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Gastroenterology Flashcards

1
Q

Describe the CAGE questionnaire

A

Do you think you should cut down your drinking?

Do you get annoyed at others commenting on your drinking?

Do you ever feel guilty about drinking?

Do you need a drink in the morning to help your hangover

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2
Q

List the complications of alcohol

A 
Alcoholic liver disease
Cirrhosis and complications including HCC
Alcohol dependence and withdrawal 
Wernicke - Korsakoff syndrome 
Pancreatitis 
Alcoholic cardiomyopathy
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3
Q

What is the weekly recommended limit of alcohol

A

14 units a week, no more than 5U a day, spread evenly over 3 or more days

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4
Q

Describe the AUDIT score

A

10 questions, score >8 indicates harmful drinking

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5
Q

List some signs of liver disease

A 
Jaundice 
Hepatomegaly
Spider naevi
Palmar erythema
Gynaecomastia
Bruising 
Ascites
Caput medusae 
Asterixis - flapping tremor
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6
Q

What investigations would you do for alcoholic liver disease

A

FBC - raised MCV

LFTs - elevated ALT and AST, low albumin due to reduced synthetic function of the liver, elevated bilirubin in cirrhosis

Clotting - elevated prothrombin time due to reduced synthetic function

U&Es - may be deranged in hepatorenal syndrome

USS - fatty change early on (increased echogenicity)

Fibro scan - used to check the elasticity of the liver by sending high frequency sound waves into the liver - helps to assess the degree of cirrhosis

Endoscopy - to assess and treat varices when portal hypertension is suspected

CT and MRI - look for fatty infiltration of the liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites

Liver biopsy - used to confirm the diagnosis of alcohol related hepatitis or cirrhosis where steroid treatment is being considered

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7
Q

Who can be referred for liver transplant in alcoholic liver disease

A

Severe disease if abstained from alcohol for 3 months prior to referral

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8
Q

Describe the nutritional support for alcoholic patients

A

High protein diet and B vitamins

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9
Q

Describe alcohol withdrawal symptoms

A

6-12hrs - tremor, sweating, headache, craving, anxiety

12-24hrs - hallucinations

24-48hrs - seizures

24-72hrs - delirium tremens

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10
Q

Describe the pathophysiology of delirium tremens

A

Medical emergency associated with alcohol withdrawal (35% mortality)

Alcohol stimulates GABA receptors in the brain causing a relaxing effect on the rest of the brain,
Alcohol inhibits glutamate receptors having further inhibitory effect on electrical activity

Chronic alcohol leads to GABA system becoming down regulated and glutamate system being upregulated. When alcohol is removed, GABA under functions and glutamate over functions causing extreme excitability of the brain with excess adrenergic activity

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11
Q

List the symptoms of delirium tremens

A 
Acute confusion 
Severe agitation 
Delusions and hallucinations
Tremor
Tachycardia
Hypertension 
hyperthermia
Ataxia
Arrhythmia
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12
Q

How is alcohol withdrawal treated?

A

Chlordiazepoxide - benzodiazepine reducing regime titrated to the required dose based on local protocol and continued for up to a week

IV high dose B vitamins - pabrinex

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13
Q

What causes Wernicke’s - Korsakoff’s syndrome?

A

Thiamine (B1) deficiency

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14
Q

List the features of Wernicke’s encephalopathy

A

Confusion
Oculomotor disturbances
Ataxia

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15
Q

List the features of Korsakoff’s syndrome

A

Memory impairment

Behavioural changes

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16
Q

How does liver cirrhosis cause portal hypertension

A

Increased resistance in the vessels leading into the liver as a result of fibrosis and scar tissue

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17
Q

List some causes of liver cirrhosis

A

Alcoholic liver disease
Non-alcoholic fatty liver disease
Hepatitis B
Hepatitis C

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18
Q

List some signs of liver cirrhosis

A 
Jaundice
Asterixis 
Caput medusae
Spider naevi
Hepatomegaly 
Splenomegaly 
Gynaecamastia and testicular atrophy 
Palmar erythema 
Bruising 
Ascites
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19
Q

