Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Finals > Gastroenterology > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What would LFT’s show in decompensated cirrhosis?

A

Raised Bilirubin, ALT, AST, ALP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the tumour marker for hepatocellular carcinoma ?

A

Alpha-fetoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Ultrasound = Increased echogenicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

Transient elastography (FibroScan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

E.coli
Klebsiella pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is spontaneous bacterial peritonitis managed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What toxin builds up to cause hepatic encephalopathy?

A

Ammonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is hepatic encephalopathy managed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the stepwise progression of alcohol-related liver disease

A
  1. Alcoholic fatty liver (hepatic steatosis)
  2. Alcoholic hepatitis
  3. Cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Name 2 screening tools for harmful alcohol consumption

A

CAGE
AUDIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are some presenting features of delirium tremens?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

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

A

CIWA-Ar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

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

A

Chlordiazepoxide
Pabrinex (to prevent Wernicke-Korsakoff)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

State 3 features of Wernicke’s encephalopathy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What causes Wernicke-Korsakoff syndrome ?

A

Thiamine (B1) deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

State 2 features of Korsakoff syndrome

A

Memory impairment (retrograde and anterograde)
Behavioural changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is metabolic syndrome a combination of?

A

hypertension, obesity and diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How is autoimmune hepatitis managed?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the inheritance pattern of Haemochromatosis?

A

autosomal recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is haemochromatosis?

A

excessive total body iron and deposition of iron in tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What mutation relates to haemochromatosis?

A

C282Y mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What investigations can be done for haemochromatosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How is haemochromatosis managed?

A

Venesection
monitoring serum ferritin
Monitoring and treating complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the inheritance pattern of Wilson’s disease ?

A

autosomal recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Excessive accumulation of what causes Wilsons disease ?

A

Copper

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

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?

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?

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions