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MCEM Pharmacology

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Penicillin / Ampicillin / Methicillin. 2nd & 3rd Generation Cephalosporins. Nitrofurantoin ... Ampicillin. Ibuprofen. Aspirin. Morphine. Something similar has ... – PowerPoint PPT presentation

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Title: MCEM Pharmacology


1
MCEM Pharmacology
2
Core Content
  • Need to have a detailed knowledge of the
    principles underlying the pharmacological
    management of conditions in the ED. In
    particular
  • CNS Analgesics anaesthetics sedatives
  • Respiratory Beta agonists anti-cholinergic
    agents
  • Cardiac anti-arhythmics inotropes nitrates
  • Infection antibiotics and antiviral agents
  • GI antacids proton pump inhibitors anti
    spasmodics laxatives anti diarrhoeal
  • Coagulation Heparin warfarin thrombolysis
    FFP protamine aspirin
  • Anti inflamm. NSAID steroids
  • Diabetes oral hypoglycaemic agents anti
    hyperglycaemic agents glucagon insulin
  • Antidotes

3
Question 1
  • The following are true of drugs used in the
    treatment of ventricular arrhythmias
  • Lignocaine toxicity is rare when used as an
    intravenous infusion as the half life is less
    than 20 minutes
  • Amiodarone may cause clinical hyperthyroidism
  • ß blockers increase automaticity by blocking the
    effects of endogenous catacholamines
  • Lignocaine is a negative inotrope

4
Q1. Answer - F T F T
  • Lignocaine is a class Ib antiarrhythmic drug. It
    blocks the sodium channel. It depresses
    conduction of premature beats and conduction
    through ischaemic tissue. It shortens the action
    potential, although this is not associated with
    changes on the 12 lead ECG. . The half life is
    approximately 1.5 hours, although this is
    extended to up to 10 hours in severe cardiac
    failure or shock. Steady state following
    infusion is not achieved for 6 hours
    (approximately four elimination half lives). As
    such lignocaine toxicity is not uncommonly seen
    in association with intravenous infusions. The
    most common features associated with lignocaine
    toxicity are neurological, but lignocaine also
    has negatively inotropic effects and may cause AV
    block.
  • ß blockers reduce automaticity of the SA and AV
    nodes by competitively inhibiting intrinsic
    catecholamine binding to ß adrenoreceptors.
  • Amiodarone is a highly effective treatment for
    many ventricular and supraventricular
    arrhythmias. This efficacy is compromised by the
    wide range of side effects, including pulmonary
    infiltrates and fibrosis, corneal deposits,
    photosensitivity, neuropathy and hyper or
    hypothyroidism

5
Question 2
  • The following drugs may cause acute haemolytic
    anaemia
  • Trimethoprim
  • Nitrofurantoin
  • Nalidixic acid
  • Methicillin

6
Q.2 Answer F T T T
  • Common Antibiotic Causes of drug-induced
    haemolytic anaemias
  • Penicillin / Ampicillin / Methicillin
  • 2nd 3rd Generation Cephalosporins
  • Nitrofurantoin

7
Question 3
  • Anticoagulation in patients taking warfarin may
    be affected by treatment with
  • Ampicillin
  • Ibuprofen
  • Aspirin
  • Morphine

8
Q.3 Answer T T T F
  • Something similar has been asked in past
  • The interactions with NSAIDs and Aspirin are
    somewhat debatable but are considered to
    enhance.
  • Most antibiotics will enhance effect
  • Those NOT
  • Trimethoprim / Tetracyclines
  • Rifampicin REDUCES EFFECT

9
Question 4
  • Acute dystonic reactions may occur following oral
    admistration of
  • Prochlorperazine
  • Diazepam
  • Metoclopramide
  • Haloperidol

10
Q.4 Answer T F T T
  • Although dystonic reactions are occasionally dose
    related, these reactions are more often
    idiosyncratic and not predictable.
  • They appear to result from drug-induced
    alteration of dopaminergic-cholinergic balance in
    the basal ganglia.
  • Most drugs produce dystonic reactions by dopamine
    D2 receptor blockade, which leads to an excess of
    striatal cholinergic output.
  • Agents that balance dopamine blockade with
    muscarinic M1 receptor blockade are less likely
    to produce a dystonic reaction.

