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269 Cards in this Set
- Front
- Back
What biochemical markers occur in chronic liver failure
|
1) high oestogen
2) high ammonia 3) low clotting factors 4) low albumin 5) impaired secretion of bile (jaundice) |
|
What are specific signs of portal congestion
|
1) ascites
2) splenomegaly 3) oesophageal varices |
|
What are the 3 stages of alcoholic liver disease
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1) faty liver (reversible)
2) steatohepatitis 3) cirrhosis |
|
What are teh non-alcohol causes of steatosis
|
1) obesity
2) diabetes 3) amiodarone |
|
Which 4 viral groups cause hepatitis
|
1) Hep
2) EBV 3) Herpes 4) CMV |
|
Which Hep's cause acutem fulminant and/or chronic hepatitis
|
Acute: ABCE
Fulminant: ABC Chronic: BCD |
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Which Hep's can be varried asymptomatically
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B and C
|
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What are liver segments
|
Anatomical regions based on branches of the portal vein
|
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Describe the features of cirrhosis
|
loss of normal architecture
fibrous bands with inflammation compression and destruction of branches of the portal vein Nodules of regeneration of parenchyma with steatosis |
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List 3 causes of cirrhosis
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Alcoholic metabolic
Infection Biliary obstruction |
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What are the bodies formed in alcoholic liver disease
|
Mallory's hyaline, precipitation of cytoskeleton from hepatocytes
|
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What cause of hepatitis should be considered in immunosupressed patients
|
EBV
CMV |
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What are the likely outcomes of Hep C
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Chronic hepatitis
cirrhosis hepatocellular carcinoma |
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What are the features of hep B chronic
|
portal inflammation
interface hepatitis (portatract interface encroachment of lymphocytes into lobule causing necrosis) lobular inflammation portal fibrosis linkage cirrhosis |
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What are the primary biliary diseases
|
Primary biliary cirrhosis: antimictochondrial antibodies against intrahepatic bile ductules
Primary schlerosing cholengitis (autoimmune, IBD scarring around and occlusion of large bile ducts) Congenital biliary atresia (common bile duct fails to form fully, can be bypassed surgically) |
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What does the liver look like with biliary cirrhosis
|
green, destruction of bile ducts and fibrosis around small and medium bile ducts.
Collections of granulomas and lymphocytes around bile ducts |
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What are the sites causing secondary biliary cirrhosis
|
Lumen: Gallstones, CF
Wall Obstruction: Pancreatic carcinoma obstructing common bile duct |
|
Hereditary haemachromatosis causes
|
Excessive absorption of iron from the GI, failure of regulatory mechanisms causing "rusted liver" and eventual cirrhosis
|
|
Alpha 1 antitrypsin ZZ phenotype causes
|
Liver parenchyma is destroyed causing cirrhosis. The abnormal alpha 1 antitrypsin precipitates as lobules
|
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What does Wilson's disease cause. How is it diagnosed
|
Deposition of copper in liver causing cirrhosis. KF brown ring surrounding iris
|
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What is absent in hepatocellular adenoma
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Portatracts but hepatocytes are present
|
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What are the major complications of hep B and C
|
Hepatocellular carcinoma
Cirrhosis |
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Why does lactic acid rise in liver failure
|
Glucose homeostasis unable to be maintained and muscle doesn't have G6p ase, but releases lactate into Cory cycle
|
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How are LFTs indicative of liver v skeletal muscle injury
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AST is present in skeletal muscle and can be elevated alone without liver damage
AST/ALT around 1 for viral hepatitis AST/ALT is 2 for ALD |
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In acute hepatitis, what is the effect on bile metabolism and excretion
|
Conjugation preserved
Conjugated hyperbilirubinaemia Liver oedema blocks biliary canniliculi, hence unable to excrete bile Urine and blood has high levels of conjugated bilirubinaemia |
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In fulminant liver disease, what are the principal biochemical derangements
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Hypoglycaemia and lactic acidosis
Ammonia encephalopathy Bleeding due to reduced clotting factors |
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How is AFP used to indicate liver disease
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Raised 10x if hepatocellular gegeneration, very high and increasing if cancer
|
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What is the likely cause of high indirect bilirubin and low direct with normal LFTs
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Gilbert's syndrome: congenital defective glucuronidase. Can worsen if blood glucose fall
|
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What are the markers of long standing biliary obstruction
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ALP, GGT produced by bile ducts
|
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What is raised in end stage alcoholic liver disease
|
Biliary obstruction, ALP, GGT
Raised cholesterol Normal ALT, AST due to prior damage to hepatocyted and destruction in prior waves Hypercalcaemia |
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What are the two methods of talking about the liver functional units
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lobule(pathology) v acinar (toxicolgists/pharmacists)
|
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What are the two features of cirrhosis
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Nodules of fibrosis surrounding a central core of regeneration
|
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What is the pathogenesis of fibrosis
|
Insult, nflammation, kuppfer cells release cytokines, stelate cells causes fibrosis in spaces of disse, loss of fenestrations, migration of lymphocytes, activation of bibroblasts causing loss of architecture and resistance of blood flow in sinusoids
|