List the investigations for cirrhosis

A

LFTs - decreased albumin
Prothrombin time - increased
U&Es - hyponatraemia (fluid retention), Ur and Cr deranged in hepatorenal syndrome
Viral markers and antibodies - see cause
Alpha fetoprotein - hepatocellular carcinoma
Ultrasound
Enhanced lifer fibrosis blood test - 1st line for testing for fibrosis in non-alcohlic fatty liver disease
Liver biopsy - cirrhosis
CT/MRI - vessel and organ changes
Endoscopy - oesophageal varices

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20
Q

How often is AFP checked?

A

Every 6 months along with USS

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21
Q

Describe the changes which may be seen on USS in people with cirrhosis

A

Nodularity of surface of the liver
Corkscrew appearance to arteries with increased flow as they compensate for reduced portal flow
Enlarged portal vein with reduced blood flow
Ascites
Splenomegaly

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22
Q

Who should fibroscans be done 2 yearly for?

A

Hep C
Heavy alcohol drinkers (>50U men, >35 U women)
Diagnosed alcoholic liver disease
Non alcoholic fatty liver and evidence of fibrosis on ELF blood test
Chronic hep B (yearly)

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23
Q

Describe the child-pugh score for liver disease

A

Estimates the severity and prognosis of liver cirrhosis
Min score - 5
Max score - 15

  • bilirubin
  • Albumin
  • INR
  • Ascites
  • Encephalopathy
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24
Q

Describe the MELD score

A

Guides transplant management - estimates the 3 month mortality for compensated cirrhosis

  • Bilirubin
  • Cr
  • INR
  • Na
  • Dialysis
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25
Q

Describe the management of liver cirrhosis

A 
USS and AFP every 6 months
Endoscopy ever 3 years 
High protein, low Na diet 
MELD score every 6 months - see if need referral for transplant 
Treat complications 
Liver transplant
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26
Q

List some complications of liver cirrhosis

A 
Malnutrition 
Portal hypertension 
Varices and variceal bleeding 
Hepatorenal syndrome
Hepatic encephalopathy 
Hepatocellular carcinoma
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27
Q

How does cirrhosis cause malnutrition and muscle wasting

A

Increased use of muscle tissue as fuel
Disrupts metabolism of protein in liver
Reduces ability to store glucose as glycogen

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28
Q

How do you manage malnutrition in cirrhosis

A 
Regular meals (every 2-3hrs) 
Low sodium (minimise fluid retention
High protein diet and high calorie
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29
Q

Describe portal hypertension

A

Portal vein comes from the superior mesenteric and splenic vein and delivers blood to the liver.
Liver cirrhosis increases the resistance of blood flow in the liver and as a reuslt there is increased back pressure into the portal system

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30
Q

Describe the development of varices

A

Portal hypertension and back pressure causes vessels where portal system anastomoses with systemic venous system to become swollen and tortous

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31
Q

Where do varices occur?

A

Gastro-oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via umbilical vein - caput medusae

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32
Q

Describe the treatment of stable varices

A

Propranolol - reduce pressure
Elastic band ligation of varices
Injection of sclerosant
Transjugular intrahepatic portosystemic shunt (TIPS)

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33
Q

Describe TIPS procedure

A

IR inserts wire under Xray guidance into jugular, down vena cava and into the liver via the hepatic vein. They make a connection through the liver tissue between the portal and hepatic vein and puts a stent in place to allow blood to flow directly from portal to hepatic vein and relieves pressure on the portal system

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34
Q

Describe the management of bleeding oesophageal varices

A

Vasopressin analogues - terlipressin (cause vasoconstriction and slow bleeding)
Correct coagulopathy - Vit K and FFP
Prophylactic broad spectrum antibiotics
Consider intubation and ICU
Endoscopy - injecting sclerosant to cause inflammatory obliteration of vessel or elastic band ligation.
Sengstaken-blakemore tube - inflatable tube inserted into oesophagus to tamponade the bleeding varices - used when endoscopy fails

