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Gastroenterology Flashcards

1
Q

What are the 4 most common causes of liver cirrhosis ?

A

Alcohol-related liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Hepatitis C

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2
Q

What are some rarer causes of liver cirrhosis?

A

Autoimmune hepatitis
Primary biliary cirrhosis
Haemochromatosis
Wilsons disease
Alpha-1 antitrypsin deficiency
Cystic fibrosis
Drugs (e.g., amiodarone, methotrexate and sodium valproate)

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3
Q

What are some findings on examination of a patient with liver cirrhosis?

A

Cachexia
Jaundice
Hepatomegaly
small nodular liver
splenomegaly
palmar erythema
Gynaecomastia and testicular atrophy
bruising
excoriations
ascites
caput medusae
Leukonychia
asterixis

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4
Q

What does a non-invasive liver screen involve?

A

USS
Hep B & C serology
Autoantibodies
Immunoglobulins
Caeruloplasmin
Alpha-1 antitrypsin levels
Ferritin and transferrin saturation

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5
Q

What autoantibodies are relevant to liver disease ?

A

Antinuclear antibodies
Smooth muscle antibodies
Antimitochondrial antibodies
Antibodies to liver and kidney microsome type-1

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6
Q

What would LFT’s show in decompensated cirrhosis?

A

Raised Bilirubin, ALT, AST, ALP

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7
Q

Apart from LFT’s what other blood tests may be deranged in cirrhosis?

A

Low albumin
Increase prothrombin time
Thrombocytopenia
Hyponatraemia
Urea and creatinine deranged in hepatorenal syndrome

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8
Q

What is the tumour marker for hepatocellular carcinoma ?

A

Alpha-fetoprotein

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9
Q

What is the first line investigation for assessing fibrosis in non-alcoholic fatty liver disease?

A

Enhanced liver fibrosis blood test (ELF)
10.51 or above = advanced fibrosis

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10
Q

What is used to diagnose non-alcoholic fatty liver disease?

A

Ultrasound = Increased echogenicity

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11
Q

What type of scan can be used to determine the degree of fibrosis to test for liver cirrhosis?

A

Transient elastography (FibroScan)

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12
Q

What is the MELD score?

A

Model for End-Stage Liver Disease
formula considers the bilirubin, creatinine, INR and sodium and whether they require dialysis, giving an estimated 3-month mortality as a percentage
score every 6 months

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13
Q

What is the Child-Pugh score and what are the components?

A

Assesses the severity of cirrhosis and prognosis
A - albumin
B - bilirubin
C - clotting (INR)
D - dilation (ascites)
E - encephalopathy

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14
Q

What is the monitoring protocol for liver cirrhosis?

A

MELD score every 6 months
Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
Endoscopy every 3 years for oesophageal varices

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15
Q

What are the 4 key features of decompensated liver disease?

A

A - Ascites
H - Hepatic encephalopathy
O- Oesophageal varices bleeding
Y - Yellow (Jaundice)

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16
Q

What is the overall 5 year survival rate in liver cirrhosis?

A

50%

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17
Q

What are some important complications of cirrhosis?

A

Malnutrition and muscle wasting
Portal hypertension, oesophageal varices and bleeding varices
Ascites and spontaneous bacterial peritonitis
Hepatorenal syndrome
Hepatic encephalopathy
Hepatocellular carcinoma

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18
Q

What is the prophylaxis management of varices?

A

Non-selective beta blockers (e.g., propranolol) first-line
Variceal band ligation (if beta blockers are contraindicated)

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19
Q

What is the initial management of bleeding oesophageal varices?

A

Immediate senior help
Consider blood transfusion (major haemorrhage protocol)
Treat any coagulopathy (fresh frozen plasma)
Vasopressin analogues (terlipressin or somatostatin)
Prophylactic broad-spectrum antibiotics
Urgent endoscopy with variceal band ligation
Consider intubation and intensive care

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20
Q

What are the management options for ascites?

