GI and Liver Flashcards

1
Q

What infections can occur in the oesophagus?

A

Candida albicans (fungus) and herpes simplex virus.

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2
Q

What is achalasia?

A

Failure of lower oesphageal sphincter to open during swallowing.

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3
Q

What is Schatzki ring?

A

A narrowing of the lower oesphagus that cause cause difficulty swallowing (dysphagia).

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4
Q

What is a Curling’s ulcer?

A

An acute gastric erosion resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa.

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5
Q

Name some acute causes of gastritis

A

Alcohol, medications eg. NSAIDs, severe trauma, burns (curlings ulcer), surgery.

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6
Q

Name some chronic causes of gastritis

A

A:Autoimmune
B:Bacterial (H. pylori)
C:Chemical

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7
Q

What is achlorhydria?

A

Absence of hydrochloric acid in the gastric secretions.

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8
Q

What is autoimmune gastritis?

A

Autoimmune destruction of parietal cells due to auto-antibodies against intrinsic factor and parietal cell antibodies in blood. Leads to complete loss of parietal cells and pyloric and intestinal metaplasia. Achlorhydria which leads to bacterial overgrowth. Persistent inflammation which can lead to epithelial dysplasia and may lead to cancer.

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9
Q

What are the patterns of gastritis that H. pylori cause?

A

1) Antral-predominant gastritis. Hypergastrinaemia and duodenal ulceration. Associated with lower IL-8 levels.
2) Pangastritis. Hypochlorhydria, multifocal atrophic gastritis, intestinal metaplasia and cancer. Associated with higher IL-8 levels.

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10
Q

What are the consequences of peptic ulceration?

A

Haemorrhage, perforation and fibrosis (leading to stenosis).

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11
Q

What is chemical gastritis?

A

Few inflammatory cells. Surface congestion oedema, elongation of gastric pits, tortuosity, reactive hyperplasia/atypia, ulceration. Seen in antrum more than corpus. Causes include bile reflux, NSAIDs, ethanol, oral iron.

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12
Q

How do you morphologically class gastric cancer?

A

Lauren classification into ‘intestinal’ or ‘diffuse’ types.

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13
Q

Diffuse gastric cancer

A

Individual malignant cells with mucin vaculous “signet ring” cells. May invade extensively without being endoscopically obvious, so called linitis plastica. Weaker link with gastritis. Metastasis to ovaries (Krukenberg tumour).

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14
Q

What is a Krukenberg tumour?

A

A malignancy in the ovary that metastasized from a primary site, classically the gastrointestinal tract, although it can arise in other tissues such as the breast. Gastric adenocarcinoma, especially at the pylorus, is the most common source.

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15
Q

What is Virchow’s node?

A

Virchow’s node, or Troisier’s node, refers to carcinomatous involvement of the supraclavicular nodes at the junction of the thoracic duct and the left subclavian vein. Usually, nodal enlargement is caused by metastatic gastric carcinoma.

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16
Q

What is melaena?

A

Refers to the dark black, tarry faeces that are associated with upper gastrointestinal bleeding. The black colour and characteristic strong odor are caused by haemoglobin in the blood being altered by digestive enzymes and intestinal bacteria.

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17
Q

Upper gastrointestinal bleeding

A

Major acute medical emergency. Presents with haematemesis (vomiting blood), “coffee ground” vomiting or melaena. Due to a bleeding source in oesophagus, stomach or duodenum.

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18
Q

What are the causes of upper GI bleeding?

A

Peptic ulcer, oesphagitis, gastriis, duodenitis, varices, malignancy, mallory-weiss tear.

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19
Q

What is a Mallory-Weiss tear?

A

Characterised by a tear or laceration often along the right border of, or near, the gastro-oesophageal junction. Patients present with non-variceal upper GI bleeding. The haemorrhage is usually self-limited, ceasing spontaneously in 80% to 90% of patients.

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20
Q

What scores can be used to assess upper GI bleeding?

A

Rockall score (full and admission) predict mortality. Glasgow Blatchford score- predicts needs for intervention or death. GBS less than or equal to 1 identifies those at very low risk of poor outcome: can be discharged for out patient endoscopy.

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21
Q

What can be done in endoscopic therapy of upper GI bleeding?

A

Adrenaline injection, heater probe, endoscopic clips, (thrombin, laser).

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22
Q

How can Hep. B be transmitted?

A

Mother to baby, contaminated needles and syringes, child to child, organs and tissue transplantation, fluids (blood, semen), transfusion (blood, blood products).

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23
Q

How can you prevent mother to child transmission of HBV?

A

1) HBV vaccination to newborn- 6 doses in first year
2) HBV immunoglobulin if eAg+ or high VL
3) Tenofovir during the last trimester if high viral load.