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35
Q

Describe ascites in cirrhosis

A

Increased portal system pressure causes fluid to leak out of the capillaries in the bowel and liver into the peritoneal space. The drop of fluid causes a reduced flood flow entering the kidneys. The kidneys sense the lower pressure and release renin which leads to increased aldosterone secretion and reabsorption of fluid and sodium in the kidneys. Cirrhosis causes a transudative ascites (low protein|)

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36
Q

Describe the management of ascites

A

Low sodium diet
Anti-aldosterone diuretics - spironolactone
Paracentesis - ascitic drain/tap
Prophylactic antibiotics - ciprofloxacin for prevention of SBP in patients with <15g/L protein in fluid
TIPS procedure or transplantation

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37
Q

How do patients with spontaneous bacterial peritonitis present?

A

Asymptomatic - low threshold for ascitic fluid culture
Fever
Abdominal pain
Deranged bloods - raised WCC, CRP, Cr, Metabolic acidosis
Ileus
Hypotension

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38
Q

Name the common organisms which cause spontaneous bacterial peritonitis

A

E.coli
Klebsiella pneumoniae
Gram positive cocci - staphylococcus and enterococcus

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39
Q

What is spontaneous bacterial peritonitis

A

Infection develops ion the peritoneal fluid

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40
Q

How do you manage spontaneous bacterial peritonitis

A

Ascitic culture taken prior to Abx

Give IV cephalosporin - cefotaxime

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41
Q

Describe hepatorenal syndrome

A

Pooling of blood in portal system causes reduction in blood supply to kidneys, vasoconstriction activates RAAS causing renal vasoconstriction and rapidly deterioating kidney function

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42
Q

Describe the treatment of hepatorenal syndrome

A

Liver transplant otherwise fatal within a week

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43
Q

Describe the pathophysiology of hepatic encephalopathy

A

Build up of ammonia which is produced by intestinal bacteria when they break down proteins and is absorbed in the gut

  • liver cells prevent the metabolism of ammonia
  • collateral vessels mean ammonia bypasses the liver
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44
Q

Describe the management of hepatic encephalopathy

A

Laxatives - lactulose

Antibiotics - rifaximin - reduce bacteria producing ammonia Nutritional support - NG feed

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45
Q

List the precipitating factors for hepatic encephalopathy

A 
Constipation#
Electrolyte disturbance
Infection 
GI bleed 
High protein diet
Medications - sedatives
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46
Q

What can non-alcoholic fatty liver disease progress to

A

Hepatitis
Fibrosis
Cirrhosis

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47
Q

List the stages of non-alcoholic fatty liver disease

A

1 - NAFLD
2 - Non-alcoholic steatohepatitis
3 - Fibrosis
4 - cirrhosis

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48
Q

List the risk factors for NAFLD

A 
Obestity 
Poor diet and low activity levels 
T2DM
High cholesterol 
Middle aged 
Smoking
High BP
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49
Q

List the components of a non-invasive liver screen

A

LFTs
USS liver
Hepatitis B and C serology
Autoantibodies - ANA, SMA, AMA, LKM-1

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50
Q

List the investigations in non-alcoholic fatty liver disease

A

Liver ultrasound
Enhanced liver fibrosis (ELF) blood test - 1st line for fibrosis in NAFLD but not available everywhere, Indicates the severity of fibrosis
NAFLD fibrosis score - 2nd line based on age, BMI< liver enzymes, platelets, albumin and diabetes
Fibroscan - 3rd line, ultrasound that assess the stiffness of liver and gives indication of fibrosis

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51
Q

Describe the management of NAFLD

A 
Diet
Exercise
Weight loss
Stop smoking
Control DM, HTN, hypercholesterolaemia
Avoid alcohol 
Refer to liver specialist if needing Vit E and pioglitazone
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52
Q

What is the triad in Budd-Chiari syndrome

A

Sudden onset abdominal pain

Ascites and tender hepatomegaly

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53
Q

What is Budd-Chiari syndrome

A

Obstruction to hepatic venous outflow

Occurs in patients in hypercoagulable state but can occur from physical obstruction

