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Phase 3 > GI/Liver > Flashcards

GI/Liver Flashcards

1
Q

List the broad causes of liver injury.

A

drugs, toxins, alcohol, abnormal nutrition, infection, obstruction to bile or blood flow, autoimmune, genetic, neoplasia

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2
Q

Name a liver disease which can be described as ‘acute-on-chronic.’ Discuss what this term means.

A

fibrosis

presents with acute exacerbation plus evidence of underlying chronicity

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3
Q

Give the three-fold definition of cirrhosis.

A

diffuse process with fibrosis and nodule formation

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4
Q

Name two causes of acute cholestasis and describe the histology.

A 
extrahepatic biliary obstruction and drug injury e.g. antibiotics
brown bile (bilirubin) pigment +/- acute hepatitis
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5
Q

Ground glass cytoplasm is the specific feature of which liver disease?

A

hepatitis B virus

= accumulation of ‘surface antigen’

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6
Q

Name two causes of chronic biliary disease and describe the histology.

A

primary biliary cirrhosis and primary sclerosing cholangitis

focal, portal predominant inflammation and fibrosis with bile duct injury; granulomas in PBC

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7
Q

Name three examples of genetic/deposition liver disease.

A

haemochromatosis (iron)
Wilson’s disease (copper)
alpha-1-antitrypsin deficiency

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8
Q

Focal liver lesions are space occupying lesions and can be split in to non-neoplastic and neoplastic. Can you give two examples of each?

A

non-neoplastic - developmental/degenerative e.g. cysts and inflammatory e.g. abscess
neoplastic - benign and malignany

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9
Q

What is the name given the commonest liver cyst? Describe it and its appearance.

A

Von Meyenberg complex - simple biliary hamartoma

can resemble metastases by naked eye - but no treatment is required

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10
Q

Name the benign and malignant neoplasms associated with:

  1. Liver cells
  2. Bile duct
  3. Blood vessel
  4. Non-liver tissue
A
  1. B = hepatocellular adenoma. M = hepatocellular carcinoma
  2. B = bile duct adenoma. M = cholangiocarcinoma
  3. B = haemangioma. M = angiosarcoma
  4. B = N/A. M = metastases
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11
Q

List the normal liver functions.

A

protein, carbohydrate and fat metabolism, plasma protein and enzyme synthesis, production of bile, detoxification, storage of proteins, glycogen, vitamins and metals, immune functions

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12
Q

What are the standard LFTs?

A 
bilirubin (isolated might be haemolysis)
AST (may also be muscle) and ALT
GGT
ALP (may also be bone)
albumin
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13
Q

Describe the histological progression of fatty liver disease.

A
  • macrovascular steatosis with lipid vacuole filling the hepatocyte cytoplasm
  • steatohepatitis: neutrophils and lymphocytes surrounding hepatocytes with Mallory hyaline
  • pericellular fibrosis as well as bands of fibrous tracts between portal tracts
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14
Q

What are the three main associations of NAFLD?

A

obesity, T2DM, hyperlipidaemia

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15
Q

What are the differences in ALT, AST, AST/ALT ratio and GGT seen in NAFLD and ALD?

A

ALT: NAFLD raised/N, ALD raised/N
AST: NAFLD normal, ALD raised
AST/ALT ratio: NAFLD <0.8, ALD > 1.5
GGT: NAFLD raised/N, ALD markedly raised

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16
Q

Discuss the clinical spectrum of alcohol liver disease.

A

malaise, nausea, hepatomegaly, fever, jaundice, sepsis, encephalopathy, ascites, renal failure, death

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17
Q

What are the four characteristic features of acute alcohol hepatitis?

A

hepatomegaly, fever, leucocytosis, hepatic bruit

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18
Q

In a newly jaundiced ALD patient, what features would make you concerned about alcohol hepatitis?

A
  • excess alcohol within 2 months
  • bilirubin > 80 umol/L for less than 2 months
  • exclusion of other liver disease
  • treatment of sepsis/GI bleeding
  • AST < 500 (AST:ALT ratio > 1.5)
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19
Q

List the four main risk factors for hepatitis C.

A

IVDU, sexual transmission, vertical transmission, needle-stick transmission

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20
Q

What are the clinical signs of chronic liver disease?

