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Local anaesthetics: chirality, differential blockade and dose-dependent lignocaine effects.
- (a)Giving few drugs as an example, compare and contrast concentration dependent and time dependent antibiotics.6 marks
- (b)Local anaesthetics should not be used in septic patients. Discuss your opinion regarding this statement.4 marks
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- (a)Describe the basic chemical structure of a typical local anaesthetic molecule.3 marks
- (b)Explain the Structure-Activity Relationship (SAR) of local anaesthetics with respect to their potency, onset and duration of action.4 marks
- (c)Compare the metabolism of the two (2) local anaesthetic groups, including the clinical implications of their metabolic products.3 marks
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7 SBAs on local anaesthetics
Viva
5 viva questions
Does S always mean levorotatory or safer?
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No. R/S is absolute configuration and is independent of (+)/(−) optical rotation. Safety must be established for the individual molecule and target; it is not a universal property of every S-enantiomer.
Why is levobupivacaine less cardiotoxic than racemic bupivacaine?
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Removal of the R-enantiomer reduces stereoselective, persistent interaction with cardiac ion channels, particularly voltage-gated sodium channels.
Why is ropivacaine less lipid soluble than bupivacaine?
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Its N-substituent is propyl rather than butyl. That structural difference, not S configuration alone, lowers lipid solubility.
Why can pain be blocked while motor power is retained?
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The delivered concentration can exceed the minimum blocking concentration of nociceptive fibres yet remain below that of many larger motor fibres; firing frequency and nodal geometry add selectivity.
Why may LAST occur without the classic early neurological sequence?
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A rapid intravascular bolus can raise arterial concentration so quickly that severe CNS or cardiovascular toxicity occurs before warning symptoms are recognised.