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54
Q

List the causes of hepatitis

A 
Alcoholic 
Viral
Autoimmune
NAFLD
Drug induced
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55
Q

How does hepatitis present

A 
Abdo pain 
Jaundice 
Nausea and vomiting 
Pruitis 
Muscle aches 
Fever
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56
Q

Describe the LFT picture in hepatitis

A

High AST and ALT with proportionally high ALP

High bilirubin

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57
Q

Describe Hepatitis A

A

RNA virus
Faecal oral route
Presents with nausea, vomiting, anorexia and jaundice. May cause cholestasis - pale stools and dark urine
Resolves without treatment in 1-3 months
Manage with basic analgesia
Vaccination before travel
Notifiable disease

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58
Q

Describe hepatitis B

A

DNA virus
Blood borne disease and vertical transmission
Most people recover in 2 months but some become carriers - continue to produce viral proteins as viral DNA integrated into persons DNA

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59
Q

What is HBsAg

A

Hep B surface antigen

Demonstrates active infection

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60
Q

What is HBeAg

A

E antigen - marker of viral replication and implies high infectivity

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61
Q

What is HBcAb

A

Core antibodies

Implies past or current infection

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62
Q

What is HBsAb

A

Surface antibody

Implies past or current infection

63
Q

What is HBV DNA

A

Hep B virus DNA - direct count of the viral load

64
Q

What do you test for when you screen for hepatitis B

A

HBcAb - previous infection
HBsAg - active infection - if positive do HBEAg and viral load
HBcAb - IgM version implies acute if high titrre and low titre if chronic and IgG indicates past infection

65
Q

What is given in hep B vaccine?

A

HBsAg - immune system creates response and HBsAb
3 doses at different intervals
Part of routine UK vaccine scale and 6 in 1 vaccine

66
Q

How is Hep B managed?

A 
Notify public health 
Refer for specialist management
Screen for other blood borne diseases
Advise lifestyle changes
Educate to reduce risk of transmission Test for complications - fibroscan and USS (HCC) 
treat complications 
liver transplant for end stage disease
Antiviral medication to slow disease
67
Q

Describe Hep C

A

RNA virus
Curable with direct acting medications
1 in 4 full recovery
3 in 4 chronic hep C

68
Q

LIst the complications of Hep C

A

HCCC and cirrhosis

69
Q

How is Hep C diagnosed

A

Hepatitic C antibody screening test then if positive do hepatitis C RNA testing to calculate viral load and assess genotype

70
Q

Describe the management of Hep C

A 
Low threshold for screening 
Notify public health
Screen for other blood borne disease
Refer
Lifestyle changes
Advise on reducing transmission 
Test for complications 
Antiviral treatment - direct acting antivirals - tailored to genotype - taken for 8-12 weeks 
Liver transplant in end stage
71
Q

Describe hepatitis D

A 
RNA virus
Concurrent hep B infection - requires the hep B antigen
Notify public health 
Increased risk of hep B complications 
No treatment
72
Q

Describe Hepatitis E

A 
RNA virus 
Faceal oral route, seafood and pork 
Mild illness - virus cleared within a month, no treatment
Rarely progresses to liver failure
Notifiable disease
73
Q

Describe autoimmune hepatitis

A

Genetic predisposition and trigger such as viral infection creating T cell response to attack liver cells

Two types - Type 1 occur in adults (woman in late 40s-50s, post menopausal, less acutely with fatigue and features of liver disease), anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (anti-actin), anti soluble liver antigen (anti-SLA/LP)

Type 2 occurs in children (teenage, acute hepatitis with high transaminases and jaundice), Anti-LKM1, anti-LC1

Diagnosis with biopsy

74
Q

How is autoimmune hepatitis treated?

A

Prednisolone
Azathioprine
Liver transplant if end stage liver disease but autoimmune hepatitis can recur in the transplanted liver.

75
Q

What is the AST:ALT ratio in alcoholic hepatitis

A

2:1

76
Q

Which hepatitis vaccine should gay men be offered?