A

Low sodium diet
Aldosterone antagonists
Paracentesis
Prophylactic antibiotics
Transjugular intrahepatic portosystemic shunt (if refractory)
Liver transplantation

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21
Q

What are some presenting features of spontaneous bacterial peritonitis ?

A

Fever
Abdo pain
Deranged bloods (raised WBC, CRP, creatinine, metabolic acidosis)
Ileus (reduced movement in intestines)
Hypotension

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22
Q

What are the 2 most common organisms in spontaneous bacterial peritonitis?

A

E.coli
Klebsiella pneumoniae

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23
Q

How is spontaneous bacterial peritonitis managed?

A

Take sample of ascitic fluid for culture before antibiotics
IV broad spectrum antibiotics

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24
Q

What toxin builds up to cause hepatic encephalopathy?

A

Ammonia

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25
Q

What are some factors that can trigger or worsen hepatic encephalopathy?

A

Constipation
Dehydration
Electrolyte disturbance
Infection
GI bleeding
High protein diet
Medications

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26
Q

How is hepatic encephalopathy managed?

A

Lactulose (aim for 2-3 soft stools a day)
Antibiotics e.g. Rifaximin
Nutritional support

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27
Q

Describe the stepwise progression of alcohol-related liver disease

A
  1. Alcoholic fatty liver (hepatic steatosis)
  2. Alcoholic hepatitis
  3. Cirrhosis
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28
Q

State 5 complications of alcohol consumption

A

Alcohol-related liver disease
Wernicke-Korsakoff syndrome
Pancreatitis
Alcoholic cardiomyopathy
Alcoholic myopathy
Increased risk of CVD and cancer

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29
Q

What blood test results would be suggestive of alcoholic-related liver disease?

A

Raised MCV
Raised ALT and AST
AST: ALT ratio above 1.5
Raised gamma-GT
Raised ALP
Raised bilirubin
Low albumin
Increased prothrombin time
Deranged U&E’s in hepatorenal syndrome

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30
Q

Name 5 other investigations besides bloods that may be done in suspected alcohol-related liver disease

A

Liver USS
FibroScan
Endoscopy (oesophageal varices)
CT/MRI
Liver biopsy

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31
Q

What are the general principles of managing alcohol-related liver disease?

A

Stop drinking
Psychological interventions
Nutritional support (thiamine, high protein diet)
Corticosteroids (may improve inflammation in short term)
Treat complications
Liver transplant (6 months of abstinence required)

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32
Q

What are the CAGE questions?

A

C – CUT DOWN? Do you ever think you should cut down?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Do you ever feel guilty about drinking?
E – EYE OPENER? Do you ever drink in the morning to help your hangover or nerves?

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33
Q

Name 2 screening tools for harmful alcohol consumption

A

CAGE
AUDIT

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34
Q

Describe the timeline of alcohol withdrawal symptoms

A

6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: delirium tremens

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35
Q

What are some presenting features of delirium tremens?

A

Acute confusion
Severe agitation
delusions and hallucinations
tremor
tachycardia
hypertension
hyperthermia
ataxia
arrhythmias

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36
Q

What can be used to score a patient on the alcohol withdrawal symptoms?

A

CIWA-Ar

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37
Q

What medications are given to combat the effects of alcohol withdrawal?

A

Chlordiazepoxide
Pabrinex (to prevent Wernicke-Korsakoff)

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38
Q

State 3 features of Wernicke’s encephalopathy

A

Confusion
Oculomotor disturbances (disturbances of eye movements)
Ataxia (difficulties with coordinated movements)

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39
Q

What causes Wernicke-Korsakoff syndrome ?

A

Thiamine (B1) deficiency

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40
Q

State 2 features of Korsakoff syndrome

A

Memory impairment (retrograde and anterograde)
Behavioural changes

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41
Q

What are the stages of non-alcoholic fatty liver disease ?

A

Non-alcoholic fatty liver disease
Non-alcoholic steatohepatitis (NASH)
Fibrosis
Cirrhosis

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42
Q

State 5 risk factors for non-alcoholic fatty liver disease

A

Middle age onwards
Obesity
Poor diet and low activity levels
Type 2 diabetes
High cholesterol
High blood pressure
Smoking

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43
Q

What is metabolic syndrome a combination of?