A

stigmata: spider naevi, foetor, encephalopathy

‘synthetic dysfunction’: prolonged prothrombin time, hypoalbuminaemia

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21
Q

Give four signs of portal hypertension.

A

caput medusa
ascites
oesophageal varices
splenoemegaly (thrombocytopenia)

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22
Q

How is severity of liver disease assessed?

A

child-turcotte-pugh score: encephalopathy, ascites, bilirubin, albumin, PTTP

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23
Q

Discuss how MELD scores indicate prognosis of liver disease.

A

mild < 10
moderate 10-15
severe > 15

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24
Q

Describe the pathophysiology of portal hypertension leading to its clinical features.

A
  • liver cirrhosis
  • raised portal pressure - hypersplenism
  • porto-systemic shunting - oesophageal varices, encephalopathy
  • vasodilation (NO) - further increases portal pressure
  • reduced effective circulating volume - hyperdynamic circulation
  • compensatory vasopressors (RAAS, catecholamimes)
  • sodium retention - ascites
  • renal vasoconstriction - hepato-renal syndrome
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25
Q

Discuss the assessment of ascites following a diagnostic tap.

A

CELL COUNT
- >500 WBC/cm3 and/or >250 neutrophils/cm3 = spontaneous bacterial peritonitis
- lymphocytosis = TB or peritoneal carcinomatosis
ALBUMIN
- SAAG = serum albumin - ascitic albumin g/L
- SAAG > 11g/L = portal hypertension

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26
Q

How is ascites managed?

A

low salt diet, diuretics (spironolactone, furosemide), paracentesis, transjugular intrahepatic portosystemic shunt (TIPSS), liver transplant, monitor renal function and electrolytes

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27
Q

List 5 precipitating factors of hepatic encephalopathy. Give 3 explanations of how these lead to encephalopathy.

A

GI bleeding, infections, constipation, electrolyte imbalance, excess dietary protein

  1. Reduction of hepatic or cerebral function
  2. Stimulation of an inflammatory response
  3. Increasing ammonia levels
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28
Q

Describe the Conn Score for grading mental state in hepatic encephalopathy.

A

0: no abnormality
1: lack of awareness, euphoria or anxiety, shortened attention span
2: lethargy, subtle personality change, inappropriate behaviour, minimal disorientation for time or place
3: somnolence to semi-stupor, confusion, gross disorientation
4: coma

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29
Q

What is hepatitis? List some of the symptoms.

A

inflammation of the liver

malaise, fever, headaches, anorexia, nausea, vomiting, RUQ pain, dark urine, jaundice

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30
Q

Give 5 causes of acute hepatitis.

A
  • infections e.g. Hep A-E, EBV, CMV, Q fever, syphilis, malaria
  • toxins
  • drugs
  • alcohol
  • autoimmune
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31
Q

How is hepatitis A diagnosed?

A

acute: IgM positive or RNA in blood or stool

previous or vaccinated: IgG positive

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32
Q

Which Hep virus is commonly spread in pork products?

A

E

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33
Q

What are the neurological manifestations of Hep E?

A

Guillaine Barre syndrome, encephalitis, ataxia, myopathy

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34
Q

What problems are associated with hepatitis B?

A

weight loss, abdo pain, fever, cachexia, mass in abdomen, bloody ascites, cirrhosis develops in 25%, HCC, death

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35
Q

What is detected during hepatitis B lab tests?

A 
sAg - marker of infection
sAb - marker of immunity
cAb - core antibody
eAg - suggests high infectivity
eAb - suggests low infectivity
HBV DNA
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36
Q

What treatments are available for hep B?

A

chronic
only treat those with liver inflammation or fibrosis
immunomodulatory - inferferon
suppress viral replication - tenofovir or entecavir

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37
Q

Which virus does Hep D require to replicate?

A

Hep B

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38
Q

Discuss HCV diagnosis through screening and blood tests.

A

most diagnosed by screening of high risk groups - drug users, immigrants to UK from high prevalence countries

  • anti HCV IgG +ve = chronic or cleared infection
  • PCR or antigen +ve = current infection
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39
Q

What treatment is available for HCV?

