Choosing and stopping drugs

Correct answer: B. Obtain a culture and sensitivity test

• A. Raising the dose of an agent the organism may be resistant to achieves nothing beyond increasing toxicity.
• B. Correct. Failure of empirical therapy is the definitive indication for culture and sensitivity. It identifies the organism and shows which agents it is susceptible to, converting guesswork into targeted therapy. The same test answers the question of which antibiotic to prescribe when the organism is unknown and the infection is not straightforward.
• C. Persisting with a failing regimen allows the infection to progress and is how odontogenic infections reach the fascial spaces.
• D. Adding another empirical agent broadens exposure and side effects without addressing the fundamental uncertainty about the organism.

Note: Culture is most useful when combined with adequate surgical drainage and removal of the source. No antibiotic substitutes for drainage.

Correct answer: D. Doxycycline

• A. Penicillin V is a beta-lactam and bactericidal. The useful generalisation is that agents acting on the cell wall or on DNA kill, while most that act on the ribosome only inhibit.
• B. Correct, and this is the exception. Tetracyclines including doxycycline are bacteriostatic. They bind the 30S ribosomal subunit and block aminoacyl-tRNA attachment, halting protein synthesis and arresting growth without killing the organism, so host immunity must clear the infection.
• C. Cephalexin is a first-generation cephalosporin and a beta-lactam, so it is bactericidal through inhibition of cell wall cross-linking.
• D. Amoxicillin is a beta-lactam and bactericidal.

Correct answer: D. Pseudomonas aeruginosa

• A. Viridans streptococci are generally susceptible to clindamycin, which is why it was long used for endocarditis prophylaxis in penicillin allergy.
• B. Peptostreptococcus is an anaerobic gram-positive coccus, well within clindamycin's spectrum.
• C. Prevotella is an anaerobe and generally susceptible.
• D. Correct. Clindamycin has no useful activity against aerobic gram-negative bacilli, and Pseudomonas aeruginosa is intrinsically resistant. Its strength is against gram-positive cocci and anaerobes, which is why it suits odontogenic infection in penicillin-allergic patients.

Correct answer: C. Andexanet alfa, or prothrombin complex concentrate if unavailable

• A. Plasma contains the factors but is not an effective reversal for a direct oral anticoagulant and carries volume and transfusion risks.
• B. Vitamin K reverses warfarin by restoring synthesis of the vitamin K dependent factors II, VII, IX and X. Rivaroxaban does not act on that pathway, so vitamin K is useless against it.
• C. Correct. Rivaroxaban is a direct factor Xa inhibitor. Its specific reversal agent is andexanet alfa, a decoy factor Xa molecule; where that is unavailable, four-factor prothrombin complex concentrate is used. For routine dental extractions no reversal is needed at all, and local haemostatic measures suffice.
• D. Protamine sulfate reverses unfractionated heparin and partially reverses low molecular weight heparin.

Note: The recall keyed this as vitamin K with the author noting real uncertainty. Vitamin K is incorrect. Match the reversal to the mechanism: warfarin with vitamin K, heparin with protamine, dabigatran with idarucizumab, and the Xa inhibitors with andexanet alfa.

Correct answer: A. They are the first choice for severe chronic pain requiring escalating doses

• A. Correct, and this is the exception. NSAIDs are not the answer to severe pain requiring dose escalation, precisely because of the ceiling effect. Raising the dose past that point adds gastrointestinal, renal and bleeding risk without adding analgesia.
• B. This is true. They inhibit COX-1 and COX-2, reducing prostaglandin synthesis, which produces both the therapeutic effect and the gastric and renal adverse effects.
• C. This is true. NSAIDs are the first-line analgesic for odontogenic pain because the pain is prostaglandin-mediated, and they outperform opioids for it.
• D. This is true and is the defining pharmacological limitation of the class. Opioids, by contrast, have no analgesic ceiling.

Correct answer: A. An adverse drug reaction

• A. Correct. Stevens-Johnson syndrome is a severe mucocutaneous hypersensitivity reaction, most often triggered by drugs: sulfonamides, anticonvulsants such as carbamazepine and lamotrigine, allopurinol and NSAIDs are the usual culprits. Target lesions, extensive mucosal ulceration and epidermal detachment define it, and it is a medical emergency.
• B. Mycoplasma pneumoniae infection can trigger a related reaction, particularly in children, but drugs are the dominant cause overall.
• C. Nutritional deficiency causes glossitis and angular cheilitis, not epidermal necrolysis.
• D. Autoimmune connective tissue disease causes other mucosal patterns; SJS is a hypersensitivity reaction, not a connective tissue disorder.

Correct answer: A. Achieves the same effect at a lower dose, appearing as a leftward-shifted curve

• A. Correct. Potency is a statement about dose. The drug whose curve sits to the left produces a given effect at a lower dose, so it has a lower EC50 and is more potent. Potency alone says nothing about how good a drug is, since it can be adjusted by changing the dose.
• B. That describes efficacy, the maximum achievable effect, which is the clinically more important property. A drug can be highly potent yet have low efficacy.
• C. Duration is a pharmacokinetic property determined by metabolism and elimination, unrelated to potency.
• D. Slope reflects the number of receptors that must be occupied and cooperativity, not potency.

Correct answer: A. They are derived from coagulation factor VIII

• A. Correct, and this is the exception. Platelets are not derived from factor VIII. They are fragments of megakaryocyte cytoplasm. Factor VIII is a plasma protein of the intrinsic coagulation pathway, deficient in haemophilia A; it circulates bound to von Willebrand factor, which is a separate matter from platelet production.
• B. This is true. Megakaryocytes in the marrow shed cytoplasmic fragments under the influence of thrombopoietin.
• C. This is true. Platelets survive about 7 to 10 days, which is why aspirin's irreversible effect on cyclo-oxygenase lasts for the life of the exposed platelet pool.
• D. This is true, and surgical bleeding risk rises appreciably below about 50,000 per microlitre.

Note: The recall also listed a claim that men have higher platelet counts than women. In fact women tend to have slightly higher counts, so that option is false too. The unambiguous error is the factor VIII derivation.

Correct answer: B. Cataract formation

• A. Corticosteroids cause hyperglycaemia, not hypoglycaemia, by stimulating gluconeogenesis and antagonising insulin. This is why they can unmask or worsen diabetes.
• B. Correct. Posterior subcapsular cataract and raised intraocular pressure are established complications of prolonged corticosteroid use. The wider list includes adrenal suppression, osteoporosis, hyperglycaemia, immunosuppression, thin fragile skin, poor wound healing, peptic ulceration and the cushingoid habitus.
• C. Weight gain with central redistribution of fat is characteristic, not weight loss.
• D. Steroids do cause hirsutism, but the distribution is generalised and it is a minor feature next to the ocular, skeletal and metabolic effects.