Semester 2 Pharmacology

18 Questions

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Pharmacology Quizzes & Trivia

Questions and Answers
  • 1. 
    What are the side effects of B2-adrenoceptor agonists?
    • A. 

      Fine skeletal muscle tremor, tachycardia, arrhythmia, hypokalaemia, headache

    • B. 

      ? Dry mouth, nausea, constipation, headache, urinary retention in men with prostatism (tiotropium), exacerbation of angle-closure glaucoma

    • C. 

      ? GI upset, CNS stimulation, hypotension, arrhythmia, hypokalaemia, interaction with CYP1A2 inhibitors

  • 2. 
    What are the short-term effects of corticosteroid treatment in asthma?
    • A. 

      Mast cell stabilisation, sensory C-fibre inhibition, inhibition of eosinophil accumulation in lungs, decreases IgE

    • B. 

      Decreased T-cell cytokine production, decreased dendritic cell signalling, decreased eosinophil/mast cell deposition in bronchial mucosa, suppression of epithelial shedding/goblet cell hyperplasia

    • C. 

      Decreased inflammatory cell activation, decreased mucosal oedema, decreased local generation of prostaglandins and leukotrienes, upregulation of B2-adrenoceptors and improved adenyl cyclase coupling, increased activity of M2 receptors

  • 3. 
    Which antibacterials disrupt the bacterial cell wall and how?
    • A. 

      Quinolones (ciprofloxacin), metronidazole, nitrofurantoin

    • B. 

      B-lactams (penicillin, cephalosporins, monobactams, carbapenam), glycopeptides (vancomycin), lipopeptides (daptomycin)

    • C. 

      Macrolides (erythromycin), aminoglycosides (gentamicin), tetracyclines, chloramphenicol, lincosamides, fusidic acid, oxazolidinones,

    • D. 

      Sulfonamides

  • 4. 
    What is the mechanism of action of diuretics in antihypertensive treatment
    • A. 

      Act at presynaptic autoreceptors in nucleus of tractus solitarius to stimulate RVLM (reduce sympathetic outflow) and increase vagal outflow

    • B. 

      Increases activity in rostral ventrolateral medulla (RVLM) which leads to decreased sympathetic outflow, which causes a decrease in vasoconstriction, heart rate and myocardial contractility

    • C. 

      Direct arterial dilation by reduced Ca2+ entry to smooth muscle cells due to intracellular Na+ depletion

  • 5. 
    What are the side-effects of diuretics?
    • A. 

      Postural hypotension, lethargy, headache, dizziness, nausea, rhinitis, urinary frequency/incontinence, palpitation

    • B. 

      ? Dilutional hyponatraemia, hypokalaemia (not spironolactone), hypomagnesaemia, hyperuricaemia, incontinence, ototoxicity, vertigo, impotence, nocturia, hyperlipidaemia, hyperkalaemia (spironolactone), GI upset, antiandrogenic (spironolactone)

    • C. 

      Acute heart failure with pre-existing poor left ventricular function, Raynaud’s phenomenon, excessive bradycardia with heart block, bronchospasm, hypoglycaemia with diabetes, raised lipid levels, sleep disturbance, vivid dreams, hallucinations, withdrawal syndrome, interactions with calcium channel blockers

  • 6. 
    What is the mechanism of action of bupropion in smoking cessation?
    • A. 

      Weak inhibitor of neuronal reuptake of noradrenaline and dopamine thus enhancing mesolimbic and dopaminergic activity, started 1-2 weeks before a quit date, makes quitter less likely to gain weight.

    • B. 

      Partial agonist at nicotine receptors, highly selective for CNS subtype involved in addiction, blocks the effect of added nicotine, started 1-2 weeks before a quit date

    • C. 

      Maintains plasma nicotine levels above those at which withdrawal symptoms occur

  • 7. 
    What is the mechanism of action of opioid analgesics?
    • A. 

      Depressing rate of PGE2 formation in hypothalamus in response to circulating IL-1

    • B. 

      ? Inhibit production of prostaglandins by COX-1/-2 isoenzymes (prostaglandins increase ability of thermal, mechanical and chemical stimuli to generate action potentials in nociceptive neurons) reduce sensitivity of nociceptive neurons to bradykinin and substance P (released by damaged tissue)

    • C. 

      Inhibition of GABA neurons which normally inhibit serotonergic neurons which connect to presynaptic afferent nociceptive fibres in the dorsal horn of the spinal cord and prevent release of pain initiating substance P, glutamate and nitric oxide from the nociceptive neuron

  • 8. 
    What are the side-effects of heparins? 
    • A. 

      Haemorrhage (greater in elderly/alcohol intake, reversed by IV protamine sulphate (less effective against LMWH), osteoporosis (unfractionated binds to osteoblasts), thrombocytopenia (2% 5-15 days after due to antibodies against heparin-platelet factor 4 complex), hyperkalaemia ( 7 days after due to inhibition of aldosterone secretion)

    • B. 

      Haemorrhage, thrombocytopenia, oedema, GI upset

    • C. 

      Haemorrhage, fever, hypersensitivity reactions

  • 9. 
    What is the mechanism of action of warfarin? 
    • A. 

      Bind to substrate binding site and catalytic site on thrombin and so inactivate circulating and clot-bound thrombin, used when heparins have induced thrombocytopenia

    • B. 

      LMWH: forms complex with antithrombin III, inactivates factor Xa (4x more potent than unfractionated), promotes tissue factor pathway inhibitor release from vascular wall (inhibits Xa formation), activation of lipoprotein lipase (decrease platelet adhesiveness), unfractionated: binds to platelet factor 4, inhibits platelet aggregation, conformationally alters antithrombin III then forms complex, inactivates thrombin, factors IXa, Xa, XIa, XIIa,

    • C. 

      Inhibits hepatic vitamin K epoxide reductase (converts vit K to active form) vitamin K used to synthesise factors II, VII, IX and X

  • 10. 
    Which drugs will increase the effect of warfarin
    • A. 

      Broad spec antibiotics, amiodarone, cimetidine (CYP2C9 inhibitors), ibuprofen

    • B. 

      Phenobarbital, alcohol

    • C. 

      Phenytoin

  • 11. 
    What INR is indicated for mechanical replacement valve?
    • A. 

      0.9-1.3

    • B. 

      3.5-4

    • C. 

      2-2.5

  • 12. 
    What is the mechanism of action of tirofiban/abciximab?
    • A. 

      Irreversibly inhibits COX-1 and so prevents the synthesis of the platelet aggregating agent thromboxane A2 by platelets throughout their lifespan

    • B. 

      Bind to GPIIb/IIIa receptors and block binding of fibrinogen thus reducing platelet aggregation

    • C. 

      Irreversibly bind to purinergic ADP receptors on platelet surface, reduces mobilisation of Ca2+ from intracellular stores and reduces expression of GPIIb/IIIa receptors

  • 13. 
    What is the best description of the different advantages/disadvantages of different fibrinolytics?
    • A. 

      Haemorrhage less common with streptokinase, tenecteplase binds longest and is least sensitive to inhibitors

    • B. 

      Alteplase can cause allergic reaction, hypotension is less common with streptokinase

    • C. 

      Reteplase is derived from bacteria, tenecteplase is an analogue of tPA

  • 14. 
    What is the mechanism of action of benzafibrate?
    • A. 

      50% reduction in absorption of cholesterol at brush border of small intestine, reduces plasma cholesterol by 15%, LDL by 20%

    • B. 

      Bind bile salts in the gut, bile acid reabsorption is impaired, so synthesis is increased from hepatic cholesterol, upregulation of LDL receptors, 15% fall in circulating LDL

    • C. 

      Increased free fatty acid uptake in liver, reduces availability for triglyceride synthesis, increased mitochondrial free fatty acid uptake in heart and skeletal muscle, increased lipoprotein lipase activity, enhanced apolipoprotein production leads to increased plasma HDL

    • D. 

      Inhibit enzyme which catalyses rate-limiting step of cholesterol synthesis, upregulation of LDL receptors on hepatocytes, increased clearance of LDL (25-50%)

  • 15. 
    What are the problems with bile-acid binding resins?
    • A. 

      GI upset, dizziness, blurred vision, headaches, disturbance of LFTs, hepatitis, myalgia, myositis, rhabdomyolysis

    • B. 

      GI upset, rash, dizziness, headache, inhibition of warfarin

    • C. 

      Unpalatability, constipation, diarrhoea, interference with absorption of acidic drugs

  • 16. 
    What factors can exacerbate digitalis toxicity?
    • A. 

      Headache, flushing, dizziness, ankle oedema, heart failure with poor left ventricular function, tachycardia, palpitations, bradycardia, heart block, constipation, nausea, heartburn, gum hyperplasia

    • B. 

      Dilutional hyponatraemia, hypokalaemia (not spironolactone), hypomagnesaemia, hyperuricaemia, incontinence, ototoxicity, vertigo, impotence, nocturia, hyperlipidaemia, hyperkalaemia (spironolactone), GI upset, antiandrogenic (spironolactone)

    • C. 

      Hypokalaemia due to decreased competition for Na+/K+ pump (diuretics), renal impairment (elderly), hypoxaemia, hypothyroidism (reduced glomerular filtration rate), verapamil and quinidine displace from binding sites and interfere with renal excretion thus raising plasma concentration

  • 17. 
    What is the mechanism of action of digoxin in heart failure?
    • A. 

      Gradual introduction can reduce workload of ischaemic myocardium, restore excitation-contraction coupling, reduce cardiac hypertrophy and fibrosis, reduce myocyte apoptosis and counteract arrhythmias

    • B. 

      Inhibit Na+/K+ ATPase in cardiac myocyte membrane, thereby reducing passive Na+/Ca2+ exchange thus retaining Ca2+ inside cell, enhancing myocardial contractility

    • C. 

      Inhibits cleavage of ATI to ATII and breakdown of bradykinin by ACE, prevents arterial vasoconstrictive effects of ATII and enhances vasodilatory effects of bradykinin, reduces release of aldosterone

  • 18. 
    WHich of these are mechanisms by which antihypertensive drugs cause vasodilation?
    • A. 

      Direct arterial dilation by reduced Ca2+ entry to smooth muscle cells due to intracellular Na+ depletion

    • B. 

      Reduced Ca2+ entry and reduced release from ER to smooth muscle cells due to blockage of L-type calcium channels

    • C. 

      Inhibits cleavage of ATI to ATII and breakdown of bradykinin by ACE, prevents arterial vasoconstrictive effects of ATII and enhances vasodilatory effects of bradykinin,

    • D. 

      Blocks ATII mediated arterial vasoconstriction