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24
Q

How do you diagnose acute pancreatitis?

A

2/3 of:

  • Pain in keeping with pancreatitis
  • Amylase 3 times upper limit of normal
  • Characteristic CT appearance
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25
Q

What are potential causes of acute pancreatitis?

A

Gallstones, alcohol, trauma/ERCP, other.

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26
Q

How do know if there is pancreatic necrosis?

A

Non enhancing pancrease on venous phase CT. Predicts complicated idsease but initial management not altered. Serial CT for resolution, or repeat if deteritration in organ function/ increse in organ support. Infected pancreatic necrosis- ongoing sepsis and progression to MODS. Requires intervention.

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27
Q

Management of infected pancreatic necrosis

A

Open necrosectomy, percutaneous necrosectomy, radiological drainage.

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28
Q

What is a pancreatic pseudocyst?

A

A circumscribed collection of fluid rich in pancreatic enzymes, blood, and necrotic tissue, typically located in the lesser sac of the abdomen. Pancreatic pseudocysts are usually complications of pancreatitis, although in children they frequently occur following abdominal trauma.

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29
Q

What is mucocoele of gallbladder?

A

A gallbladder mucocele is the distention of the gallbladder by an inappropriate accumulation of mucus.

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30
Q

What is acute haemorrhagic pancreatitis?

A

Characterised by acute inflammation and necrosis of pancreas parenchyma, focal enzymic necrosis of pancreatic fat and vessel necrosis (haemorrhage). These are produced by intrapancreatic activation of pancreatic enzymes.

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31
Q

Signs and symptoms of carcinoma of pancreas

A

Painless obstructive jaundice, new onset diabetes, abdominal pain due to pancreatic insufficiency or nerve invasion. Tumours in head may obstruct pancreatic duct and bile duct- “double duct sign” on radiology.

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32
Q

What is the “double duct sign” and what causes it?

A

In radiology, double duct sign is simultaneous dilation of the common bile duct and pancreatic ducts. 2 most common causes are carcinoma in head of pancreas and ampullary tumours.

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33
Q

What is Whipple’s resection?

A

Operation to remove tumours in head of pancreas. Only 10% of patients suitable for operation. 75% incompletely excised. Average life expectancy following operation is 20 months.

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34
Q

Neoadjuvant therapy for carcinoma of pancreas

A

Folfirinox chemotherapy associated with (limited) improvement in metastatic disease. Early data suggests that neoadjuvant therapy improved margin status and may be associated with longer survival.

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35
Q

Carcinoma of gallbladder

A

Rare. Gallstones present in 80% of cases. Adenocarcinoma.

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36
Q

What are the most common causes of abnormal liver blood tests?

A

Fatty liver (alcoholic or non-alcoholic), chronic viral hepatitis, autoimmune liver disease, haemochromatosis.

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37
Q

What are the characteristic features of alcoholic hepatitis?

A

Hepatomegaly +/- fever +/- leucocytosis +/- hepatic bruit. Short term mortality as high as 60%.

38
Q

Management of ascites

A

Low salt diet, diuretics (spironolactone and frusemide), paracentesis, transjugular intrahepatic portosystemic shunt (TIPSS), liver transplant.

39
Q

Common precipitating factors of hepatic encephaolopathy

A

Gastrointesntial bleeding, infections, constipation, electrolyte imbalance, excess dietary (esp. animal) protein.

40
Q

How do you treat hepatic encephalopathy?

A
  • Non absorbable disaccharides eg. lactulose. Aim for 2-3 soft stool/day.
  • Non (minimally)- absorbable antibiotics. Gut ‘decontamination’ reduces urease and protease activity.
41
Q

What causes peptic ulcers?

A

Too much acid, NSAIDs, H. Pylori

42
Q

Role of beta blockers in variceal bleeding

A

Beta blockers reduce portal pressure- primary prevent of variceal bleeding.

43
Q

What is Terlipressin?

A

A vasopressin agonist used to treat variceal bleeding. Causes constriction of portal circulation.

44
Q

Primary prophylaxis of cirrhotic patients to prevent variceal bleeding

A

Beta blockers or banding

45
Q

How do you prevent re-bleeding after variceal bleeding?

A

Beta blockers and repeat banding

46
Q

What is the best scoring system for assessing severity of upper GI bleeds?

A

Glasgow Blatchford Score. 2 blood tests required- haemoglobin and urea.

47
Q

Why have upper GI bleeding cases risen in the UK?

A

Due to a rise in alcohol, hepatitis C and fatty liver disease which lead to cirrhosis and portal hypertension.

48
Q

How do you manage acute upper GI bleeding?