A

hypertension, obesity and diabetes

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44
Q

What investigations can be done in suspected non-alcoholic fatty liver disease

A

ALT (raised)
Liver USS - confirms diagnosis
ELF bloods (1st line to assess fibrosis)
NAFLD Fibrosis score, Fibrosis 4
FibroScan
Liver biopsy

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45
Q

What are the management options for non-alcoholic fatty liver disease?

A

weight loss
healthy diet
exercise
stop smoking
avoid/limit alcohol
control diabetes, BP and cholesterol
vitamin E, pioglitazone, bariatric surgery, liver transplantation

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46
Q

What is the type of virus, transmission, vaccine and treatment for hepatitis A ?

A

type: RNA
transmission: Faecal-oral
vaccine: yes
treatment: supportive

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47
Q

What is the type of virus, transmission, vaccine and treatment for hepatitis B?

A

type: DNA
transmission: Blood/bodily fluids
vaccine: yes
treatment: supportive/antivirals

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48
Q

What is the type of virus, transmission, vaccine and treatment for hepatitis C?

A

type: RNA
transmission: blood
vaccine: no
treatment: direct-acting antivirals

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49
Q

What is the type of virus, transmission, vaccine and treatment for hepatitis D?

A

type: RNA
transmission: always with hepatitis B
vaccine: no
treatment: Pegylated interferon alpha

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50
Q

What is the type of virus, transmission, vaccine and treatment for hepatitis E?

A

type: RNA
transmission: faecal-oral
vaccine: no
treatment: supportive

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51
Q

What symptoms of viral hepatitis may a patient present with?

A

Abdominal pain
Fatigue
Flu-like illness
Pruritus (itching)
Muscle and joint aches
Nausea and vomiting
Jaundice

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52
Q

Describe the key viral markers in hepatitis B

A

Surface antigen (HBsAg) – active infection
E antigen (HBeAg) – a marker of viral replication and implies high infectivity
Core antibodies (HBcAb) – implies past or current infection
Surface antibody (HBsAb) – implies vaccination or past or current infection
Hepatitis B virus DNA (HBV DNA) – a direct count of the viral load

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53
Q

What are the differences between the 2 types of autoimmune hepatitis?

A

Type 1 typically affects women in their late forties or fifties. It presents around or after menopause with fatigue and features of liver disease on examination. It takes a less acute course than type 2.

Type 2 usually affects children or young people, more commonly girls. It presents with acute hepatitis with high transaminases and jaundice.

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54
Q

What would blood tests show in autoimmune hepatitis?

A

Investigations will show high transaminases (ALT and AST) and minimal change in ALP levels (a “hepatitic” picture). Raised immunoglobulin G (IgG) levels are an important finding.

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55
Q

What are the autoantibodies in type 1 autoimmune hepatitis?

A

Anti-nuclear antibodies (ANA)
Anti-smooth muscle antibodies (anti-actin)
Anti-soluble liver antigen (anti-SLA/LP)

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56
Q

What are the autoantibodies in type 2 autoimmune hepatitis?

A

Anti-liver kidney microsomes-1 (anti-LKM1)
Anti-liver cytosol antigen type 1 (anti-LC1)

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57
Q

How is autoimmune hepatitis managed?

A

High-dose steroids
immunosuppression e.g. azathioprine
Liver transplant in end-stage

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58
Q

What is the inheritance pattern of Haemochromatosis?

A

autosomal recessive

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59
Q

What is haemochromatosis?

A

excessive total body iron and deposition of iron in tissues

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60
Q

What gene is associated with hemochromatosis and where is it located?

A

human haemochromatosis protein (HFE) gene is located on chromosome 6

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61
Q

What mutation relates to haemochromatosis?

A

C282Y mutations

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62
Q

How may Haemochromatosis present?

