GI and Liver Flashcards

1
Q

How long does hepatitis persist for to be deemed chronic?

A

6 months.

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

Give 3 infective causes of acute hepatitis.

A
  1. Hepatitis A to E infection.
  2. EBV.
  3. CMV.
  4. Toxoplasmosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give 3 non-infective causes of acute and chronic hepatitis.

A
  1. Alcohol.
  2. Drugs.
  3. Toxins.
  4. Autoimmune.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Give 3 symptoms of acute hepatitis.

A
  1. General malaise.
  2. Myalgia.
  3. GI upset.
  4. Abdominal pain.
  5. Raised AST, ALT.
  6. +/- jaundice.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Give 3 infective causes of chronic hepatitis.

A
  1. Hepatitis B (+/-D).
  2. Hepatits C.
  3. Hepatitis E.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the potential complications of chronic hepatitis?

A

Uncontrolled inflammation -> fibrosis -> cirrhosis -> HCC.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Is HAV a RNA or DNA virus?

A

HAV is a RNA virus.

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

How is HAV transmitted?

A

Faeco-oral transmission. E.g. contaminated food/water; shellfish.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Who could be at risk of HAV infection?

A

Travellers and food handlers.

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

Is HAV acute or chronic?

A

Acute! There is 100% immunity after infection.

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

How might you diagnose someone with HAV infection?

A

Viral serology: initially anti-HAV IgM and then anti-HAV IgG.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the management of HAV infection.

A
  1. Supportive.
  2. Monitor liver function to ensure no fulminant hepatic failure.
  3. Manage close contacts.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the primary prevention of HAV.

A

Vaccination.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Is HEV a RNA or DNA virus?

A

HEV is a small RNA virus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is HEV transmitted?

A

Faeco-oral transmission.

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

Is HEV acute or chronic?

A

Usually acute but there is a risk of chronic disease in the immunocompromised.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How might you diagnose someone with HEV infection?

A

Viral serology: Initially anti-HEV IgM and then anti-HEV IgG.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the primary prevention of HEV.

A
  1. Good food hygiene.

2. A vaccine is in development.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Is HBV a RNA or DNA virus?

A

HBV is a DNA virus! It replicates in hepatocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is HBV transmitted?

A

Blood-borne transmission e.g. IVDU, needle-stick, sexual, MTCT.

HBV is highly infectious!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the natural history of HBV in 4 phases.

A
  1. Immune tolerance phase: unimpeded viral replication -> high HBV DNA levels.
  2. Immune clearance phase: the immune system ‘wakes up’. There is liver inflammation and high ALT.
  3. Inactive HBV carrier phase: HBV DNA levels are low. ALT levels are normal. There is no liver inflammation.
  4. Reactivation phase: ALT and HBV DNA levels are intermittent and inflammation is seen on the liver -> fibrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What HBV protein triggers the initial immune response?

A

The core proteins.

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

How might you diagnose someone with HBV?

A

Viral serology: HBV surface antigen can be detected from 6w - 3m or anti-HBV core IgM after 3 months.

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

Describe the management of HBV infection.

A
  1. Supportive.
  2. Monitor liver function.
  3. Manage contacts.
  4. Follow up at 6 months to see if HBV surface Ag has cleared. If present -> chronic hepatitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How would you know if someone had acute or chronic HBV infection?

A

You would do a follow up appointment at 6 months to see if HBV surface Ag had cleared. If it was still present then the person would have chronic hepatitis.

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

What are the potential consequences of chronic HBV infection?

A
  1. Cirrhosis.
  2. HCC.
  3. Decompensated cirrhosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How can HBV infection be prevented?

A

Vaccination - injecting a small amount of inactivated HbsAg.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe two treatment options for HBV infection.

A
  1. Alpha interferon - boosts immune system.

2. Antivirals e.g. tenofovir. They inhibit viral replications.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

HBV treatment: give 3 side effects of alpha interferon treatment.

A
  1. Myalgia.
  2. Malaise.
  3. Lethargy.
  4. Thyroiditis.
  5. Mental health problems.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Is HDV a RNA or DNA virus?

A

It is a defective RNA virus. It required HBsAG to protect it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Infection with what virus is needed for HDV to survive?

A

HDV can’t exist without HBV infection! It needs HBsAg to protect it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is HDV transmitted?

A

Blood-borne transmission, particularly IVDU.

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

Is HCV a RNA or DNA virus?

A

HCV is a RNA virus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is HCV transmitted?

A

Blood borne.

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

Give 4 risk factors for developing HBV/HCV infection.

A
  1. IVDU.
  2. People who have required blood products e.g. blood transfusion.
  3. Needle-stick injuries.
  4. Unprotected sexual intercourse.
  5. Materno-foetal transmission.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How might you diagnose someone with current HCV infection?

A

Viral serology - HCV RNA tells you if the infection is still present.

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

You want to find out if someone has previously been infected with HCV. How could you do this?

A

Viral serology - anti-HCV IgM/IgG indicates that someone has either a current infection or a previous infection.

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

Describe the treatment for HCV.

A

Lots of new drugs have been developed recently for HCV infection. Direct acting antivirals (DAA) are currently in use e.g. NS5A and NS5B.

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

What percentage of people with acute HCV infection will progress onto chronic infection?

A

Approximately 70%.

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

What percentage of people with acute HBV infection will progress onto chronic infection?

A

Approximately 5%.

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

How can HCV infection be prevented.

A
  1. Screen blood products.
  2. Lifestyle modification.
  3. Needle exchange.

There is currently no vaccination and previous infection does not confer immunity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What types of viral hepatitis are capable of causing chronic infection?

A

Hepatitis B (+/-D); C and E in the immunosuppressed.

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

What is acute pancreatitis?

A

An inflammatory process with release of inflammatory cytokines (TNF alpha, IL-6) and pancreatic enzymes (trypsin, lipase).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the 3 different types of acute pancreatitis?

A
  1. 70% are oedematous; acute fluid collection.
  2. 25% are necrotising.
  3. 5% are hemorrhagic.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Give 5 causes of acute pancreatitis.

A
  1. Gallstones.
  2. Alcohol.
  3. Hyperlipidaemia.
  4. Direct damage e.g. trauma.
  5. Idiopathic.
  6. Toxic e.g. drugs, infection, venom.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Give 4 symptoms of acute pancreatitis.

A
  1. Severe epigastric pain that radiates to the back.
  2. Anorexia.
  3. Nausea, vomiting.
  4. Signs of septic shock e.g. fever, dehydration, hypotension, tachycardia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How can acute pancreatitis be diagnosed?

A

Pancreatitis is diagnosed on the basis of 2 out of 3 of the following:

  1. Characteristic severe epigastric pain radiating to the back.
  2. Raised serum amylase.
  3. Abdominal CT scan pathology.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Name a scoring system that can be used a prognostic tool in acute pancreatitis.

A

The abbreviated glasgow scoring system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What 8 points make up the glasgow scoring system?

A
PaO2 < 8kPa.
Age > 55 years.
Neutrophils > 15x10^9.
Calcium < 2mmol/L.
Raised urea > 15mmol/L.
Elevated enzymes.
Albumin < 32g/L.
Sugar - serum glucose > 15mmol/L.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Describe the treatment for acute pancreatitis.

A
  1. ANALGESIA!
  2. Catheterise and ABC approach for shock patients.
  3. Drainage of oedematous fluid collections.
  4. Antibiotics.
  5. Nutrition.
  6. Bowel rest.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Give 2 potential complications of acute pancreatitis.

A
  1. Systemic inflammatory response syndrome.

2. Multiple organ dysfunction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is chronic pancreatitis?

A

Chronic inflammation of the pancreas leads to irreversible damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe the pathogenesis of chronic pancreatitis.

