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SU1.1-3 | Metabolic Response and Surgical Homeostasis — Practice Quiz
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A 28-year-old man is admitted six hours after a road-traffic crash with a closed femoral shaft fracture and a splenic laceration. He is cold, pale and quiet, his cardiac output is reduced and his core temperature is low. According to Cuthbertson's classical description of the metabolic response to injury, which phase is he MOST likely in at this point?
Correct. Cuthbertson described an early ebb phase in the first hours after major injury, dominated by hypovolaemia and intense neuroendocrine vasoconstriction: the patient is cool, the metabolic rate falls and cardiac output is reduced. The flow phase, with its hypermetabolism and catabolism, follows once the circulation is restored.
Cuthbertson's biphasic model: an early hypometabolic ebb phase (hypovolaemia, vasoconstriction, cool periphery, low cardiac output) precedes the hypermetabolic flow phase.
Re-read the early picture: a cold patient with a low metabolic rate and reduced cardiac output in the first hours after trauma is in the ebb phase. The flow phase (hypermetabolic/catabolic then anabolic) comes later, after resuscitation.
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Forty-eight hours after major abdominal surgery a previously well patient is found to have a blood glucose of 11 mmol/L despite having received no exogenous glucose load and having no prior history of diabetes. Which combination of mediators is the PRINCIPAL driver of this post-injury hyperglycaemia?
Correct. The 'diabetes of injury' is driven by the counter-regulatory hormones — cortisol, catecholamines and glucagon — which promote gluconeogenesis and glycogenolysis, combined with peripheral insulin resistance. The result is hyperglycaemia despite no carbohydrate intake.
Post-injury hyperglycaemia ('diabetes of injury') results from counter-regulatory hormones (cortisol, catecholamines, glucagon) plus peripheral insulin resistance.
Post-injury hyperglycaemia is driven by the counter-regulatory (catabolic) hormones — cortisol, catecholamines and glucagon — plus peripheral insulin resistance. ADH/aldosterone govern salt and water; insulin lowers glucose.
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In the hours after major haemorrhage, a fall in circulating volume and a rise in plasma osmolality trigger hormonal changes that conserve salt and water. Which hormone is released directly in response to reduced effective circulating volume and acts to retain sodium by the kidney?
Correct. Reduced renal perfusion activates the renin-angiotensin-aldosterone system; aldosterone acts on the distal nephron to retain sodium (and therefore water), while ADH retains free water. Together they defend the circulating volume after injury.
After injury, ADH retains water and aldosterone (via RAAS) retains sodium, conserving the circulating volume.
Reduced effective circulating volume activates renin-angiotensin-aldosterone; aldosterone retains sodium. Atrial natriuretic peptide does the opposite (promotes sodium loss); glucagon and thyroxine are not the salt-retaining hormones here.
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Two patients undergo the same elective major operation. One is a well-nourished 40-year-old; the other is a malnourished 75-year-old with poorly controlled diabetes and an untreated wound infection. Which statement BEST describes how these factors affect the magnitude of the metabolic response to injury?
Correct. The magnitude and duration of the response are modifiable: the severity and extent of tissue injury, the presence of sepsis, nutritional and comorbid state, age, and factors such as pain, cold and hypovolaemia all influence it. Sepsis in particular amplifies and prolongs the catabolic flow phase. This is why good perioperative care (warming, analgesia, infection control, nutrition) blunts the response.
The metabolic response is modifiable: tissue injury severity, sepsis, nutrition, age and afferent stimuli (pain, cold, hypovolaemia) change its magnitude and duration; good perioperative care attenuates it.
The response is not fixed. Sepsis, the size of the injury, nutritional state, age and afferent stimuli (pain, cold, hypovolaemia) all modify it — and crucially, sepsis amplifies and prolongs the catabolic response. This is the rationale for attenuating it with good perioperative care.
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A 55-year-old man with hypertension and well-controlled diabetes, fully independent and able to climb two flights of stairs without chest pain, is being consented for an elective inguinal hernia repair. Using the American Society of Anesthesiologists physical status classification, which ASA grade BEST describes him?
Correct. Well-controlled mild systemic disease (controlled hypertension and diabetes) with no functional limitation is ASA II. ASA III implies severe, substantively limiting systemic disease; ASA IV implies disease that is a constant threat to life.
ASA classification: I = healthy; II = mild well-controlled systemic disease; III = severe limiting disease; IV = severe disease that is a constant threat to life; V = moribund.
Mild, well-controlled systemic disease without functional limitation is ASA II. ASA I is a wholly healthy patient; ASA III is severe disease that limits function; ASA IV is disease that constantly threatens life.
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A healthy adult is listed for elective surgery on a morning list. Applying standard preoperative fasting guidance ('2-4-6'), which instruction is correct?
Correct. Standard fasting guidance is 2 hours for clear fluids, 4 hours for breast milk, and 6 hours for solids, formula and non-human milk, minimising aspiration risk while avoiding unnecessary dehydration. Encouraging clear fluids up to 2 hours is part of ERAS.
Preoperative fasting '2-4-6': clear fluids 2 h, breast milk 4 h, solids/formula/non-human milk 6 h. Permitting clear fluids to 2 h reduces dehydration and is an ERAS principle.
The rule is 2-4-6: clear fluids up to 2 hours, breast milk up to 4 hours, solids/formula/milk up to 6 hours. Stopping clear fluids early (6-8 h) causes needless dehydration; solids are never allowed at 2 hours.
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