A

direct acting antiviral inhibits different stages of the replication cycle

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40
Q

Acute cholecystitis is initiated by stone obstruction of cystic duct causing supersaturation of bile and chemical irritation. What symptoms will this lead to?

A

severe RUQ pain, tenderness and fever

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41
Q

Leucocytosis and normal serum amylase are blood results of which acute condition?

A

cholecystitis.

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42
Q

Acute pancreatitis is most commonly caused by gallstone, alcohol abuse, trauma/ERCP, drugs etc. How does it present?

A

severe upper abdo pain, fever, leucocytosis, raised serum amylase

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43
Q

What are potential complications of acute pancreatitis?

A

pancreatic abscess

pseudocyst

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44
Q

How would you manage a pancreatic abscess?

A

drainage or necrosectomy plus antibiotics

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45
Q

List some differentials of pancreatic cysts.

A
  1. Intraductal papillary mucinous neoplasm
  2. Mucinous cystic neoplasm (‘ovarian-type’ stroma)
  3. Serous cystadenoma
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46
Q

What is the 5 year survival rate of pancreatic cancer?

A

7%

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47
Q

What are the risk factors to develop pancreatic cancer?

A

smoking
alcohol
germline mutations e.g. BRCA

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48
Q

Discuss the signs and symptoms of pancreatic cancer.

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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49
Q

What is the name given to the process of excising a head of pancreas tumour?

A

Whipple’s resection

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50
Q

What is the commonest pancreatic neuroendocrine tumour and how does it present?

A

insulinoma - hypoglycaemia

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51
Q

Differentiate between intra and extra hepatic cholangiocarcinoma.

A

intra: needs to be distinguished from metastatic adenocarcinoma and HCC
extra: similar to pancreatic carcinoma. Treatment = Whipple’s to remove common bile duct and involved pancreas/duodenum

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52
Q

What are the criteria for diagnosis of 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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53
Q

What investigations should be carried out in acute pancreatitis?

A
  • US to assess gallstones
  • MRCP to assess for CBD stones
  • CT if diagnostic doubt or concern about complications
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54
Q

Give 2 DDx for acute pancreatitis.

A

perforated duodenum

ischaemic bowel

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55
Q

What does non-enhancing pancreas on venous phase CT suggest?

A

pancreatic necrosis

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56
Q

How would you manage infected pancreatic necrosis?

A
  • open necrosectomy
  • percutaneous necrosectomy
  • radiological drainage
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57
Q

Give complications associated with pancreatic necrosis.

A

bleeding

erosion to surrounding structures

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58
Q

Discuss the use of interventional radiology for bleeding following pancreatic necrosis.

A
  • access via groin
  • selective cannulation of coeliac trunk
  • commonly splenic artery aneurysm
  • usually coils placed before and after blood, can be stunted
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59
Q

Pancreatic pseudocysts may settle without intervention. However if they remain symptomatic, how are they resolved?

A

drain to stomach laparoscopically or endoscopically

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60
Q

What is a pancreatic fistula?

A

an abnormal communication between the pancreas and other organs due to leakage of pancreatic secretions from damaged pancreatic ducts

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61
Q

How is pancreatic fistula managed?

A
  • may require period of parenteral nutrition
  • endoscopic treatment
  • may require salvage distal pancreatectomy
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62
Q

What is the initial treatment of acute pancreatitis?

A

fluids, oxygen, organ support, antibiotics? early enteral feeding superior to parenteral feeding

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63
Q

What type of epithelium lines the oesophagus?

A

non-keratinising stratified squamous

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64
Q

What histological changes occur to the epithelium in reflux oesophagitis?

A

increased number of inflammatory cels

basal zone becomes hyperplastic

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65
Q

Which two pathogens most commonly cause infection of the oesophagus?

A

candida albicans

herpes simplex virus

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66
Q

What causes inflammation of oesophageal tissue?

A
  • peptic oesophagitis/GORD: reflux of acid/bile
  • lye
  • pills: iron, bisphosphonates, tetracyclines
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67
Q

Describe Barrett’s oesophagus.

A
  • a metaplastic response to mucosal injury e.g. long term GORD
  • squamous epithelium becomes glandular, usually intestinal with goblet cells
  • associated with the development of benign strictures and adenocarcinoma
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68
Q

Describe the typical epithelial appearance of Candida oesophagitis.