A

The pathogenesis is not fully understood but the current theory is that pancreatic duct obstruction leads to activation of pancreatic enzymes -> necrosis -> fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe how alcohol can cause chronic pancreatitis.

A

Alcohol -> proteins precipitate in the ductal structure of the pancreas (obstruction) -> pancreatic fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?

A

IgG4.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How is autoimmune chronic pancreatitis treated?

A

It is very steroid responsive.

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

Give 5 symptoms of chronic pancreatitis.

A
  1. Severe abdominal pain.
  2. Epigastric pain radiating to the back.
  3. Nausea, vomiting.
  4. Decreased appetite.
  5. Exocrine/endocrine dysfunction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

A sign of chronic pancreatitis is exocrine dysfunction. What can be a consequence of this?

A
  1. Malabsorption.
  2. Weight loss.
  3. Diarrhoea.
  4. Steatorrhoea.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

A sign of chronic pancreatitis is endocrine dysfunction. What can be a consequence of this?

A

Diabetes mellitus.

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

What is the treatment for chronic pancreatitis?

A

Opiates in a controlled environment for severe pain.

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

Give 4 functions of the liver.

A
  1. Glucose and fat metabolism.
  2. Detoxification and excretion.
  3. Protein synthesis e.g. albumin, clotting factors.
  4. Defence against infection.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Name 3 things that liver function tests measure.

A
  1. Serum bilirubin.
  2. Serum albumin.
  3. Pro-thrombin time.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Name an enzyme that increases in the serum in cholestatic liver disease (duct and obstructive disease).

A

Alkaline phosphatase.

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

What enzymes increase in the serum in hepatocellular liver disease?

A

Transaminases e.g. AST and ALT.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Name two hepatocellular enzymes.

A

Transaminases e.g. AST and ALT.

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

Name a cholestatic enzyme.

A

Alkaline phosphatase.

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

Give 4 causes of hepatitis.

A
  1. Viral e.g. A, B, C, D, E.
  2. Drug induced.
  3. Alcohol induced.
  4. Autoimmune.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Give 2 possible outcomes of acute liver disease.

A
  1. Recovery.

2. Liver failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Give 5 causes of acute liver disease.

A
  1. Viral hepatitis.
  2. Drug induced hepatitis.
  3. Alcohol induced hepatitis.
  4. Vascular.
  5. Obstruction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Give 3 symptoms of acute liver disease.

A
  1. Malaise.
  2. Lethargy.
  3. Anorexia.
  4. Jaundice may develop later on.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Give 2 possible outcomes of chronic liver disease.

A
  1. Cirrhosis.

2. Liver failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Give 5 causes of chronic liver disease.

A
  1. Alcohol.
  2. NAFLD.
  3. Viral hepatitis (B, C, E).
  4. Autoimmune diseases.
  5. Metabolic e.g. haemochromatosis.
  6. Vascular e.g. Budd-Chiari.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is Budd-Chiari syndrome?

A

A vascular disease associated with occlusion of hepatic veins that drain the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Give 5 signs of chronic liver disease.

A
  1. Ascites.
  2. Oedema.
  3. Malaise.
  4. Anorexia.
  5. Bruising.
  6. Itching.
  7. Clubbing.
  8. Palmar erythema.
  9. Spider naevi.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Drug induced liver injury is common. What question should you remember to ask in a patient history?

A

Have you started taking any new medication recently?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Name a drug that can cause drug induced liver injury.

A
  1. Co-amoxiclav.
  2. Flucloxacillin.
  3. Erythromyocin.
  4. TB drugs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Name 3 drugs that are not known to cause drug induced liver injury.

A
  1. Low dose aspirin.
  2. NSAIDS.
  3. Beta blockers.
  4. HRT.
  5. CCB.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What enzyme is responsible for ‘mopping up’ reactive intermediates of paracetamol and so prevents toxicity and liver failure?

A

Glutathione transferase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the potential consequences of hepatocyte regeneration in someone with liver cirrhosis?

A

Neoplasia and therefore HCC. Hepatocyte regeneration is liable to errors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Give 3 causes of iron overload.

A
  1. Genetic disorders e.g. haemochromatosis.
  2. Multiple blood transfusions.
  3. Haemolysis.
  4. Alcoholic liver disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

90% of people with haemochromatosis have a mutation in which gene?

A

HFE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Haemochromatosis is a genetic disorder. How is it inherited?

A

Autosomal recessive inheritance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Describe the pathophysiology of haemochromatosis.

A

Uncontrolled intestinal iron absorption leads to deposition in the liver, heart and pancreas -> fibrosis -> organ failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What protein is responsible for controlling iron absorption?

A

Hepcidin.

Levels of this protein are decreased in haemochromatosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How might you diagnose someone with haemochromatosis?

A
  1. Raised ferritin.
  2. HFE genotyping.
  3. Liver biopsy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Name 3 metabolic disorders that can cause liver disease.

A
  1. Haemochromatosis - iron overload.
  2. Alpha 1 anti-trypsin deficiency.
  3. Wilson’s disease - disorder of copper metabolism.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Describe the mechanism by which alpha 1 anti-trypsin deficiency can lead to chronic liver disease.

A

Alpha 1 anti-trypsin deficiency results in protein retention in the liver -> eventually cirrhosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is Wilson’s disease?

A

An autosomal recessive disorder of copper metabolism; there is excessive deposition of copper in the liver. This can lead to fulminant hepatic failure and cirrhosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What can cause raised unconjugated bilirubin?

A

A pre-hepatic problem e.g. haemolysis due to sickle cell disease, spherocytosis, hypersplenism etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Describe the urine and stools in someone with pre-hepatic jaundice?

A

Urine and stools are normal. There is no itching and the LFT’s are normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What can cause raised conjugated bilirubin?

A

Raised conjugated bilirubin indicates a cholestatic problem e.g. liver disease (hepatic) or bile-duct obstruction (post-hepatic).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Describe the urine and stools in someone with cholestatic jaundice?

A

Dark urine and pale stools. There may be itching and LFT’s are abnormal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Give 3 causes of duct obstruction.

A
  1. Gallstones.
  2. Stricture (narrowing) e.g. malignant, inflammatory.
  3. Carcinoma.
  4. Blocked stent.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Give 4 causes of hepatic jaundice.

A
  1. Viral hepatitis.
  2. Alcoholic hepatitis.
  3. Drugs.
  4. Cirrhosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Give 3 symptoms of jaundice.

A
  1. Biliary pain.
  2. Rigors - indicate an obstructive cause.
  3. Abdomen swelling.
  4. Weight loss.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is ascites?

A

An accumulation of fluid in the peritoneal cavity that leads to abdominal distension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Give 4 pathophysiological causes of ascites and an example for each.

A
  1. Local inflammation e.g. peritonitis.
  2. Leaky vessels e.g. imbalance between hydrostatic and oncotic pressures.
  3. Low flow e.g. cirrhosis, thrombosis, cardiac failure.
  4. Low protein e.g. hypoalbuminaemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Describe the pathogenesis of ascites.

A
  1. Increased intra-hepatic resistance leads to portal hypertension -> ascites.
  2. Systemic vasodilation leads to secretion of RAAS, NAd and ADH -> fluid retention.
  3. Low serum albumin also leads to ascites.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What are the 3 phases of alcoholic liver disease.

A
  1. Fatty change: hepatocytes contain triglycerides.
  2. Alcohol hepatitis.
  3. Alcoholic cirrhosis: destruction of liver architecture and fibrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What might be seen histologically that indicates a diagnosis of alcoholic liver disease?

A

Neutrophils and fat accumulation within hepatocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is non alcoholic steato-hepatitis (NASH)?