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What are the consequences of portal hypertension
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There are shunts between the portal and systemic veins, collaterals form around the oesophagus and abdomen forming varices, backward congestion to the spleen, ascites
|
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How is steatohepatitis different to steatosis
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Inflammation, necrosis, Mallory bodies
|
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An alcoholic stops drinking, can he develop cirrhosis
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Past the point of steatohepatitis, the liver may continue to degenerate to cirrhosis
|
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What is the histological pattern of paracetamol toxicity
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Paradoxically zone 3 is most likely because of low oxygen in zone 3
|
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What are 3 metabolic liver disease
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Wilson's disease
Haemochromatosis G6P deficiency |
|
Describe the classifications of haemochromatosis
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Haemosiderosis (secondary, transfusion type with macrophage accumulation) - will not cause cirrhosis
HFE gene defect, primary disease with accumulation of iron in hepatocytes - cirrhosis |
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What is piecemeal hepatitis
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Hepatitis around the interface of the portal triad
|
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What histological sign is distinctive of hep B
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Ground glass bodies caused by accumulation of surface antigen
|
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What is the distinctive feature of autoimmune hepatitis
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Plasma cell infiltrate
|
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What is budkiari syndrome
|
Hepatic vein occlusion causing ascites, acute abdominal pain
|
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What is the cause of nutmeg liver
|
Heart failure
|
|
What are the commonest nodules of the liver
|
Haemangioma (blood vessel neoplasms)
Focal nodular hyperplasia Nodular regenerative hyperplasia (contraceptice pill) Diffuse nodular regeneration with obliteration of architecture) Bile duct adenoma |
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What are the neoplasms of the liver
|
Hepatocellular carcinoma
Haemangiosarcoma (endothelial origin) Cholangiocarcinoma Carcinoid Metastases |
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What are the risk factors for cholangiocarcinoma
|
hep c
? ? ? |
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Describe primary biliary cirrhosis
|
autoimmune destruction of intrahepatic bile ducts by antimitochondrial antibodies. Bile ducts are obliterated and absent from portal triad
|
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How is biliary schlerosis different from primary biliary cirrhosis
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Onion skin rings of fibrosis surrounding bile ducts
|
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Describe the pathology of reflux oesophagitis. What are 2 complications
|
oedema in epithelium, inflammatory cells, esp eosinophils
Complications are ulceration and Barretts oesophagus |
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Describe the pathogenesis of Barretts
|
Reflux and oesophagitis
glandular intestinal metaplasia with presence of goblet cells dysplasia with risk of high grade dysplasia and risk of adenocarcinoma of the glandular epithelium |
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Describe early oesophageal cancer
|
Early microinvasive adenocarcinoma with glands invafing the submucosa
|
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Multinucleated giant cells are found in an oesophageal biopsy. What is happening
|
Herpes virus infection
|
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A child has difficulty swallowing bolus and an oespophageal biopsy shows many eosinophils. What gives?
|
Eosinophilic oesophagitis
|
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What type of cancer is likely in the oesophagus of a heavy smoker/drinker. What is the course of the disease
|
SCC with likely invasion into the mediastinum
|
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What are risk factors for acute gastritis
|
H.pylori, age, alcohol, caffeine, burns, steroids, NSAIDS
|
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Describe autoimmune atrophic gastritis
|
Antibodies against crypt glandular cells with destruction of parietal cells and loss of intrinsic factor. Patient develops pernicious anaemia (glossitis, neuropathy, megaloblastic anaemia)
|
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What are the layers of a peptic ulcer
|
Exudate (necrosis)
Granulation tissue Fibrosis |
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AWhat are complications of a peptic ulcer
|
Perforation and possible adhesion with underlying pancreas or liver
Haemorrage Fibrosis and obstruction Carcinoma |
|
List gastrointestinal tumours
|
GIST (gastrointestinal stromal tumours (metastatic) made up of spindle cells - can be malignant)
Adenocarcinoma derived from adenomous polyps (villous, serrated) Lymphoma derived from MALT Mucocoele, haemangioma |
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What are the two types of stomach adenocarcinoma and what are the risk factors
|
Intestinal and diffuse
Diet, nitrosamines Tobacco H.pylori |
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What cells morphology is typical of adenocarcinoma, why?
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Signet ring cells. Cells are filled with mucin, pushing the nucleus to the extremity
|
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What haematological malignancy can occur in the stomach
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MALT lymphome forming very undifferentiated masses
|
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How has the prevalence of hepatitis A changed in developed countries
|
Hygeine has shifted the burden to older age groups with more a serious disease response
|
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How effective is the Hep B vaccine
|
Monovalent but does not cover against 20-30% escape mutants with weak binding of the surface antigen (may be in pre S region)
|
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What is the marker present in Hep B patients infected perinatally. What is the mechanism of infection of the foetus?
