GI/Liver Flashcards
(182 cards)
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
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
3
Q
Give the three-fold definition of cirrhosis.
A
diffuse process with fibrosis and nodule formation
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
5
Q
Ground glass cytoplasm is the specific feature of which liver disease?
A
hepatitis B virus
= accumulation of ‘surface antigen’
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
7
Q
Name three examples of genetic/deposition liver disease.
A
haemochromatosis (iron)
Wilson’s disease (copper)
alpha-1-antitrypsin deficiency
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
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
10
Q
Name the benign and malignant neoplasms associated with:
- Liver cells
- Bile duct
- Blood vessel
- Non-liver tissue
A
- B = hepatocellular adenoma. M = hepatocellular carcinoma
- B = bile duct adenoma. M = cholangiocarcinoma
- B = haemangioma. M = angiosarcoma
- B = N/A. M = metastases
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
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
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
14
Q
What are the three main associations of NAFLD?
A
obesity, T2DM, hyperlipidaemia
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
16
Q
Discuss the clinical spectrum of alcohol liver disease.
A
malaise, nausea, hepatomegaly, fever, jaundice, sepsis, encephalopathy, ascites, renal failure, death
17
Q
What are the four characteristic features of acute alcohol hepatitis?
A
hepatomegaly, fever, leucocytosis, hepatic bruit
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)
19
Q
List the four main risk factors for hepatitis C.
A
IVDU, sexual transmission, vertical transmission, needle-stick transmission
20
Q
What are the clinical signs of chronic liver disease?
A
stigmata: spider naevi, foetor, encephalopathy
‘synthetic dysfunction’: prolonged prothrombin time, hypoalbuminaemia
21
Q
Give four signs of portal hypertension.
A
caput medusa
ascites
oesophageal varices
splenoemegaly (thrombocytopenia)
22
Q
How is severity of liver disease assessed?
A
child-turcotte-pugh score: encephalopathy, ascites, bilirubin, albumin, PTTP
23
Q
Discuss how MELD scores indicate prognosis of liver disease.
A
mild < 10
moderate 10-15
severe > 15
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
25
Discuss the assessment of ascites following a diagnostic tap.
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
26
How is ascites managed?
low salt diet, diuretics (spironolactone, furosemide), paracentesis, transjugular intrahepatic portosystemic shunt (TIPSS), liver transplant, monitor renal function and electrolytes
27
List 5 precipitating factors of hepatic encephalopathy. Give 3 explanations of how these lead to encephalopathy.
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
28
Describe the Conn Score for grading mental state in hepatic encephalopathy.
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
29
What is hepatitis? List some of the symptoms.
inflammation of the liver
| malaise, fever, headaches, anorexia, nausea, vomiting, RUQ pain, dark urine, jaundice
30
Give 5 causes of acute hepatitis.
- infections e.g. Hep A-E, EBV, CMV, Q fever, syphilis, malaria
- toxins
- drugs
- alcohol
- autoimmune
31
How is hepatitis A diagnosed?
acute: IgM positive or RNA in blood or stool
| previous or vaccinated: IgG positive
32
Which Hep virus is commonly spread in pork products?
E
33
What are the neurological manifestations of Hep E?
Guillaine Barre syndrome, encephalitis, ataxia, myopathy
34
What problems are associated with hepatitis B?
weight loss, abdo pain, fever, cachexia, mass in abdomen, bloody ascites, cirrhosis develops in 25%, HCC, death
35
What is detected during hepatitis B lab tests?
```
sAg - marker of infection
sAb - marker of immunity
cAb - core antibody
eAg - suggests high infectivity
eAb - suggests low infectivity
HBV DNA
```
36
What treatments are available for hep B?
chronic
only treat those with liver inflammation or fibrosis
immunomodulatory - inferferon
suppress viral replication - tenofovir or entecavir
37
Which virus does Hep D require to replicate?
Hep B
38
Discuss HCV diagnosis through screening and blood tests.
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
39
What treatment is available for HCV?
direct acting antiviral inhibits different stages of the replication cycle
40
Acute cholecystitis is initiated by stone obstruction of cystic duct causing supersaturation of bile and chemical irritation. What symptoms will this lead to?
severe RUQ pain, tenderness and fever
41
Leucocytosis and normal serum amylase are blood results of which acute condition?
cholecystitis.