A

An advanced form of non-alcoholic fatty liver disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Give 3 causes of non-alcoholic fatty liver disease.

A
  1. Type 2 diabetes mellitus.
  2. Hypertension.
  3. Obesity.
  4. Hyperlipidaemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is cirrhosis?

A

A chronic disease of the liver resulting from necrosis of liver cells followed by fibrosis. The end result is impairment of hepatocyte function and distortion of liver architecture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Give 3 causes of cirrhosis.

A
  1. Alcohol!
  2. Hepatitis B and C.
  3. Any chronic liver disease e.g. autoimmune, metabolic, vascular etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is the treatment of liver cirrhosis?

A
  1. Deal with the underlying cause e.g. stop drinking alcohol.
  2. Screening for HCC.
  3. Consider transplant.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Approximately what percentage of blood flow to the liver is provided by the portal vein?

A

75%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Portal hypertension can lead to varices. Explain why.

A

Obstruction to portal blood flow e.g. cirrhosis leads to portal hypertension. Blood is diverted into collaterals e.g. the gastro-oesophageal junction and so causes varices.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Give 3 causes of portal hypertension.

A
  1. Cirrhosis and fibrosis (intra-hepatic causes).
  2. Portal vein thrombosis (pre-hepatic).
  3. Budd-Chiari (post-hepatic cause).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the potential consequences of varices?

A

If they rupture -> haemorrhage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What is the primary treatment for varices?

A

Endoscopic therapy - banding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is peritonitis?

A

Inflammation of the peritoneum often due to infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What can cause peritonitis?

A
  1. Bacterial infection due to a perforated organ; spontaneous bacterial peritonitis; infection secondary to peritoneal dialysis.
  2. Non-infective causes e.g. bile leak; blood from ruptured ectopic pregnancy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What is the commonest serious infection in those with cirrhosis?

A

Spontaneous bacterial peritonitis.

It can also affect immunocompromised people and those undergoing peritoneal dialysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Name a bacteria that can cause spontaneous bacterial peritonitis.

A
  1. E.coli.

2. S.pneumoniae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

How can spontaneous bacterial peritonitis be diagnosed?

A

By looking for the presence of neutrophils in ascitic fluid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Give 3 symptoms of peritonitis.

A
  1. Pain.
  2. Tenderness.
  3. Systemic symptoms e.g. nausea, chills, rigor.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Name a cause of pelvic inflammatory disease.

A

A complication of chlamydial infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Give 4 reasons why liver patients are vulnerable to infection.

A
  1. They have impaired reticulo-endothelial function.
  2. Reduced opsonic activity.
  3. Leukocyte function is reduced.
  4. Permeable gut wall.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is primary biliary cirrhosis?

A

An autoimmune disease where there is progressive lymphocyte mediated destruction of intra-hepatic bile ducts -> cholestasis -> cirrhosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Describe 2 features of the epidemiology of primary biliary cirrhosis.

A
  1. Females affected more than men.

2. Familial - 10 fold risk increase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Describe the pathophysiology of primary biliary cirrhosis.

A

Lymphocyte mediated attack on bile duct epithelia -> destruction of bile ducts -> cholestasis -> cirrhosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Give 3 diseases associated with primary biliary cirrhosis.

A
  1. Thyroiditis.
  2. RA.
  3. Coeliac disease.
  4. Lung disease.

(Other autoimmune diseases).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Give 5 symptoms of primary biliary cirrhosis.

A
  1. Itching.
  2. Fatigue.
  3. Dry eyes,
  4. Joint pains.
  5. Variceal bleeding.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is the treatment for primary biliary cirrhosis?

A

Ursodeoxycholic acid; improves liver enzymes; reduces inflammation and portal pressure and therefore the rate of variceal development.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Give 3 risk factors for gallstone development.

A
  1. Female.
  2. Obese (fat).
  3. Fertile.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

How can gallstones be removed from the gall bladder?

A

Laproscopic cholecystectomy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Give 4 potential complications of gallstones in the bile duct.

A
  1. Biliary pain.
  2. Obstructive jaundice.
  3. Cholangitis (infection of the biliary tract).
  4. Pancreatitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is ascending cholangitis?

A

Obstruction of biliary tract causing bacterial infection. Regarded as a medical emergency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Name the triad that describes 3 common symptoms of ascending cholangitis.

A

Charcot’s triad:

  1. Fever.
  2. RUQ pain.
  3. JAUNDICE (cholestatic)!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What is charcot’s triad?

A

It describes 3 common symptoms of ascending cholangitis:

  1. Fever.
  2. RUQ pain.
  3. Jaundice (cholestatic)!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What investigations might you do in someone who you suspect might have ascending cholangitis?

A
  1. Ultrasound.
  2. Blood tests - LFT’s.
  3. ERCP - definitive investigation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Describe the management of ascending cholangitis.

A
  • IV fluid.
  • IV antibiotics e.g. cefotaxime and metronidazole.
  • ERCP to remove stone.
  • Stenting.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is the difference between ascending cholangitis and acute cholecystitis?

A

A patient with acute cholecystitis would not have signs of jaundice!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is acute cholecystitis?

A

Inflammation of the gall bladder caused by blockage of the bile duct -> obstruction to bile emptying.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Give 3 symptoms of acute cholecystitis.

A
  1. RUQ pain.
  2. Fever.
  3. Raised inflammatory markers.
    - NO JAUNDICE!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Give 2 risk factors for acute cholecystitis.

A
  1. Obesity.

2. Diabetes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Describe the pathophysiology of primary sclerosing cholangitis.

A

Inflammation of the bile duct -> strictures and hardening -> progressive obliterating fibrosis of bile duct branches -> cirrhosis -> liver failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Give 3 symptoms of primary sclerorsing cholangitis.

A
  1. Itching.
  2. Rigor.
  3. Pain.
  4. Jaundice.

75% also have IBD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What is biliary colic?

A

Gallbladder attack - RUQ pain due to a gall stone blocking the bile duct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What can trigger biliary colic?

A

Eating a heavy meal especially one that is high in fat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Give 5 causes of diarrhoeal infection.

A
  1. Traveller’s diarrhoea.
  2. Viral e.g. rotavirus, norovirus.
  3. Bacterial e.g. E.coli.
  4. Parasites e.g. helminths.
  5. Nosocomial e.g. c.diff.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Give 5 causes of non-diarrhoeal infection.

A
  1. Gastritis/peptic ulcer disease e.g. h.pylori.
  2. Acute cholecystitis.
  3. Peritonitis.
  4. Typhoid/paratyphoid.
  5. Amoebic liver disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Give 3 ways in which diarrhoea can be prevented.

A
  1. Access to clean water.
  2. Good sanitation.
  3. Hand hygiene.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What is the diagnostic criteria for traveller’s diarrhoea?

A

> 3 unformed stools per day and at least one of:

  • Abdominal pain.
  • Cramps.
  • Nausea.
  • Vomiting.

It occurs within 3 days of arrival in a new country.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Give 3 causes of traveller’s diarrhoea.

A
  1. Enterotoxigenic e.coli (ETEC).
  2. Campylobacter.
  3. Norovirus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Describe the pathophysiology of traveller’s diarrhoea.

A

Heat labile ETEC modifies Gs and it is in a permanent ‘locked on’ state. Adenylate cyclase is activated and there is increased production of cAMP. This leads to increased secretion of Cl- into the intestinal lumen, H2O follows down as osmotic gradient -> diarrhoea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Which type of e.coli can cause bloody diarrhoea and has a shiga like toxin?

A

Enterohaemorrhagic e.coli (EHEC) aka e.coli 0157.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What does EIEC stand for?

A

Enteroinvasive e.coli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Which type of e.coli is responsible for causing large volumes of watery diarrhoea?