A

Hep A

77
Q

Describe ischaemic hepatitis

A

Reduced perfusion of liver

Grossly elevated transaminases with AKI

78
Q

Describe haemachromatosis and its inheritance

A

Iron storage disorder
Autosomal recessive
Chromosome 6 human haemochromatosis protein (HFE) mutation

79
Q

How does haemachromatosis present?

A

> 40yo or later in females (menstruation)
Chronic tiredness
Joint pain
Bronze discolouration
Hair loss
Sexual problems - amenorrhea and erectile dysfunction
Memory and mood

80
Q

How is haemochromatosis diagnosed

A

Serum ferritin
Transferrin saturation (high)
Genetic test
Liver biopsy and pearls stain but this replaced by genetics
CT abdomen - increased attenuation of liver - iron overload
MRI - liver iron deposits and heart

81
Q

What is serum ferritin

A

Acute phase protein - inflammation

82
Q

List some complications of haemochromatosis

A 
DM
Liver damage and cirrhosis and HCC 
Chrondrocalcinosis - iron in joints
Pituitary gland and gonads - hypogonadism or impotence or amenorrhoea or infertility 
Cardiomyopathy - heart failure 
Hypothyroidism
83
Q

How is haemachromatosis managed

A

Venesection - weekly
Serum ferritin monitor
Monitor and treat complications

84
Q

Describe Wilsons disease and its inheritance

A

Accumulation of copper
Autosomal recessive
Mutation in wilsons disease protein on chromosome 13 - ATP7B copper binding protein

85
Q

Describe the symptoms of wilsons disease

A

Hepatic - hepatitis, cirrhosis
Neurological - concentration, coordination, dystonia, Parkinsonism (symmetrical)
Psychiatric - depression to psychosis

Kayser-Fleischer rings - copper deposition in descements corneal membrane - brown circles surrounding iris

Haemolytic anaemia
Renal tubular acidosis
Osteopenia

86
Q

How is wilsons disease diagnosed

A 
Low serum caeruloplasmin 
Liver biopsy 
24hr urine copper assay 
Low serum copper 
Kayser fleischer rings 
MRI brain showing non specific changes
87
Q

How is wilsons disease managed

A

Copper chelation with penicillamine or trientene

88
Q

What is alpha-1-antitrypsin deficiency

A

Autosomal recessive defect in gene for alpha-1-antitrypsin which usually prevents the neutrophil elastase enzyme breaking down the connective tissues
Liver cirrhosis >50
Lung bronchiectasis and emphysema >30yo

89
Q

How is alpha-1-antitrypsin diagnosed?

A

Low serum alpha-1-antitrypsin
Liver biopsy shows cirrhosis and acid schiff positive staining globules
Genetic testing for A1AT gene
High resolution CT thorax

90
Q

Describe the management of alpha-1-antitrypsin

A

Stop smoking
Symptom management
Organ transplant
Monitor for complications

91
Q

Describe primary biliary cirrhosis

A

Autoimmune condition which attacks the small bile ducts in the liver (intralobar ducts)

92
Q

Describe the presentation of primary biliary cirrhosis

A 
Middle aged women 
Other autoimmune or rheumatoid conditions 
Fatigue
Pruitis
GI disturbance and abdominal pain 
Jaundice
Pale and greasy stools
Xanthoma and xanthelasma 
Signs of cirrhosis and liver failure - ascites, splenomegaly, spider naevi
93
Q

How is primary biliary cirrhosis diagnosed?