A

active chronic inflammation with many neutrophils especially near the luminal surface

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69
Q

How is a PAS stain used to confirm Candida albicans?

A

spores and hyphae present

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70
Q

Differentiate between low grade and high grade dysplastic epithelium seen in Barrett’s oesophagus.

A

low grade: cells polarised, nuclei stratified

high grade: polarity lost, nuclei rounder, prominent nucleoli, abnormal mitoses, necrosis

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71
Q

What is the main risk of Barrett’s oesophagus? How is risk of developing to this stage avoided?

A

carcinoma
radiofrequency ablation
radical surgery

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72
Q

Squamous carcinoma and adenocarcinoma are the two main oesophageal cancers. How do their associated factors differ?

A
  1. smoking and drinking

2. GORD and obesity

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73
Q

Gastritis may be acute or chronic. Give three examples of how each is caused.

A

acute: alcohol, NSAIDs, burns
chronic: autoimmune, bacterial (H. pylori), chemical

74
Q

Define autoimmune gastritis.

A

autoimmune destruction of parietal cells due to auto-antibodies against intrinsic factor and parietal cell antibodies in blood

75
Q

List four consequences of autoimmune gastritis.

A
  1. Complete loss of parietal cells with pyloric and intestinal metaplasia
  2. Achlorhydia - bacterial overgrowth
  3. Hypergastrinaemia - endocrine cell hyperplasia/carcinoids
  4. Persistent inflammation which can lead to epithelial dysplasia and may lead to cancer
76
Q

Discuss how H. pylori leads to gastritis and peptic ulceration.

A
  • colonises gastric mucosa causing active inflammation: IL-8 from epithelial cells attracts neutrophils
  • antral-predominant gastritis: hypergastrinaemia and duodenal ulceration
  • pangastritis: hypochlorhydia, multifocal atrophic gastritis, intestinal metaplasia, cancer
77
Q

What three factors can lead to peptic ulcers?

A
  • too much acid
  • impaired mucosal defence (due to NSAID interfering with mucosal PG synthesis; bile reflux)
  • microbe factors (CagA + variants ass. w/ more severe inflammation)
78
Q

What is the typical presentation of peptic ulcer?

A

haematemesis, melena, abdo pain

79
Q

List three consequences of peptic ulceration.

A

haemorrhage, perforation, fibrosis (leading to stenosis)

80
Q

Describe the histological appearance of chemical gastritis.

A

few inflammatory cells, surface congestion oedema, elongation of gastric pits, tortuosity, reactive hyperplasia/atypia, ulceration

81
Q

Bile reflux, NSAIDs, ethanol and oral iron are all causes of which type of gastritis?

A

chemical

82
Q

Name two causes of chronic gastritis which are strongly associated with gastric cancer.

A

H. pylori

autoimmune

83
Q

Discuss the Lauren classification of gastric cancer.

A
  • ‘intestinal’: environmental, gastric atrophy, intestinal metaplasia, increasing incidence with age, men>women, haematogenous spread, differentiated
  • ‘diffuse’: familial, blood type A, women>men, younger age group, transmural/lymphatic spread, undifferentiated
84
Q

Name three areas where diffuse gastric cancer may metastases.

A
  • ovaries (Kurkenburg tumour)
  • supraclavicular lymph node (Virchow’s node)
  • Sister Joseph’s nodule (umbilical metastasis)
85
Q

Which three signs/symptoms indicate the major acute medical emergency of an upper GI bleed?

A

haematemesis
‘coffee ground’ vomiting
melaena

86
Q

List the 5 main causes of an upper GI bleed.

A

peptic ulcer, oesophagitis, gastritis, duodenitis, varices

87
Q

Outline the basics in upper GI bleed management.

A 
resuscitate if required
risk assessment and timing of endoscopy:
- high risk = emergency endoscopy
- moderate = admit and next day
- low = out patient management?
drug therapy and transfusion
88
Q

Which scoring systems are used to identify patients at risk of adverse outcome following acute upper GI bleeding?