A

Enteropathogenic e.coli (EPEC).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What does EAEC stand for?

A

Enteroaggregative e.coli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What does DAEC stand for?

A

Diffusely adherent e.coli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What is the leading cause of diarrhoeal illness in young children?

A

Rotavirus.

There is a vaccine - rotarix.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Name a helminth responsible for causing diarrhoeal infection.

A

Schistosomiasis.

154
Q

Give 5 symptoms of helminth infection.

A
  1. Fever.
  2. Eosinophilia.
  3. Diarrhoea.
  4. Cough.
  5. Wheeze.
155
Q

Briefly describe the reproductive cycle of schistosomiasis.

A
  1. Fluke matures in blood vessels and reproduces sexually in human host.
  2. Eggs expelled in faeces and enter water source.
  3. Asexual reproduction in an intermediate host.
  4. Larvae expelled and penetrate back into human host.
156
Q

Why is c.diff highly infectious?

A

It is a spore forming bacteria.

Gram positive

157
Q

Give 5 risk factors for c.diff infection.

A
  1. Increasing age.
  2. Co-morbidities.
  3. Antibiotic use.
  4. PPI.
  5. Long hospital stays.
158
Q

Describe the treatment for c.diff infection.

A

Metronidazole and vancomyocin (PO).

159
Q

Name 5 antibiotics prone to causing c.diff infection.

A
  1. Ciprofloxacin.
  2. Co-amoxiclav.
  3. Clindamycin.
  4. Cephlasporins.
  5. Carbapenems.

RULE OF C’s!

160
Q

What can helicobacter pylori infection cause?

A

H.pylori produces urease -> ammonia -> damage to gastric mucosa -> neutrophil recruitment and inflammation. This can cause gastritis; peptic ulcer disease and gastric cancer.

161
Q

Describe h.pylori.

A

A gram negative bacilli with a flagellum.

162
Q

Describe the treatment for H.pylori infection.

A

Triple therapy: 2 antibiotics and 1 PPI e.g. omeprazole, clarithromyocin and amoxicillin.

163
Q

Who is most likely to be affected by diverticular disease?

A

Older patients and those with low fibre diets.

164
Q

Describe the pathophysiology of diverticulitis.

A

Out-pouching of bowel mucosa -> faeces can get trapped here and obstruct the diverticula -> abscess and inflammation -> diverticulitis.

165
Q

What part of the bowel is most likely to be affected by diverticulitis?

A

The descending colon.

166
Q

What is acute diverticulitis?

A

A sudden attack of swelling in the diverticula. Can be due to surgical causes.

167
Q

Describe the signs of acute diverticulitis.

A

Similar to the signs of appendicitis but on the left side e.g. pain in the left iliac fossa region, fever, tachycardia.

168
Q

Name the 3 broad categories that describe the causes of intestinal obstruction.

A
  1. Blockage.
  2. Contraction.
  3. Pressure.
169
Q

Intestinal obstruction: give 3 causes of blockage.

A
  1. Tumour.
  2. Diaphragm disease.
  3. Gallstones in ileum (rare).
170
Q

Intestinal obstruction: what is thought to cause diaphragm disease?

A

NSAIDS.

171
Q

Intestinal obstruction: give 3 causes of contraction.

A
  1. Inflammation.
  2. Intramural tumours.
  3. Hirschprung’s disease.
172
Q

Describe how Crohn’s disease can cause intestinal obstruction.

A

Crohn’s disease -> fibrosis -> contraction -> obstruction.

173
Q

Describe how Diverticular disease can cause intestinal obstruction.

A

Out-pouching of mucosa -> faeces trapped -> inflammation in bowel wall -> contraction -> obstruction.

174
Q

What is Hirschprung’s disease?

A

A congenital condition where there is a lack of nerves in the bowel and so motility is affected. This leads to obstruction and gross dilatation of the bowel.

175
Q

Intestinal obstruction: give 3 causes of pressure.

A
  1. Adhesions.
  2. Volvulus.
  3. Peritoneal tumour.
176
Q

Intestinal obstruction: what are adhesions?

A

Adhesions often form secondary to abdominal surgery. Loops of bowel stick together and the bowel is pulled and distorted. 40% of intestinal obstructions are due to adhesions.

177
Q

Intestinal obstruction: what causes adhesions?

A

Adhesions often form secondary to abdominal surgery.

178
Q

Intestinal obstruction: what is volvulus?

A

Volvulus is a twist/rotation in the bowel; closed loop obstruction. There is a risk of necrosis.

179
Q

Intestinal obstruction: which areas of the bowel are most likely to be affected by volvulus?

A

Volvulus occurs in free floating areas of the bowel e.g. bowel with mesentery. The sigmoid colon has a long mesentery and so can twist on itself.

180
Q

Give 4 common causes of small bowel obstruction in adults.

A
  1. Adhesions.
  2. Hernias.
  3. Crohn’s disease.
  4. Malignancy.
181
Q

Which is more common: small bowel obstruction or large bowel obstruction?

A

Small bowel obstruction is more common; it makes up 75% of intestinal obstruction.

182
Q

Give 3 common causes of small bowel obstruction in children.

A
  1. Appendicitis.
  2. Volvulus.
  3. Intussusception.
183
Q

Intestinal obstruction: what is intussusception?

A

Intussusception is when part of the intestine invaginates into another section of the intestine -> telescoping. It is caused by force in-balances.

184
Q

Define hernia.

A

The abnormal protrusion of an organ into a body cavity it doesn’t normally belong.

185
Q

What are the risks of hernia’s if left untreated?

A

They can become strangulated and you may not be able to return them into their correct body cavity - irreducible.

186
Q

Give 2 symptoms of hernia.

A
  1. Pain.

2. Palpable lump.

187
Q

Give 5 symptoms of small bowel obstruction.

A
  1. Vomiting.
  2. Pain.
  3. Constipation.
  4. Distension.
  5. Tenderness.
188
Q

Would dilatation, distension and increased secretions be seen proximal or distal to an intestinal obstruction?

A

Proximal.

189
Q

Give 4 signs of small bowel obstruction.

A
  1. Vital signs e.g. increased HR, hypotension, raised temperature.
  2. Tenderness and swelling.
  3. Resonance.
  4. Bowel sounds.
190
Q

What investigations might you do in someone who you suspect to have a small bowel obstruction?

A
  1. Take a good history - ask about previous surgery (adhesions)!
  2. FBC, U+E, lactate.
  3. X-ray.
  4. CT, ultrasound, MRI.
191
Q

What is the management/treatment for small bowel obstruction?

A
  1. Fluid resuscitation.
  2. Bowel decompression.
  3. Analgesia and anti-emetics.
  4. Antibiotics.
  5. Surgery e.g. laparotomy, bypass segment, resection.
192
Q

Give 2 common causes of large bowel obstruction.

A
  1. Colorectal malignancy.

2. Volvulus (especially in the developing world).

193
Q

Give 5 symptoms of large bowel obstruction.

A
  1. Tenesmus.
  2. Constipation.
  3. Abdominal discomfort.
  4. Bloating.
  5. Vomiting.
  6. Weight loss.
194
Q

What investigations might you do in someone who you suspect to have a large bowel obstruction?

A
  1. Digital rectal examination.
  2. Sigmoidoscopy.
  3. Plain X-ray.
  4. CT scan.
195
Q

Describe the management for a large bowel obstruction.

A
  1. Fast the patient.
  2. Supplement O2.
  3. IV fluids to replace losses and correct electrolyte imbalance.
  4. Urinary catheterisation to monitor urine output.
196
Q

Give 3 consequences of untreated intestinal obstructions.