A

LFTs - ALP is first liver enzyme to be raised, other liver enzymes and bilirubin are raised in later disease
Auto antibodies - Anti-mitochondrial antibodies, Anti-nuclear antibodies
ESR raised
IgM raised
Liver biopsy - diagnosing and staging disease

94
Q

Describe the treatment of primary biliary cirrhosis

A

Ursodeoxycholic acid - reduces intestinal absorption of cholesterol
Colestyramine - bile acid sequestrate in that it binds to bile acids and prevents absorption in the gut and can help with pruitis (raised bile acids)
Liver transplant
Immunosuppression

95
Q

Describe the disease progression of primary biliary cirrhosis

A 
Advanced liver cirrhosis 
Portal hypertension 
Symptomatic pruitis
Fatigue
Steatorrhoea 
Distal renal tubular acidosis
Hypothyroidism
Osteoporosis
Hepatocellular carcinoma
96
Q

Describe primary sclerosing cholangitis

A

Stricturing and fibrosis of the intrahepatic or extrahepatic ducts causing obstruction to bile

97
Q

Describe the presentation of primary sclerosing cholangitis

A 
Jaundice
Chronic right upper quadrant pain
Pruitis
Fatigue
Hepatomegaly
98
Q

Describe the diagnosis of primary sclerosisng cholangitis

A

Deranged ALP and high bilirubin, other liver function off in later disease
Auto antibodies to see if autoimmune component - p-ANCA, ANA, aCL
Gold standard is MRCP

99
Q

Describe the management of primary sclerosing cholangitis

A

ERCP - stenting of strictures
Colestyramine - prevents pruitis
Monitor for complications
Liver transplant

100
Q

List the complications of primary sclerosisng cholangitis

A 
Acute bacterial cholangitis 
Cholangiocarcinoma
Colorectal cancer
Liver cirrhosis and failure
Biliary strictures
Fat soluble vitamin deficiency
101
Q

Which other GI disease is primary sclerosising cholangitis linked to?

A

Ulcerative colitis

102
Q

Where does the endoscope travel in ERCP

A

Through duodenum into the sphincter of oddi and into the ampulla of vater to bile ducts

103
Q

What are the two types of primary liver cancer?

A

Hepatocellular (80%)

Cholangiocarcinoma (20%) - bile ducts

104
Q

What are the risk factors for hepatocellular carcinoma

A

Liver cirrhosis due to viral hep B &C, alcohol, NAFLD

105
Q

What are the risk factors for cholangiocarcinoma

A

Primary sclerosing cholangitis

106
Q

What is the presentation of liver cancer

A 
WEight loss
Abdo pain but no pain in cholangiocarcinoma 
Anorexia
Nausea and vomiting 
Jaundice 
Pruitis
107
Q

How is liver cancer diagnosed

A 
Alpha fetoprotein - hepatocellular 
CA19-9 - cholangiocarcinoma
Liver USS 
CT/MRI 
ERCP and biopsy
108
Q

Describe the treatment of hepatocellular cancer

A

Resistant to chemo/radiotherapy
Surgical resection or liver transplant if refined to liver
Kinase inhibitors - reduce proliferation - sorafenib, regorafenib, lenvatinib

109
Q

Describe the treatment of cholangiocarcinoma

A

ERCP and stent
Resistant to chemo and radiotherapy
Surgical resection in very early disease

110
Q

What is a haemangioma

A

Common benign tumour of liver

No symptoms and no cancerous potential so no treatment or monitoring

111
Q

What is focal nodular hyperplasia?

A 
Benign liver tumour made of fibrotic tissue 
Found incidentally 
No symptoms and no malignant potential 
More common in women taking COCP 
No treatment or monitoring required
112
Q

Name the two types of incision in liver transplant

A

Roof top

Mercedes benz

113
Q

List some contraindications of liver transplant

A 
Significant co morbidity - severe kidney or heart disease
Excessive weight loss and malnutrition
Active hepB and C or other infection 
End stage HIV
Active alcohol use
114
Q

What is the lining to the oesophagus

A

Squamous epithelial lining

115
Q

What is the lining to the stomach

A

Columnar epithelial lining

116
Q

Describe the symptoms of GORD

A 
Heart burn
Acid regurgitation
Pain in retrosternal area or epigastrium
Bloating 
Bowels
Nocturnal cough 
Hoarse voice
117
Q

When would you refer a GORD patient for endoscopy

A

Bleed (malaena and coffee ground vomit) - urgent admission and endoscopy

2 week wait - 
Dysphagia
Age >55
Weight loss
Upper abdominal pain/reflux
Treatment resistant dyspepsia
Low Hb 
Raised platelet count
118
Q