A

Chronic tiredness
Joint pain
Pigmentation (bronze skin)
Testicular atrophy
Erectile dysfunction
Amenorrhoea (absence of periods in women)
Cognitive symptoms (memory and mood disturbance)
Hepatomegaly

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63
Q

What are some causes of a raised ferritin?

A

Haemochromatosis
Infections (it is an acute phase reactant)
Chronic alcohol consumption
Non-alcoholic fatty liver disease
Hepatitis C
Cancer

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64
Q

What investigations can be done for haemochromatosis?

A

Ferritin
Transferrin saturation
Genetic testing
Liver biopsy with Perl’s stain
MRI

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65
Q

What are some complications of haemochromatosis?

A

Secondary diabetes
Liver cirrhosis
Endocrine and sexual problems (hypogonadism, erectile dysfunction, amenorrhea and reduced fertility)
Cardiomyopathy
Hepatocellular carcinoma
Hypothyroidism
Chondrocalcinosis

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66
Q

How is haemochromatosis managed?

A

Venesection
monitoring serum ferritin
Monitoring and treating complications

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67
Q

What is the inheritance pattern of Wilson’s disease ?

A

autosomal recessive

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68
Q

Excessive accumulation of what causes Wilsons disease ?

A

Copper

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69
Q

What mutation causes Wilsons disease?

A

Wilson disease protein gene on chromosome 13 (also called the ATP7B copper-binding protein)

70
Q

What are some features of Wilsons disease ?

A

Liver - chronic hepatitis then cirrhosis
Neurological - tremor, dysarthria, dystonia, parkinsonism
Psychiatric - abnormal behaviour, depression, cognitive impairment, psychosis
Kayser-Fleischer rings in the cornea
Haemolytic anaemia
renal tubular damage

71
Q

When does Wilson’s disease usually present?

A

teenagers or young adults

72
Q

How is Wilsons disease investigated?

A

Serum caeruloplasmin (low is suggestive of Wilsons)
24-hour urine copper assay (shows high urinary copper)
Liver biopsy

73
Q

How is Wilson’s disease managed?

A

copper chelation using either: Penicillamine or Trientine
others: zinc salts. liver transplant

74
Q

What are the two main organs affected by alpha-1 antitrypsin deficiency?

A

Chronic obstructive pulmonary disease and bronchiectasis in the lungs (typically after 30 years old)
Dysfunction, fibrosis and cirrhosis of the liver (depending on the specific genotype)

75
Q

What is the inheritance pattern of alpha-1 antitrypsin deficiency?

A

Autosomal co-dominant

76
Q

What gene codes for alpha-1 antitrypsin and where is it found?

A

SERPINA1 gene
chromosome 14

77
Q

How is alpha-1 antitrypsin deficiency diagnosed

A

Low serum alpha-1 antitrypsin (the screening test)
Genetic testing

78
Q

What will liver biopsy show in alpha-1 antitrypsin deficiency ?

A

periodic acid-Schiff positive staining globules in hepatocytes, resistant to diastase treatment.

79
Q

What are the management options for alpha-1 antitrypsin deficiency?

A

Stop smoking
Symptomatic management (e.g., standard treatment of COPD)
Organ transplant for end-stage liver or lung disease
Monitoring for complications (e.g., hepatocellular carcinoma)
Screening of family members

80
Q

What is primary biliary cholangitis?

A

autoimmune condition where the immune system attacks the small bile ducts in the liver, resulting in obstructive jaundice and liver disease

81
Q

How may a patient with primary biliary cholangitis present?

A

Fatigue
Pruritus (itching)
Gastrointestinal symptoms and abdominal pain
Jaundice
Pale, greasy stools
Dark urine

82
Q

What may be seen on examination in a patient with primary biliary cholangitis?

A

Xanthoma and xanthelasma (cholesterol deposits)
Excoriations
Hepatomegaly
Signs of liver cirrhosis and portal hypertension in end-stage disease (e.g., splenomegaly and ascites)

83
Q

What investigations can be done for primary biliary cholangitis and what will they show?