A
  • Antibiotics and terlipressin (in A&E)
  • Banding first line for oesophageal variceal bleeding
  • Tissue glue injection for gastric variceal bleeding
  • TIPS for uncontrolled variceal bleeding
  • Balloon tamponade (as temporary salvage)
49
Q

What is Dermatitis Herpetiformis?

A

A chronic skin condition linked to coeliac disease. Blistering rash on extensor surfaces.

50
Q

What is faecal calprotectin?

A

Can be used in investigation of GI problems. It is a protein produced in the gut as a result of any inflammatory process. It is sensitive but non-specific and can be elevated due to any cause of underlying inflammation eg. coeliac, NSAIDs, IBD or infection.

51
Q

Functional hyposplenism

A

Diagnosed by the presence of Howell-Jolly bodies on blood film. Patients must be encouraged to have vaccinations- pneumococcus and influenza.

52
Q

What type of cancer is associated with coeliac disease?

A

Enteropathy- associated T cell lymphoma.

53
Q

What is decompensated liver disease?

A

Decompensated cirrhosis is defined by the development of jaundice, ascites, variceal hemorrhage, or hepatic encephalopathy.

54
Q

What are the key laboratory findings of autoimmune hepatitis?

A
  • Elevated serum ALT and AST
  • Raised serum immunoglobulins
  • Negative serum tests for viral hepatitis
  • High titres of circulating autoantibodies (titres of >1:40).
55
Q

What is interface hepatitis and what condition is it associated with?

A

Inflammation of hepatocytes at the junction of the portal tract and hepatic parenchyma is a typical feature of autoimmune hepatitis.

56
Q

What is the treatment of autoimmune hepatitis?

A

Immunosuppressive glucocorticoids with or without azathioprine. Remission can be achieved in up to 60-80% of cases and long term immunosuppression is often required.

57
Q

What is ‘acute abdomen’?

A

Rapid onset of severe symptoms that may indicate potentially life-threatening intra-abdominal pathology that require urgent surgical intervention.

58
Q

What is ultrasound good for seeing in the abdomen?

A

Gallstones, appendicitis, hydronephrosis.

59
Q

What is Chilaiditi syndrome?

A

Chilaiditi syndrome is a rare condition when pain occurs due to transposition of a loop of large intestine (usually transverse colon) in between the diaphragm and the liver, visible on plain abdominal X-ray or chest X-ray. Normally this causes no symptoms, and this is called Chilaiditi’s sign.

60
Q

In patients with liver cirrhosis, what are oesophageal varices?

A

Portosystemic collateral venous channels related to portal hypertension.

61
Q

What chronic changes do you get in chronic inflammatory bowel disease?

A

Crypt distortion, loss of crypts, submucosal fibrosis, paneth cell hyperplasia, neuronal hyperplasia.

62
Q

What acute changes are seen during active chronic inflammatory bowel disease?

A

Cryptitis, loss of goblet cells, crypt abscess formation, ulceration.

63
Q

What are the symptoms of ulcerative colitis?

A

Relapsing, bloody mucoid diarrhoea (stringy mucus) with pain/cramps relieved by defecation. Lasts days/months, then remission for months/years; initial attack may cause medical emergency for fluid and electrolyte imbalance.

64
Q

What are extraintestinal manifestations of UC?

A

Migratory polyarthritis, sacroiliitis, ankylosing spondylitis, erythema nodosum, clubbing of fingertips, primary sclerosing cholangitis, pericholangitis, cholangiocaricnoma (rare), uveitis.

65
Q

What are the potential complications of UC?

A

Perforation, toxic megacolon, iliac vein thrombosis, carcinoma and lymphoma.

66
Q

What is toxic megacolon?

A

Toxic colitis with dilated colon is referred to as toxic megacolon; dilatation may be segmental or generalised. Toxic colitis can develop without megacolon.

67
Q

What is Crohn’s disease?

A

IBD. Transmural granulomatous disease affecting oesophagus to anus but discontinuous, usually involves small intestine and colon with rectal sparing, less severe in distal vs. proximal colon (ie. preferential right-sided involvement).

68
Q

What are the symptoms of Crohn’s disease?

A

Episodic mild diarrhoea, fever, pain, may be precipitated by stress, if colon involved, may have anaemia. 20% have an abrupt onset, resembling acute appendicitis or bowel perforation.

69
Q

What are some of the potential complications of Crohn’s disease?

A

Fibrosing strictures (common in terminal ileum), fistula, malabsorption, toxic megacolon, carcinoma (but lower risk than UC).

70
Q

What are the long term risks associated with IBD?

A

IBD= Crohn’s and ulcerative colitis. Associated with increased risk of colonic carcinoma.