42
Acute pancreatitis is most commonly caused by gallstone, alcohol abuse, trauma/ERCP, drugs etc. How does it present?
severe upper abdo pain, fever, leucocytosis, raised serum amylase
43
What are potential complications of acute pancreatitis?
pancreatic abscess
| pseudocyst
44
How would you manage a pancreatic abscess?
drainage or necrosectomy plus antibiotics
45
List some differentials of pancreatic cysts.
1. Intraductal papillary mucinous neoplasm
2. Mucinous cystic neoplasm ('ovarian-type' stroma)
3. Serous cystadenoma
46
What is the 5 year survival rate of pancreatic cancer?
7%
47
What are the risk factors to develop pancreatic cancer?
smoking
alcohol
germline mutations e.g. BRCA
48
Discuss the signs and symptoms of pancreatic cancer.
- 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
49
What is the name given to the process of excising a head of pancreas tumour?
Whipple's resection
50
What is the commonest pancreatic neuroendocrine tumour and how does it present?
insulinoma - hypoglycaemia
51
Differentiate between intra and extra hepatic cholangiocarcinoma.
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
52
What are the criteria for diagnosis of acute pancreatitis?
2/3 of:
- pain in keeping with pancreatitis
- amylase 3 times upper limit of normal
- characteristic CT appearance
53
What investigations should be carried out in acute pancreatitis?
- US to assess gallstones
- MRCP to assess for CBD stones
- CT if diagnostic doubt or concern about complications
54
Give 2 DDx for acute pancreatitis.
perforated duodenum
| ischaemic bowel
55
What does non-enhancing pancreas on venous phase CT suggest?
pancreatic necrosis
56
How would you manage infected pancreatic necrosis?
- open necrosectomy
- percutaneous necrosectomy
- radiological drainage
57
Give complications associated with pancreatic necrosis.
bleeding
| erosion to surrounding structures
58
Discuss the use of interventional radiology for bleeding following pancreatic necrosis.
- access via groin
- selective cannulation of coeliac trunk
- commonly splenic artery aneurysm
- usually coils placed before and after blood, can be stunted
59
Pancreatic pseudocysts may settle without intervention. However if they remain symptomatic, how are they resolved?
drain to stomach laparoscopically or endoscopically
60
What is a pancreatic fistula?
an abnormal communication between the pancreas and other organs due to leakage of pancreatic secretions from damaged pancreatic ducts
61
How is pancreatic fistula managed?
- may require period of parenteral nutrition
- endoscopic treatment
- may require salvage distal pancreatectomy
62
What is the initial treatment of acute pancreatitis?
fluids, oxygen, organ support, antibiotics? early enteral feeding superior to parenteral feeding
63
What type of epithelium lines the oesophagus?
non-keratinising stratified squamous
64
What histological changes occur to the epithelium in reflux oesophagitis?
increased number of inflammatory cels
| basal zone becomes hyperplastic
65
Which two pathogens most commonly cause infection of the oesophagus?
candida albicans
| herpes simplex virus
66
What causes inflammation of oesophageal tissue?
- peptic oesophagitis/GORD: reflux of acid/bile
- lye
- pills: iron, bisphosphonates, tetracyclines
67
Describe Barrett's oesophagus.
- 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
68
Describe the typical epithelial appearance of Candida oesophagitis.
active chronic inflammation with many neutrophils especially near the luminal surface
69
How is a PAS stain used to confirm Candida albicans?
spores and hyphae present
70
Differentiate between low grade and high grade dysplastic epithelium seen in Barrett's oesophagus.
low grade: cells polarised, nuclei stratified
high grade: polarity lost, nuclei rounder, prominent nucleoli, abnormal mitoses, necrosis
71
What is the main risk of Barrett's oesophagus? How is risk of developing to this stage avoided?
carcinoma
radiofrequency ablation
radical surgery
72
Squamous carcinoma and adenocarcinoma are the two main oesophageal cancers. How do their associated factors differ?
1. smoking and drinking
| 2. GORD and obesity
73
Gastritis may be acute or chronic. Give three examples of how each is caused.
acute: alcohol, NSAIDs, burns
chronic: autoimmune, bacterial (H. pylori), chemical
74
Define autoimmune gastritis.
autoimmune destruction of parietal cells due to auto-antibodies against intrinsic factor and parietal cell antibodies in blood
75
List four consequences of autoimmune gastritis.
