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2a > GI and Liver > Flashcards

GI and Liver Flashcards

1
Q

How long does hepatitis persist for to be deemed chronic?

A

6 months.

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2
Q

Give 3 infective causes of acute hepatitis.

A
  1. Hepatitis A to E infection.
  2. EBV.
  3. human herpes virus
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3
Q

Give 5 (6) non-infective causes of acute and chronic hepatitis.

A
  1. Alcohol
  2. Drugs.
  3. Toxins.
  4. Autoimmune.
  5. non alcoholic fatty liver disease
  6. pregnancy (acute)
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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.
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5
Q

Give 3 infective causes of chronic hepatitis.

A
  1. Hepatitis B (+/-D).
  2. Hepatits C.
  3. Hepatitis E.
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6
Q

What are the potential complications of chronic hepatitis?

A

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

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7
Q

Is HAV a RNA or DNA virus?

A

HAV is a RNA virus.

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8
Q

How is HAV transmitted?

A

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

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9
Q

Who could be at risk of HAV infection?

A

Travellers and food handlers.

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10
Q

Is HAV acute or chronic?

A

Acute! There is 100% immunity after infection.

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11
Q

How might you diagnose someone with HAV infection?

A

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

also

  • serum transaminases: raised
  • serum bilirubin: raised
  • prothrombin time: prolonged
  • serum creatinine: raised
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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.
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13
Q

Describe the primary prevention of HAV.

A

Vaccination.

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14
Q

Is HEV a RNA or DNA virus?

A

HEV is a small RNA virus.

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15
Q

How is HEV transmitted?

A

Faeco-oral transmission.

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16
Q

Is HEV acute or chronic?

A

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

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17
Q

How might you diagnose someone with HEV infection?

A

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

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18
Q

Describe the primary prevention of HEV.

A
  1. Good food hygiene.

2. A vaccine is in development.

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19
Q

Is HBV a RNA or DNA virus?

A

HBV is a DNA virus! It replicates in hepatocytes.

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20
Q

How is HBV transmitted?

A

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

HBV is highly infectious!

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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.
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22
Q

What HBV protein triggers the initial immune response?

A

The core proteins.

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23
Q

what do the different immunoglobulin levels and antigens mean in hepatitis?

IgG, IgM, antigens present

A
  • IgM (means currently ongoing acute infection)
  • IgG (chronic current or Previous infection)
  • Any antigens present => current infection (chronic or acute)
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24
Q

Describe the management of HBV infection.

A
  • Screen at risk patients for hep B/C + HIV, notify public health, stop smoking + alcohol
  • Antiviral med (entecavir), slows progression and decrease infectivity
  • test for complications: fibroscan (cirrhosis), ultrasound (HCC)
  • Follow up at 6 months to see if HBV surface Ag has cleared. if present -> chronic hepatitis
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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.

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26
Q

What are the potential consequences of chronic HBV infection?

A
  1. Cirrhosis.
  2. HCC.
  3. Decompensated cirrhosis.
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27
Q

How can HBV infection be prevented?

A

Vaccination - injecting a small amount of inactivated HbsAg.

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28
Q

Describe treatment options for HBV infection.

A

Antivirals e.g. entecovir. They inhibit viral replications.

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29
Q

What is HBV treatment

A
  • screen at risk patients for hep b/c + HIV
  • notify public health
  • stop smoking and drinking
  • antivirals (entecavir)
  • test for complications (fibroscan, ultrasound)
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30
Q

Is HDV a RNA or DNA virus?

A

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

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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.

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32
Q

How is HDV transmitted?

A

Blood-borne transmission, particularly IVDU.

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33
Q

Is HCV a RNA or DNA virus?

A

HCV is a RNA virus.

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34
Q

How is HCV transmitted?

A

Blood borne.

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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.
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36
Q

How might you diagnose someone with current HCV infection?

A

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

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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.

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38
Q

Describe the treatment for HCV.

