GI IV Flashcards
Gilberts
Gilbert’s syndrome is associated with an isolated elevation of unconjugated bilirubin due to mild deficiency of glucuronyl transferase, with normal liver architecture and consequently no elevation in urobilinogen.
Alkaline phosphatase is normal. Bilirubin concentrations are variable, and jaundice can be precipitated by drugs and infection.
It is the commonest form of familial non-haemolytic hyperbilirubinaemia affecting 2-5% of the population, and is now thought to be inherited in an autosomally recessive manner, although other abnormalities may contribute to phenotype.
Budd-Chiari syndrome: Cause of splenomegaly
Hepatic vein thrombosis/Budd-Chiari results in portal hypertension and splenomegaly.
Colonic carcinoma is not associated with splenomegaly.
Other causes include infections such as
Infectious mononucleosis
Lymphoma.
Splenomegaly is not a feature of congestive cardiac failure.
AXR useful for….
Sigmoid volvulus
Up to 30% of patients with end-stage chronic pancreatitis will have diffuse calcification within the pancreas gland, best visualised by an oblique abdominal view.
Caecal carcinoma is only reliably demonstrated on double-contrast barium enema or colonoscopy. The ‘parrot’s beak’ sign is the characteristic appearance on plain films with the distended sigmoid loop arising out of the pelvis.
Cholesterol stones are typically radiolucent. Only 10% of all gallstones are radio-opaque (c.f. 90% of renal stones).
Black pigment stones are more commonly calcified and therefore visible on the AXR. The plain AXR is perhaps the most useful investigation in fulminant colitis. Serial AXRs will demonstrate toxic dilatation of the colon (>6 cm diameter, usually the transverse colon), which is an indication for surgery.
Pharmacological causes of pancreatitis
Drugs associated with pancreatitis include
Steroids Oestrogens Thiazides Valproate Azathioprine. The most notable precipitant is alcohol.
Chemotherapy with cisplatin/vinca alkaloids may produce acute pancreatitis but radiotherapy is not associated with acute but is associated with chronic pancreatitis.
Which does not predispose to gastro-oesophageal reflux disease (GORD)?
Predisposing factors include
Alcohol
Smoking
Antral disorders and disorders of emptying (Pyloric stenosis)
Previous vagal surgery
Obesity
yet there does not appear to be an association with H. pylori, in fact data would suggest an increase in GORD associated with H pylori eradication.
Pyloric stenosis
The characteristic radiological feature is the ‘string sign’, which comprises a thin contracted pyloric canal, containing a central streak of barium.
The clinical symptoms commonly appear in this time frame.
The vomiting is not bile stained but consists of large volumes of curdled milk. Appetite and feeding are normal or increased.
The characteristic metabolic abnormality is hypochloraemic hypokalaemic alkalosis.
Achalasia cardia
Achalasia cardia is a neuromuscular failure of relaxation at the lower end of the oesophagus due to loss of ganglia from the Auerbach’s plexus (absence of ganglion cells in the neural plexus of the intestinal wall leads to Hirschsprung’s disease).
It is more common in females (3:2) and is frequently seen during the third decade of life.
There is progressive dysphagia to solids and liquids, chest pain and regurgitation of old food from the dilated oesophageal sac.
x Ray reveals a dilated oesophagus with a tapering lower oesophageal segment, likened to a bird’s beak, which fails to relax.
There is absence of gastric air bubbles because the dilated oesophagus never completely empties and therefore swallowed air cannot pass into the stomach.
Chest x ray shows air or fluid level behind the heart and the expanded oesophagus gives the appearance of a ‘double right heart border’.
Genetic associations
Coeliac disease and HLA B8
Haemochromatosis and HLA A3
Primary sclerosing cholangitis and HLA B8
Ulcerative colitis and HLA B27
HLA B8 is also associated with polymyalgia rheumatica.
Haemochromatosis is also associated with HLA B14.
Primary biliary cirrhosis is associated with HLA DR8.
Malabsorption association
Malabsorption may be associated with numerous disorders but typically occurs with:
Pancreatic exocrine deficiency
Short bowel
Coeliac disease: dermatitis herpetiformis is an association that responds to dapsone.
Inflammatory bowel disease.
Diverticular disease may be associated with bacterial overgrowth and malabsorption.
Helicobacter is associated with peptic ulceration not malabsorption.
Mesenteric ischaemia is associated with malabsorption but pain after eating is the main feature. Patients lose weight because eating is painful and from an element of malabsorption.
Regarding the rectum
The rectum lies in the posterior part of the pelvic cavity.
It is continuous with the sigmoid colon at the rectosigmoid junction where there is often an acute angulation (not constriction) in the intestine which may hamper the passage of the colonoscope.
When the rectum pierces the pelvic floor it turns abruptly downwards and backwards, and terminates at the anorectal junction where it is continuous with the anal canal.
Unlike the colon, the rectum is devoid of appendices epiploicae and has no taeniae, the longitudinal muscle being distributed uniformly around its circumference.
The upper third of the rectum is covered anteriorly and on both sides by peritoneum while the middle third, lying behind the rectouterine or rectovesical pouch, has peritoneum only on its anterior surface.
The arterial supply of the rectum is derived principally from the superior rectal artery, the continuation of the inferior mesenteric artery. This supply may be supplemented by middle rectal branches from the internal iliac arteries.
Regarding laparotomy
Intra-abdominal sepsis should be considered in all patients with MODS of unknown cause.
Bacteraemia caused by laparotomy initially worsens MODS causing a temporary (occasionally permanent) deterioration in the patient’s condition.
Septic patients are safer in theatre than in the radiology department and CT gives little information which will not be obtained at laparotomy.
Coagulopathy will be exacerbated by surgery and blood transfusion and will result in poor haemostasis or worse, no haemostasis.
Leaving the abdomen open initially allows for re-inspection of the wound, the abdomen should be closed when the patient’s condition has improved.
Abdominal drains inserted when…
Drains should be used prudently and not prophylactically. A wound should not be closed until adequate haemostasis has been achieved, with excessive / uncontrollable bleeding the abdomen should be packed with gauze. Adequate peritoneal lavage should be performed with soiling. Anastomotic breakdown is diagnosed clinically, drain outputs can be misleading. A drain in the gallbladder bed may cause a bile leak. The common bile duct is repaired around a T-tube, most surgeons place a drain close to the repair.
h2 receptors
H2 receptors mediate gastric acid secretion and are also present in human heart, blood vessels, uterus and the brain although their exact function is not clearly defined.
The H2 receptors in the stomach are situated on the basolateral aspect of the parietal cell.
The receptor complex spans the cell membrane and contains an adenylcyclase enzyme (without the need for a linked transmembrane protein). When the receptor is activated by histamine (not gastrin) the net result is an increase in intracellular cAMP which stimulates acid secretion and release from the parietal cell.
Omeprazole is a proton pump inhibitor and as the name suggests specifically inhibits the proton pump.
in ascites complicating cirrhosis
It should be remembered that a patient with ascites complicating cirrhosis will have hyperaldosteronism, i.e. sodium retention with consequent potassium loss.
There is:
Decreased vascular resistance,
Increased plasma volume, and
Low serum sodium.
Free fatty acids
Free fatty acid (such as alpha ketoglutarate and 3OH butyrate) release in starvation (and diabetic ketoacidosis) is responsible for ketosis.
Insulin inhibits the release of free fatty acids.
FFA stimulates hepatic gluconeogenesis and inhibits metabolism via the hexose monophosphate shunt and anaerobic glycolysis.