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HBeAg which has been passed on through the placenta and the foetus becomes immune tolerant
|
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Why are combination antivirals more effective than monotherapy against Hep B
|
Cross resistance occurs where one antiviral results in a mutation that affects the target epitope of another. Combinations with different targets greatly reduce the probability that the right sequence of mutations will occur to decrease the inhibition caused by both vaccines.
|
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Hoe does proglumide treat Zollinger-Ellison syndrome
|
Blocks gastrin receptors, effective because ZE involves neuroendocrine tumours secrting gastrin
|
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What drug counters the GI effects of NSAIDS, explain
|
NSAIDS inhibit the conversion of arachadonic acid to prostaglandin (which normally inhibits H+ secretion and promotes mucin secretion). Misoprostol is a prostaglandin agonist.
|
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A diabetic patient complains food is stuck in his oesophagus. What is happenning
|
Achalasia occurs because of vagal nerve lesions causing reduced oesophageal motility, increased LOS tone, decreased LOS relaxation
|
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What is typical in the herpes infected oesophagus
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Large multinucleated cells and numerous neutrophils
|
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Where does eosinic oesophagitis occur
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Throughout the entire length
|
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How is Barretts diagnosed
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Biopsy showing intestinal epithelium with goblet cells. Classification is short segment (<3cm) and long with shifting of the gastrooesophageal junction
|
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What is evident in advancing dysplasia followed by neoplasia in Barretts
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At the GE junction, adenocarcinoma forms with increase in glandular looking aggregations of abnormal cells
|
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How do the cell types differ between the antrum and fundus
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Antrum is absent of parietal cells and high in ECL cells
Fundus has high chief and parietal cell content |
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A bout of salmonella will cause what in the stomach
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Acute gastritis with small flat erosions (muscularis isn't penetrated). There is no fibrosis and evidence of contractile puckering around the erosions
|
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What does a PAS stain of H.pylori show
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Flagellated rods on the mucosal surface
|
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The diffuse type of adenocarcinoma shows what? What are signs on examination
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It is linitus plastica with a stiff, thickened submucosa reducing the lumen size. Shows signet ring cells. Identified by Virchows node and Sister Mary Joseph nodule at the periumbilicar region
|
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Do carcinoid tumours cause carcinoid syndrome
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Not in the GI tract because it secretes into the portal system causing first pass breakdown of vasoactive amines
|
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How do we grade GIST
|
Mitotic bodies
Size greater than 10cm |
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Who is at risk of gallstones
|
The F's: fair, fat, female, flatulant, family and resected or distal ileal disease eg Crohns wth decreased bile salt reabsorption
Gall bladder stasis Haemoglobinopathies eg thallassemia, sickle-cell Bile duct colonisation of SE Asians eg Ascaris lumbracoides |
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How likely are asymptomatic gallstones likely to cause symptoms. How likely that these will be serious
|
3% per year. 3-5% of these will develop complicated biliary disease eg cholestatic liver disease
|
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Describe the pathogenesis of gallstones
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Precipitation of bile constituents (mixed cholesterol) from a supersaturated solution. Small's triangle shows that stones form when the cholesterol content of bile rises or the lecithin or bile salt content falls.
|
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What is the role of an xray in diagnosis of gallstones
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None, cholesterol and mixed stones are not radio opaque
|
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How are brown pigment stones formed
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Deconjugation of bilirubin diglucuronidide, typically by pathogenic flukes and worms
|
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Describe the pain from a gallstone
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Epigastric, RUQ, infrascapular radiation (Boas sign), typically 1 hour after a fatty meal. Asociated with nausea.
|
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What are the complications of gallstones
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Fulminant necrotising pancreatitis due to choledocolythiasis
Septicaemia from cholangitis Cholecystitis, ulceration, perforation, fistula, empyema, emphysematous gall bladder, carcinoma |
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What is the likely cause of painless jaundice
|
Pre-hepatic: haemolysis (thallasaemia, sickle cell, G6P dehydrogenase deficiency, hereditary spherocytosis)
Hepatic, pancreatic or biliary tract cancers as opposed to a biliary calculus, NASH, Primary biliary cirrhosis |
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How is the function of a gallbladder tester
|
HIDA scan pre and following a fatty meal. Expect 80% ejection fraction
|
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An ultrasound shows a thickened gallbladder wall. What is likely
|
Gallstone causing inflammation of the gallbladder wall
|
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What are complications of a gallbladder from a stone
|
choledocolythiasis: (Cholangitis, pancreatitis, biliary cholic disease)
acute and chronic cholesystitis hydrops (mucus) Infection: empyema perforation gangrene emphysematous (gas filled wall - surgical emergency) Carcinoma (porcelaine gallbladder) |
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What is Charcod's triad
|
Cholangitis: ruq pain, fever jaundice
|
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What is Reynolds pentad
|