A
  1. Ischaemia.
  2. Necrosis.
  3. Perforation.
197
Q

Describe the progression from normal epithelium to colorectal cancer.

A
  1. Normal epithelium.
  2. Adenoma.
  3. Colorectal adenocarcinoma.
  4. Metastatic colorectal adenocarcinoma.
198
Q

Define adenocarcinoma.

A

A malignant tumour of glandular epithelium.

199
Q

What is familial adenomatous polyposis?

A

Familial adenomatous polyposis is a genetic condition where you develop thousands of polyps in your teens.

200
Q

Describe the pathophysiology of familial adenomatous polyposis.

A

There is a mutation in apc protein and so the apc/GSK complex isn’t formed -> beta catenin levels increase -> up-regulation of adenomatous gene transcription.

201
Q

Describe the pathophysiology of HNPCC.

A

There are no DNA repair proteins meaning there is a risk of colon cancer and endometrial cancers.

202
Q

How can adenoma formation be prevented?

A

NSAIDS are believed to prevent adenoma formation.

203
Q

What is the treatment for adenoma?

A

Endoscopic resection.

204
Q

What is the treatment for colorectal adenocarcinoma?

A

Surgical resection can be done when there is no spread. Remember to balance risks v benefits. The patient has a pre-op assessment.

205
Q

What is the treatment for metastatic colorectal adenocarcinoma?

A

Chemotherapy and palliative care.

206
Q

Give 3 reasons why bowel cancer survival has increased over recent years.

A
  1. Introduction of the bowel cancer screening programme.
  2. Colonoscopic techniques.
  3. Improvements in treatment options.
207
Q

Give 5 risk factors for colorectal cancer.

A
  1. Low fibre diet.
  2. Diet high in red meat.
  3. Alcohol.
  4. Smoking.
  5. A PMH of adenoma or ulcerative colitis.
  6. A family history of colorectal cancer; FAP or HNPCC.
208
Q

What can affect the clinical presentation of a colorectal cancer?

A

How close the cancer is to the rectum affects its clinical presentation.

209
Q

Give 3 signs of rectal cancer.

A
  1. PR bleeding.
  2. Mucus.
  3. Thin stools.
  4. Tenesmus.
210
Q

Give 2 signs of a left sided/sigmoid cancer.

A
  1. Change of bowel habit e.g. diarrhoea, constipation.

2. PR bleeding.

211
Q

Give 3 signs of a right sided cancer.

A
  1. Anaemia.
  2. Mass.
  3. Diarrhoea that doesn’t settle.
212
Q

Describe the emergency presentation of a left sided colon cancer.

A

The LHS of the colon is narrow and so the patient is likely to present with signs of obstruction e.g. constipation; colicky abdominal pain; abdominal distension; vomiting.

213
Q

Describe the emergency presentation of a right sided colon cancer.

A

The RHS of the colon is wide and so the patient is likely to present with signs of perforation.

214
Q

What investigations might you do in someone who you suspect might have colorectal cancer?

A

Colonoscopy = gold standard!
It permits biopsy and removal of small polyps.
- Tumour markers are good for monitoring progress.
- Faecal occult blood is used in screening but not diagnosis.

215
Q

Give 5 non-infective causes of diarrhoea.

A
  1. Neoplasm.
  2. Inflammatory.
  3. Irritable bowel.
  4. Anatomical.
  5. Chemical.
  6. Hormonal.
  7. Radiation.
216
Q

Give 3 infective causes of dysentery.

A
  1. Shigella.
  2. Salmonella.
  3. Campylobacter.
  4. E.coli 0157.
217
Q

Give 2 infective causes of non-bloody diarrhoea.

A
  1. Rotavirus.

2. Norovirus.

218
Q

Describe the chain of infection.

A

Reservoir -> agent -> transmission -> host -> person to person spread.

219
Q

Give 3 ways in which infection can be transmitted.

A
  1. Direct e.g. faeco-oral.
  2. Indirect e.g. vectorborne (malaria).
  3. Airborne e.g. respiratory route.
220
Q

What is the treatment for vibrio cholerae infection?

A

HYDRATE e.g. ORS. What goes out must be replaced.

221
Q

Describe the management of c.diff infection.

A
  1. Control antibiotic use.
  2. Infection control measures.
  3. Isolate the case.
  4. Case finding.
  5. Test stool samples for toxin.
222
Q

Give 4 groups at risk of diarrhoeal infection.

A
  1. Food handlers.
  2. Health care workers.
  3. Children who attend nursery.
  4. Persons of doubtful personal hygiene.
223
Q

Give 3 causes of peptic ulcers.

A
  1. Prolonged NSAID use -> decreased mucin production.
  2. H.pylori infection.
  3. Hyper-acidity.
224
Q

Give 3 symptoms of peptic ulcers.

A

Often acute onset of symptoms:

  1. Pain.
  2. Bleeding.
  3. Perforation.
225
Q

What investigations might you do in someone who you suspect to have peptic ulcers?

A
  1. H.pylori test e.g. urease breath test and faecal antigen test.
  2. Gastroscopy.
  3. Barium meal.
226
Q

Give 3 treatments for peptic ulcers.

A
  1. Stop NSAIDS.
  2. PPI’s e.g. omeprazole.
  3. H.pylori eradication.
227
Q

Give 2 potential complications of oesophago-gastroduodenoscopy (OGD).

A
  1. Cardiopulmonary.

2. Small risk of bleeding or perforation.

228
Q

Give 3 indications for OGD.

A
  1. Dyspepsia.
  2. Dysphagia.
  3. Anaemia.
  4. Suspected coeliac disease.
229
Q

Give 3 indications for colonoscopy.

A
  1. Altered bowel habit.
  2. Diarrhoea +/- dysentery.
  3. Anaemia.
230
Q

Give 3 symptoms of GORD.

A
  1. Heart burn.
  2. Acid reflux.
  3. Dysphagia.
231
Q

Describe the pathophysiology of coeliac disease.

A

Gliadin (product of gluten digestion) = immunogenic. It can have direct toxic effects by up-regulating the innate immune system or HLADQ2 can present it to T helper cells in the lamina propria -> inflammation -> villi atrophy -> malabsorption.

232
Q

Give 5 symptoms of coeliac disease.

A
  1. Diarrhoea.
  2. Weight loss.
  3. Irritable bowel.
  4. Iron deficiency anaemia.
  5. Mouth ulcers.
  6. Abnormal liver function.
233
Q

What investigations might you do in someone who you suspect to have coeliac disease?

A
  1. Serology - look for auto-antibodies - TTG and EMA.

2. Gastroscopy - duodenal biopsies.

234
Q

What part of the bowel is commonly affected by Crohn’s disease?

A

Can affect anywhere from the mouth to anus.

235
Q

What part of the bowel is commonly affected by ulcerative colitis?

A

It only affects the rectum. It spreads proximally but only affects the colon.

236
Q

Give 5 complications of Crohn’s disease.

A
  1. Malabsorption.
  2. Fistula.
  3. Obstruction.
  4. Perforation.
  5. Anal fissures.
  6. Neoplasia.
  7. Amyloidosis (rare).
237
Q

Give 5 complications of ulcerative colitis.

A
  1. Colon: blood loss and colorectal cancer.
  2. Arthritis.
  3. Iritis and episcleritis.
  4. Fatty liver and primary sclerosing cholangitis.
  5. Erythema nodosum.
238
Q

Give an example of a functional bowel disorder.

A

IBS.

239
Q

Describe the multi-factorial pathophysiology of IBS.

A

The following factors can all contribute to IBS:

  • Psychological morbidity e.g. trauma in early life.
  • Abnormal gut motility.
  • Genetics.
  • Altered gut signalling (visceral hypersensitivity).
240
Q

Give 3 symptoms of IBS.

