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2550 Advanced Life Sciences Final Exam Review.docx

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NURS 2550H
Ellen Buck- Mc Fadyen

2550 Advanced Life Sciences Final Exam Review Pharmacodynamics - Principles of drug action Teratogenesis: o Drug interacts with receptor -> bind to receptor -> response A – remote risk o Drug alters physiological response B – slightly more risk o Drug always has more than one effect C – more risk - Drugs bind to receptors instead of natural ligand D – proven risk o Mimic neurotransmitter, trick the body into allowing the drug to bind X - CONTRAINDICATION - D (drug) R(receptor)D – R Complex  Response - Receptor function is normally regulated by molecules supplied by the body - A drug cannot make the body do something new, only help the body to help itself 1. Cell membrane-embedded enzymes - Fast-acting (ex. Insulin) - increase catalytic activity 2. Ligand-gated ion channels - Concentration gradient (ex. Acetylcholine) - span cell membrane 3. G protein-coupled receptor systems (ex. NE, serotonin, histamine); binding of endogenous ligand or antagonistic drug activates receptors -> G protein -> effector 4. Transcription factors (ex. Steroids) - regulate protein synthesis - Very slow acting, delayed response (hrs -> days) Lock-and-key: If a drug interacts with one type of receptor and that receptor type regulates Lock = receptor only a few processes, the effects of the drug are relatively selective. Non- - Key = drug selective drugs either interact with multiple receptors or one receptor type that - Affinity = fit regulates multiple processes. Selectivity doesn’t guarantee safety. The more - Intrinsic activity = open selective the drug, the more desirable (min. side effects). Receptors are dynamic: With long-term use of drugs the number and sensitivity of receptors can increase/decrease. Dose-response relationship - Increase dose = increase response Three phases: o Bind more receptors 1. Low doses – doesn’t elicit measurable response o Max efficacy 2. Increase dose, increased response (graded) o Allows comparison between medications 3. Increased dose doesn’t increase response Types of Drug-Drug Interactions Pharmacological Non-pharmacological - Based on drug-response interaction - Not predictable - Predictable (side effects, dependence) Alters Blood Level of Drug – Pharmacokinetics Alters Effect of Drug Alters absorption – increases or decreases time/speed of drug Additive – final effect = sum of two drugs - ex. Ion trapping/partitioning – antacid = change pH Potentiative – effect of 1 drug increased by Alters distribution – competing for same receptor another Alters metabolism – ex. Enzymes, inducers Synergistic – final effect > sum of effects nd Alters excretion – change in cardiac output = GFR Antagonistic – 1 drug blocks effect of 2 drug Central Nervous System Pharmacology Neurotransmitters of the CNS All sedatives/hypnotics effect inhibitory neurotransmitter – GABA - Inhibitory (ex. GABA) by either mimicking GABA as an agonist or increasing effect of GABA. - Excitatory (ex. Norepinephrine) - Both (ex. Acetylcholine) ADHD - 3 Types: inattentive, hyperactive-impulsive, combination - Frontal cortex, basal ganglia, brainstem, cerebellum - Neurotransmitters – dopamine, norepinephrine, serotonin - Methylphenidate (Ritalin) – similar to amphetamines o Increases release and prevents re-uptake of NE and dopamine Pharmacotherapy of Depression - SSRI’s - Kinetics o Active metabolite o Long half life o Highly bound to plasma proteins - Effects of fluxoxetine o Immediate – increases 5-HT (serotonin) levels at synapses o 1 month – receptor changes; restore balance of 5-HT and R (receptors) - Adverse effects – decreased sensitivity of serotonin receptors over time Opioids Therapy to Manage Pain - Excitatory neurotransmitters of pain - Opioid analgesics o ex. Substance P, glutamate - decrease neurotransmitter, interfere with substance P - Primary afferent nerve fibers - NSAIDS – decrease prostaglandins o C fibers – Unmyelinated o A-delta fibers – myelinated - Pentazazine Advantages: o Narcotic agonist-antagonists - decreased respiratory depression o If given to someone with opioid dependence - decreased dependence (full agonist), would provide withdrawal symptoms - decreased euphoria o Agonist at kappa Disadvantages: o Antagonist at mu - Increased sedation o Analgesic without respiratory depression - Increased dysphoria - 10% of codeine is converted to morphine in liver - Increased cardiac work o lacking CYP206 -> ineffective o multiple copies CYP206 -> ineffective Benzodiazepine Pharmacology Mechanism - Enhance actions of GABA (inhibitory neurotransmitter); no GABA, no effect - GABA binds at receptor-chloride channel complex o Cl channel opens -> Cl influx - BDZ binds to another site on receptor o Increase frequency of channel opening, increases Cl influx and inhibiting action potential - - When Cl flows into cell, hyperpolarizes, decreases ability to fire (inhibitory) Adverse effects Antagonist - Anterograde amnesia - Flumazenil - Some cross-tolerance with other depressants - May reverse sedative but not respiratory depression Contraindications - Pregnancy (category D) - Lactation – breastmilk - Fetal malformations Over-the-Counter Pain Medications One central mechanism: inhibition of cyclooxygenase (COX), enzyme, responsible for synthesis of prostanoids. Synthesis of PG Aspirin (ASA) Injury - Metabolism: short half-life, converted to active metabolite salicylic acid Arachidonic Acid - Distribution: 80-90% bound to albumin; 10-20% can (released from lipid bilayer) cross the BBB -> enter placenta, breastmilk, etc. - low albumin=toxic effects of drug (elderly, Cyclo-oxygenase (COX) malnourished) Leukotrienes (converts acid to PG) - competition for binding sites -inflammation - Salicylism – overdose (tinnitus, sweating, dizzy) -allergic reactions Prostaglandins - acid-base disturbance -smooth muscle contraction (TXA2, PGI2, PGE2) - Hypersensitivity resembles anaphylaxis - D-D interactions: ACE inhibitors/ARB’s – kidney func Ibuprofen - Contraindications: pregnancy – Cat. C, D in 3 trimest. - COX1 and COX2 inhibitor - risk of bleeding in delivery - Reversi
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