Sepsis due to infrcted biliary tree - shows sign of Charcods yriad plus confusion and other signs of sepsis (changes in vitals and urine output)
|
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What are the prognostic criteria and imaging of acute pancreatitis
|
Ransons indices eg wcc > 15, AST, age > 55, raised glucose 11+, raised urea (declining renal function)
Need contrast CT of pancreas |
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What is a porcelain gallbladder indicative of
|
Cancer in up to 40% of cases
GB 5th commonest GI cancer Cholesystectomy is compulsory |
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What are complications of a gallbladder from a stone
|
biliary colic
acute and chronic cholesystitis hydrops (mucus) Empyema perforation gangrene emphysematous (gas filled wall - surgical emergency) Cholangitis (inflammation of the bile duct) Carcinoma |
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What is Charcod's triad
|
Cholangitis: ruq pain, fever jaundice
|
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What is Reynolds pentad
|
Sepsis due to infected biliary tree - shows sign of Charcods triad (RUQ pain, jaundice, fever due to cholangitis) plus confusion and other signs of sepsis (changes in vitals and urine output)
|
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What are the prognostic criteria and imaging of acute pancreatitis
|
Poor if 3 or more of Ransons indices eg wcc > 15, decreased renal function ie raised urea, age > 55, glucose 11+, raised LDH, raised AST
Need contrast CT of pancreas |
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What is a porcelain gallbladder indicative of
|
Cancer in up to 40% of cases
GB 5th commonest GI cancer Cholesystectomy is compulsory |
|
Where is located
|
rectum to splenic flexure
|
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Where is Crohns located
|
From perineum to perianium
Colonic disease |
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How does Crohns present on colonoscopy
|
Transmural disease with pseudopolyps, dysplasia, exudate
|
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What tissue does UC affect and what do blood tests show
|
mucosa and submucosa, less mucosal damage than Crohns, hence CRP, platelets and haemoglobin are normal. May be positive to HLA-B27, especially if ankylosing spondilitis is present
|
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What does UC show on histology
|
Depletion of goblet cells
Crypt architecture distortion |
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What does Crohns show on histology
|
Granulomata with numerous mucin containing goblet cells (different to UC with absence of goblet cells)
Cobblestone mucosa Deep ulcerated mucosa Deep fissures and fistulas, sometimes to the abdominal wall |
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What are UC symptoms
|
Tenesmus causing trauma to anus, fissures
Urgency because of non compliant rectum Colic due to obstruction Infection of anal glands Fistula in ano discharge |
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What are Crohns disease
|
Colic due to ileal obstruction
Diarrhoea |
|
What other diseases are associated with Crohns
|
Primary schlerosing cholangitis
Ankyloding spondilitis |
|
Eye conditions associated with UC
|
Uveitis, scleritis due to thinning, injection
|
|
What skin conditions are associated with UC
|
pyoderma gangrenosum
erythema nodosum |
|
What types of arthritis are associated with UC
|
seronegative arthritis
ankylosing spondylitis Type 1 arthritis is polyarthritis |
|
What are the main serious complications of IBD
|
Fistulas and strictures in CD
Colorectal cancer Iron deficiency anaemia and anaemia of chronic inflammation B12 deficiency and bile dalt wasting due to ileal resection of CD |
|
What is the pathophys of UC
|
Mucosal dysfunction causing inappropriate immune response possibly to benign bacteria but also associated with the HLA-B27 antigen. the inflammation begins towards the rectum and proceeds without break along the sigmoid colon, possibly affecting the entire mucosa and sub-mucosa of the large intestine while sparing the muscularis and serosa. erosions and pseudopolyps line the mucosa, causing bloody diarrhoea.
|
|
Wha are protective factors for UC
|
Smoking and appendicectomy are protective
|
|
What are triggers for UC
|
Stress
Infection Smoking cessation Constipation (causes more proximal flareups) |
|
What is the association of UC and goblet cells
|
Improper unfolding of mucin causing apoptosis of goblet cells
|
|
What are the targets of treatments for IBDs
|
1) Modulate NK T cell function, hence, budesonide, hydrocortisone, prednisolone, cyclosporin
2) Aminsalicylates: released in different parts of the colon 3) Purine analogues, azathiopurine hijacking the purine salvage pathway causing abnormal ribonucleoside formation inhibiting t cell production. Take 6 months to work so need to start on steroids |
|
What is the Paed treatment for UC
|
Exclusive enteral treatment followed by biologics (azathioprine)
|
|
What surgical treatments are used for CD
|
Ileal resection
Stricturoplasty or resection Colectomy Temporary diversion ileostomy to allow healing on rectum, anus and perianum |
|
What are the common viruses casing colitis
|
rota
norwalk, noro astro herpes (cmv, herpes simplex) |
|
What are the types of enterotoxins
|
secretogogues (travellers)
Cytotoxins (shigella) with invasion Staphylcoccal exotoxin |
|
Describe the pathogenesis and complications of campylobacter
|
uncooked chicken, faecal oral route
neutrophil infiltrate exudes into lumen, severe inflammation and sloughing of mucosa complications include reactive arthritis and Guillian-Barre |
|
What are the complications of c.difficile
|
Watery diarrhoea, dehydration, fever
Ulcerations and volcano lesions |
|
What gene is associated with IBD
|
NOD2
|
|
In UC, what is the pattern of colon involvement
|
Rectum to distal colon with no ulceration. Serosal surface is normal. Inflammation is continuous
|
|
A section of bowel shows a fissuring ulcer affecting the muscularis. What is the likely disease
|
CD
|
|
How does cancer risk increase with UC
|
10 years 2%
20 years 10% 30 years 20% Higher risk with pan colitis |
|
What type of cancer occurs with UC
|
Signet ring adenocarcinoma
|
|
What is the difference between collagenous colitis and lymphocytc colitis
|
Collagenos collitis is thickening of collafen of lamina propria with lymphocitic infiltate. Lymphocytic collitis is less severe with less thickening of the epithelium
|
|
What comon dysplatic lesions are present in UC
|
Villous adenoma. Can develop into adenocarcenoma when it penetrates the basement membrane
|
|
What is the pathophysiology of serrated polyps
|
Generally have either BRAF or KRAS mutations ihibiting apoptosis and forming serrated lesions. Sessile serrated polyps appear as innoculous raised lesions. Dysplasia can arise leading to adenoma.
|
|
What are the main pathways to colon cancer
|
1) Chromosomal instability pathway causing adenoma leading to adenocarcinoma.
