GI Flashcards
what factors are red flags for endoscopy with upper GI disease
> 55, >4 weeks symptoms, dysphagia, persistent symptoms despite treatment, relapsing symptoms, weight loss
what investigations may be useful in a patient with GORD symptoms
barium swallow, demonstrate hernia, 24 hr luminal pH monitoring, confirm GORD when endoscopy normal
what associations are there wth GORD?
hiatus hernia, smoking, alcohol, pregnancy, obesity, drugs (anticholinergics, tricyclic antidepressants, nitrates), systemic sclerosis
what conditions can cause dysphagia?
malignancy (oesophageal/gastric/pharyngeal), benign strictures, external pressure (lymph nodes, aortic aneurysm, mediastinal mass, L atrial enlargement, bulbar palsy, oesophagitis from infection/reflux, scleroderma (thickening of oesophageal wall?immune) achalsia
what questions could be asked to differentiate causes of dysphagia?
liquids and/or solids? Difficulty swallowing both from start? (yes, suspect neurological/pharyngeal cause/motlty cause eg achalsia, no suspect malignancy),
difficult to make swallowing motion? yes, suspect bulbar palsy especially if coughing
painful to swallow? yes suspect Ca, oesophagitis, achalasia/oesophageal spasm
intermittent or getting worse and constant? if constant suspect Ca
neck bulge/gurgle on swallowing? pharangeal pouch
What are the common causes of jaundice
Prehepatic (gilbert’s, haemoglobinopathies, malaria)
Intrahepatic (metabolic (Alcohol,fatty liver) infectious (viral hepatitis,leptospirosis) autoimmune (PBC, autoimmune hepatitis, hereditary (wilsons), malignancy of liver or secondaries
Post hepatic (gallstones, malignancy, pancreatitis)
What patterns would be expected in bilirubin tests with pre/intra/post hepatic jaundice
Pre; Tot bilirubin normal/raised, conj normal, unconjugated normal/raised, urobilinogin normal/raised, urine bili normal
Intra; Total bili raised, conjugated raised, unconjugated raised, urobilinogen decreased, urine conjugated raised
Post Total bil raised, conj raised, unconj normal, urobilinogen decreased/-ve, urine conj raised
what are the components of autoimmune screen for the liver
Anti-mitocondrial antibody (PBC), anti sm antibody (autoimmune hepatitis)
what tests diagnose wilson’s
caeruloplasmin (reduced)
if inconclusive 24hr urinary copper
What tests should be done on a patient with signs of CLD
FBC, LFT, U and E, clotting (pTT/INR), amylase and lipase, consider viral and autoimmune, bloods for malabsorption, a-1 antitryptase and AFP
abdo US, consider ERCP if suspect stone, consider liver biopsy
what conditions caused a raised AFP
hepatocellular carcinoma, germ cell carcinoma, mets to liver
What are the symptoms of carcinoid syndrome? what tests can be done to dx?
Flushing
Abdominal pain
Diarrhoea – this can be severe, some people have diarrhoea 15 or more times a day
Loss of appetite
Wheezing
Fast heart rate
Dizziness due to blood pressure that may go up or down - this can be triggered by having an anaesthetic
tests will include one to measure the amount of serotonin in the blood and one to measure the amount of a protein called chromogranin A (CgA). Chromogranin A
what are the recommended number of alcohol units per week
21 men 14 women
what drugs commonly cause liver damage
amioderone, methotrexate
what are the treatment options for oesophageal varices
ABCDE, IV access and CVP, urinary catheter, Maintain bp no more than 90 systolic, cross match 6 units, transfuse hb >8 and haematocrit >0.3, correct platelet/clotting abnormalities with vit K/FFP/Platelets
IV b-blocker (carvidolol), antibiotic prophylaxis, vasoactives eg terlipressin (avoid diabetics/vasculophaty), endoscopy and banding.
Failure to control balloon tamponade with segstaken-blakemore tube or TIPPS (shunt between portal and hepatic veins. No clearance by liver so increased encephalopathy)
Liver transplant
1 unit of alcohol = ….of pure alcohol
10ml
rough amounts of units in alcoholic drinks
Pint of lager,2.5, pint of beer 3, large wine 3 small wine 1, regular 2. Bottle of wine 10, bottle of spirit approx. 30/40, bottle of 1l cider approx. 5
features of haemocromatosis
- Liver disease (hepatomegaly, 13%; cirrhosis, 13%, usually late in the disease)
- Skin bronzing or hyperpigmentation (70%)
- Diabetes mellitus (48%)
- Arthropathy
- Amenorrhea, impotence, hypogonadism
- Cardiomyopathy
- Osteopenia and osteoporosis[5]
- Hair loss
- Koilonychia (spoon nails)
causes of haematemasis
The most important cause of major life threatening acute gastrointestinal bleeding is peptic ulcer. Significant haemorrhage is due to erosion of an underlying artery and the magnitude of bleeding is related to the size of the arterial defect and the diameter of the artery; consequently bleeding from a large posterior duodenal ulcer which may erode the gastroduodenal artery and high, lesser curve gastric ulcers involving branches of the left gastric artery can be particularly severe. The majority of cases present with little or no history of dyspepsia, while a history of aspirin or non-steroidal anti-inflammatory drug (NSAID) consumption is common.
Oesophagogastric varices are a less common cause but because the patient often has other features of decompensated cirrhosis and because bleeding is often high volume the impact on hospital resources is high. Prognosis is related to the severity of liver disease rather than to the magnitude of bleeding.
Mallory-Weiss tears are usually associated with alcohol abuse but other causes of vomiting including drugs (chemotherapy, digoxin toxicity, etc), renal failure, or advanced malignancy may be responsible. Bleeding usually stops spontaneously and endoscopic therapy only required in rare severe cases.
Oesophagitis is a common finding in elderly patients who present with “coffee ground” haematemesis. Bleeding is never life threatening and conservative supportive therapy combined with the use of proton pump acid inhibitor drugs is all that is necessary.
Gastritis, duodenitis, and gastroduodenal erosions are often linked to NSAID use and to Helicobacter pylori infection. Circulatory support, stopping NSAIDs, and H pylori eradication are required.
management of haematemasis
The principles of “airway, breathing, and circulation” apply. Patients who present with major bleeding are frequently elderly and have significant cardiorespiratory, renal, and cerebrovascular co-morbidity. It is crucial that this is recognised and supported since most deaths are due to decompensation of general medical diseases precipitated either by the bleed itself or postoperative complications which are much more likely when medical co-morbidity is present.7 Central venous pressure monitoring is useful in the elderly and in patients with cardiac disease to optimise decisions concerning fluid replacement. Intravenous fluids should be given through a large cannula inserted in an anticubital vein. Crystalloids (principally normal saline) are used to normalise blood pressure and urine output; colloids (such as gelefusin) are often employed in the presence of major hypotension. Saline should be used with care in patients with liver disease.
Blood transfusion is administered to patients who are shocked and are actively bleeding. Blood is also transfused when the haemoglobin concentration is less than 100 g/l. The evidence base for this transfusion threshold is rather poor, but it is known in the intensive care setting that a haemoglobin concentration of less than 70 g/l has significant adverse cardiac effects and it is reasonable to pre-empt this by employing a value of 100 g/l in bleeding patients.
Appropriate monitoring includes measurement of pulse, blood pressure, urine output (through an indwelling catheter), and central venous pressure. Actively bleeding, shocked patients are managed in a high dependency environment.