71
Q

Colorectal cancer risk factors

A

Adenoma (benign glandular neoplasm)- size and number, IBD, family history, other carcinomas, polyposis syndrome- FAP (associated with APC gene) and Lynch syndrome (associated with mismatch repair defects).

72
Q

What is ulcerative colitis?

A

Diffuse mucosal inflammation limited to the colon. Defined by extent eg. distal colitis limited to rectum (proctitis) or rectum and sigmoid (proctosigmoiditis).

73
Q

What history would you take when investigating IBD?

A
  • Stool frequency, consistency, urgency, blood.
  • Abdo pain, malaise, fever
  • Weight loss
  • Extraintestinal symptoms (joint, eyes, skin).
  • Travel
  • Family Hx
  • Smoking
74
Q

What examinations would you do when investigating IBD?

A

Weight, pulse, temperature, anaemia, abdominal tenderness, perineal examination.

75
Q

What is erythema nodosum?

A

Characterised by painful, erythematous, and sometimes bruised-looking, nodules on the anterior surface of the legs. Can be seen in IBD.

76
Q

What is pyodermic gangrenosum?

A

A rare, neutrophilic dermatosis, commonly associated with systemic disease. Although there are a number of PG variants, the typical presentation is a painful ulcer (or ulcers) that grows rapidly and develops an irregular, undermined, purple edge. It is important to exclude other causes of ulcers including infection and factitious disease. Associated with IBD.

77
Q

What is orafacial granulomatosis?

A

A rare chronic inflammatory condition characterised by lip swelling, a histological finding of non-caseating granulomas in mucosal or skin biopsies taken from the mouth or face, and the absence of a recognised systemic condition known to cause granulomas such as Crohn’s disease, sarcoidosis, and granulomatosis with polyangiitis.

78
Q

How do you investigate IBD?

A

FBC, ESR, U&Es, LFTs, CRP, stool culture + C. Diff toxin. Faecal calprotectin. AXR.

79
Q

What are the side effects of steroids?

A

Immunosuppression, impaired glucose tolerance, osteoporosis, weight gain, cushinoid appearance.

80
Q

What are aminosalicylates used for?

A

eg. Mesalazine. Induction of remission of mild-moderate ulcerative colitis. Maintenance of remission in UC.

81
Q

What metabolites are you monitoring when prescribing thiopurines?

A
  • 6TGN (6-Thioguanine nucleotides)- checked to ensure drug within therapeutic window. Used as an assessment of compliance.
  • 6MMP (6-methylmercaptopurine). Associated with risk of hepatotoxicity.
82
Q

What are the side effects of thiopurines?

A

Side effects are common:

  • leucopenia
  • nausea, vomiting
  • arthralgia
  • pancreatitis
  • hepatitis
  • squamous skin cancers
  • haematological malignancy
83
Q

What are the side effects of methotrexate?

A

GI upset, hepatotoxicity, immunosuppression, sepsis, pulmonary fibrosis.

84
Q

What is Budd-Chiara syndrome?

A

A very rare condition, affecting one in a million adults. The condition is caused by occlusion of the hepatic veins that drain the liver. It presents with the classical triad of abdominal pain, ascites, and liver enlargement.

85
Q

What are some of the issues with Anti TNF drugs (used to treat IBD)?

A
  • Infection risk-reactivation of TB or hep B.
  • Neurological- incidence of MS, progressive multifocal leucoencephalopathy.
  • Malignancy- possible increased lymphoma risk.
86
Q

How do you treat acute severe colitis?

A

-Prophylactic LMW heparin
-IV hydrocortisone 100mg QDS or methylprednisolodine 30mg bd.
Treat for 72 hours, if improvements then give oral prednisolone 40mg. If no improvement give rescue therapy.

87
Q

What is the ‘rescue therapy’ for acute severe colitis?

A
  • Ciclosporin 2mg/kg/day IV
  • Infliximab 5mg/kg single dose
  • Surgery
88
Q

When is surgery indicated in Crohn’s?

A

Surgery is sparing. If medical therapy doesn’t work, surgery indicated for stricturing, perforation and fistulizing disease.

89
Q

What are the complications of cirrhosis?

A

Ascites, variceal bleeding, encephalopathy, hepatocellular carcinoma.

90
Q

What is refractory ascites?

A

Occurs in less than 10% of patients. Fluid overload unresponsive to:

  • Sodium restriction
  • 400mg/day spironolactone
  • 160mg/ day frusemide
91
Q

Define an ulcer

A

ulcers are characterised by segmental or more extensive loss of the epidermis, including the BM with exposure of the underlying dermis.

92
Q

Define an erosion

A

Erosion is characterised by partial loss of the epithelium, with the BM left intact.