Describe the treatment of GORD

A

Lifestyle - reduce tea, coffee, alcohol, weight loss, avoid smoking, avoid heavy meals, stay upright after eating
Gaviscon and rennie
PPI - lansoprazole and omeprazole
Ranitidine - H2 receptor antagonist (antihistamine), reduce acid secretion
Surgery - laparoscopic fundoplication - tie fundus around the lower oesophageal sphincter to narrow it

119
Q

What tyype of bacteria is Helicobacter pylori

A

Gram negative aerobic bacteria

120
Q

Describe H pylori

A

Lives in stomach
Causes damage to the epithelial lining resulting in gastritis, ulcers and increases risk of stomach cancer

Evades the stomach acid by forcing its way into the gastric mucosa and creating breaks in the mucosa to expose the epithelial cells under the acid

Produces ammonia to neutralise the acid - this directly damages the epithelial lining

121
Q

How is H.pylori tested for?

A

Urea breath test - radiolabelled carbon 13
Stool antigen test
Rapid urease test (CLO) test - performed during endoscopy and involves taking biopsy of stomach mucosa, adding urea. If H.pylori is present then this produces urase enzymes that convert the urea to ammonia - ammonia makes the solution more alkali giving a positive result when pH is tested

122
Q

How is H.pylori eradicated?

A

Triple therapy - PPI and 2 antibiotics (amoxicillin and clarithromycin) for 7 days
Urea breath test after treatment to test for eradication

123
Q

What is Barrett’s oesophagus

A

Pre-malignant condition for development of adenocarcinoma of the oesophagus
Changing of the squamous epithelium to columnar epithelium (metaplasia) this is then at risk of dysplasia

124
Q

How is Barrett’s oesophagus treated?

A

PPI

Ablation treatment - photo-dynamic therapy, laser therapy and cyrotherapy in dysplasia

125
Q

Which ulcer is worsened by eating food?

A

Peptic ulcer

126
Q

Which ulcer is improved by eating food?

A

Duodenal ulcer

127
Q

How are peptic/duodenal ulcers treated?

A

High dose PPI

128
Q

List some complications of duodenal/peptic ulcers

A

Bleeding
Perforation
Scarring/strictures

129
Q

List some causes of Upper GI bleed

A

Oeosphageal varices
Mallory weiss tear - tear of oesophagus mucous membrane
Ulcers
Cancer

130
Q

How do peopl with upper GI bleeds present

A

Haematemeiss
Coffee ground comit
malaena
Haemodynamic instability - hypotension, tachycardia, sign of shocj (young people compensate)

131
Q

Name the scoring system used in predicting upper GI bleeds

A 
Glasgow blatchford score 
Score >0 indicates high risk of GI bleed
- Drop in Hb
- Raised ur - breakdown of blood by acid and digestive enzyme 
- BP
- HR
-Melaena
Syncope
132
Q

Name the scoring system used to predict mortality and risk of re bleeding after endoscopy

A 
Rockall score
- age
- comorbidity 
- shock 
cause of bleed
- endoscopic stigmata of recent haemorrhage - visible bleeding vessels and clots
133
Q

Describe the management of upper GI bleed

A

ABCDE approach
Access - 2 large bore cannulae
Bloods - FBC (Hb, plts), U&Es (Ur), coagulation (INR), LFTs (liver disease), cross match 2 Units.
Transfuse - depending on individual presentation, blood, platelets and clotting factors (FFP) to patients with massive haemorrhage, prothrombin complex in someone taking warfarin
Endoscopy - urgent if unstable, within 24hrs if stable - OGD - provide interventions to stop bleeding (banding and cauterisation)
Drugs - stop NSAIDs and anticoagulants, some senior doctors give PPI
If oesophageal varices - give terlipressin and prophylactic broad spectrum antibiotics

134
Q

Describe the features of crohns disease

A 
No blood or mucus 
Entire GI tract 
Skip lesions 
Terminal ileum and Transmural thickness inflammation 
Smoking is a RF 
Weight loss, strictures and fistula
135
Q