Serrated neoplasia pathway where serated polyps undergo mutatios in BRAF and KRAS, dysplasia folliwed by gene methylation of DNA repair and gene (silencing) followed by rapid progression of adenocarcinoma |
|
What is the prognosis of FAP
|
Colon is carpeted with polyps and 100% risk of cancer development, hence early colon resection
|
|
With rectal bleeding, what are the examination requirements
|
Anaemia (may not show as occult)
Jaundice for metastaces and lymphadenopathy Abdo palpation of enlarged organs and masses or tenderness Rectal blood, masses, fissures DRE, look at any residual stool, blood, mucus |
|
How can you interpret bloody faeces in a DRE
|
Blood mixed with stool Ca
Surface blood with pain: fissure Blood with mucus IBD |
|
What are the investigations for rectal bleeding
|
Colonoscopy
CT for identifying masses but not fine enough for polyps Double contrast barium enema picks up gross changes but not subtle mucosal changes |
|
What could be visualised by barium enema for lower GI bleed. Why is there risk involved with the procedure
|
Diverticular disease
Strictures Masses Baloon in anus and air inflation of abdomen can perfrate the bowel |
|
What are red blood cell scans used for
|
RBC scintography to find a bleeding point
|
|
Describe anal fissures
|
Tear in rectal epithelium (may involve ischemia in acute fissures) exacerbated by constipation and bowrl motions. Rectogesic relaxes the sphincter and Proctosedyle reduces ischemia. High fibre diet recommended
|
|
Describe the aetiology and pathophys of diverticular disease
|
Normally fibre retains water in stools. In western low fibre diets, usually after 40yo, the bowel has to generate high pressures to move the dry stool. Points of weakness occur where blood vessels enter the bowel, diverticula (outpouching) form that can perforate, become infected. Pain may be present in LLQ. Bleeding points arise causing dark red stools.
|
|
What is angiodysplasia
|
Enlarged veins in right colon. Usually patients with valvular disease, renal failure. Can bleed at different rates.
|
|
Describe pancreatitis
|
Acute inflammation of pancreas with regional tissue involvement and remote organ systems. Can be fatal.
|
|
List the causes of pancreatitis
|
Alcohol 25%, gallstones 50%
Post ERCP trauma idiopathic 25% |
|
Describe the clasification of acute pancreatitis
|
Mild w no organ failure
Moderate w transient organ failure Severe persistent organ failure Critical - persistent multi organ failure |
|
Describe the pain and symptoms of acute pancreatitis
|
Severe epigastric pain with radiation through to back. Vomiting, fever
|
|
What is the score system used for acute pancreatitis
|
Ranson criteria
|
|
What investigations are used for acute pancreatits
|
Lipase and amylase
Ranson score tests (glucose, urea, AST, LDH, WCC) Imaging: High def ultrasound to find cholesystitis, bile duct enlargement. CT ERCP if Ranson score >3 ie severe plus jaundice plus cholengitis CRP LFTs |
|
Describe the phases of acute pancreatitis
|
Acute phase: inflammatory phase with minimal necrosis but organ failure, ischaemia, SIRS
Necrotic phase with deterioration of Ranson score, infection, sepsis, pseudocyst forming in lesser sac |
|
What are the causes of chronic pancreatitis
|
Chronic alcohol abuse
Hereditary pancreatic disorder Pancreas divisum with narrow accessory papilla formed by non fusion of dorsal and ventral buds. |
|
What are the clinical features of chronic pancreatitis
|
Endocrine and exocrine insufficiency, steatorrhoea, diabetes, malabaorption of fat soluble vitamins with bruising & bleeding
|
|
Why is xray and ultrasound not an effective investigation of chronic pancreatitis
|
Colon gas obscures pancreas. Better to use ERCP (2% mortality), CT and MRI
|
|
What are the risk factors and predispositions of developing pancreatic cancer
|
tobacco
obesity chronic pancreatitis tooth or gum disease hereditary pancreatitis polyposis coli |
|
What are the areas responsible for emesis
|
ctz (5ht3, dopamine D3)
Vestibular (Ach) GI (H1) Medullary vomiting centre |
|
A patient post GI surgery requires a laxative. Which are used
|
Stool softeners to reduce peristaltic effort eg docusate
|
|
A patient reveals his diet is very high in fat and protein and low in vegetables. Is a stimulant or stool softener appropriate
|
Neither is appropriate, need bulking agent to increase size and water content of stool to decrease colonic forces and mucosal injury
|
|
What agents in addition to proton pump inhibitors are used in GORD, why?
|
Prokinetics increase tone of LOS and increase gastric emptying
|
|
What are the congenital gi abnormalities
|
Atresia of bowel or anus
Hirschprung with loss of ganglion cells of myenteric plexus, megacolon, dilation, ischemia Duplication Meckel's diverticulum and congenital diverticulitis |
|
Dilation of colon is caused by.