A 
ROCKALL: predicts mortality
A: age
B: blood pressure fall (shock)
C: co-morbidity
D: diagnosis
E: evidence of bleeding

GLASGOW-BLATCHFORD: predicts need for intervention or death
Hb level, BP, pulse, blood urea nitrogen level, melena or syncope, past or present liver disease or heart failure

89
Q

Which class of drugs are most commonly used in upper GI bleeding?

A

IV proton pump inhibitors

90
Q

Should adjustments be made to dosage of antiplatelet drugs following GI bleed?

A
  • continue low dose aspirin once haemostasis is achieved

- stop NSAIDs

91
Q

Why should you assess risks and benefits of continuing anticoagulant drugs following GI bleed?

A

mortality high from CVD

92
Q

Blood should be transfused following upper GI bleeding once Hb <7-8 g/dL. Name 3 other occasions where transfusion is indicated.

A
  • transfuse platelets if actively bleeding and platelet count < 50x10^9/L
  • FFP if INR > 1.5
  • prothrombin complex concentrate if on warfarin and active bleeding
93
Q

Outline the process by which oesophageal varices are formed due to liver cirrhosis.

A
  1. Increased hepatic resistance
    - mechanical: architectural changes, fibrosis, vascular occlusion
    - dynamic: endothelial dysfunction, increased vascular tone
  2. Increased portal pressure
  3. Increased portal flow: splanchnic vasodilation
    - increased NO, CO, glucagon
    - hyperkinetic syndrome
  4. Angiogenesis
  5. Portal systemic collaterals i.e. varices
94
Q

Give three methods of treatment of varices.

A

endoscopic banding
TIPS - transjugular intrahepatic portosystemic shunt
B-blocker drugs

95
Q

What is the therapy for acute variceal bleeding?

A

antibiotics early, vasopressors - terlipressin, endoscopic band ligation, rescue TIPS

96
Q

What name is given to the tube that is passed down into the oesophagus and the gastric balloon is inflated inside the stomach in uncontrolled variceal bleeding?

A

sengstaken tube

97
Q

What is Mallory-Weiss syndrome?

A

bleeding from a laceration in the mucosa at the junction of the stomach and oesophagus

98
Q

What are the causes of MW syndrome and how does it present?

A
  • severe vomiting due to alcoholism or bulimia

- haematemesis

99
Q

Describe the pathological histology appearance of the intestinal epithelium in coeliac disease.

A

crypt hyperplasia
villous atrophy
intraepithelial lymphocytes

100
Q

Crohn’s disease and ulcerative colitis are examples of which type of disease?

A

chronic inflammatory bowel disease

101
Q

Describe 5 chronic histological changes seen in IBD due to regeneration following ulceration.

A

crypt distortion, loss of crypts, submucosal fibrosis, Paneth cell metaplasia, neuronal hyperplasia

102
Q

Give four acute changes seen during active IBD.

A

cryptitis, loss of goblet cells, crypt abscess formation, ulceration

103
Q

What are the symptoms of ulcerative colitis?

A
  • relapsing, bloody mucoid diarrhoea with pain/cramps relieved by defecation
  • lasts days/months, then remission for months/years
104
Q

List 5 extraintestinal manifestations of ulcerative colitis.

A 
migratory polyarthritis
ankylosing spondylitis
sacroilitis
erythema nodosum
primary sclerosing cholangitis
uveitis
105
Q

What are the main complications of ulcerative colitis?

A

perforation, toxic megacolon, iliac vein thrombosis, carcinoma, lymphoma

106
Q

Patients with UC are given local or systemic steroids as treatment. What other ways of management may be required?

A
  • 30% require colectomy during first 3 years

- regular colonoscopy with biopsy to detect precancerous dysplastic changes

107
Q

Define Crohn’s disease.

A

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

108
Q

List the symptoms of Crohn’s disease.

A

episodic mild diarrhoea
fever
pain
may be precipitated by stress

109
Q

What are the 5 most common complications of Crohn’s disease?

A 
fibrosing strictures
fistula
malabsorption
toxic megacolon
carcinoma
110
Q

What is the eventual treatment of Crohn’s disease?

A

surgery

involvement of resection margins doesn’t correlate with recurrence

111
Q

In addition to the histological features common to both IBDs, Crohn’s has some additional features. Can you give three?