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
Discuss how H. pylori leads to gastritis and peptic ulceration.
- 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
What three factors can lead to peptic ulcers?
- 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
What is the typical presentation of peptic ulcer?
haematemesis, melena, abdo pain
79
List three consequences of peptic ulceration.
haemorrhage, perforation, fibrosis (leading to stenosis)
80
Describe the histological appearance of chemical gastritis.
few inflammatory cells, surface congestion oedema, elongation of gastric pits, tortuosity, reactive hyperplasia/atypia, ulceration
81
Bile reflux, NSAIDs, ethanol and oral iron are all causes of which type of gastritis?
chemical
82
Name two causes of chronic gastritis which are strongly associated with gastric cancer.
H. pylori
| autoimmune
83
Discuss the Lauren classification of gastric cancer.
- '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
Name three areas where diffuse gastric cancer may metastases.
- ovaries (Kurkenburg tumour)
- supraclavicular lymph node (Virchow's node)
- Sister Joseph's nodule (umbilical metastasis)
85
Which three signs/symptoms indicate the major acute medical emergency of an upper GI bleed?
haematemesis
'coffee ground' vomiting
melaena
86
List the 5 main causes of an upper GI bleed.
peptic ulcer, oesophagitis, gastritis, duodenitis, varices
87
Outline the basics in upper GI bleed management.
```
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
Which scoring systems are used to identify patients at risk of adverse outcome following acute upper GI bleeding?
```
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
Which class of drugs are most commonly used in upper GI bleeding?
IV proton pump inhibitors
90
Should adjustments be made to dosage of antiplatelet drugs following GI bleed?
- continue low dose aspirin once haemostasis is achieved
| - stop NSAIDs
91
Why should you assess risks and benefits of continuing anticoagulant drugs following GI bleed?
mortality high from CVD
92
Blood should be transfused following upper GI bleeding once Hb <7-8 g/dL. Name 3 other occasions where transfusion is indicated.
- 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
Outline the process by which oesophageal varices are formed due to liver cirrhosis.
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
Give three methods of treatment of varices.
endoscopic banding
TIPS - transjugular intrahepatic portosystemic shunt
B-blocker drugs
95
What is the therapy for acute variceal bleeding?
antibiotics early, vasopressors - terlipressin, endoscopic band ligation, rescue TIPS
96
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?
sengstaken tube
97
What is Mallory-Weiss syndrome?
bleeding from a laceration in the mucosa at the junction of the stomach and oesophagus
98
What are the causes of MW syndrome and how does it present?
- severe vomiting due to alcoholism or bulimia
| - haematemesis
99
Describe the pathological histology appearance of the intestinal epithelium in coeliac disease.
crypt hyperplasia
villous atrophy
intraepithelial lymphocytes
100
Crohn's disease and ulcerative colitis are examples of which type of disease?
chronic inflammatory bowel disease
101
Describe 5 chronic histological changes seen in IBD due to regeneration following ulceration.
crypt distortion, loss of crypts, submucosal fibrosis, Paneth cell metaplasia, neuronal hyperplasia
102
Give four acute changes seen during active IBD.
cryptitis, loss of goblet cells, crypt abscess formation, ulceration
103
What are the symptoms of ulcerative colitis?
- relapsing, bloody mucoid diarrhoea with pain/cramps relieved by defecation
- lasts days/months, then remission for months/years
104
List 5 extraintestinal manifestations of ulcerative colitis.
```
migratory polyarthritis
ankylosing spondylitis
sacroilitis
erythema nodosum
primary sclerosing cholangitis
uveitis
```
105
What are the main complications of ulcerative colitis?
perforation, toxic megacolon, iliac vein thrombosis, carcinoma, lymphoma
106
Patients with UC are given local or systemic steroids as treatment. What other ways of management may be required?
- 30% require colectomy during first 3 years
| - regular colonoscopy with biopsy to detect precancerous dysplastic changes
107
Define Crohn's disease.
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
List the symptoms of Crohn's disease.
episodic mild diarrhoea
fever
pain
may be precipitated by stress
109
What are the 5 most common complications of Crohn's disease?