A
  • Screen at risk patients for Hep B/C + HIV, notify public health, stop drinking and smoking
  • antiviral med (glecaprevir) slows progression and decrease infectivity
  • test for complications: fibroscan (cirrhosis), ultrasound (HCC)
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39
Q

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

A

Approximately 70%.

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40
Q

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

A

Approximately 5-10%.

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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.

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42
Q

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

A

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

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43
Q

What is acute pancreatitis?

A

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

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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.
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45
Q

Give 5 causes of acute pancreatitis.

A

IGETSMASHED

  • Idiopathic
  • Gallstones
  • Ethanol/ alcohol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion venom
  • Hyperlipidaemia
  • ERCP
  • Drugs (methotrexate)
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46
Q

Give 4 symptoms of acute pancreatitis.

A
  1. Severe epigastric pain that radiates to the back, worse with movement.
  2. Anorexia.
  3. Nausea, vomiting.
  4. Signs of septic shock e.g. fever, dehydration, hypotension, tachycardia.
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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 (necrosis, abscesses + fluid collection)
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48
Q

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

A

The abbreviated glasgow scoring system.

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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.
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50
Q

Describe the treatment for acute pancreatitis.

A
  1. ANALGESIA! (ibuprofen, opioids)
  2. IV fluids, nil by mouth
  3. Drainage of oedematous fluid collections.
  4. treat underlying cause (IGETSMASHED)
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51
Q

Give 2 potential complications of acute pancreatitis.

A
  1. Systemic inflammatory response syndrome.
  2. Multiple organ dysfunction.
  3. necrosis of pancreas
  4. chronic pancreatitis
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52
Q

What is chronic pancreatitis?

A

Chronic inflammation of the pancreas leads to irreversible damage.

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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.

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54
Q

Describe how alcohol can cause chronic pancreatitis.

A

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

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55
Q

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

A

IgG4.

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56
Q

How is autoimmune chronic pancreatitis treated?

A
  • stop drinking and smoking

It is very steroid responsive.

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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 (diabetes, steatorrhoea, malnutrition).
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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.
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59
Q

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

A

Diabetes mellitus.

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60
Q

What is the treatment for chronic pancreatitis?

A
  1. analgesia - Opiates in a controlled environment for severe pain.
  2. stop smoking and alcohol
  3. replacement of pancreatic enzymes, sub cut insulin, ERCp with stunting (biliary obstruction), surgery
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61
Q

Give 4 functions of the liver.

A
  1. Bile production and excretion
  2. Excretion of bilirubin, cholesterol and drugs
  3. Metabolism of fat, proteins + carbs
  4. Enzymes activation
  5. Storage of glycogen, vitamins + minerals
  6. Synthesis of plasma proteins (albumin) + clotting factors
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62
Q

Name 4 things that liver function tests measure.

A
  1. Serum bilirubin.
  2. Serum albumin.
  3. Pro-thrombin time
  4. liver enzymes (ALT, ALP, AST)
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63
Q

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

A

Alkaline phosphatase.

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64
Q

What enzymes increase in the serum in hepatocellular liver disease?

A

Transaminases e.g. AST and ALT.

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65
Q

Name two hepatocellular enzymes.

A

Transaminases e.g. AST and ALT.

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66
Q

Name a cholestatic enzyme.

A

Alkaline phosphatase.

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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
  5. metabolic - haemochromatosis
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68
Q

Give 2 possible outcomes of acute liver disease.

A
  1. Recovery.

2. Liver failure.

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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.
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70
Q

Give 3 symptoms of acute liver disease.

A
  1. Malaise.
  2. Lethargy.
  3. Anorexia.
  4. Jaundice may develop later on.
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71
Q

Give 2 possible outcomes of chronic liver disease.

A
  1. Cirrhosis.

2. Liver failure.

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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.
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73
Q

What is Budd-Chiari syndrome?

A

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

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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.
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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?

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76
Q

Name a drug that can cause drug induced liver injury.