A

LFT’s = raised alkaline phosphatase
autoantibodies = anti-mitochondrial antibodies, anti-nuclear antibodies
raised immunoglobulins
liver biopsy = staging

84
Q

What is the treatment of primary biliary cholangitis?

A

Ursodeoxycholic acid

85
Q

What are some complications of primary biliary cholangitis?

A

Liver cirrhosis - carcinoma, portal hypertension
Fat-soluble vitamin deficiency (A, D, E and K)
Osteoporosis
Hyperlipidaemia (raised cholesterol)
Sjögren’s syndrome (dry eyes, dry mouth and vaginal dryness)
Connective tissue diseases (e.g., systemic sclerosis)
Thyroid disease

86
Q

What is primary sclerosing cholangitis?

A

intrahepatic and extrahepatic bile ducts become inflamed and damaged, developing strictures that obstruct the flow of bile out of the liver and into the intestines

87
Q

What other condition is associated with primary sclerosing cholangitis?

A

Ulcerative colitis

88
Q

State 4 risk factors for primary sclerosing cholangitis

A

Male
Aged 30-40
Ulcerative colitis
Family history

89
Q

How may primary sclerosing cholangitis present?

A

Abdominal pain in the right upper quadrant
Pruritus (itching)
Fatigue
Jaundice
Hepatomegaly
Splenomegaly

90
Q

What LFT will be raised in primary sclerosing cholangitis?

A

alkaline phosphatase

91
Q

What investigation is used to diagnose primary sclerosing cholangitis?

A

Magnetic resonance cholangiopancreatography (MRCP)

92
Q

How is primary sclerosing cholangitis managed?

A

Endoscopic retrograde cholangio-pancreatography (ERCP)
liver transplant

93
Q

What are some complications of primary sclerosing cholangitis?

A

Biliary strictures
Acute bacterial cholangitis
Cholangiocarcinoma develops in 10-20% of cases
Cirrhosis and the related complications (e.g., portal hypertension and oesophageal varices)
Fat-soluble vitamin deficiency (A, D, E and K)
Osteoporosis
Colorectal cancer in patients with ulcerative colitis

94
Q

What is the main type of primary liver cancer?

A

Hepatocellular carcinoma

95
Q

State 4 risk factors for hepatocellular carcinoma

A

Alcohol-related liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Hepatitis C
Rarer causes (e.g., primary sclerosing cholangitis)

96
Q

Patients with liver cirrhosis are offered screening for hepatocellular carcinoma every 6 months with what investigations?

A

Ultrasound
Alpha-fetoprotein

97
Q

What non-specific features are associated with liver cancer?

A

Weight loss
Abdominal pain
Anorexia
Nausea and vomiting
Jaundice
Pruritus
Upper abdominal mass on palpation

98
Q

State 4 investigations that may be carried out to assess liver cancer?

A

Alpha-fetoprotein
Liver ultrasound is the first-line imaging investigation
CT and MRI scans are used for further assessment and staging of the cancer
Biopsy is used for histology

99
Q

What are the management options for hepatocellular carcinoma?

A

Surgery (resection/transplant)
radiofrequency ablation
microwave ablation
transarterial chemoembolisation
Radiotherapy
targeted drugs

100
Q

Where to Cholangiocarcinoma’s originate?

A

Bile ducts

101
Q

What condition is Cholangiocarcinoma associated with?

A

Primary sclerosing cholangitis

102
Q

What is the key presenting feature of cholangiocarcinoma?

A

Obstructive jaundice:

Pale stools
Dark urine
Generalised itching

103
Q

What is the tumour marker for cholangiocarcinoma?

A

CA19-9

104
Q

State 3 contraindications in referring for a liver transplant

A

Significant co-morbidities (e.g., severe kidney, lung or heart disease)
Current illicit drug use
Continuing alcohol misuse (generally 6 months of abstinence is required)
Untreated HIV
Current or previous cancer (except certain liver cancers)

105
Q

What are the names of the 2 incisions in a liver transplant?

A

Rooftop
Mercedes Benz

106
Q

What is gastro-oesophageal reflux disease?