Describe the features of ulcerative colitis

A 
Continuous inflammation 
Limited to Rectum and colon 
Only the superficial mucosa affected 
Smoking is protective
Excrete blood and mucus 
Use of aminosalicylates 
Primary sclerosisng cholangitis
136
Q

List the tests for IBD

A

Bloods - FBC, U&E, LFT, CRP
Faecal calprotectin
Endoscopy - OGD and colonoscopy
Imaging - USS, CT, MRI - fistulas, abscesses and strictures

137
Q

How do you induce remission in crohns

A

Oral prednisolone or IV hydrocortisone

138
Q

How do you maintain remission in crohns

A 
Azathioprine
Mercaptopurine
Methotrexate
Infliximab 
Adalinumab

Surgery when affecting distal ileum

139
Q

How do you induce remission in mild/moderate UC

A

Aminosalicylate - mesalazine PO/PR or corticosteroids (prednisolone)

140
Q

How do you induce remission in severe disease

A 
IV corticosteroids (hydrocortisone) 
IV ciclosporin
141
Q

How do you maintain remission in UC

A

Aminosalciylates - mesalazine PO/PR
Azathioprine
Mercaptopurine

Panproctocolectomy (remove the colon and rectum), ileostomy or J-pouch (ileo-anal anastomosis where the ileum is folded back into itself and fashioned into a larger pouch that functions like a rectum)

142
Q

Which scoring system is used for the severity of IBD flare

A

Truelove and Witts criteria

143
Q

List some symptoms which are suggestive of IBD

A

Abdominal pain relieved on opening bowels or associated with a change in bowel habit, abnormal stool passage, bloating, worse symptoms after eating and PR mucus

144
Q

Describe the management of IBD

A

Adequate fluid intake
Regular small meals
Reduced processed food
Limit caffeine and alcohol
Low FODMAP diet
Trial of probiotic supplement 4 weeks
Loperamide for diarrhoea and laxatives (not lactulose for constipation as causes bloating)
Antispasmodics - hyoscine butylbromide (buscopan)
Tricyclic antidepressants (amitriptyline) or SSRI antidepressants and CBT

145
Q

Describe coeliac disease

A

Autoantibodies produced in response to exposure to gluten

Lead to inflammation of the epithelial cells in intestine

146
Q

How is coeliac diagnosed

A

Total immunoglobulin A levels - exclude IgA deficiency
Raised anti-TTG (tissue transglutaminase antibodies) antibodies
Raised anti-EMA (endomysial antibodies) antibodies
Deaminated gliadin peptide antibodies (anti-DGPs)
Endoscopy and intestinal biopsy - crypt hypertrophy and villous atrophy

147
Q

Which genes are implicated in coeliac disease

A

HLA-DQ2 and HLA-DQ8

148
Q

Describe the presentation of coeliac disease

A 
Failure to thrive 
Diarrhoea
Fatigue
Weight loss
Mouth ulcers 
Anaemia secondary to B12 and folate deficiency 
Dermatitis herpetiformis 
Peripheral neuropathy
Cerebellar ataxia
Epilepsy
149
Q

List the associations of coeliac disease

A 
T1DM
Thyroid disease
Autoimmune hepatitis 
Primary biliary cirrhosis
Primary sclerosing cholangitis
150
Q

List the complications of untreated coeliac disease

A 
Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis 
Enteropathy associated T cell lymphoma 
Non-Hodgkin lymphoma
Small bowel adenocarcinoma
151
Q

What is the treatment for coeliac disease

A

Life long gluten free diet

Pneumococcal vaccine every 5 yrs

152
Q

Which anti-emetic should be avoided in bowel obstruction

A

Metoclopramide - increases the peristalsis and can precipitate perforation

153
Q

What is the treatment of C.difficle

A

Oral vancomycin

154
Q

What is Plummer Vinson syndrome

A

Oesophageal web associated with iron deficiency anaemia

Finals (18 decks)

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