A
  1. ABDOMINAL PAIN!
  2. Pain is relieved on defecation.
  3. Bloating.
  4. Change in bowel habit.
  5. Mucus.
  6. Fatigue.
241
Q

Give an example of a differential diagnosis for IBS.

A
  1. Coeliac disease.
  2. Lactose intolerance.
  3. Bile acid malabsorption.
  4. IBD.
  5. Colorectal cancer.
242
Q

What investigations might you do in someone who you suspect has IBS?

A
  1. Bloods - FBC, U+E, LFT.
  2. CRP.
  3. Coeliac serology.
243
Q

Describe the treatment for mild IBS.

A

Education, reassurance, dietary modification e.g. FODMAP.

244
Q

Describe the treatment for moderate IBS.

A

Pharmacotherapy and psychological treatments:

  • Antispasmodics for pain.
  • Laxatives for constipation.
  • Anti-motility agents for diarrhoea.
  • CBT and hypnotherapy.
245
Q

Describe the treatment for severe IBS.

A

MDT approach, referral to specialist pain treatment centres.
- Tri-cyclic anti-depressants.

246
Q

Why are all gastric ulcers re-scoped 6-8 weeks after treatment?

A

All peptic ulcers are re-scoped to ensure they’ve healed. If they haven’t healed it could be a sign of malignancy.

247
Q

What is the criteria for dyspepsia?

A

> 1 of the following:

  • Postprandial fullness.
  • Early satiation.
  • Epigastric pain/burning.
248
Q

Give 5 causes of dyspepsia.

A
  1. Excess acid.
  2. Prolonged NSAIDS.
  3. Large volume meals.
  4. Obesity.
  5. Smoking/alcohol.
  6. Pregnancy.
249
Q

Give 5 red flag symptoms that you might detect when taking a history from someone with dyspepsia.

A
  1. Unexplained weight loss.
  2. Anaemia.
  3. Dysphagia.
  4. Upper abdominal mass.
  5. Persistent vomiting.
250
Q

What investigations might you do in someone with dyspepsia?

A
  1. Endoscopy.
  2. Gastroscopy.
  3. Barium swallow.
  4. Capsule endoscopy.
251
Q

What is the management for dyspepsia if the red flag criteria has been met?

A
  1. Suspend NSAID use and review medication.
  2. Endoscopy.
  3. Refer malignancy to specialist.
252
Q

What is the management for dyspepsia without red flag symptoms?

A
  1. Review medication.
  2. Lifestyle advice.
  3. Full dose PPI for 1 month.
  4. Test and treat h.pylori infection.
253
Q

What kind of lifestyle advice might you give to someone with dyspepsia?

A
  1. Lose weight.
  2. Stop smoking.
  3. Cut down alcohol.
  4. Dietary modification.
254
Q

Describe the treatment for GORD.

A
  1. PPI.
  2. Lifestyle modification.
  3. Anti-reflux surgery.
255
Q

Give a potential consequence of anterior ulcer haemorrhage.

A

Acute peritonitis.

256
Q

Give a potential consequence of posterior ulcer haemorrhage.

A

Pancreatitis.

257
Q

Name 5 things that can break down the mucin layer in the stomach and cause gastritis.

A
  1. Not enough blood - mucosal ischaemia.
  2. H.pylori.
  3. Aspirin, NSAIDS.
  4. Increased acid - stress.
  5. Bile reflux - direct irritant.
  6. Alcohol.
258
Q

Describe the treatment for gastritis.

A
  1. Reduced mucosal ischaemia.
  2. PPI.
  3. H2RA.
  4. Enteric coated aspirin.
259
Q

Give 5 broad causes of malabsorption.

A
  1. Defective intra-luminal digestion.
  2. Insufficient absorptive area.
  3. Lack of digestive enzymes.
  4. Defective epithelial transport.
  5. Lymphatic obstruction.
260
Q

Malabsorption: what can cause defective intra-luminal digestion?

A
  1. Pancreatic insufficiency due to pancreatitis, CF. There is a lack of digestive enzymes.
  2. Defective bile secretion due to biliary obstruction or ileal resection.
  3. Bacterial overgrowth.
261
Q

Why can pancreatitis cause malabsorption?

A

Pancreatitis results in pancreatic insufficiency and so a lack of pancreatic digestive enzymes. There is defective intra-luminal digestion which leads to malabsorption.

262
Q

Malabsorption: what can cause insufficient absorptive area?

A
  1. Coeliac disease.
  2. Crohn’s disease.
  3. Extensive parasitisation.
  4. Small intestine resection.
263
Q

Malabsorption: give an example of when there is a lack of digestive enzymes.

A

Lactose intolerance - disaccharide enzyme deficiency.

264
Q

Malabsorption: what can cause lymphatic obstruction?

A
  1. Lymphoma.

2. TB.

265
Q

Describe the distribution of inflammation seen in Crohn’s disease.

A

Patchy, granulomatous, transmural inflammation (can affect just the mucosa or go through the bowel wall).

266
Q

Describe the distribution of inflammation seen in ulcerative colitis.

A

Continuous inflammation affecting only the mucosa.

267
Q

Histologically, what part of the bowel wall is affected in ulcerative colitis?

A

Just the mucosa.

268
Q

Histologically, what part of the bowel wall is affected in crohn’s disease?

A

Can affect just the mucosa or can go all the way through to the bowel wall -> transmural inflammation.

269
Q

What is the treatment for crohn’s disease and ulcerative colitis?

A

Anti-inflammatories.

270
Q

Name the break down product of gluten that can trigger coeliac disease.

A

Gliadin.

271
Q

What part of the small intestine is mainly affected by coeliac disease?

A

Duodenum.

272
Q

What disorders might be associated with coeliac disease?

A

Other autoimmune disorders:

  1. T1 diabetes.
  2. Thyroxoicosis.
  3. Hypothyroidism.
  4. Addisons disease.

Osteoporosis is also commonly seen in people with coeliac disease.

273
Q

What is the prevalence of coeliac disease?

A

1%.

274
Q

What cells normally line the oesophagus?

A

Stratified squamous non-keratinising cells.

275
Q

What is Barrett’s oesophagus?

A

When squamous cells undergo metaplastic changes and become columnar cells.

276
Q

What can cause Barrett’s oesophagus?

A
  1. GORD.

2. Obesity.

277
Q

Give a potential consequence of Barrett’s oesophagus.

A

Adenocarcinoma.

278
Q

Describe how Barrett’s oesophagus can lead to oesophageal adenocarcinoma.

A
  1. GORD damages normal oesophageal squamous cells.
  2. Glandular columnar epithelial cells replace squamous cells (metaplasia).
  3. Continuing reflux leads to dysplastic oesophageal glandular epithelium.
  4. Continuing reflux leads to neoplastic oesophageal glandular epithelium - adenocarcinoma.
279
Q

Give 5 symptoms of oesophageal carcinoma.

A
  1. Dysphagia.
  2. Odynophagia (painful swallowing).
    People often present very late.
  3. Vomiting.
  4. Weight loss.
  5. Anaemia.
  6. GI bleed.
  7. Reflux.
280
Q

Give 3 causes of squamous cell carcinoma.

A
  1. Smoking.
  2. Alcohol.
  3. Poor diet.
281
Q

What can cause oesophageal adenocarcinoma?

A

Barrett’s oesophagus.

282
Q

Give 3 causes of gastric cancer.

A
  1. Smoked foods.
  2. Pickles.
  3. H.pylori infection.
  4. Pernicious anaemia.
283
Q

Describe how gastric cancer can develop from normal gastric mucosa.

A

Smoked/pickled food diet leads to intestinal metaplasia of the normal gastric mucosa. Several genetic changes lead to dysplasia and then eventually intra-mucosal and invasive carcinoma.