A
  1. Co-amoxiclav.
  2. Flucloxacillin.
  3. Erythromyocin.
  4. TB drugs.
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77
Q

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

A
  1. Low dose aspirin.
  2. Beta blockers.
  3. HRT.
  4. CCB.
  5. paracetamol
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78
Q

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

A

Glutathione transferase.

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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.

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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.
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81
Q

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

A

HFE - human haemochromatosis gene

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82
Q

Haemochromatosis is a genetic disorder. How is it inherited?

A

Autosomal recessive inheritance.

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83
Q

Describe the pathophysiology of haemochromatosis.

which organs it affects ?

A

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

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84
Q

What protein is responsible for controlling iron absorption?

A

Hepcidin.

Levels of this protein are decreased in haemochromatosis => loss of control

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85
Q

How might you diagnose someone with haemochromatosis?

A
  1. Raised ferritin and raised transferratin.
    - ferritin can be raised in inflamm so if both high then distinguishes iron overload from inflammation)
  2. HFE genotyping.
  3. Liver biopsy.
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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.
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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.

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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.

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89
Q

What can cause raised unconjugated bilirubin?

A

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

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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.

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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).

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92
Q

Describe the urine and stools in someone with cholestatic jaundice?

A

Dark urine and pale stools. There may be itching (pruritus due to bile salts) and LFT’s are abnormal.

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93
Q

Give 3 causes of duct obstruction.

A
  1. Gallstones (cholelithiasis)
  2. Stricture (narrowing) e.g. malignant, inflammatory.
  3. Carcinoma.
  4. Blocked stent.
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94
Q

Give 4 causes of hepatic jaundice.

A
  1. Viral hepatitis.
  2. Alcoholic hepatitis.
  3. Drugs.
  4. Cirrhosis.
  5. autoimmune hepatitis
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95
Q

Give 3 symptoms of jaundice.

A
  1. Biliary pain.
  2. Rigors - indicate an obstructive cause.
  3. Abdomen swelling.
  4. Weight loss.
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96
Q

What is ascites?

A

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

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97
Q

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

A
  1. Portal hypertension (cirrhosis)
  2. hypoalbuminaemia (nephrotic syndrome)
  3. malignant ascites (peritoneal mesothelioma)
  4. infectious peritonitis (TB)
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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.
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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.
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100
Q

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

A

Neutrophils and fat accumulation within hepatocytes.

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101
Q

What is non alcoholic steato-hepatitis (NASH)?

A

An advanced form of non-alcoholic fatty liver disease.

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102
Q

Give 3 causes of non-alcoholic fatty liver disease.

A

the usual stuff

  1. Type 2 diabetes mellitus.
  2. Hypertension.
  3. Obesity.
  4. Hyperlipidaemia.
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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.

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104
Q

Give 3 causes of cirrhosis.

A
  1. Alcohol!
  2. Hepatitis B and C.
  3. Autoimmune hepatitis
  4. Metabolic (haemachromotosis)

any chronic liver disease

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105
Q

What is the treatment of liver cirrhosis?

A
  1. Treat underlying cause (stop drinking alcohol, hep b) and manage complications (portal hypertension, hepatic encephalopathy, ascites)
  2. Screening for HCC (alphafetoprotein and ultrasound)
  3. High protein, low salt diet
  4. Consider transplant (MELD score)
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106
Q

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

A

75%.

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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.

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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).
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109
Q

What are the potential consequences of varices?

A

If they rupture -> haemorrhage.

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110
Q

What is the primary treatment for varices?

A

Endoscopic therapy - elastic band ligation

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111
Q

What is peritonitis?

A

Inflammation of the peritoneum often due to infection.

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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.
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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.

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114
Q

Name a bacteria that can cause spontaneous bacterial peritonitis.

A
  1. E.coli.
  2. klebsiella .pneumoniae.
  3. s.aureus
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115
Q

How can spontaneous bacterial peritonitis be diagnosed?

A

Is there ascites?

By looking for the presence of neutrophils in ascitic fluid.

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116
Q

Give 3 symptoms of peritonitis.

