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Pharmacological Principles MCQ’s explained1. What is the half life of a drug given: clearance = 8.4L/min; weight = 70kg; Vd = 5L/kg?a. 24 hrb. 12 hrc. 30+ hrd. ?e. ? t1/2 = 0.7 x Vd (in L/70kg) / CL (L/h/70kg)…. mL/min -> L/h/70kg by dividing by 16.6 thus 8.4L/min = 8400ml/min = 506L/h/70kg. t1/2 = 0.7 x (5 x 70) / 506 = approx 30mins. This clearance seems very high (hydralazine has the highest clearance on the table at 234L/h/70kg)2. With regard to a drug:a. LD50 is 50% of the dose necessary to kill experimental animalsb. Efficacy is the maximum response produced by a drug <- true, “In pharmacology, efficacy refers to the maximum response achievable from a drug. It is often described by the parameter Emax.”c. Spare receptors are present if Kc50 is the same as EC50 – if EC50 < Kdd. Potency is the same as affinitye. TD50 is the concentration of a drug necessary to produce toxic effects 50% of the time -is borderline/ambiguous, the correct definition would be “to produce toxic effects in 50% of the subjects receiving it” – 50% of the time could apply to individuals3. Half lifea. May not be a good indication of clearanceb. Does not increase with agec. Is not dependent on Vdd. ?e. ?4. 2mL of 0.5% wv is equal toa. 1mgb. 10mg – 0.1% = 1:1000 = 1mg/ml, so 0.5% = 5mg x 2 ml = 10mgc. 100mgd. 20mge. ?5. What is an example of a phase II biotransformation?a. Oxidation – phase Ib. Reduction – phase I, also hydrolysisc. Glycolysis - glyclolysis is not a phase II reaction, it is a 10 step reaction glucose -> pyruvate. The phase II rections are glucuronidation, acetylation, glutathione conjugation, glycine conjugation, sulfation, methylation, water conjugationd. ?e. ?6. Regarding enzyme inductiona. It is irreversibleb. It takes 4 months to developc. Causes increase in smooth endoplasmic reticulum <= correct ?steroidd. Causes increase in rough endoplasmic reticulume. ?7. Clearancea. Is proportional to liver blood flowb. ?c. ?d. ?e. ?8. Regarding pharmacokinetics and pharmacodynamicsa. Diffusion is inversely proportionate to surface area and directly proportionate to thickness – Fick’s law of diffusion: Flux = (C1-C2) x area x permeability coef. / thickness, i.e the opposieb. The LD50 is 50% of the dose that kills most peoplec. The LD50 is 50% of the dose at which toxicity occursd. Efficacy is the maximum response produced by a drug <= correcte. ?9. Regarding bioavailabilitya. PR drugs have no first pass – assume 50%b. Transdermal drugs have first pass – possible, they don’t have hepatic first pass, bioavailabilty = 80-100%c. IV drugs undergo first pass – bioavailability by definition = 100%d. ?e. ?10. Volume of distributiona. Is inversely proportional to clearance – CL = elimination/Conc, CL = Vd x kel (elimination rate constant), or CL = t1/2 x Vd / 0.7, thus it is proportionalb. Is measured in mg/L – is in L/70kgc. Is used to work out the maintenance dose – maintenance dose = dosing rate/F (bioavailability) x dosing interval, dosing rate = rate of elimination (to reach steady state) = CL x target conc. The loading dose is related to the Vd: Loading dose = Vd x target concentrationd. Is high in warfarin - lowe. Is proportional to half life - correct11. 5mL of 2% wv is equal to:a. 10mgb. 100mg 0.1% = 1:1000 = 1mg/mL, thus 2% = 20mg x 5mL = 100mgc. 200mgd. 20mge. 40mg12. Volume of distributiona. Is calculated by dividing the amount of drug by its clearance – Vd = amount of drug/blood or plasma concentrationb. If high suggests homogeneous distribution through tissues – cannot determine exactly where or how the drug is distributed, just the ratio of intravascular to extravascular.c. If low suggests homogeneous distribution through tissuesd. Of aspirin is greater than that of pethidine – aspirin is low (12), pethidine high (280)e. Of midazolam is greater than that of warfarin – correct, warfarin ~ 10L/70kg, midaz = 77L/70kg13. The volume of distributiona. Is less than 70L for fluoxetine – is 2,500L/70kg (which is 35L/kg… question is likely missing units)b. Is calculated by dividing rate of elimination by concentrarion – this is CLc. Is inversely proportional to half life – is proportional tod. Is about 5L/kg for pethidine – true, pethidine has a high Vd, and is listed as 4L/kge. Is affected by the route of drug administration – no, bioavailability is14. By limiting liver blood flow, cardiac disease might inhibit the metabolism of all of the following