```
fibrosing strictures
fistula
malabsorption
toxic megacolon
carcinoma
```
110
What is the eventual treatment of Crohn's disease?
surgery
| involvement of resection margins doesn't correlate with recurrence
111
In addition to the histological features common to both IBDs, Crohn's has some additional features. Can you give three?
```
skip lesions
fistulas/sinus tracks
malabsorption
granulomas
deep ulcerations
marked lymphcytic infiltration
serositis
```
112
What is the major long term risk associated with IBD?
colonic carcinoma
113
The majority of adenomas of the colon are dysplastic and are polyps, but what is an adenoma?
benign glandular neoplasms
114
How are adenomas prevented from progressing to malignant potential?
identified and removed
115
Give four differentials of adenomas.
hyperplastic polyps
hamartomatous polyps
inflammatory polyps
submucosal lesions
116
What are the main risk factors for developing CRC?
- 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
What features of benign polyps would make you worried about it becoming malignant?
- > 2cm
- flat polyps with a villous pattern - larger SA and no stalk
- increased no. of polyps
- epithelial dysplasia
118
Discuss TNM classification of malignant tumours.
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
Describe the staging for the tumour component of TNM.
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
Describe the staging for the nodal component of TNM.
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
Describe the staging of the metastases component of TNM.
M0: no distant metastasis
M1: metastasis to distant organs
122
Outline Dukes' classification of colon cancer.
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
Describe the impact that staging has on treatment offered to patients with colorectal cancer.
Dukes' A and B: better prognosis, no need to give CTx
124
What methods are used to detect colorectal cancer early?
- 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
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.
- increased risk of Crohn's
| - reduced risk of UC
126
Describe the pathophysiological differences between UC and Crohn's.
- UC: cytokine response vaguely ass. w/ Th2
| - Crohn's: cytokine response ass. w/ Th17
127
What features of a history and examination are crucial in diagnosing IBD?
- 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
How would you investigate suspected IBD?
- rigid sigmoidoscopy
- colonoscopy preferable
- small bowel radiology
- labelled WCC scanning
129
Name three treatments which are common to both UC and Crohn's.
corticosteroids e.g. hydrocortisone, prednisolone, beclometasone,
thiopurines
biologics
130
Mesalazine (5ASA) is a drug used to treat which type of IBD? How does it work?
ulcerative colitis
| anti-inflammatory - induction and maintenance of remission in UC
131
Which two drugs are limited to Crohn's type of IBD?
methotrexate
| immune modulating diets
132
List five significant side effects of steroids.
immunosuppression, impaired glucose tolerance, osteoporosis, weight gain, Cushingoid appearance
133
Describe the efficacy of thiopurine in maintenance therapy for UC and Crohn's.
- purine anti-metabolites
- steroid sparing agent
- immune modulating drugs
- prevent T cell clonal expansion in response to antigenic stimuli, allow T cell apoptosis
134
Name two thiopurines and 3 common side effects.
azathioprine, mercaptopurine
bone marrow suppression (leukopenia), N+V, arthralgia, pancreatitis, hepatitis, squamous skin cancers, haematological malignancy
135
Which two metabolites must be closely monitored while on thiopurines and why?
- 6TGN: assessment of compliance
| - 6MMP: associated with hepatotoxicity
136
List 5 side effects of methotrexate.
```
GI upset
hepatotoxicity
immunosuppression
sepsis
pulmonary fibrosis
```
137
Name 3 anti-TNFa monoclonal antibodies used in IBD.
- infliximab, adalumimab, golimumab
| - severe or fistulating Crohn's, rescue acute severe UC
138
Give 3 disadvantages to the use of infliximab in IBD.
loss of efficacy
allergic reactions
expensive
139
What are the three main concerns with prescribing anti-TNF drugs?
- infection risk (reactivation of TB and hep B)
- neurological (MS, progrressive multifocal leucoencephalopathy)
- malignancy (possible increased lymphoma risk)
140
Describe the initial management plan of an admitted patient due to IBD.
- 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
How would acute severe colitis be treated?
- 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
Can surgery cure IBD?
- in UC, technically yes
| - Crohn's - no, often returns following removal of the affected part
143
If surgery does not cure Crohn's, then when is it indicated?
stricturing, perforation, fistulising disease.
144
Where is the most common site for neuroendocrine tumour along the GI tract?
appendix
145
What is the name of the spindle cell tumour derived from interstitial cells of Cajal?