|
Inflammation of submucosa due to toxic megacolon in UC
Chagas Hirschprung |
|
Protozoal causes of diarrhoea
|
Cryptosporidium
Entamoeba hystolitica Giardia |
|
Viral causrs of diarrhoea
|
rota
adeno astro calci |
|
Enterotoxin bacteria
|
Vibrio
Clostridium perfringens E.coli |
|
What neoplasia causes diarrhoea
|
Villous adenoma (lots of excess goblet cells) producing mucin
Carcinoid (eg seratonin, prostaglandin, peptides) |
|
What type of diarrhoea is caused by pancreatitis
|
Osmolar, cf intraluminal malabsorption eg lactose intolerance
|
|
What are the complications of pseudomembranous colitis
|
Diarrhoea due to epithelial destruction, bleeding, inflammation and sepsis
|
|
What causes large amoebic ulcers. What is the main presentation
|
Entamoeba hystolitica. Diarrhoea with blood
|
|
Small round structures (smaller than lymphocytes) are seen attached to the intestinal lumen. Who is likely to be infected by what
|
Cryptosporidium infecting immunosuppressed patients
|
|
Explain radiation colitis
|
Radiation therapy of uterine cancer causes damage to blood vessels causing ischemia plus damage to enterocytes
|
|
What is the classic inflammatory feature of Crohn's
|
Non caseating geanulomas made up of epitheloid macrophages and giant cells
|
|
Most common causes of ischemic bowel disease
|
Atheroma, Angiodysplasia, embolus, strangulated hernia, volvulus
|
|
Complications of diverticula
|
Fistulae
Infection, abcesses Rupture Hypertrophy of neck muscularis making the lumen smaller causing impaction |
|
What clinical conditions cause haemorroids
|
Portal hypertension
Pregnancy compressing the IVC |
|
What painful complication occurs with haemorroids
|
Infarct
|
|
What polyps are of most concern
|
Adenomatous polyps
|
|
What would a surgeon do with hyperplastic polyps
|
Nothing, benign
|
|
What types of bowel adenomas are there
|
tubular
villous (most prone to hyperplasia) Tubulovillous sessile serrated |
|
What congenital condition predisposes to bowel anenocarcinoma
|
familial adenomatous polyposis
|
|
A mutation in DNA repair causes what bowel cancer
|
Hereditary non-polyposis colorectal cancer
|
|
Risk factors for colorectal carcinoma
|
Excessive calorie intake
low fibre refined carbohydrates hugh meat |
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What does a typical advanced colorectal cancer lesion look like
|
Inflamed raised irregular borders, central necrosis with either fibrotic repair or perforation of the ulcer. Prognosis is poor.
|
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An alcoholic shows shadows on an xray in the peritoneum. What is this
|
Fat necrosis due to pancreatitis
|
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What colon abnormality occurs with laxative abuse
|
Melanosis coli due to high turnover and prolferation of immature pigmented epithelial cells
|
|
What are the broad types of diarrhoea and give examples
|
Secretory (Cholera enterotoxin, rotavirus)
inflammatory (C.jejuni) osmotic (lastase) motility (diabetes) |
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What is the most common infective cause of diarhoea in adults and children
|
adults - norovirus
children - rotavirus (notifiable) |
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What are the most common causes of dyesntry
|
Campilobacter
Salmonella Yersinia Shigella |
|
Commonest cause of acute bacterial in children and travellers
|
Enterotoxogenic E.coli
|
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What are forgotten questions regarding diarrhoea in history taking
|
Abdo pain, vomiting, contacts, mucus in addition to the usual history of duration, volume, frequency, blood
|
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A person returns with travellers diarrhoea. Are antibiotics and loperimide indicated
|
Resolves in days but no loperimide with blood, fever or children
|
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An elderly person presents for the first time with chronic diarrhoea. Causes?
|
Microscopic colitis
Faecal impaction Colon cancer |
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What are the broad causes of acute diarrhoea. What are the alarm signs
|
Infective
Blood, systemic illness, dehydration |
|
What are entero invasive bacteria
|
Shigella
EIEC Salmonella |
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What are the 3 classes of toxins
|
Neurotoxins
Secretory Cytotoxins |
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Indicate the three classes of GI infection. Where does each occur and give examples
|
Non inflammatory infection of upper GI - watery eg cholera, rota, noro, staph, cerius, clostridium, giardia, EPEC
Inflammatory of colon causing dysentry, shigella, campylobacter, salmonella, entamoeba histolytica, EIEC Imvasive of distal SI causing enteric fever, typhoid, yersinia |
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How does bacillus mediate GI clinical features
|
In starchy foods - ingestion releases emetotoxin
In other cooked foods the toxin causes diarrhoea |
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A patient's stool dample cultured ETEC, what do you advise the patient
|
Traveller's diarrhoea, self limiting in 3 days
|
|
Weenling diarrhoea is caused by. . .