EXCEPT:a. Verapamilb. Labetalolc. Propoxyphened. Lignocainee. Trimethoprim <= 100% bioavailabilty… other drugs with 100% bioavailability are: chlordiazepoxide, diazepam, lithium, phenobarbital, salicylic acid, sulfamethoxazole, valproic acid15. The bioavailability of a druga. Must be 100% if given by inhalation – no lungs can metaboliseb. Is typically about 75% for IV administration – 100% by definitionc. Is high if the drug is hydrophilic – no, a balance between hydrophilic/lipophlic needed.d. Is equal to 1- the extraction ratio – close, it is = F x (1-ER) where F is the extent of absorption, so this is correct if the absorption is 100% (e.g. morphine 100% absorbed, ER = 0.67, ~33% bioavailable – actually listed as 24%)e. Is 70% for orally administered digoxin <= correct16. For a specific effect, drug A is more potent than drug B. It follows that:a. Drug B is a partial agonist acting at the same receptor as drug Ab. Drug A causes a greater maximal effect than drug Bc. When present in identical concentrations, drug A causes a greater effect than drug Bd. Drug A has a lower ED50 than drug B <= this is the definition of potencye. Drug B will have a steeper dose response curve than drug A17. The volume of distribution of a drug:a. Relates its dose to its clearance – incorrect, no relationshipb. Is not an apparent volume – it isc. If high, implies greater concentration of drug in extravascular tissue <= true d. If high, implies greater plasma protein binding of the drug - lowere. If high, implies easier clearance of the drug by haemodialysis in overdose – no harder, less in intravascular compartment18. Regarding receptors, the following statements are true EXCEPT:a. Most are proteinsb. They largely determine quantitative relations between dose of a drug and pharmacologic effectc. They are responsible for selectivity of a drug reactiond. Mediate actions of pharmacologic antagonistse. Spare receptors produce effect without the need for a drug <= incorrect, agonisism still required, just more sensitive19. Regarding elimination kinetics, which statement is INCORRECT?a. In first-order kinetics, the rate of elimination is directly proportional to drug concentration - trueb. Ethanol displays dose-dependent kinetics <= no, zero-order (aspirin also)c. In zero-order kinetics, the rate of elimination is constant - trued. Most drugs display first-order kinetics - truee. Phenytoin can display zero-order kinetics – true, usually does20. For a drug that is present in a concentration 4 times its EC50a. The time course of effect is linear, initially – true, from 1/4-4x EC50b. The time course of effect will follow the exponential decline in concentration – if 1/4th EC50c. Toxicity can be expected – can’t inferd. All of the above may be true depending on the drug – not b…e. Toxicity would not be expected – can’t infer21. All of the following statements about spare receptors are correct EXCEPT:a. Spare receptors are identical, in the absence of drug, to non spare receptorsb. Spare receptors do not bind drug when the maximal drug effect occurs – they bind the drug beyond this point, ambiguous… especially since the concept of spareness is just that – a conceptc. Spare receptors influence the sensitivity of the receptor system to the drug - trued. Spare receptors activate the effector machinery of the cell without the need for a drug – not true, need agoniste. Spare receptors may be detected by finding that the EC50 is less than the Kd for the agonist - true22. Which of the following drug metabolising systems has been shown to differ in populations in genetically pre-determined ways?a. Reductionsb. Acetylations of amines – isoniazid -> peripheral neuropathy, also oxidation (codeine -> reduced analgesia, EtOH -> toxicity, nortriptyline -> toxicity, s-warfarin -> bleeding), ester hydrolysis (succinylcholine -> prolonged apnea), o-demethylation (omeprazole -> increased efficacy)c. Methylationd. Glucuronidatione. Sulfate conjugation23. Regarding receptor actiona. High concentrations of an agonist can never surmount a competitive antagonist – incorrect, they compete..b. Partial agonists do not occupy all receptor sites – do not bind c. EC50 refers to the clinical effect at 50% of the maximal dose – no, the dose to achieve 50% Emaxd. Second messengers explain “spare receptors” – they do, providing non-linear or temporally increased relationshipse. B-blockers and adrenaline exhibit physiological antagonism – incorrect, this is pharmacologic antagonism – they compete for the same