurotropic Hypothesis of Depression - Hallucinogens - Addiction Pathways |
| Why does it take several weeks for antidepressants to work, even though they increase serotonin levels immediately? | The brain must adapt to sustained increases in serotonin. |
| Why can drugs that treat psychosis also cause movement disorders? | Antipsychotics block D2 receptors to reduce excess dopamine activity linked to psychosis. This same blockade disrupts motor control. |
| Why is L-DOPA given with Carbidopa instead of by itself? | Carbidopa prevents L-DOPA from converting to dopamine outside the brain, allowing more L-DOPA to cross the BBB. |
| Why are dopamine D₂ receptors important in addiction? | They control reward and motivation in the mesolimbic pathway. Addictive drugs overstimulate these receptors producing euphoria and reinforcing drug use. |
Created by:
beccaalvarado5
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