284
Q

Give 3 causes of oesophageal carcinoma.

A
  1. GORD -> Barrett’s.
  2. Smoking.
  3. Alcohol.
285
Q

What investigations might you do in someone who you suspect to have oesophageal carcinoma?

A
  1. Barium swallow.

2. Endoscopy.

286
Q

Describe the 2 treatment options for oesophageal cancer.

A
  1. Medically fit and no metastases = operate. The oesophagus is replaced with stomach or sometimes the colon. The patient often has 2/3 rounds of chemo before surgery.
  2. Medically unfit and metastases = palliative care. Stents can help with dysphagia.
287
Q

Give 3 signs of gastric cancer.

A
  1. Weight loss.
  2. Anaemia.
  3. Vomiting blood.
  4. Melaena.
  5. Dyspepsia.
288
Q

A mutation in what gene can cause familial diffuse gastric cancer?

A

CDH1 - 80% chance of gastric cancer.

Prophylactic gastrectomy is done in these patients.

289
Q

What investigations might you do in someone who you suspect has gastric cancer?

A
  1. Endoscopy.
  2. CT.
  3. Laparoscopy.
290
Q

What is the advantage of doing a laparoscopy in someone with gastric cancer?

A

It can detect metastatic disease that may not be detected on ultrasound/endoscopy.

291
Q

What is the treatment for proximal gastric cancers that have no spread?

A

3 cycles of chemo and then a full gastrectomy. Lymph node removal too.

292
Q

What is the treatment for distal gastric cancers that have no spread?

A

3 cycles of chemo and then a partial gastrectomy if the tumour is causing stenosis or bleeding. Lymph node removal too.

293
Q

What vitamin supplement will a patient need following gastrectomy?

A

They will be deficient in intrinsic factor and so will need vitamin B12 supplements to prevent pernicious anaemia.

294
Q

Give 3 symptoms of spontaneous bacterial peritonitis.

A
  1. Dull to percussion.
  2. Temperature.
  3. Abdominal pain.
295
Q

What investigations might you do in someone who you suspect could have peritonitis?

A
  1. Blood tests: raised WCC, platelets, CRP, amylase. Reduced blood count.
  2. CXR: look for air under the diaphragm.
  3. Abdominal x-ray: look for bowel obstruction.
  4. CT: can show inflammation, ischaemia or cancer.
  5. ECG: epigastric pain could be related to the heart.
  6. B-HCG: a hormone secreted by pregnant ladies.
296
Q

Give 5 potential complications of peritonitis.

A
  1. Hypovolaemia.
  2. Kidney failure.
  3. Systemic sepsis.
  4. Paralytic ileus.
  5. Pulmonary atelectasis (lung collapse).
  6. Portal pyaemia (pus in the portal vein).
297
Q

Explain how paralytic ileus can lead to respiratory problems.

A

Peristaltic waves stop -> dilation of bowel -> distended abdomen therefore increased pressure -> pushes on diaphragm -> respiration affected.

298
Q

What is the management for peritonitis?

A
  1. ABC.
  2. Treat the underlying cause!
  3. Call a surgeon.
  4. Set up post-management support.
299
Q

What can cause exudative ascites?

A

Increased vascular permeability secondary to infection; inflammation (peritonitis) or malignancy.

300
Q

What can cause transudative ascites?

A

Increased venous pressure due to cirrhosis, cardiac failure or hypoalbuminaemia.

301
Q

Give 2 signs of ascites.

A
  1. Flank swelling.

2. Dull to percuss and shifting dullness.

302
Q

What investigations might you do in someone who you suspect has ascites?

A
  1. Ultrasound.

2. Ascitic tap.

303
Q

Describe the treatment for ascites.

A
  1. Restrict sodium.
  2. Diuretics.
  3. Drainage.
304
Q

Where in the colon do the majority of colon cancers occur?

A

In the descending/sigmoid colon and rectum.

305
Q

Why do proximal colon cancers have a worse prognosis?

A

They have fewer signs and so people often present with them at a very advanced and late stage.

306
Q

What 3 histological features are needed in order to make a diagnosis of coeliac disease?

A
  1. Raised intraepithelial lymphocytes.
  2. Crypt hyperplasia.
  3. Villous atrophy.
307
Q

What investigation is it important to do in someone with chronic liver disease and ascites? Explain why it is important.

A

It is important to do an ascitic tap so you can rule out spontaneous bacterial peritonitis as soon as possible.

308
Q

What would be raised in the blood tests taken from someone with primary biliary cirrhosis?

A
  1. Raised IgM.
  2. Raised ALP.
  3. Positive AMA.
309
Q

What 4 features would you expect to see in the blood test results taken from someone who has overdosed on paracetamol.

A
  1. Metabolic acidosis.
  2. Prolonged pro-thrombin time (due to coagulability).
  3. Raised creatinine (renal failure).
  4. Raised ALT.
310
Q

What 3 symptoms make up the triad of Wernicke’s encephalopathy?

A
  1. Ataxia.
  2. Opthalmoplegia.
  3. Confusion.
311
Q

How can Wernicke’s encephalopathy be reversed?

A

Give IV thiamine.

312
Q

What histological stain can be used for haemochromatosis?

A

Perl’s stain.

313
Q

Name 4 fat soluble vitamins.

A

A, D, E and K.

314
Q

What is the main difference between biliary colic and acute cholecystitis?

A

Acute cholecystitis has an inflammatory component!

315
Q

What is the treatment for acute cholecystitis?

A

Laparoscopic cholecystectomy.

316
Q

Why might someone with primary biliary cirrhosis experience itching as a symptom?

A

Because there is a build up of bilirubin.

317
Q

Give 3 components of gallstones.

A
  1. Cholesterol.
  2. Bile pigment.
  3. Phospholipid.
318
Q

What investigations might you do in someone who you suspect has gallstones?

A

Ultrasound!

ERCP.

319
Q

Are most liver cancers primary or secondary?

A

Secondary - they have metastasised to the liver from the GI tract, breast and bronchus.

320
Q

Where have most secondary liver cancers arisen from?

A
  1. The Gi tract.
  2. Breast.
  3. Bronchus.
321
Q

Describe the aetiology of HCC.

A

Most HCC is in patients with cirrhosis. This is often due to HBV/HCV and alcohol.

322
Q

Give 5 symptoms of HCC.

A
  1. Weight loss.
  2. Anorexia.
  3. Fever.
  4. Malaise.
  5. Ascites.
323
Q

What investigations might you do on someone who you suspect has HCC?

A
  1. Bloods: serum AFP may be raised.
  2. US or CT to identify lesions.
  3. MRI.
  4. Biopsy if diagnostic doubt.
324
Q

Describe the treatment for HCC.

A
  1. Surgical resection of solitary tumours.
  2. Liver transplant.
  3. Percutaneous ablation.
325
Q

How long after infection with hepatitis B virus is HBsAg present in the serum for?

A

HBsAg will be present in the serum from 6 weeks - 3 months after infection.

326
Q

How long after infection with hepatitis B virus is anti-HBV core (IgM) present in the serum for?

A

Anti-HBV core (IgM) slowly rises from 6 weeks after infection and its serum level peaks at about 4 months.

327
Q

Give 3 symptoms of haemochromatosis.

A
  1. Hepatomegaly.
  2. Cardiomegaly.
  3. Diabetes mellitus.
  4. Hyperpigmentation of skin.
  5. Lethargy.
328
Q

Name 3 diseases that lead to heamolytic anaemia and so a raised unconjugated bilirubin and pre-hepatic jaundice.

A

Causes of haemolytic anaemia:

  1. Sickle cell disease.
  2. Hereditary spherocytosis/elliptocytosis.
  3. GP6D deficiency.
  4. Hypersplenism.
329
Q

Give 3 causes of liver failure.

