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Post gastrectomy management
Q) A 60-year-old woman presents with chronic postprandial epigastric pain, nausea, and bilious vomiting. She had a Billroth II gastrectomy 8 years ago. Despite medical therapy with proton pump inhibitors, sucralfate, and cholestyramine, her symptoms persist. Endoscopy and biopsy confirm ongoing bile reflux gastritis with reactive gastropathy. She is nutritionally declining and has poor quality of life.
What is the most appropriate next step in management?
Shock
Clinical vignette
Answer: b) Neurogenic shock due to spinal cord injury
Explanation: The classic triad in neurogenic shock is hypotension, warm dry skin (due to peripheral vasodilatation) and relative bradycardia resulting from loss of sympathetic tone with unopposed vagal activity. The history of acute spinal cord injury (inability to move lower limbs with sensory level) strongly supports spinal shock with sympathetic disruption. Low JVP argues against cardiogenic causes; hypovolemia typically causes tachycardia and cold, clammy skin; septic shock is unlikely immediately post-trauma and usually causes tachycardia. Initial management includes cervical spine immobilization (if relevant), airway protection, judicious IV fluids, and vasopressors (norepinephrine) for persistent hypotension—atropine may be required for severe bradycardia. Consideration for definitive spinal stabilization and early neuro-monitoring is essential.
Key points: loss of sympathetic tone → decreased systemic vascular resistance; bradycardia is characteristic; treat with vasopressors and supportive care.
Retinoblastoma
Q) Retinoblastoma, the most common ocular malignancy of childhood, has the following features. Which statement is TRUE?
Esophagectomy Chyle leak
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Body response to Trauma
Which of the following best explains his condition?
🔍 Explanation:
Trauma and major surgery cause tissue necrosis, ischemia, and cellular injury. Intracellular molecules such as HMGB1, mitochondrial DNA, ATP, uric acid, and heat shock proteins are released and act as DAMPs (damage-associated molecular patterns).
These activate innate immune receptors like Toll-like receptors and inflammasomes (e.g., NLRP3), triggering a robust inflammatory response even in the absence of infection. This explains sterile SIRS, which can mimic sepsis but with negative cultures.
🧠 Key Point: DAMP-driven sterile inflammation is common after trauma, burns, pancreatitis, and ischemia-reperfusion injuries. It must be differentiated from infection-driven SIRS (PAMP-mediated sepsis).
Pancreas Embryology
Q) Regarding pancreas embryology what is true
IPMN Pancreas
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MEN 1 (click the topic to see answer)
- Serum calcium: 11.6 mg/dL (elevated)
- PTH: inappropriately elevated
- Serum prolactin: normal
- Fasting glucose: elevated, HbA1c: 7.2%
Her brother had a gastrinoma and hyperparathyroidism in his 30s.
A MEN1 mutation is detected on genetic testing.
Which of the following is the most appropriate next step in her evaluation?
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Cystic neoplasm of pancreas
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Ulcerogenic cause of hypergastrinemia
🔍 Explanation:
Zollinger–Ellison syndrome (ZES) is caused by a gastrinoma (a gastrin-secreting tumor), typically located in the pancreas or duodenum.
It leads to massive hypergastrinemia, increased gastric acid secretion, and multiple, recurrent, or atypical peptic ulcers.
Diarrhea and steatorrhea are common due to acid inactivation of pancreatic enzymes.
Other Options:
A. Atrophic gastritis:
Leads to hypochlorhydria/achlorhydria with secondary hypergastrinemia, but non-ulcerogenic (low acid state).
C. Chronic PPI use:
Causes compensatory hypergastrinemia due to acid suppression, but again non-ulcerogenic unless stopped abruptly in predisposed individuals.
D. Helicobacter pylori infection:
May increase gastrin levels mildly, but ulcers are primarily due to mucosal damage and inflammation, not from gastrin hypersecretion.
🧠 Key Point: Zollinger–Ellison syndrome is the only ulcerogenic cause of hypergastrinemia. Fasting gastrin >1000 pg/mL with low gastric pH is diagnostic.
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