A 
skip lesions
fistulas/sinus tracks
malabsorption
granulomas
deep ulcerations
marked lymphcytic infiltration
serositis
112
Q

What is the major long term risk associated with IBD?

A

colonic carcinoma

113
Q

The majority of adenomas of the colon are dysplastic and are polyps, but what is an adenoma?

A

benign glandular neoplasms

114
Q

How are adenomas prevented from progressing to malignant potential?

A

identified and removed

115
Q

Give four differentials of adenomas.

A

hyperplastic polyps
hamartomatous polyps
inflammatory polyps
submucosal lesions

116
Q

What are the main risk factors for developing CRC?

A
  • adenoma: size, number
  • IBD: UC, Crohn’s
  • family history
  • other carcinomas
  • polyposis syndromes e.g. FAP (ass. w/ APC gene), Lynch syndrome (ass. w/ MMR defects)
117
Q

What features of benign polyps would make you worried about it becoming malignant?

A
  • > 2cm
  • flat polyps with a villous pattern - larger SA and no stalk
  • increased no. of polyps
  • epithelial dysplasia
118
Q

Discuss TNM classification of malignant tumours.

A

T: size of the original (primary) tumour and whether it has invaded nearby tissue,
N: nearby (regional) lymph nodes that are involved,
M: distant metastasis (spread of cancer from one part of the body to another).

119
Q

Describe the staging for the tumour component of TNM.

A

TX unable to assess primary tumour
T0 no evidence of tumour
Tis carcinoma in situ
T1 - T4 size and/or extension of primary tumour

120
Q

Describe the staging for the nodal component of TNM.

A

Nx: lymph nodes cannot be assessed
N0: no regional lymph node metastasis
N1: regional lymph node metastasis
N2: tumour spread to an extent between N1 and N3
N3: tumout spread to more distant or numerous regional lymph nodes

121
Q

Describe the staging of the metastases component of TNM.

A

M0: no distant metastasis
M1: metastasis to distant organs

122
Q

Outline Dukes’ classification of colon cancer.

A

Dukes A: Invasion into but not through the bowel wall
Dukes B: Invasion through the bowel wall penetrating the muscle layer but not involving lymph nodes
Dukes C: Involvement of lymph nodes
Dukes D: Widespread metastases

123
Q

Describe the impact that staging has on treatment offered to patients with colorectal cancer.

A

Dukes’ A and B: better prognosis, no need to give CTx

124
Q

What methods are used to detect colorectal cancer early?

A
  • bowel screening program 50-75 y/o
  • if +ve go for colonoscopy
  • patient education of symptoms e.g. PR bleeding, change in bowel habits
125
Q

Aetiology of IBD is widely unknown, with thoughts it is linked to genetic and environmental factors. Describe the effect that smoking has on pathogenesis of IBD.

A
  • increased risk of Crohn’s

- reduced risk of UC

126
Q

Describe the pathophysiological differences between UC and Crohn’s.

A
  • UC: cytokine response vaguely ass. w/ Th2

- Crohn’s: cytokine response ass. w/ Th17

127
Q

What features of a history and examination are crucial in diagnosing IBD?

A
  • history: stool frequency, consistency, urgency, blood, abdo pain, malaise, fever, weight loss, extraintestinal symptoms (joint, eyes, skin), travel, family Hx, smoking
  • exam: weight, pulse, temperature, anaemia, abdominal tenderness, perineal exam
128
Q

How would you investigate suspected IBD?

A
  • rigid sigmoidoscopy
  • colonoscopy preferable
  • small bowel radiology
  • labelled WCC scanning
129
Q

Name three treatments which are common to both UC and Crohn’s.

A

corticosteroids e.g. hydrocortisone, prednisolone, beclometasone,
thiopurines
biologics

130
Q

Mesalazine (5ASA) is a drug used to treat which type of IBD? How does it work?

A

ulcerative colitis

anti-inflammatory - induction and maintenance of remission in UC

131
Q

Which two drugs are limited to Crohn’s type of IBD?

A

methotrexate

immune modulating diets

132
Q

List five significant side effects of steroids.