11
Question 5
  • With respect to the clotting cascade
  • Warfarins main action is on the Intrinsic
    pathway
  • Warfarin affects production of Factors III,
    VII,IX, X
  • Heparin affects thrombin and the Intrinsic
    pathway
  • Prothrombin Complex Concentrate contains factors
    IX and X

12
Q.5 Answer F F T T
  • Warfarins main effects are on the extrinsic
    pathway and Vitamin K dependent factors II, VII,
    IX X
  • Heparins main effects act via potentiation of
    Antithrombin III

13
Question 5
  • Regarding oral hypoglycemic agents
  • Metformin is cleared by hepatic metabolism
  • Metformin acts by stimulating insulin release
  • Glipizide has its main effects by improving
    insulin sensitivity
  • Glucophages are more likely to cause hypoglycemic
    episodes than sulphonylureas

14
Q.5 Answers F F F F
  • Glipizide (sulfonylurea) acts by stimulating
    insulin release and is cleared by hepatic
    hydroxylation can cause hypoglycemia
  • Metformin (biguanide) reduces hepatic release,
    gut absorption of glucose and peripheral
    utilisation. It is cleared by renal excretion and
    does not cause hypoglycemia in isolation.

15
Question 6
  • The following drugs have their main direct
    effects at the receptors listed
  • Adrenaline alpha-1, beta-12
  • Noradrenaline alpha-1 beta-2
  • Phenylephrine alpha-1 beta-1
  • Dobutamine beta-12

16
Q.6 Answers T F F F
  • Adrenaline has effects on all alpha/beta
    receptors.
  • Noradrenaline has effects on all but beta 2
  • Dobutamine has its main effects on beta1
  • Phenylephrine on alpha 1 receptors

17
Question 7
  • The following statements regarding local
    anaesthetics are correct
  • They work by decreasing the resting action
    potential of nerve cells
  • They work by blocking sodium channels
  • The maximum dose of bupivacaine is 2mg/kg
  • The initial signs of overdose is cardiac
    dysrhythmias

18
Q.7 Answer F T T F
  • Local anaesthetics act mainly on sodium channels,
    but do not effect the resting or threshold
    potential, they prolong the repolarisation phase.
  • In overdose, neurological sequelae are noted
    first
  • Maximum dose of common drugs

19
  • Suxamethonium is a non depolarising neuromuscular
    blocker
  • The normal dose of suxamethonium is 10-20 mg/kg
  • Suxamethonium is associated with bradycardia
  • Ketamine is a bronchodilator
  • Propofol is not associated with cardiovascular
    depression

20
  • Suxamethonium is a non depolarising neuromuscular
    blocker
  • FALSE - is a depolarising blocker producing
    profound paralysis within 30-45 s
  • The normal dose of suxamethonium is 10-20 mg/kg
  • FALSE 1.5-2mg/kg
  • Suxamethonium is associated with bradycardia
  • TRUE esp in children who are sensitive to
    muscarinic effects of suxamethonium
  • Ketamine is a bronchodilator
  • TRUE
  • Propofol is not associated with cardiovascular
    depression
  • FALSE

21
  • The following anti-dotes and poisons are
    correctly paired
  • Ethylene Glycol Ethanol/ Fomepizole
  • B Blockers Glucagon/Atropine
  • Cyanide Sodium Nitrite/Sodium thiosuphate/Dicobat
    e Edetate
  • Methanol Ethanol/Folmepizole
  • Organophosphates Fomepazole

22
  • The following anti-dotes and poisons are
    correctly paired
  • Ethylene Glycol Ethanol/ Fomepizole
  • TRUE
  • B Blockers Glucagon/Atropine
  • TRUE
  • Cyanide Sodium Nitrite/Sodium thiosuphate/Dicobat
    e Edetate
  • TRUE (also ?)
  • Methanol Ethanol/Fomepazole
  • TRUE
  • Organophosphates Fomepazole
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