A
  1. Pain.
  2. Tenderness.
  3. Systemic symptoms e.g. nausea, chills, rigor.
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117
Q

Name a cause of pelvic inflammatory disease.

A

A complication of chlamydial infection.

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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.
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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.

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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.

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121
Q

Describe the pathophysiology of primary biliary cirrhosis.

A

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

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122
Q

Give 3 diseases associated with primary biliary cirrhosis.

A
  1. Thyroiditis.
  2. RA.
  3. Coeliac disease.
  4. UC
  5. Crohns

(Other autoimmune diseases).

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123
Q

Give 5 symptoms of primary biliary cirrhosis.

A
  1. Itching.
  2. Jaundice
  3. Fatigue
  4. Joint pains.
  5. Variceal bleeding.
  6. Xanthelasma (cholesterol deposits in skin)
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124
Q

What is the treatment for primary biliary cirrhosis?

A
  • Bile acid analogue (ursodeoxycholic acid)
  • immunosuppression steroids (prednisolone)
  • Anti pruritus (cholestyramine)
  • If end stage liver failure => Liver transplant
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125
Q

Give 5 risk factors for gallstone development.

A
  1. Female.
  2. Obese (fat).
  3. Fertile.
  4. Forties
  5. Flatulent
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126
Q

How can gallstones be removed from the gall bladder?

A

Laproscopic cholecystectomy.

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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.
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128
Q

What is ascending cholangitis?

A

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

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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)!
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130
Q

What is charcot’s triad?

A

It describes 3 common symptoms of ascending cholangitis:

  1. Fever.
  2. RUQ pain.
  3. Jaundice (cholestatic)!
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131
Q

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

A
  1. abdominal Ultrasound.
  2. Blood tests - LFT’s (raised transaminases)
  3. ERCP - definitive investigation.
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132
Q

Describe the management of ascending (acute) cholangitis.

A
  • Nil by mouth
  • IV fluid.
  • take blood cultures
  • IV antibiotics e.g. cefotaxime and metronidazole.
  • ERCP to remove stone blocking the bile duct
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133
Q

What is the difference between ascending cholangitis and acute cholecystitis?

A

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

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134
Q

What is acute cholecystitis?

A

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

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135
Q

Give 3 symptoms of acute cholecystitis.

A
  1. RUQ pain (+ guarding)
  2. Fever.
  3. Nausea, vomiting
  4. Raised inflammatory markers.
  5. NO JAUNDICE! (less common)
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136
Q

Give 3 risk factors for acute cholecystitis.

A
  1. History or gallstones
  2. Diabetes.
  3. prolonged episodes of fasting
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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.

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138
Q

Give 3 symptoms of primary sclerorsing cholangitis.

A
  1. Pruritus
  2. Fatigue
  3. Chronic RUQ pain
  4. Jaundice.

75% also have IBD.

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139
Q

What is biliary colic?

A

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

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140
Q

What can trigger biliary colic?

A

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

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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.
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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.
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143
Q

Give 3 ways in which diarrhoea can be prevented.

A
  1. Access to clean water.
  2. Good sanitation.
  3. Hand hygiene.
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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.

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145
Q

Give 3 causes of traveller’s diarrhoea.

A
  1. Enterotoxigenic e.coli (ETEC).
  2. Campylobacter.
  3. Norovirus.
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146
Q

Describe the pathophysiology of traveller’s diarrhoea.

A

ETEC => increased production of cAMP => increased secretion of Cl- into the intestinal lumen, H2O follows down as osmotic gradient -> diarrhoea.

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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.

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148
Q

What does EIEC stand for?

A

Enteroinvasive e.coli.

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149
Q

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

A

Enteropathogenic e.coli (EPEC).

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150
Q

What does EAEC stand for?

A

Enteroaggregative e.coli.

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151
Q

What does DAEC stand for?

A

Diffusely adherent e.coli.

152
Q

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

A

Rotavirus.

There is a vaccine - rotarix.

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 or 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.

gram stain

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.

can rupture => peritonitis

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 and inflammation in the diverticula. Can be due to surgical causes or infection

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.