A
  1. Infection e.g. viral hepatitis B, C.
  2. Induced e.g. alcohol, drug toxicity.
  3. Inherited e.g. autoimmune.
330
Q

Hepatic encephalopathy is a complication of liver failure. Describe the pathophysiological mechanism behind this.

A

The liver can’t get rid of ammonia and so ammonia crosses the BBB -> cerebral oedema.

331
Q

Give 4 complications of liver failure.

A
  1. Hepatic encephalopathy.
  2. Abnormal bleeding.
  3. Jaundice.
  4. Ascites.
332
Q

Describe the treatment for liver failure.

A
  1. Nutrition.
  2. Supplements.
  3. Treat complications.
  4. Liver transplant.
333
Q

You do an ascitic in someone with ascites. The neutrophil count comes back as - Neutrophils > 250/mm3. What is the likely cause of the raised neutrophils?

A

Spontaneous bacterial peritonitis.

334
Q

Describe the treatment for spontaneous bacterial peritonitis.

A

Cefotaxime and metronidazole.

335
Q

Give 5 symptoms of ruptured varices.

A
  1. Haematemesis.
  2. Melaena.
  3. Abdominal pain.
  4. Dysphagia.
  5. Anaemia.
336
Q

How would you know if an individual had been vaccinated against hepatitis B?

A

They would have anti-HBVs IgG in their serum.

337
Q

What type of anaemia do you associate with alcoholic liver disease?

A

Macrocytic anaemia.

338
Q

Name a protozoa that can cause amoebic liver abscess?

A

Entemoeba histolytica.

339
Q

What are the symptoms of entemoeba histolytica?

A
  • RUQ pain.
  • Bloody diarrhoea.
  • Fever and malaise.

Often the patient has a history of foreign/rural travel.

340
Q

What is the treatment for entemoeba histolytica?

A

Metronidazole.

341
Q

What is the treatment for mild/moderate UC?

A

Mesalazine.

342
Q

A 4-year-old girl presents with diarrhoea and is hypotensive. What is the physiological reason that fluid moves from the interstitium to the vascular compartment in this case?

A

Reduced hydrostatic pressure.

Fluid will move from the interstitium into the plasma if there is an increase in osmotic pressure or a decrease in hydrostatic pressure. As this patient is hypotensive it is more likely to be the latter.

343
Q

What drug would you give to someone that has overdosed on paracetamol?

A

IV N-Acetyl-Cysteine.

344
Q

With which disease would you associate Reynold’s pentad?

A

Ascending cholangitis.

345
Q

Describe Reynold’s pentad.

A
  • Charcot’s triad (fever, RUQ pain and jaundice).
    • hypotension.
    • altered mental state.
346
Q

What is a potential consequence of h.pylori infection in a person with decreased gastric acid?

A

Gastric cancer.

347
Q

What is a potential consequence of h.pylori infection in a person with increased gastric acid?

A

Duodenal ulcer.

348
Q

What might pain radiating to the back be a sign of?

A

Pancreatitis or AAA.

349
Q

What blood test might show that someone has alcoholic liver disease?

A

Serum GGT (gamma-glutamyl transferase) will be elevated.

350
Q

What distinctive feature is often seen on biopsy in people suffering from alcoholic liver disease?

A

Mallory bodies.

351
Q

What feature seen on liver biopsy is diagnostic of cirrhosis?

A

Nodular regeneration.

352
Q

A man has his ascites drained and is advised to restrict his diet. Which non-hormonal substance will promote re-accumulation of the ascites?

A

Salt.

353
Q

What is the treatment for Wilson’s disease.

A

Lifetime treatment with penicillamine.

354
Q

Name the 2 main pathophysiological factors that contribute to the formation of ascites.

A
  1. High portal venous pressure.

2. Low serum albumin.

355
Q

Give 2 indications for the need of immediate surgical intervention in someone with a small bowel obstruction.

A
  1. Signs of perforation (peritonitis).

2. Signs of strangulation.

356
Q

Why is morphine contraindicated in acute pancreatitis?

A

Morphine increases sphincter of Oddi pressure and so aggravates pancreatitis.

357
Q

What two enzymes, if raised, suggest pancreatitis?

A

LDH and AST.

358
Q

Where is folate absorbed?

A

In the jejunum.

359
Q

Where is vitamin B12 absorbed?

A

In the terminal ileum.

360
Q

Where is iron absorbed?

A

In the duodenum.

361
Q

In someone with coeliac disease, what are they most likely to be deficient in - iron, folate, or B12?

A

Iron.

Coeliac disease mainly affects the duodenum and iron is absorbed in the duodenum. Folate is absorbed in the jejunum and B12 in the terminal ileum.

362
Q

Give 5 histological features of a malignant neoplasm.

A
  1. High mitotic activity.
  2. Rapid growth.
  3. Border irregularity.
  4. Necrosis.
  5. Poor resemblance to normal tissues.
363
Q

What lymph nodes can oesophageal carcinoma commonly metastasise to?

A

Para-oesophageal lymph nodes.

364
Q

What hormone is responsible for the production of gastric acid?

A

Gastrin.

365
Q

State two pathological changes that occur in the liver with continued consumption of excessive amounts of alcohol.

A
  1. Fatty liver.
  2. Alcoholic hepatitis.
  3. Cirrhosis.
366
Q

A patient’s oedema is caused solely by their liver disease. State one possible pathophysiological mechanism for their oedema.

A

Hypoalbuminaemia.

367
Q

List 5 important questions a GP should ask when taking a history to establish a cause of diarrhoea.

A
  1. Blood or mucus in the stools.
  2. Family history of bowel problems?
  3. Abdominal pain.
  4. Recent foreign travel history.
  5. Bloating.
  6. Weight loss.
368
Q

List two blood tests a GP might perform to help differentiate between the different causes of diarrhoea.

A
  1. FBC.

2. ESR/CRP.

369
Q

List two stool tests a GP might request to help differentiate between the different causes of diarrhoea.

A
  1. Stool culture.

2. Faecal calprotectin.

370
Q

State one histological feature that will be seen in ulcerative colitis.

A
  1. Crypt abscess.

2. Increase in plasma cells in the lamina propria.

371
Q

What investigations might you do in someone with inflammatory bowel disease?

A
  1. Bloods - FBC, ESR, CRP.
  2. Faecal calprotectin - shows inflammation but is not specific for IBD.
  3. Flexible sigmoidoscopy.
  4. Colonoscopy.
372
Q

Name 3 drugs or classes of drugs that can cause acute pancreatitis.

A
  1. NSAIDs.
  2. Diuretics.
  3. Steroids.
373
Q

What 2 products does haem break down in to?

A

Haem -> Fe2+ and biliverdin.

374
Q

What enzyme converts biliverdin to unconjugated bilirubin?

A

Biliverdin reductase.

375
Q

What is the function of glucuronosyltransferase?

A

It transfers glucuronic acid to unconjugated bilirubin to form conjugated bilirubin.

376
Q

What protein does unconjugated bilirubin bind to and why?

A

Albumin.

It isn’t H2O soluble therefore it binds to albumin so it can travel in the blood to the liver.

377
Q

What does conjugated bilirubin form?

A

Urobilinogen.

378
Q

What is responsible for the conversion of conjugated bilirubin into urobilinogen?

A

Intestinal bacteria.

379
Q

What can urobilinogen form?

A
  1. It can go back to the liver via the enterohepatic system.
  2. It can go to the kidneys forming urinary urobilin.
  3. It can form stercobilin which is excreted in the faeces.
380
Q

What disease could be caused by a non-functioning mutation in NOD2?

A

Crohn’s.