Gastro 2 Flashcards
Types o/f bariatric surgery
Primarily restrictive operations
laparoscopic-adjustable gastric banding (LAGB)
it is normally the first-line intervention in patients with a BMI of 30-39kg/m^2
produces less weight loss than malabsorptive or mixed procedures but as it has fewer complications
sleeve gastrectomy
stomach is reduced to about 15% of its original size
intragastric balloon
the balloon can be left in the stomach for a maximum of 6 months
Primarily malabsorptive operations
biliopancreatic diversion with duodenal switch
usually reserved for very obese patients (e.g. BMI > 60 kg/m^2)
Mixed operations
Roux-en-Y gastric bypass surgery
is both restrictive and malabsorptive in action
What is the urea breath test?
patients consume a drink containing carbon isotope 13 (13C) enriched urea
urea is broken down by H. pylori urease
after 30 mins patient exhale into a glass tube
mass spectrometry analysis calculates the amount of 13C CO2
should not be performed within 4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)
sensitivity 95-98%, specificity 97-98%
may be used to check for H. pylori eradication
What is the CLO test?
Rapid urease test (e.g. CLO test)
biopsy sample is mixed with urea and pH indicator
colour change if H pylori urease activity
sensitivity 90-95%, specificity 95-98%
what is haemochromatosis?
Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by the inheritance of mutations in the HFE gene on both copies of chromosome 6.
How is Haemochromatosis investigated?
There is continued debate about the best investigation to screen for haemochromatosis.
general population
transferrin saturation is considered the most useful marker
ferritin should also be measured but is not usually abnormal in the early stages of iron accumulation
testing family members
genetic testing for HFE mutation
These guidelines may change as HFE gene analysis become less expensive
Typical iron study profile in patient with haemochromatosis
transferrin saturation > 55% in men or > 50% in women
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC
Further tests - LFTs, MRI, liver biopsy
How is haemacromatosis managed?
venesection is the first-line treatment
monitoring adequacy of venesection: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
desferrioxamine may be used second-line
Investigations for pancreatic cancer?
ultrasound has a sensitivity of around 60-90%
high-resolution CT scanning is the investigation of choice if the diagnosis is suspected
imaging may demonstrate the ‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts
features of pancreatic cancer?
painless jaundice
pale stools, dark urine, pruritus
cholestatic liver function tests
the following abdominal masses may be found (in decreasing order of frequency)
hepatomegaly: due to metastases
gallbladder: Courvoisier’s law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
epigastric mass: from the primary tumour
many patients present in a non-specific way with anorexia, weight loss, epigastric pain
loss of exocrine function (e.g. steatorrhoea)
loss of endocrine function (e.g. diabetes mellitus)
atypical back pain is often seen
migratory thrombophlebitis (Trousseau sign) is more common than with other cancers
what is Zollinger-Ellison syndrome?
Zollinger-Ellison syndrome is a condition characterised by excessive levels of gastrin secondary to a gastrin-secreting tumour. The majority of these tumours are found in the first part of the duodenum, with the second most common location being the pancreas.
Around 30% of gastrinomas occur as part of MEN type I syndrome.
what are the features of Zollinger Ellison syndrome?
And how is it diagnosed?
Features
multiple gastroduodenal ulcers
diarrhoea
malabsorption
Diagnosis
fasting gastrin levels: the single best screen test
secretin stimulation test
How do you diagnose bile acid malabsorption
the test of choice is SeHCAT
nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT)
scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT
how is bile acid malabsorption managed?
bile acid sequestrants e.g. cholestyramine
Prophylaxsis against variceal haemorrhage?
Propranolol - reduced rebreeding and mortality - non selective beta blocker which decreases portal venous pressure by reducing cardiac output and splanchnic blood flow
Endoscopic variceal band ligation (superior to endoscopic sclerotherapy)
Offer endoscopic variceal band ligation for the primary prevention of bleeding for people with cirrhosis who have medium to large oesophageal varices.’
it should be performed at two-weekly intervals until all varices have been eradicated
proton pump inhibitor cover is given to prevent EVL-induced ulceration
Transjugular Intrahepatic Portosystemic Shunt (TIPSS) may be used if the above measures are unsuccessful in preventing further episodes
what are the causes of Budd-Chiari syndrome?
polycythaemia rubra vera
thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
pregnancy
combined oral contraceptive pill: accounts for around 20% of cases
features of Budd chairi syndrome?
The features are classically a triad of:
abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly
what is Budd chair syndrome?
Budd-Chiari syndrome, or hepatic vein thrombosis, is usually seen in the context of underlying haematological disease or another procoagulant condition.
investigations for Budd Chiari syndrome?
ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation
what happens in referring syndrome?
hypophosphataemia
this is the hallmark symptom of refeeding syndrome
may result in significant muscle weakness, including myocardial muscle (→ cardiac failure) and the diaphragm (→ respiratory failure)
hypokalaemia
hypomagnesaemia: may predispose to torsades de pointes
abnormal fluid balance
what is the pathophysiology of hypophosphataemia in referring syndrome?
Shift from Fat to Carbohydrate Metabolism: In refeeding syndrome, the reintroduction of carbohydrates leads to a shift from fat to carbohydrate metabolism. This switch activates insulin secretion, which in turn increases cellular uptake of glucose.
Intracellular Movement of Phosphate: Insulin and increased glucose uptake stimulate the intracellular movement of phosphate, which is used in the synthesis of ATP and 2,3-diphosphoglycerate in erythrocytes. This intracellular shift reduces serum phosphate levels.
Decreased Phosphate Stores: Patients with chronic malnutrition often have depleted phosphate stores, although their serum phosphate levels may initially be normal. When refeeding starts, the sudden demand for phosphate in anabolic processes exceeds the supply, leading to hypophosphatemia.
clinical consequences of hypophphopshataemia in referring syndrome?
Cardiac Dysfunction: Hypophosphatemia can impair myocardial contractility, leading to heart failure. It may also cause arrhythmias due to its role in maintaining normal cellular electrophysiology.
Respiratory Failure: Phosphate is essential for ATP production, necessary for respiratory muscle function. Severe hypophosphatemia can lead to muscle weakness, including the diaphragm and intercostal muscles, potentially resulting in acute respiratory failure.
Neurological Complications: These can range from confusion and seizures to coma, attributable to disturbed ATP metabolism in the central nervous system.
Haematological Effects: Reduced 2,3-diphosphoglycerate levels in erythrocytes affect oxygen release from haemoglobin, leading to tissue hypoxia. Hypophosphatemia can also result in hemolysis.
Rhabdomyolysis: Phosphate depletion impairs ATP production in muscles, which can lead to muscle breakdown and rhabdomyolysis.
how is familial adenomatous polyposis inherited?
Familial adenomatous polyposis (FAP) is an autosomal dominant disorder
what is ischaemic colitis?
Ischaemic colitis describes an acute but transient compromise in the blood flow to the large bowel. This may lead to inflammation, ulceration and haemorrhage.
what sit is most commonly affected in ischaemic colitis?
It is more likely to occur in ‘watershed’ areas such as the splenic flexure that are located at the borders of the territory supplied by the superior and inferior mesenteric arteries.
what would an XR show in ischaemic colitis?
‘thumbprinting’ may be seen on abdominal x-ray due to mucosal oedema/haemorrhage
What is Wilson’s disease and how is is inherited?
Wilson’s disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues. Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion.
where is the gene defect located in Wilsons disease?
Wilson’s disease is caused by a defect in the ATP7B gene located on chromosome 13.