  • fever, diarrhoea, nausea + vomiting, rectal bleeding
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 2 causes of contraction.

A
  1. Inflammation.

2. Intramural tumours.

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

Intestinal obstruction: give 3 causes of pressure.

A
  1. Adhesions.
  2. Volvulus.
  3. Peritoneal tumour.
175
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.

176
Q

Intestinal obstruction: what causes adhesions?

aetiology

A

Adhesions often form secondary to abdominal surgery.

177
Q

Intestinal obstruction: what is volvulus?

A

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

178
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.

179
Q

Give 4 common causes of small bowel obstruction in adults.

A
  1. Adhesions (surgery)
  2. Hernias.
  3. Crohn’s disease (gum to bum)
  4. Malignancy.
180
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.

181
Q

Give 3 common causes of small bowel obstruction in children.

A
  1. Appendicitis.
  2. Volvulus.
  3. Intussusception.
182
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.

183
Q

Define hernia.

A

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

184
Q

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

A

incarceration: can’t go back from herniated position
obstruction
strangulation: base of hernia becomes so tight => cuts of blood supply => ischaemia

185
Q

Give 2 symptoms of hernia.

A
  1. Pain.

2. Palpable lump.

186
Q

Give 5 symptoms of small bowel obstruction.

A
  1. Vomiting.
  2. Pain.
  3. Constipation.
  4. Distension.
  5. Tenderness.
187
Q

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

A

Proximal.

188
Q

Give 4 signs of small bowel obstruction.

A
  1. Vital signs e.g. increased HR, hypotension, raised temperature.
  2. Tenderness and swelling.
  3. dehydration
  4. Bowel sounds (early => hyperactive, late => hypoactive)
189
Q

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

A

Take good history (prep surgery => adhesions)

  1. CT
  2. ABG (raised lactate => poor tissue perfusion
  3. FBC (raised WBC)
  4. elevated inflammatory markers
190
Q

What is the management/treatment for small bowel obstruction?

A
  1. Fluid resuscitation
  2. Analgesia (morphine)
  3. Nasogastric decompression
  4. treat underlying cause
  5. Surgery e.g. laparotomy, bypass segment, resection.
191
Q

Give 2 common causes of large bowel obstruction.

A
  1. Colorectal malignancy.

2. Volvulus (especially in the developing world).

192
Q

Give 5 symptoms of large bowel obstruction.

A
  1. Tenesmus.
  2. Constipation.
  3. Abdominal discomfort.
  4. Bloating.
  5. Vomiting.
  6. Weight loss.
193
Q

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

A 
lifethreatening surgical emergency
1. CT scan (urgent)
2 .Lower gastrointestinal endoscopy or flexible sigmoidoscopy (confirm diagnosis)
3. FBC (raised WBC)
4. CRP: raised
194
Q

Describe the management for a large bowel obstruction.

A
  1. Nil by mouth
  2. Supplement O2.
  3. IV fluids to replace losses and correct electrolyte imbalance.
  4. Urinary catheterisation to monitor urine output.
  5. emergency surgery
195
Q

Give 2 consequences of untreated intestinal obstructions.

A
  1. Ischaemia => necrosis

2. Perforation.

196
Q

Describe the progression from normal epithelium to colorectal cancer.

A
  1. Normal epithelium.
  2. Adenoma.
  3. Colorectal adenocarcinoma.
  4. Metastatic colorectal adenocarcinoma.
197
Q

Define adenocarcinoma.

A

A malignant tumour of glandular epithelium.

198
Q

How can adenoma formation be prevented?

A

NSAIDS are believed to prevent adenoma formation.

199
Q

What is the treatment for adenoma?

A

removal - Endoscopic resection.

200
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.

201
Q

What is the treatment for metastatic colorectal adenocarcinoma?

A

Chemotherapy and palliative care.

202
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.
203
Q

Give 5 risk factors for colorectal cancer.