A

immunosuppression, impaired glucose tolerance, osteoporosis, weight gain, Cushingoid appearance

133
Q

Describe the efficacy of thiopurine in maintenance therapy for UC and Crohn’s.

A
  • purine anti-metabolites
  • steroid sparing agent
  • immune modulating drugs
  • prevent T cell clonal expansion in response to antigenic stimuli, allow T cell apoptosis
134
Q

Name two thiopurines and 3 common side effects.

A

azathioprine, mercaptopurine
bone marrow suppression (leukopenia), N+V, arthralgia, pancreatitis, hepatitis, squamous skin cancers, haematological malignancy

135
Q

Which two metabolites must be closely monitored while on thiopurines and why?

A
  • 6TGN: assessment of compliance

- 6MMP: associated with hepatotoxicity

136
Q

List 5 side effects of methotrexate.

A 
GI upset
hepatotoxicity
immunosuppression
sepsis
pulmonary fibrosis
137
Q

Name 3 anti-TNFa monoclonal antibodies used in IBD.

A
  • infliximab, adalumimab, golimumab

- severe or fistulating Crohn’s, rescue acute severe UC

138
Q

Give 3 disadvantages to the use of infliximab in IBD.

A

loss of efficacy
allergic reactions
expensive

139
Q

What are the three main concerns with prescribing anti-TNF drugs?

A
  • infection risk (reactivation of TB and hep B)
  • neurological (MS, progrressive multifocal leucoencephalopathy)
  • malignancy (possible increased lymphoma risk)
140
Q

Describe the initial management plan of an admitted patient due to IBD.

A
  • IV steroid therapy
  • investigations: daily bloods, stool cultures (C. diff?), daily AXR, sigmoidoscopy?
  • liaison with colorectal surgeon
  • stool frequency >8/day / CRP>45 on day 3 predicts colectomy in 85%
141
Q

How would acute severe colitis be treated?

A
  • prophylactic LMWH
  • IV hydrocortisone
  • treat for 72 hours: if improving then switch to oral prednisolone, no improvement = rescue therapy
  • rescue therapy: ciclosporin, infliximab, surgery
142
Q

Can surgery cure IBD?

A
  • in UC, technically yes

- Crohn’s - no, often returns following removal of the affected part

143
Q

If surgery does not cure Crohn’s, then when is it indicated?

A

stricturing, perforation, fistulising disease.

144
Q

Where is the most common site for neuroendocrine tumour along the GI tract?

A

appendix

145
Q

What is the name of the spindle cell tumour derived from interstitial cells of Cajal?

A

GI stromal tumour

146
Q

Imatinib is commonly used as a target for GIST. Why?

A

majority have abnormalities of tyrosine-kinase receptor

147
Q

Hodgkin’s and NHL are rare in the colon. Which type of lymphomas are common?

A

enteropathy associated T cell lymphoma

148
Q

How can coeliac disease increased risk of lymphoma in the colon?

A

untreated/refractory coeliac disease results in over stimulation of T cells leading to high risk of malignant transformation

149
Q

Name three common viral infections in the intestines.

A

adenovirus
CMV
HSV (multinucleate giant cells with nuclear inclusions)

150
Q

Describe pseudomembranous colitis.

A

membrane of fibrin and inflammatory exudate formed over lining of mucosa

151
Q

What is the most common cause of pseudomembraneous colitis?

A

C. difficile. - usually following antibiotic therapy

152
Q

Discuss the pathophysiology of ischaemic damage to the intestines.

A
  • superficial ulceration
  • congestion of mucosal/submucosal vessels
  • oedema of submucosa and muscularis propria
  • eventually progresses to full thickness necrosis
  • may be due to decreased local blood flow secondary to stretching wall in obstruction
153
Q

Chronic non-bloody, watery diarrhoea, with normal endoscopy associated with autoimmune disease is characteristic of which type of colitis?

A

lymphocytic and collagenous

154
Q

How is lymphocytic colitis treated?

A

sulfasalazine

corticosteroids

155
Q

Describe the histological appearance of lymphocytic colitis.

A

colonic epithelial lymphocytosis with surface epithelial damage but without thickened subepithelial collagen
increased chronic inflammatory cells in lamina propria

156
Q

Which type of colitis has patchy thickening of subepithelial basement membrane of 10 microns or more on histology?

