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Pharm Exam #1
Concepts and Definitions
| Question | Answer |
|---|---|
| Compare Pharmacokinetics to Pharmacodynamics. | Pharmacokinetics: What the body does to the drug (movement of drugs through the body) Pharmacodynamics: What the drug does to the body (the effects of the drug at its site of action) |
| How do we get a drug discovery? | Identifying a new target / modifying existing molecule , testing them for efficacy selectively and toxicity then moving onto clinical trials |
| How do we get drug approval? | Requires preclinical testing then clinical trial testing |
| Role of post-market surveillance. *Vioxx example | Post-market surveillance monitors drugs after approval for defects, long-term side effects, that were not found in the trials *Vioxx was withdrawn due to double the risks for heart attacks in the long run. |
| What is an off-label usage? | When an FDA-approved drug is prescribes for a condition or purpose other than the one originally approved for |
| Compare prescription meds to OTC. | Prescription Meds: require a Doctors approval due to more specific condition treatment Over The Counter: considered safer |
| Types of receptors. | - Ion channels - Protein tyrosine kinase - Cytokine receptors - G protein coupled receptors - Steroid receptors |
| How receptors “couple” to intracellular events: - Ion channels - Protein tyrosine kinase - Cytokine receptors - G protein coupled receptors - Steroid receptors | IC- opening or closing channels to change ion flow PTK- auto-phosphorylate CR- recruit kinase to trigger similar pathways GPCR- activate second messengers SR- enter the nucleus to regulate gene transcription |
| What are the properties of an agonist? | Affinity Intrinsic efficacy Receptor to bind too |
| Compare agonists to antagonists. | Agonist- Affinity, intrinsic efficacy Antagonist- Affinity, little to no intrinsic efficacy |
| Types of antagonists. | Competitive Non-Competitive |
| Dose response curves and their various profiles. | Dose increases... response increases to maximal response - sigmoidal curve on a log scale |
| Receptor selectivity | ability of a drug to bind to one type of receptor over others -some may be "promiscuous" causing more toxicity |
| Allosteric sites | Alternative receptor binding sites that alter receptor activity - can enhance or block responses w/o binding to the main site |
| Receptor up-regulation vs. down regulation | Receptor-Down Regulation: fewer receptors , chronic high agonist activation (tolerance) Receptor-Up Regulation: more receptors , reduced activation (supersensitivity) |
| Receptor desensitization *(what is it, compare to down regulation, how does it happen?) | Fast reversible reduction in receptor activity (via phosphorylation) *Down-regulation is slower long-term decrease in receptor number |
| What is the CHF example? | Chronic High Catecholamines cause B-receptor down-regulation, reducing heart responsiveness |
| What is drug tolerance? | Higher doses are required to achieve the same effect, often due to receptor down-regulation, desensitization, or faster drug metabolism |
| What is drug dependence? | Stopping a drug causes withdrawal syndrome |
| What is Supersensitivity? | Reduced activation causes more receptors and heightened response to agonists, making sudden drug withdrawal risky |
| EC50 vs. ED50 | EC50: concentration for half-max response ED50: dose effective in half the population |
| What is meant by absorption, distribution, metabolism, elimination? | Absorption: Drug enters the bloodstream Distribution: Spreads through the body's fluids and tissue Metabolism: The body chemically changes the drug (in liver) Elimination: Drug removed from the body |
| What things impact drug travel in body? | Absorption, Distribution, Metabolism, and Elimination |
| How do drugs cross barriers? | Pharmacokinetics - Absorption, Distribution, Metabolism, and Elimination |
| What role does a drug’s pKa have on membrane crossing? | Determines the proportion of the drug that is ionized versus non-ionized at a given pH - ONLY non-ionized drugs cross the lipid membrane via passive diffusion |
| Enteral vs. parenteral admin? | Enteral: in GI tract Parenteral: non-GI administration |
| What are enteral ways? | Oral Sublingual Buccal Rectal |
| What are advantages and disadvantages of enteral ways? | Advantages: easy faster (bypasses liver), backup route Disadvantages: potent small doses, absorption is unreliable |
| 1st pass effect? | Drug metabolism that occurs before a drug reaches systemic circulation |