A
  1. Low fibre diet.
  2. Increasing age
  3. Alcohol.
  4. Smoking.
  5. A PMH of adenoma or ulcerative colitis.
  6. A family history of colorectal cancer; FAP or HNPCC.
204
Q

What can affect the clinical presentation of a colorectal cancer?

A

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

205
Q

Give 3 signs of rectal cancer.

A
  1. PR bleeding.
  2. Mucus.
  3. Thin stools.
  4. Tenesmus.
206
Q

Give 2 signs of a left sided/sigmoid cancer.

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

2. PR bleeding.

207
Q

Give 3 signs of a right sided cancer.

A
  1. Anaemia.
  2. Mass.
  3. Diarrhoea that doesn’t settle.
208
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.

209
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.

210
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.
- Staging CT scan (thorax + abdo + pelvis to look for metastases)

  • Faecal occult blood is used in screening but not diagnosis.
211
Q

Give 5 non-infective causes of diarrhoea.

A
  1. Neoplasm.
  2. Inflammatory.
  3. Irritable bowel.
  4. Radiation.
212
Q

Give 3 infective causes of dysentery.

A
  1. Shigella.
  2. Salmonella.
  3. Campylobacter.
  4. E.coli 0157.
213
Q

Give 2 infective causes of non-bloody diarrhoea.

A
  1. Rotavirus.

2. Norovirus.

214
Q

Describe the chain of infection.

A

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

215
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.
216
Q

What is the treatment for vibrio cholerae infection?

A

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

217
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.
218
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.
219
Q

Give 3 causes of peptic ulcers.

A
  1. Prolonged NSAID or steroid use -> decreased mucin production.
  2. H.pylori infection.
  3. Hyper-acidity (stress, alcohol, smoking, excess caffeine)
220
Q

Give 3 symptoms of peptic ulcers.

A
  1. epigastric discomfort, tenderness on palpation
  2. nausea and vomiting
  3. dyspepsia (indigestion)
  4. haematemesis + coffee ground vomit
  5. Iron deficiency anaemia (if prolonged bleeding)
221
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.
222
Q

Give 3 treatments for peptic ulcers.

A
  1. Stop NSAIDS.
  2. PPI’s e.g. omeprazole.
  3. H.pylori eradication.
223
Q

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

A
  1. Cardiopulmonary.

2. Small risk of bleeding or perforation.

224
Q

Give 3 indications for OGD.

A
  1. Dyspepsia.
  2. Dysphagia.
  3. Anaemia.
  4. Suspected coeliac disease.
225
Q

Give 3 indications for colonoscopy.

A
  1. Altered bowel habit.
  2. Diarrhoea +/- dysentery.
  3. Anaemia.
226
Q

Give 3 symptoms of GORD.

A
  1. Heart burn.
  2. Acid reflux.
  3. Dysphagia.
227
Q

Describe the pathophysiology of coeliac disease.

A

autoimmune antibodies made in response to gluten exposure => target epithelial cells of small intestine => inflammation (jejunum) => crypt hypertrophy + villous atrophy => malabsorption

228
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.
229
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.
  3. HLA-DQ2/HLA-DQ8 Genetic typing (good to rule out coeliac (if -ve))
230
Q

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

A

Can affect anywhere from the mouth to anus (gum to bum)

but often terminal ileum

231
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.

232
Q

Give 5 complications of Crohn’s disease.

A
  1. Malabsorption.
  2. abscess formation
  3. Obstruction.
  4. Perforation.
  5. Anal fissures.
  6. Neoplasia.
233
Q

Give 3 complications of ulcerative colitis.

A
  1. Colon: blood loss and colorectal cancer.
  2. Arthritis.
  3. primary sclerosing cholangitis.
234
Q

Give an example of a functional bowel disorder.

A

IBS.

235
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).
236
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.
237
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.
238
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.
239
Q

Describe the treatment for mild IBS.

A

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

240
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.
241
Q

Describe the treatment for severe IBS.

A

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

242
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.

243
Q

What is the criteria for dyspepsia?

A

> 1 of the following:

  • Postprandial fullness.
  • Early satiation.
  • Epigastric pain/burning.
244
Q

Give 5 causes of dyspepsia.