receptor. Physiologic antagonism is where drugs act on different receptors to stimulate different endogenous regulatory pathways with opposing effects – more difficult to control (e.g. glucocorticoids vs. insulin) and with chemical antagonism the antagonist will react directly with the drug (protamine +ve change binds to heparin –ve charge to counteract)24. Half-lifea. Is inversely proportional to Vd (volume of distribution) – directly proportional tob. Is the time required to attain 50% of steady-state concentration - truec. Is directly proportional to clearance – inversely proportionald. Is decreased in renal failure - increasede. Is decreased in hepatic failure - increased25. Regarding bioavailabilitya. Rectal administration has the same first-pass effect as oral – no, more like 50% lessb. Transdermal is up to 90% - up to 100%c. IV administration is between 95 and 100% - by definition 100%d. Is reduced in digoxin when given orally because of bacterial metabolism – it is, and ABx that kill the bacteria may increase the bioavailabiltye. Can be calculated by the extence of absorption (f) multiplied by the extraction ratio (ER) – by 1-ER26. Regarding biotransformationa. Phase I reactions lead to increased polarity for excretion by the liver – excretion by kidneysb. Phase I reactions occur solely in the liver – primarily in liver, but also GI, brain, lung, kidneys, skinc. Phase I reactions must undergo phase II reactions in order to be renally excretedd. Hydroxylation and deamination are examples of phase I reactions – other examples are: oxidations, epoxidation, dealkylation, desulfuration, reductions, hydrolysese. Rarely leads to toxic metabolites – can do27. The potency of a druga. Refers to the concentration needed to produce maximal effects – half maximalb. Depends on the efficiency of drug-receptor interaction – it doesc. Is the limit of the dose-response relation- Emax is efficacyd. Determines clinical efficacy – no efficacy doese. Determines its toxic side-effects - unrelated28. The volume of distributiona. Is proportionately related to the concentration of drug in the bodyb. Is high for those drugs retained in the vascular compartmentc. Is a measure of the apparent space available in the body to contain a drugd. For chloroquine is much smaller than that of digoxine. None of the above29. Phase II reactions in metabolic biotransformation include all of the following EXCEPT:a. Water conjugationb. Cytochrome P-450 dependent oxidations – Phase Ic. Acetylationd. Methylatione. Glucuronidation30. An example of a drug receptor includes:a. Leukotriene-B (LTB)b. Tubulin (colchicine binds to tubulin, inhibits microtubule formation arresting neutrophil activity and decreasing inflammation)c. Arachinodic acidd. Fibronectine. Tumour necrosis factor -131. The volume of distribution of a druga. Related the amount of a drug in the body to its plasma concentration – correctVd = amount in body/conc in blood or plasmab. Is large for a drug extensively bound to plasma proteins - lowc. Is large for aspirin – low, 11L/70kgd. Never exceeds 42 litres – it cane. Is not affected by albumin concentration – it will be by drugs that are protein bound32. Receptor antagonists (i.e. pharmacologic)a. Prevent agonists from binding to antagonists – to receptorsb. Progressively inhibit agonist response to decreasing concentrations of antagonist – to increasing concentrations of antagonistc. Cannot be negated at high doses of agonists – they can if competitived. Bind to the receptor and activate it – have affinity but no efficacye. Inhibit receptors to a degree proportionate to antagonist concentration - true33. Regarding second messengersa. cAMP has no role in calcium homeostasis – it doesb. cAMP exerts most of its effects by stimulating cAMP-dependent protein kinases – it doesc. inhibition of adenylyl cyclase results in increased cAMPd. phospholipase C is situated in the cell nucleus – membrane enzymee. phospholipase C catalyses IP3 into PIP2 and DAG – no PLC splits PIP2 -> IP3 and DAG34. The volume of distribution of a drug:a. Relates the amount of a drug in the body to its plasma concentrationb. Is large for a drug extensively bound to plasma proteinsc. Is large for aspirind. Never exceeds 42 litrese. Is not affected by albumin concentration35. Type I biotransformation reactions include:a. Methylationb. Acetylationc. Oxidation – phase Id. Glucuronidatione. Sulphonation ................
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