|
Rota and ETEC
|
|
What are the complications of salmonella
|
If invasive then systemic illness invading joints causing arthralgias, endocarditis and aortitis
|
|
What is the mechanism of shigella infection
|
Shigella toxin: enterotoxin, cytotoxin, neurotoxin and can cause haemolytic uraemic syndrome
|
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Why aren't antibiotics used to treat shigella
|
Attack of bacteria by antibiotic causes release of large amounts of the phage toxin
|
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Why is Salmonella typhi a concern
|
Penetrating the bowel and colonises peyer's patches, causes bacteraemia resulting in fever, splenomegaly and features of sepsis. May not cause diarrhoea
|
|
What are the forms of irritable bowel
|
spastic
diarrhoea constipation/diarrhoea |
|
What are the ckinical signs of irritable bowel
|
Pain (lower left)
altered bowel habits bloating (out of proportion) upper GI symptoms (gerd, nausea, vomiting) GU symptoms, viscera becomes irritated and presses on bladder: urgency, nocturea, frequency |
|
What are the ROME criteria
|
3 months of continuous symptoms of pain or discomfort such that:
Relieved by bowel movement Coupled with change in frequency (more than 3 per day) Mucous Bloating Incomplete feeling of evacuation, urgency, straining Extraintestinal symptoms include nausea, fatigue |
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Why is a gynae exam and xray indicated for irritable bowel syndrome suspect
|
xray indicates bowel distension
gynae hx and exam rules out pain from GU source (endometriosis) |
|
What is the aetiology of haemorroids
|
Portal hypertension
Pregnancy Chronic constipation Straining |
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What are the causes of intestinal obstruction
|
hernia
volvulus intersussception adhesion tumour |
|
FAP
|
Familial adenomatous polyposis
Autosomal dominant Mutations of APC gene |
|
What is GIST
|
GI Stromal Tumour - carcinoid
|
|
What are the fluid compartments of the body and which is the most volume. What factors change these volumes
|
intracellular 60%
Extracellular is plasma plus interstitial transcellular age and obesity reduces the fluid to weight ratio |
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If 2L are lost through a NG tube, what is needed as a replacement
|
Basal 3 L plus 2L with high NaCl content
|
|
A patient following trauma has reduced bp but haemoglobin 95. Should you transfuse
|
If blood loss caused hypotension then transfuse. Use lower limit of 70 for anaemic patients
|
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A diabetic admitted with diabetic acidosis with hyponatremia. What is the effect of administring insulin
|
Glucose is highly osmotic and shifts fluid from the extracellular space to the intravascular space, hence the decrease in sodium concentration is artifactual (dilutional). The fluid shift out of the intravascular space restores the sodium level
|
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What are the main causes of small bowel pathologies. give one specific example of each
|
obstruction (incarcerated hernia, intersussception, adhesions, tumour, ileus from a stone or meiconium)
infection (Ghiardia, Shigella, EHEC, ETEC) malabsorption (coeliac (gliaden hypersensitivity), ghiardia, Crohn's) ischaemia (strangulated hernia, volvulus, blockage of superior mesenteric arrtery by thrombus, emboli, shock, LVF) tumours (adenomas, adenocarcinoma, lymphomas, carcinoid |
|
What is the most common small bowel congenital abnormality
|
Meckels diverticulitis
Remnant of vililline duct that can become inflamed causing umbilical pain |
|
What are the 3 malabsorption syndromes
|
coeliac
tropical sprue Whipples |
|
What is the pathology of coeliac disease
|
Causes atrophy of villi with lymphocyte infiltration (plasma cells secreting anti gliaden IgA) of the lamina propria and epithelium. Partial or total villous atrophy is possible.
T cell mediated disease of gliaden sensitivity Associated to hladq2 and dq8 Cure is gluten free diet |
|
Describe the pathology of tropical sprue
|
Bacterial overgrowth of unknown pathogen causing B12 and folate depletion. Treated with broad spectrum antibiotics
|
|
Large numbers of macrophages in the lamina propria is associated with a form of sprue. What is it
|
Whipples disease caused by a bacteria that cannot be destroyrd by macrophages
|
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A patient presents with steatorrhoea and malabsorption. What is likely and what investigations
|
Giardia - stool sample to identify cysts. If villous atrophy is present then it may be compounded by coeliac disease,vrequiring antibiotic treatment and gluten free diet
|
|
What dors dog hookworm cause
|
Eosinophilic enteritis causing intestinal wass thickening, abdo pain, rectal bleeding and obstruction. Eosinophils proliferate in the intestinal wall.
|
|
What are the two main complications of hernias
|
incarceration (not reducible by pressing or lying down) and strangulation. This causes venous blockage and ischemia
|
|
What are adhesions
|
Internal hernias formed by healing adhesions of the peritoneum resulting in obstruction or ischaemia
|
|
What is the cause of intersussception in adults and what is the complication
|
Tumour. If mesentary is caught then blood flow is obstructed
|
|
what are causes of small bowel obstruction
|
tumours
strictures pseudo obstruction such as paralytic ilius or complication of Crohn's |
|
What are the modes of occlusion of the superior mesentaric artery
|
Atheroschlerosis
Embolism |
|
What is the most common cause of venous occlusion of the small bowel
|
External compression such as hernia, volvusus, adhesions causing haemorragic infarction due to continues inflow of arterial blood causing red boggy necrosed tissue
|
|
What are causes of non occlusive ischaemia of the small bowel
|
shock
chf dehydration |
|
Fibrosis and stricture can occur at the site of the iliocaecal junction. How
|
Chronic ischaemia
|
|
What are the complications of a haemangioma
|
Intersussception and obstruction
|
|
What is the most common cancer of the small bowel
|
Carcinoid tumours causing diffuse slow growing metastatic disease. Appendix carcinoids, most common, are benign.
|
|
What is the most common haematological neoplasm of the small intestine
|
Maltomas - B cell lymphoma resulting from untreated helicobacter.
