Written questions
Model answers available
- Briefly outline the role of the following investigations in critically ill patients;
- (i)serum ammonia
- (ii)serum globulin
- (iii)urine osmolarity
- (iv)C-reactive protein
- A 39-year-old female with class 3 BMI is scheduled for bariatric surgery. She gives a history of GERD which is well controlled.
- (i)Describe lower oesophageal sphincter (LOS).3 marks
- (ii)Describe the changes in LOS in this patient.1 mark
- (iii)Discuss all the factors influencing the resting LOS tone.6 marks
Single best answer
20 SBAs on gastrointestinal and hepatic physiology
Viva
15 viva questions
Your patient has a mid-thoracic epidural running for a laparotomy. What does that do to the gut, and why?
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A mid-thoracic epidural blocks the preganglionic sympathetic fibres from T5 to L2 that supply the gut. Removing that inhibition leaves the vagal supply unopposed, so enteric acetylcholine release rises, motility increases and the sphincters relax. Clinically that translates into a shorter postoperative ileus, which is one of the reasons a thoracic epidural sits in most enhanced recovery protocols for open abdominal surgery.
The second consequence is circulatory rather than gastrointestinal. The same block dilates the splanchnic resistance and capacitance vessels, so blood pools in the abdomen, venous return falls, and hypotension follows unless it is anticipated. The two effects have the same cause.
A lumbar epidural would not do the same thing. It sits below most of the gastrointestinal sympathetic outflow, so it neither improves motility to the same extent nor produces the same degree of splanchnic pooling.
Likely follow-ups
- Which fibres are you blocking?
- Would a lumbar epidural do the same thing?
Barrier pressure is 25 mmHg in one patient and 25 mmHg in another. Are they equally protected?
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Yes, as far as that number goes — and that is precisely the point of using barrier pressure rather than sphincter pressure. One may have a sphincter at 30 against a gastric pressure of 5, and the other a sphincter at 43 against a gastric pressure of 18. The subtraction is what determines whether contents move, so at this instant both are equally competent.
What differs is their reserve. The second patient is holding a normal barrier with an abnormally high gastric pressure, so a much smaller further insult — a fasciculation, a pneumoperitoneum, an induction agent that relaxes the sphincter — exhausts it. Two patients with the same barrier can be very differently placed for what happens next.
Likely follow-ups
- What would change your answer?
- Why use barrier pressure rather than sphincter pressure?
Gastrointestinal 2: Swallowing and the Lower Oesophageal Sphincter →
Your patient ate a full meal five hours ago and has a fractured femur. Are they fasted?
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No. Five hours is within the six-hour interval for solids in any case, but the more important point is that the interval assumes the emptying curve applies, and here it does not. Pain and the sympathetic response to trauma inhibit the enteric plexuses and arrest gastric emptying at about the moment of injury, and any opioid given since has arrested it further. The clock effectively stopped when the femur broke, not when the meal ended.
So this patient is a full stomach regardless of the number of hours, and should have a rapid sequence induction. Head-up positioning helps by both mechanisms in lesson 2: it restores the gravitational assistance and it does not raise intra-abdominal pressure.
A nasogastric tube is genuinely two-edged. It drains the stomach, which is why it is recommended in intestinal obstruction and should be aspirated before induction. But it also splints the lower oesophageal sphincter open across its lumen, reducing the barrier. On balance it is used where the volume to be drained is large and predictable, and it is not left in place as a substitute for a secured airway.
Likely follow-ups
- What would you do differently?
- Does a nasogastric tube help?
Your patient is having an open right hemicolectomy. What has happened to their hepatic blood flow by the time the surgeon starts mobilising the flexure?
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Several things have happened, and they are worth giving in order of size rather than in the order they occurred.
The surgical factors dominate. Retraction and packing of the liver reduce hepatic blood flow more than any anaesthetic factor does, and if this were laparoscopic the pneumoperitoneum would compress the portal vein and the hepatic veins as well. Sympathetic activity from the surgical stimulus constricts the splanchnic bed, so portal flow falls before the arterial pressure does.
The anaesthetic factors are smaller but additive. Positive-pressure ventilation raises mean intrathoracic pressure and reduces venous return and cardiac output; the volatile agent reduces mean arterial pressure and cardiac output dose-dependently; and if I have over-ventilated them, hypocapnia alone reduces hepatic blood flow by about 30% by raising portal resistance. That last one is entirely mine and entirely avoidable.
The buffer response is helping, and only partly. Most of what I have described arrives at the liver as a fall in portal flow, which is exactly what the buffer exists for: adenosine accumulates and the hepatic arteriole dilates, raising arterial flow by 22 to 100%. But it is partial, so total flow is still down; and if I were using halothane it would be abolished altogether. Alongside it, hepatic oxygen consumption is being defended by increased extraction rather than by restored flow, and that is what is actually protecting the hepatocyte.
The practical consequence is for the drugs: every high-extraction drug in the anaesthetic — propofol, and any opioid with a high extraction ratio — now has a reduced clearance, because for those drugs clearance simply is liver blood flow.
Likely follow-ups
- Which of those is the biggest single effect?
