Free UKMLA perioperative medicine and anaesthesia questions with explanations

D. 88-92%

In patients at risk of hypercapnic respiratory failure such as those with COPD, an initial target SpO2 of 88-92% is recommended pending arterial blood gas results. This balances adequate tissue oxygenation against the risk of worsening type 2 respiratory failure from loss of hypoxic drive and V/Q mismatch. Controlled oxygen should be delivered via a 24% or 28% Venturi mask rather than a non-rebreather.

C. Arterial blood gas

This patient has signs of type 2 respiratory failure (drowsiness, asterixis, respiratory rate 8/min) likely precipitated by uncontrolled high-flow oxygen in a chronic CO2 retainer, and an arterial blood gas is required immediately to confirm hypercapnia and acidosis, guide controlled oxygen titration to SpO2 88-92%, and identify the need for NIV.

D. Continue aspirin, stop clopidogrel 7 days preoperatively

Aspirin should be continued perioperatively in patients with coronary stents whenever bleeding risk permits, while stopping the P2Y12 inhibitor (clopidogrel 7 days, ticagrelor 3–5 days, prasugrel 7 days) before surgery. After 6 months from DES insertion the elective stent thrombosis risk has fallen sufficiently that this strategy balances thrombotic and bleeding risks, and elective surgery can be timed once the P2Y12 inhibitor has been held.

E. Methaemoglobinaemia

Topical prilocaine (in EMLA) is metabolised to o-toluidine, which oxidises haemoglobin iron from the ferrous to ferric state, producing methaemoglobin that cannot bind oxygen and causes cyanosis with an oxygen-refractory saturation gap. Infants under 12 months are particularly vulnerable due to immature NADH-cytochrome b5 reductase activity and higher levels of fetal haemoglobin, which is more readily oxidised. First-line treatment is IV methylene blue.

E. Secondary IgG response to a donor antigen

Pregnancy exposes a woman to fetal red cell antigens inherited from the father, such as Kidd or Rh antigens, and she may form alloantibodies. Over years these can fall below the level a pre-transfusion screen detects, while memory B cells persist. Transfused red cells carrying the antigen then trigger a secondary, anamnestic response: within several days IgG rises rapidly, coats the donor cells and causes mainly extravascular haemolysis in the spleen. About a week after transfusion the haemoglobin falls back and jaundice appears. A primary response would be slower and weaker.

Takeaway: Delayed haemolytic transfusion reactions reflect an anamnestic IgG response in a previously sensitised patient.

D. Urgent surgical debridement with broad-spectrum intravenous antibiotics

This presentation (severe pain out of proportion, crepitus, haemorrhagic bullae and septic shock in a poorly controlled diabetic) is necrotising fasciitis, a surgical emergency where survival depends on rapid source control. Definitive management is urgent theatre debridement of all necrotic tissue combined with broad-spectrum IV antibiotics (typically a carbapenem plus clindamycin for antitoxin effect, per UK sepsis and surgical infection guidance).

D. Adult epiglottitis (supraglottitis)

Acute onset of severe odynophagia, drooling, a muffled 'hot potato' voice and fever in an adult who is sitting forward with a relatively normal-looking oropharynx is the classic picture of adult epiglottitis (supraglottitis). Adults often lack the dramatic stridor seen in children because of a wider airway calibre, but airway compromise can develop rapidly. Management follows ENT UK guidance with airway monitoring in HDU or ICU, IV ceftriaxone and dexamethasone.

B. HELLP syndrome

In a pre-eclamptic woman, severe epigastric or right upper quadrant pain with nausea is the classic clinical herald of HELLP syndrome, reflecting hepatic sinusoidal microangiopathic injury and Glisson's capsule stretch before the haematological triad becomes overt. Any pre-eclamptic patient with epigastric pain warrants urgent FBC, LFTs, LDH, and a film to confirm haemolysis, elevated liver enzymes, and low platelets, with definitive management being delivery alongside magnesium sulfate prophylaxis and BP control.

E. Congestive heart failure

Chronic pressure overload from severe aortic stenosis drives concentric LV hypertrophy that eventually decompensates, producing systolic and diastolic dysfunction with pulmonary congestion (exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea). The onset of heart failure in severe AS is a class I indication for valve intervention, distinguishing it from the arrhythmic, infective, and aortic complications that present very differently.

A. Intravenous diazepam

Tetanus toxin blocks release of glycine and GABA from spinal inhibitory interneurons, so the spasms are disinhibited motor activity rather than seizures. Benzodiazepines are first-line because they enhance GABA-A signalling, restoring inhibition, and also provide sedation and anxiolysis; diazepam or midazolam are given by intravenous infusion and titrated to control spasms. Magnesium sulfate is a useful adjunct that reduces spasm and autonomic instability but is not first-line on its own, and if spasms threaten ventilation the patient is paralysed and ventilated. Anticonvulsants such as phenytoin have no role because the spasms are not epileptic.