T cell lymphomas are caused by coeliac. |
|
Pathology of acute appendix
|
Faecal nodule blocks lumen allowing colonisation by microbes, inflammation, peritonitis and perforation
|
|
What are the common causes of appendic pathology
|
Acute appendicitis
Carcinoid Parasites Adrnoma or adenocarcinoma causing mucocoele which can infiltrate the peritonium (dissrminated mucinous tumours) |
|
Why does meiconium iliem lodge in the ileum
|
Ileocoecal valve causes obstruction
|
|
What type of infarct occurs in the bowel and why
|
Red infarct because of dual blood supply
|
|
What is the typical gross appearance of Crohn's
|
Cobblestone mucosa
|
|
What infiltration is present in Coeliac
|
lymphocytes in mucosa and plasma cells in the submucosa
|
|
Cancers if the SI
|
carcinoid
metastatic lymphoma adenocarcinoma GIST |
|
What features would be visible in small bowel cancer
|
Lymphomas are white, homogenous and invades mesentary
Melanoma Metastices are irregular, polypoid and ulcerated Carcinoid are well demarcated and yellow |
|
What are the causes of chronic inflammation in the appendix
|
Crohn's
Yersinia TB |
|
What is the cause of an all white appendix
|
Mucocoele caused by adenoma or andenocarcinoma
|
|
Where can mucinous depositing tumours form
|
Mucinous myxoma in SI, pancreas and ovaries. Can develop a swiss cheese and concrete look
|
|
What does the histology of carcinoid look like
|
Nests of smal cells with lots of cytoplasm
|
|
What can happen with Meckel's
|
Ulceration
Dilatation Perforation Inflammation infection Obstruction |
|
An area of mucosa shows thickening, loss of normal mucosa and adhesions. What inflammatory process is likely to cause this
|
Crohn's
|
|
The intestine of a baby is obstructed with a green yellow mass. What is it
|
Meiconium ileus
|
|
What are the complications of intersusseption
|
Obstruction
Ischaemia Infarct |
|
An appendix has white regions. What are the ddx
|
Mucocoele
Acute appendicitis with puss and fibrin Lymphoma |
|
A small bowel has an irregular yellow mass post infection. What is it
|
Xanthogranuloma caused by foam cell macrophages accumulating lipid
|
|
What physical examinations indicate alcoholism
|
Dupytrens
Signs of Wernicke-Korsakoff (abnormal gait, nystagmus) Decreased personal hygeine and grooming |
|
Contrast different colicky pain
|
Biliary cholic is associated with meals and never completely is relieved
True colic is peristaltic and waxes and wanes every 8 minutes |
|
What is the histological picture of chronic cholesystitis
|
fibrosis, lots of macrophages, wall thickening
|
|
Describe the pathology of an indirect inguinal hernia. What are the complications.
|
In males, the testes form adjacent to the kidneys through the internal ring via the inguinal canal. This is an anatomical defect of the posterior abdominal wall allowing the samall intestine to enter, become incarcerated or strangulated causing obstruction and ischaemia
|
|
Describe the location of a femoral hernia. Who is at risk and why
|
Femoral vein, inguinal ligament and lacunar ligament form the borders with bone beneath. The region is more open in females because of hip geometry. Common cause of strangulation, incarceration
|
|
List the common groin lumps
|
Inguinal hernia
Femoral hernia Hydrocoele Cysts Lymph nodes (infection or malignancy) Skin lesions (cancers) Lipomas, seb cysts, abcess |
|
What are 3 ways to determine the cause of an enlarged femoral node
|
Fine needle
Core biopsy Gland excision Femoral aneurism (pulsatile) Varicocoele, saphino varynx (fills on standing) |
|
What can ultrasound find in the GB
|
calculus (appears opaque)
polypoidal mucosal thickening (not a polyp but indicates carcinoma) tumour (adenoma) |
|
Whar can ultrasound and CT identify in pancreatic pathology
|
Hypodense areas of necrosis
Calcifications Peripancreatic fluid shadowing Bleeding into a cavity |
|
What would ultrasound identify with a renal calculus
|
Dilated calices and the echogenic calculus itself
The ureteric junction is a likely spot for the calculus Hydroureter |
|
RIF pain ddx
|
mesenteric adenitis
appendicitis ectopic pregnancy |
|
What can ultrasound identify in appendicitis
|
faecolith
Thickened wall Increased vascularity when using doppler |
|
A CT shows a narrow lumen in an appendix with dark areas around it. Explain
|
Wall thickening and periappendicular effusions indicating acute appendix
|
|
A patient with acute llq pain shows a well defined anechoic sac adjacent to the uterus but within the abdo cacity. What's happening
|
Ectopic pregnancy
|
|
What are the ddx of RIF pain
|
appendicitis
acute appendix, ectopic preg, mesenteric adenitis infection carcinoid lymphoma |
|
What pathologies might be visible on CT with acute LIF pain
|
UC shows ulcerations
Diverticular disease Diverticular abcess Free air indicates perforated viscus Small bowrl obstruction showing proximal dilation and distal collapse (adhesions, incarcerated hernia, intersussception, Crohn's, tumour, carcinoma) |
|
What are the large bowel obstructions common in the elderly
|
Volvulus
Ischaemic cholitis (atheroschlerosis, embolus) |
|
What can US show in obstructive jaundice
|
Dilated ducts (intrahepatic and common bile)
Calculi |
|
What are the causes of ascites
|
Cirrhosis
RHF Peritonitis Pancreatitis Cancer (peritoneal, intrahepatic) |
|
List 5 GI causes of clubbing
|
Primary biliary schlerosis
liver cirrhosis Inflammatory bowel disease hepatopulmonary disorder Malabsorption (Whipples, coeliac, tropical sprue, pancreatic insufficiency) |