| What is bioavailability? | How much drug is available to have an effect (often depending on route of administration) |
| What things impact distribution in the body? | Blood Flow, Capillary Barriers, Protein Binding, Lipid Solubility |
| What is Vd? | Amount administered / Plasma Concentration |
| In general, what does metabolism do to a med? | Changes a drug's chemical structure so that the body can easily use it or eliminate it |
| Where are drugs metabolized and how? | In the liver (ER) Phase I: Oxidation, reduction, deamination, and hydrolysis Phase II: Conjugation |
| Example of acetaminophen and drug metabolism. | Normal dose... safe conjugate Overdose... toxic metabolite builds up |
| Enzyme inhibition and activation. *Plavix and Nexium example. | Inhibition stops pro-drug activation , treatment failure |
| Where are meds eliminated? Excreted? | Urine, Feces, Lungs, Sweat/Saliva, Milk |
| What sorts of things impact rate of drug elimination/half life? | Renal function, Liver metabolism, Vd, Age, Protein binding, Genetics, Disease states |
| What are advantages and disadvantages of short or long half life? | Short half-life: Rapid Adjustment of drug levels, BUT requires frequent dosing Long half-life: Less frequent dosing, BUT takes linger to reach steady state |
| What types of things impact whether a med works for someone? | Renal function, Liver metabolism, Vd, Age, Protein binding, Genetics, Disease states |
| CAMS: what are they? | Complementary and Alternative Medicines |
| CAMS: How are they regulated? | Less strictly regulated than prescription drugs |
| CAMS: What are some things to be careful of? | Drug interactions, Quality, False claims, Delay in treatment, Side effects, Uncertain doses |
| CAMS: Can they impact prescription meds? | Yes. increase/decrease side effects of prescription drug, Alter Metabolism, Risk of toxicity |
| What makes a neurotransmitter excitatory? | If it increases the likelihood that the postsynaptic neuron will fire an action potential |
| What makes a neurotransmitter inhibitory? | If it reduces the likelihood that the postsynaptic neuron will fire an action potential |
| What are sedatives, hypnotics, anxiolytics? | Sedatives: Calm or relax the patient w/o necessarily causing sleep Hypnotics: Induce or maintain sleep (used for insomnia) Anxiolytics: Reduce anxiety (technically a sedative) |
| What receptor is the most common site for sedatives? | GABA-A receptor |
| What receptor is the most common site for hypnotics? | GABA-A receptor |
| What receptor is the most common site for anxiolytics? | GABA-A receptor |
| Which subunit(s) are more related to sedatives? | Alpha-1 |
| Which subunit(s) are more related to anxiolytics? | Alpha-2 and 3 |
| What is different between benzodiazepines? | Duration (short, intermediate, long) , Potency , Clinical Use , Metabolism |
| What are the major side/adverse effects of benzos? | Ataxia , Hangover , Tolerance , Physical and Psychological dependence , Withdrawal Syndrome |
| Competitive antagonist? | Drug that binds to the same receptor site as a natural agonist but does not activate it |
| Where do zaleplon and eszoplicone act? | GABA-A receptor |
| Where are zaleplon and eszoplicone used for? | the "Z-drug" , used for insomnia |
| What are barbiturates used for? | Sedation , Hypnosis , Seizure control , Anesthesia induction |
| Compare long, short, and ultra short term usages of barbiturates. | Long: Maintain anticonvulsant levels Short: Used for insomnia Ultra-Short: Very rapid onset |
| Problems and side effects of barbiturates? | Dependence and Toxicity , Alteration of liver metabolism , Hangover effect , Tolerance |
| Ramelteon uses. | Sleep |
| Advantages of buspirone over other anxiolytics? Disadvantages? | Takes 1-2 weeks , non addictive |
| When are beta blockers used for anxiety? | Situational or performance anxiety |
| Types of depression? Which do antidepressants work for? | Reactive , Major Depression* |
| Types of antidepressants? Main side effects? | SSIR's (nausea, headaches insomnia) , SNRI's (increased BP) , TCA's (Sedation, dry mouth, hypotension) |
| What is meant by anti-cholinergics effects? | Caused by blocking Acetylcholine at muscarinic receptors |
| Advantages of heterocyclics vs tricyclics? | Fewer anticholinergic side effects , less sedation |
| Why MAO inhibitors? How do they work? | Block mono-amine oxidase to increase amine levels |
Created by:
beccaalvarado5
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