GI stromal tumour
146
Imatinib is commonly used as a target for GIST. Why?
majority have abnormalities of tyrosine-kinase receptor
147
Hodgkin's and NHL are rare in the colon. Which type of lymphomas are common?
enteropathy associated T cell lymphoma
148
How can coeliac disease increased risk of lymphoma in the colon?
untreated/refractory coeliac disease results in over stimulation of T cells leading to high risk of malignant transformation
149
Name three common viral infections in the intestines.
adenovirus
CMV
HSV (multinucleate giant cells with nuclear inclusions)
150
Describe pseudomembranous colitis.
membrane of fibrin and inflammatory exudate formed over lining of mucosa
151
What is the most common cause of pseudomembraneous colitis?
C. difficile. - usually following antibiotic therapy
152
Discuss the pathophysiology of ischaemic damage to the intestines.
- 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
Chronic non-bloody, watery diarrhoea, with normal endoscopy associated with autoimmune disease is characteristic of which type of colitis?
lymphocytic and collagenous
154
How is lymphocytic colitis treated?
sulfasalazine
| corticosteroids
155
Describe the histological appearance of lymphocytic colitis.
colonic epithelial lymphocytosis with surface epithelial damage but without thickened subepithelial collagen
increased chronic inflammatory cells in lamina propria
156
Which type of colitis has patchy thickening of subepithelial basement membrane of 10 microns or more on histology?
collagenous
157
What is the name given to a pouch of mucosa which has herniated through the muscularis propria?
diverticulum
158
How is it though that diverticular disease develops?
as a result of increased intra luminal pressure associated with low fibre diets
159
What are the main complications of diverticular disease?
inflammation
abscess formation
perforation
160
Which genes are commonly associated with coeliac disease?
HLADQ2/8
161
TTG autoantibodies are found in which disease of the colon?
coeliac disease
162
Give three possible complications of coeliac disease.
osteoporosis, IDA, small bowel malignancy
163
What is the definition of spontaneous bacterial peritonitis?
>250 neutophils/mm3 in ascites in absence of intra-abdominal source of infection or malignancy
usually gram-ve bacteria
164
How would you treat SBP?
IV antibiotics and IV albumin
165
How do you manage ascites?
salt restriction and diuretics
| oral spironolactone +/- frusemide
166
What therapies are available for refractory ascites?
- large volume paracentesis
- TIPS
- liver transplant
167
Which condition is associate with C282Y gene mutation?
genetic haemochromatosis
| autosomal recessive
168
What is haemochromatosis?
excessive absorption of dietary iron
| leads to iron overload in liver, heart, pancreas, joints, skin ('bronze diabetes')
169
How is haemochromatosis diagnosed and treated?
- raised ferritin and transferrin saturation
- HFE gene
- treated by venesection
170
What is the name of the stain used to pick up iron in haemochromatosis?
Perl's stain
171
List the causes of hyperamylasaemia.
- 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
Discuss what each of the LFTs show in jaundice.
- bilirubin increase = bilirubin in blood
- transaminase rise = destruction of hepatocytes
- Alk Phos rise = damage to bile ducts
173
What is the best initial management of pancreatitis?
IV fluids, catheter and nil by mouth, observe in ward
174
What are the surveillance tests for HCC in cirrhosis?
6 monthly US +/- AFP
175
Discuss the management of HCC.
- small: liver transplant, resect tumour, RF ablation
- larger: trans-arterial chemoembolisation, oncology drug therapy (sorafenib)
- palliative care
176
Describe the pathogenesis of coeliac disease.
- 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
Give an example of a proton pump inhibitor.
omeprazole, lansoprazole, pantoprazole
178
Describe the mechanism of action of PPIs.
- bind to H+/K+ ATPase pump on gastric parietal cells
| - reduced HCl production and hence reduced gastric acidity
179
What are the indications of PPI use?
peptic ulcers, GORD, H.pylori infection, prophylaxis in patients receiving long term NSAIDs, Zollinger-Ellison syndrome
180
Ranitidine and cimetidine are examples of which type of drug?
H2 receptor antagonists
181
How do H2 receptor antagonists reduce gastric acidity?
- 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
When should H2 antagonists be used?
peptic ulcer, GORD, zollinger-Ellison syndrome