A

acid from the stomach flows through the lower oesophageal sphincter and into the oesophagus, where it irritates the lining and causes symptoms.

107
Q

What cells line the oesophagus?

A

squamous epithelial

108
Q

What cells line the stomach?

A

Columnar epithelial

109
Q

What factors can exacerbate the symptoms of GORD?

A

Greasy and spicy foods
Coffee and tea
Alcohol
Non-steroidal anti-inflammatory drugs
Stress
Smoking
Obesity
Hiatus hernia

110
Q

State some symptoms of GORD

A

Heartburn
Acid regurgitation
Retrosternal or epigastric pain
Bloating
Nocturnal cough
Hoarse voice

111
Q

What are some red flags in a patient with GORD that require a 2WW?

A

Dysphagia (difficulty swallowing)
Aged over 55 (this is generally the cut-off for urgent versus routine referrals)
Weight loss
Upper abdominal pain
Reflux
Treatment-resistant dyspepsia
Nausea and vomiting
Upper abdominal mass on palpation
Low haemoglobin (anaemia)
Raised platelet count

112
Q

What is a hiatus hernia?

A

herniation of the stomach up through the diaphragm

113
Q

What are the 4 types of hiatus hernia?

A

Type 1: Sliding
Type 2: Rolling
Type 3: Combination of sliding and rolling
Type 4: Large opening with additional abdominal organs entering the thorax

114
Q

What is a sliding hiatus hernia?

A

stomach slides up through the diaphragm, with the gastro-oesophageal junction passing up into the thorax

115
Q

What is a rolling hiatus hernia?

A

a separate portion of the stomach (i.e., the fundus), folds around and enters through the diaphragm opening, alongside the oesophagus

116
Q

What investigations may show a hiatus hernia?

A

Chest x-ray
CT scan
Endoscopy
Barium swallow test

117
Q

What are the management options for GORD?

A

Lifestyle changes
Reviewing medications (e.g., stop NSAIDs)
Antacids (e.g., Gaviscon, Pepto-Bismol and Rennie) – short term only
Proton pump inhibitors (e.g., omeprazole and lansoprazole)
Histamine H2-receptor antagonists (e.g., famotidine)
Surgery

118
Q

What lifestyle changes may be helpful in GORD?

A

Reduce tea, coffee and alcohol
Weight loss
Avoid smoking
Smaller, lighter meals
Avoid heavy meals before bedtime
Stay upright after meals rather than lying flat

119
Q

What is the name of the surgery for reflux?

A

laparoscopic fundoplication

120
Q

When do you need to stop using a PPI before H.pylori testing?

A

2 weeks

121
Q

What are the investigations for H.Pylori ?

A

Stool antigen test
Urea breath test using radiolabelled carbon 13
H. pylori antibody test (blood)
Rapid urease test performed during endoscopy (also known as the CLO test)

122
Q

What is Barrett’s oesophagus?

A

lower oesophageal epithelium changes from squamous to columnar epithelium. This process is called metaplasia.

123
Q

What does Barrett’s oesophagus put you at risk of developing?

A

oesophageal adenocarcinoma

124
Q

What is the treatment of Barrett’s oesophagus?

A

Endoscopic monitoring for progression to adenocarcinoma
Proton pump inhibitors
Endoscopic ablation (e.g., radiofrequency ablation)

125
Q

What is Zollinger-Ellison syndrome?

A

duodenal or pancreatic tumour secretes excessive quantities of gastrin causing excess production of stomach acid resulting in severe dyspepsia, diarrhoea and peptic ulcers

126
Q

what type of peptic ulcer is most common?

A

duodenal ulcer

127
Q

What are some risk factors of peptic ulcers?

A

H.Pylori
NSAIDS
stress
alcohol
smoking
caffeine
spicy foods

128
Q

What drugs increase the risk of bleeding from a peptic ulcer?

A

Non-steroidal anti-inflammatory drugs (NSAIDs)
Aspirin
Anticoagulants (e.g., DOACs)
Steroids
SSRI antidepressants

129
Q

What are some signs of a peptic ulcer?

