Pharmacology cheat sheet PDF

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Pharmacology 1 cheat sheet for online proctored exam...

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Agonist: elicits a biological effect when it interacts with receptorspossess affinity and intrinsic/efficacy Antagonist: drug which interacts with receptor but does not elicit a biological effect and blocks/reverse effect of agonist – affinity, no efficacy Competitive: competes for binding site/receptor site Reversible competitive: emax reached by giving more drug, antagonist, same emax, ED50 shift right e.g. muscarinic Irreversible competitive: absence of dissociation of agonist, same ED50,Emax,cant be reversed by adding more of drug e.g. neurotoxins Non-competitive: bind elsewhere, ion channel/G protein linked e.g. suxamethonium, ED50 shifts right, Emax Therapeutic index= LD50/ED50 (relative margin of safety of drug) Dose-response relationship: Potency: Inherent ability of drug to combine with receptors- depends on drug affinity  Slope: relationship between change in dose and change in effect Maximal effect (Emax): where graph plateaus Efficacy :maximal possible effect which can be produced by drug pH partitioning: if not ionised in gut passes through systems, alkalisation of urine  rate of excretion of weak acids, acidification of urine  increased rate of excretion of weak bases -

acids: pKa-pH = log( [non-ionised]/[ionised] ) bases: pKa-pH= log ( [ionised]/[non-ionised] )

Difficulties with oral route: First-pass metabolism: drugs absorbed in stomach + SI  drug passes through liver before being distributed around the body

Sublingual: under the tongue, rapid absorption, avoids gastric pH and first-pass metabolism Intravenous: precise, immediate, limitations include greater risk of adverse effects, large volumes IM and subcutaneous injection: prompt absorption but slow and sustained, self-admin e.g. insulin, not suitable for large volumes Rectal: local or systemic effect, good for drugs affecting bowel e.g. laxatives Spinal: local anaesthetics/opioids for pain controls Topical: mucosal membranes, dermal, no first pass, for potent and lipophilic drugs Plasma proteins: As free fraction becomes larger, binding becomes less important, Binding proteins become saturated so there is a largein free drug, Extensive PP binding can result in greater rises in Cp following small in dose, E.g. Phenylbutazone displaces and inhibits warfarin metabolism internal bleeding Drug reservoirs: thiopentone in fat, tetracycline in bone Volume of distribution= Q(quantity of drug in mg/g in body) / Cp (concentration in plasma) – important as not all drugs distribute equally through all body fluids = Q/Cp Loading dose= Target concentration x Vd (volume of distribution) Assumptions: drug must be instantaneously distributed and no metabolism should have occurred, no portion of the drug should have been excreted, no portion of the drug should have been sequestered Drug metabolism: Phase 1: predominate, oxidation, reduction and hydrolysis, catabolic functions, generate functional/ reactive group. Phase 2: conjugation with hydrophobic groups, anabolic reactions, usually results in inactive compounds. Prodrugs: bioactivation of prodrug (inactive) to active metabolite Codeine: Absorbed from GI tract produces peak plasma conc  metabolised by O- and N-demethylation in liver  morphine  metabolised by CYP450  codeine + metabolites excreted by kidney Renal excretion: drugs filtered across glomerulus drugs secreted at proximal tubule remain in tubule unless they are lipid soluble and can be re-absorbed into blood - Key function of metabolism is to make drug less lipid soluble - OAT secrete weak acids, OCT secrete weak bases into renal tubule more rapidly excreted Biliary excretion: any unabsorbed orally drugs are excreted via faeces, low MW drugs are poorly excreted in bile, bile acids allow absorption of fats delivered to duodenum and reabsorbed in ileum portal vein delivers bile to hepatocytes which extract it Enterohepatic recirculation: B-glucuronidase from gut microflora removes glucuronide, reforming original drug that can then re-enter hepatic circulation- prolongs duration of action of affected drug, important for morphine, aspirin etc. Factors affecting drug excretion: high degree of ionisation and water solubility, non-ionised/lipid soluble substances are reabsorbed and therefore not excreted, no reabsorption=excretion Drug clearance (CL)= volume of plasma cleared of drug per unit time (L/hr) – determine

- Rate of drug elimination (mg/hr) = Cp (mg/L) x CL Renal clearance= CLfiltration + CLsecretion – CLreabsorption Elimination= excretion + metabolism (single compartment) Initial plasma concentration (Co)= Q/Vd Rate of decay= Co exp (-CL/Vd) t Repeated dosing: if dosing interval...