- Does the buffer response help you here?
How would you use blood glucose and serum ammonia as tests of liver function?
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Both are genuine functional measurements rather than markers of cellular leakage, which is what makes them interesting — and both are limited in the same way, by being late.
Blood glucose reports the capacity for glycogenolysis and gluconeogenesis. Hypoglycaemia in acute liver failure means the glycogen is exhausted and gluconeogenesis has failed, so it is a late and ominous sign. It is neither sensitive nor specific: normal until the reserve is gone, and disturbed by feeding, sepsis and exogenous insulin. Its practical importance is that encephalopathy masks the clinical signs, so it must be measured repeatedly rather than waited for.
Serum ammonia reports the capacity of the urea cycle and of perivenous glutamine synthesis, and also the degree of portosystemic shunting. A raised concentration supports a hepatic cause for an unexplained encephalopathy. But no single concentration reliably predicts neurological toxicity and the correlation with the clinical grade is poor, and the sample is unstable unless it goes on ice and is analysed promptly.
If I could have only one test of synthetic function I would take the prothrombin time, because factor VII’s half-life of about six hours means it moves within a day, whereas albumin’s three weeks means it may be entirely normal in a patient with fulminant failure.
Likely follow-ups
- What are their limitations?
- Which single test would you rather have?
Why does alkalosis worsen hepatic encephalopathy?
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Ammonia has a pKa of about 9.2. Raising the pH shifts the equilibrium from the charged NH4+, which does not cross the blood–brain barrier, towards the uncharged NH3, which does. Hyperventilation, vomiting and diuretic-induced alkalosis therefore all increase brain ammonia exposure at an unchanged serum concentration.
A patient has a total protein of 62 g/L and an albumin of 22 g/L. What have you learnt?
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The globulin is 40 g/L, so the albumin:globulin ratio is reversed at about 0.55. That combination — low albumin with raised globulin — points to chronic liver disease, since synthetic failure lowers albumin while portosystemic shunting raises γ-globulin. It would also fit a paraproteinaemia, which electrophoresis distinguishes. It does not fit protein loss, because that would lower both.
Why does the fractional excretion of urea outperform the fractional excretion of sodium in a patient on furosemide?
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Furosemide blocks the Na-K-2Cl cotransporter in the thick ascending limb, so sodium excretion is pharmacologically driven and the FeNa reports the drug rather than the kidney. Urea is reabsorbed mainly in the proximal tubule, which the loop diuretic does not act on, so the fractional excretion of urea still reflects proximal avidity and therefore perfusion. Below about 35% remains consistent with a prerenal state.
Why is a CRP taken four hours into a septic presentation of limited value?
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Synthesis has barely begun. CRP starts to rise 4 to 6 hours after the stimulus and peaks at 36 to 50 hours, so an early value reflects the patient’s state yesterday rather than today. A normal early CRP does not exclude sepsis, and the decision to treat is clinical. Its value is in the days afterwards, as a trend.
Which of these four tests is most affected by how the sample was taken?
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Ammonia, by a wide margin. A prolonged tourniquet, fist clenching, haemolysis, a warm sample or a delay before separation all raise the measured value, and a spuriously high ammonia has changed management before now. It should be free-flowing, on ice, and analysed promptly.
Why is the LOS called a physiological sphincter?
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Because there is no discrete anatomical thickening of muscle to identify at dissection. It is defined functionally, as a 2–4 cm zone of tonically contracted circular smooth muscle identified by a high-pressure zone on manometry. Contrast the upper oesophageal sphincter, which is a named muscle — cricopharyngeus — and therefore an anatomical sphincter.
Barrier pressure is 25 mmHg in one patient and 25 mmHg in another. Are they equally protected?
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Yes, as far as that number goes — which is the point of using barrier pressure rather than LOS pressure. One may have an LOS of 30 against a gastric pressure of 5, and the other an LOS of 43 against a gastric pressure of 18. The subtraction is what determines whether contents move. What differs is their reserve: the second patient loses competence with a much smaller further fall in tone.
How does a hiatus hernia reduce the barrier when the sphincter muscle is unchanged?
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It removes three of the five components at once. The intrinsic sphincter is displaced above the hiatus so it no longer acts at the same level as the crural diaphragm, and the two components can no longer summate. The intra-abdominal segment is lost, so the self-sealing effect of raised intra-abdominal pressure goes. And the angle of His is straightened, so the flap valve is abolished.
Why does the crural diaphragm matter more during coughing than at rest?
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Coughing and straining raise intra-abdominal pressure sharply, which would otherwise overwhelm the barrier. The crus contracts as part of that same effort, so the extrinsic sphincter pressure rises at the moment of threat. It is a feed-forward mechanism: the same muscular act that raises the challenge also raises the defence.
What is the dominant mechanism of reflux in obesity — low tone, or something else?
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Something else. Resting tone is often normal. The dominant mechanisms are raised intra-abdominal pressure reducing barrier pressure by the subtraction, a higher frequency of transient LOS relaxations, and a high prevalence of hiatus hernia. This is why treating the sphincter pharmacologically does not solve the problem, and why bariatric surgery itself often does.
Teaching pathway