A

Epigastric discomfort or pain
Nausea and vomiting
Dyspepsia

130
Q

What are some signs of upper gastrointestinal bleeding?

A

Haematemesis (vomiting blood)
Coffee ground vomiting
Melaena (black, tarry stools)
Fall in haemoglobin on a full blood count

131
Q

What are the characteristics of the pain with duodenal ulcers

A

improve immediately after eating, followed by pain 2-3 hours later

132
Q

How are peptic ulcers diagnosed ?

A

Endoscopy
(CLO test for H.pylori may be performed during)

133
Q

What are the key management options for peptic ulcers

A

Stopping NSAIDs
Treating H. pylori infections
Proton pump inhibitors (e.g., lansoprazole or omeprazole)

134
Q

State 3 complications of peptic ulcers

A

bleeding
Perforation -> peritonitis
scarring + strictures

135
Q

state 4 key sources of an upper GI bleed

A

Peptic ulcers (the most common cause)
Mallory-Weiss tear
Oesophageal varices
Stomach cancers

136
Q

What are the presenting features of an upper GI bleed?

A

Haematemesis
Coffee ground vomit
Melaena

137
Q

What score estimates the risk of a patient having an upper GI bleed?

A

Glasgow-Blatchford score

138
Q

What is the Rockall score used for?

A

after endoscopy to estimate the risk of rebleeding and mortality

139
Q

What is the initial management of an upper GI bleed?

A

get senior support early
A – ABCDE approach to immediate resuscitation
B – Bloods
A – Access (ideally 2 x large bore cannula)
T – Transfusions are required
E – Endoscopy (within 24 hours)
D – Drugs (stop anticoagulants and NSAIDs)

140
Q

In a patient with an upper GI bleed what should you send bloods for?

A

Haemoglobin (FBC)
Urea (U&Es)
Coagulation (INR and FBC for platelets)
Liver disease (LFTs)
Crossmatch 2 units of blood

141
Q

What are some general presenting features of IBD?

A

Diarrhoea
Abdominal pain
Rectal bleeding
Fatigue
Weight loss

142
Q

What features can help to differentiate Crohn’s ?

A

N – No blood or mucus (PR bleeding is less common)
E – Entire gastrointestinal tract affected (from mouth to anus)
S – “Skip lesions” on endoscopy
T – Terminal ileum most affected and Transmural (full thickness) inflammation
S – Smoking is a risk factor (don’t set the nest on fire)

143
Q

What features can help differentiate ulcerative colitis?

A

C – Continuous inflammation
L – Limited to the colon and rectum
O – Only superficial mucosa affected
S – Smoking may be protective
E – Excrete blood and mucus
U – Use aminosalicylates
P – Primary sclerosing cholangitis

144
Q

Sate 4 conditions associated with IBD

A

Erythema nodosum
Pyoderma gangrenosum
Enteropathic arthritis
Primary sclerosing cholangitis (particularly with UC)
Red eye conditions (e.g., episcleritis, scleritis and anterior uveitis)

145
Q

What blood tests may be done in suspected IBD?

A

FBC (for low haem and raised platelets)
CRP
U&E
LFT’s (low albumin if severe)
TFT (hyperthyroidism may cause diarrhoea)
anti-TTG (for coeliac)

146
Q

What stool investigations may be done in suspected IBD?

A

Faecal calprotectin
Stool microscopy + culture (rule out infection)

147
Q

What is the diagnostic test for IBD?

A

Colonoscopy with multiple intestinal biopsies

148
Q

How is mild to moderate acute UC treated?

A

1st: Aminosalicylate (e.g. oral or rectal mesalazine)
2nd: Corticosteroids (oral/rectal prednisolone)

149
Q

How is severe acute UC treated?

A

1st: IV steroids (hydrocortisone)
others: IV ciclosporin, infliximab, surgery

150
Q

What are some options for maintaining remission in UC?