A

collagenous

157
Q

What is the name given to a pouch of mucosa which has herniated through the muscularis propria?

A

diverticulum

158
Q

How is it though that diverticular disease develops?

A

as a result of increased intra luminal pressure associated with low fibre diets

159
Q

What are the main complications of diverticular disease?

A

inflammation
abscess formation
perforation

160
Q

Which genes are commonly associated with coeliac disease?

A

HLADQ2/8

161
Q

TTG autoantibodies are found in which disease of the colon?

A

coeliac disease

162
Q

Give three possible complications of coeliac disease.

A

osteoporosis, IDA, small bowel malignancy

163
Q

What is the definition of spontaneous bacterial peritonitis?

A

> 250 neutophils/mm3 in ascites in absence of intra-abdominal source of infection or malignancy
usually gram-ve bacteria

164
Q

How would you treat SBP?

A

IV antibiotics and IV albumin

165
Q

How do you manage ascites?

A

salt restriction and diuretics

oral spironolactone +/- frusemide

166
Q

What therapies are available for refractory ascites?

A
  • large volume paracentesis
  • TIPS
  • liver transplant
167
Q

Which condition is associate with C282Y gene mutation?

A

genetic haemochromatosis

autosomal recessive

168
Q

What is haemochromatosis?

A

excessive absorption of dietary iron

leads to iron overload in liver, heart, pancreas, joints, skin (‘bronze diabetes’)

169
Q

How is haemochromatosis diagnosed and treated?

A
  • raised ferritin and transferrin saturation
  • HFE gene
  • treated by venesection
170
Q

What is the name of the stain used to pick up iron in haemochromatosis?

A

Perl’s stain

171
Q

List the causes of hyperamylasaemia.

A
  • Pancreatitis, disruption pancreatic duct
  • Biliary conditions (gallbladder infection/ perforation, choledocolithiasis, cholangitis)
  • Enteric contents to peritoneum/ circulatory system (perforated viscus/ ischaemia)
  • Other source of amylase parotid gland (viral infection, stone parotid duct)
172
Q

Discuss what each of the LFTs show in jaundice.

A
  • bilirubin increase = bilirubin in blood
  • transaminase rise = destruction of hepatocytes
  • Alk Phos rise = damage to bile ducts
173
Q

What is the best initial management of pancreatitis?

A

IV fluids, catheter and nil by mouth, observe in ward

174
Q

What are the surveillance tests for HCC in cirrhosis?

A

6 monthly US +/- AFP

175
Q

Discuss the management of HCC.

A
  • small: liver transplant, resect tumour, RF ablation
  • larger: trans-arterial chemoembolisation, oncology drug therapy (sorafenib)
  • palliative care
176
Q

Describe the pathogenesis of coeliac disease.

A
  • inflammatory disorder of the small bowel caused by immune sensitivity to gluten
  • loss of immune tolerance to gliadin peptide antigens derived from wheat, rye, and related grains, in genetically susceptible individuals (HLA-DQ2/8)
  • malabsorption occurs because of loss of absorptive area and the presence of a population of immature surface epithelial cells
177
Q

Give an example of a proton pump inhibitor.

A

omeprazole, lansoprazole, pantoprazole

178
Q

Describe the mechanism of action of PPIs.

A
  • bind to H+/K+ ATPase pump on gastric parietal cells

- reduced HCl production and hence reduced gastric acidity

179
Q

What are the indications of PPI use?

A

peptic ulcers, GORD, H.pylori infection, prophylaxis in patients receiving long term NSAIDs, Zollinger-Ellison syndrome

180
Q

Ranitidine and cimetidine are examples of which type of drug?

A

H2 receptor antagonists

181
Q

How do H2 receptor antagonists reduce gastric acidity?

A
  • histamine binds to H2 receptors on gastric parietal cells stimulating gastric acid secretion
  • drugs antagonise the effect of histamine at these H2 receptors
  • reduced cAMP and hence reduced activity of H+/K+ ATPase pump
182
Q

When should H2 antagonists be used?

A

peptic ulcer, GORD, zollinger-Ellison syndrome

Phase 3 (10 decks)

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