A

1st: Aminosalicylate
2nd: Azothioprine or mercaptopurine

151
Q

What surgery can be used for UC?

A

panproctocolectomy

152
Q

How can you induce remission in an exacerbation of Crohn’s disease?

A

1st: Steroids (oral pred or IV hydrocortisone)
Others: Enteral nutrition, + azothioprine, mercatopurine, methotrexate, infliximab, adalimumab

153
Q

What is first line for maintaining remission in Crohn’s disease?

A

Azathioprine or
Mercaptopurine

2nd: methotrexate

154
Q

What are 3 key features of IBS?

A

I – Intestinal discomfort (abdominal pain relating to the bowels)
B – Bowel habit abnormalities
S – Stool abnormalities (watery, loose, hard or associated with mucus)

155
Q

What factors may triggers symptoms in IBS?

A

Anxiety
Depression
Stress
Sleep disturbance
Illness
Medications
Certain foods
Caffeine
Alcohol

156
Q

State 4 differential disgnoses for IBS

A

Bowel cancer
Inflammatory bowel disease
Coeliac disease
Ovarian cancer
Pancreatic cancer

157
Q

What investigations may be done in suspected IBS?

A

done to exlude red flags
FBC
ESR/CRP
anti-TTG
Faecal calprotectin
CA125

158
Q

What is the NICE criteria for diagnosing IBS?

A

differentials need to be excluded, and the patient should have at least 6 months of abdominal pain or discomfort with at least one of:

Pain or discomfort relieved by opening the bowels
Bowel habit abnormalities (more or less frequent)
Stool abnormalities (e.g., watery, loose or hard)
For a diagnosis, patients also require at least two of:

Straining, an urgent need to open bowels or incomplete emptying
Bloating
Worse after eating
Passing mucus

159
Q

How is IBS managed?

A

lifestyle advice: drink fluids, regular small meals, adjusting fibre, limit caffeine, low FODMAP diet, probiotic, exercise, reduce stress
1st line medications: Loperamide for diarrhoea, bulk forming laxatives for constipation, antispasmodics for cramps e.g. mebeverine

160
Q

What laxative should be avoided in IBS due to bloating?

A

lactulose

161
Q

what diseases are associated with Coeliacs?

A

T1DM
autoimmune thyroid disease

162
Q

What are the 3 antibodies associated with coeliacs?

A

Anti-tissue transglutaminase antibodies (anti-TTG)
Anti-endomysial antibodies (anti-EMA)
Anti-deamidated gliadin peptide antibodies (anti-DGP)

163
Q

How does coeliacs affect the bowel?

A

Inflammation particulalry in jejunum causes atrophy of intestinal villi and crypt hypertophy resulting in malabsorption

164
Q

What 2 HLA genotypes are associated with coeliacs?

A

HLA-DQ2
HLA-DQ8

165
Q

What are some presenting features of coeliacs disease?

A

Failure to thrive in young children
Diarrhoea
Bloating
Fatigue
Weight loss
Mouth ulcers
Dermatitis herpetiformis
anaemia
rarely neurological symptoms

166
Q

What are the 1st line blood tests for coeliacs?

A

Total immunoglobulin A levels (to exclude IgA deficiency)
Anti-tissue transglutaminase antibodies (anti-TTG)

167
Q

What are the biospy findings in coeliacs?

A

Crypt hyperplasia
Villous atrophy

168
Q

What is the management of coeliacs?

A

Lifelong gluten-free diet

169
Q

What are some complications of coeliac disease?

A

Nutritional deficiencies
Anaemia
Osteoporosis
Hyposplenism
Ulcerative jejunitis
Enteropathy-associated T-cell lymphoma (EATL)
Non-Hodgkin lymphoma
Small bowel adenocarcinoma

170
Q

What type of cancer are people with coeliac disease more likely to get?

A

enteropathy-associated T-cell lymphoma of small intestine

171
Q

What is the most common type of inherited colorectal cancer?

A

Hereditary non-polyposis colorectal carcinoma (HNPCC), also known as Lynch syndrome.

Finals (21 decks)

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