A
  1. Excess acid.
  2. Prolonged NSAIDS.
  3. Large volume meals.
  4. Obesity.
  5. Smoking/alcohol.
  6. Pregnancy.
245
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.
246
Q

What investigations might you do in someone with dyspepsia?

A
  1. Endoscopy.
  2. Gastroscopy.
  3. Barium swallow.
  4. Capsule endoscopy.
247
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.
248
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.
249
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.
250
Q

Describe the treatment for GORD.

A
  1. PPI.
  2. Lifestyle modification.
  3. Anti-reflux surgery.
251
Q

Give a potential consequence of anterior ulcer haemorrhage.

A

Acute peritonitis.

252
Q

Give a potential consequence of posterior ulcer haemorrhage.

A

Pancreatitis.

253
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.
254
Q

Describe the treatment for gastritis.

A
  1. Reduced mucosal ischaemia.
  2. PPI.
  3. H2RA.
  4. Enteric coated aspirin.
255
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.
256
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.
257
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.

258
Q

Malabsorption: what can cause insufficient absorptive area?

A
  1. Coeliac disease.
  2. Crohn’s disease.
  3. Extensive parasitisation.
  4. Small intestine resection.
259
Q

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

A

Lactose intolerance - disaccharide enzyme deficiency.

260
Q

Malabsorption: what can cause lymphatic obstruction?

A
  1. Lymphoma.

2. TB.

261
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).

No blood or mucus
Entire GI tract offended (gum to bum)
Smoking - risk factor
Terminal ileum most affected
Skip lesions
262
Q

Describe the distribution of inflammation seen in ulcerative colitis.

A

Continuous inflammation affecting only the mucosa, from rectum proximally

263
Q

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

A

Just the mucosa.

264
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.

265
Q

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

A

crohns: steroids

UC: aminosalicylate

266
Q

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

A

Gliadin.

267
Q

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

A

Duodenum.

268
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.

269
Q

What is the prevalence of coeliac disease?

A

1%.

270
Q

What cells normally line the oesophagus?

A

Stratified squamous non-keratinising cells.

271
Q

What is Barrett’s oesophagus?

A

When squamous cells undergo metaplastic changes and become columnar cells.

272
Q

What can cause Barrett’s oesophagus?

A
  1. GORD.

2. Obesity.

273
Q

Give a potential consequence of Barrett’s oesophagus.

A

Adenocarcinoma.

274
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.
275
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.
276
Q

Give 3 causes of squamous cell carcinoma (oesophageal)

A
  1. Smoking.
  2. Alcohol.
  3. Poor diet.
277
Q

What can cause oesophageal adenocarcinoma?

A

Barrett’s oesophagus.

278
Q

Give 3 causes of gastric cancer.

A
  1. Smoked foods.
  2. Pickles.
  3. H.pylori infection.
  4. Pernicious anaemia.
279
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.

280
Q

Give 3 causes of oesophageal carcinoma.

A
  1. GORD -> Barrett’s.
  2. Smoking.
  3. Alcohol.
281
Q

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

A
  1. Barium swallow.

2. Endoscopy.

282
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.
283
Q

Give 3 signs of gastric cancer.

A
  1. Weight loss.
  2. Anaemia.
  3. Vomiting blood.
  4. Melaena.
  5. Dyspepsia.
284
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.

285
Q

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

A
  1. Endoscopy.
  2. CT.
  3. Laparoscopy.
286
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.

287
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.

288
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.

289
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.

290
Q

Give 3 symptoms of spontaneous bacterial peritonitis.

A
  1. Dull to percussion.
  2. Temperature.
  3. Abdominal pain
  4. signs of ascites
291
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. diagnostic paracentesis
292
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).
293
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.

294
Q

What is the management for peritonitis?

A
  1. ABC.
  2. Treat the underlying cause!
  3. antibiotic therapy
  4. Analgesia
  5. Call a surgeon.
295
Q

What can cause exudative ascites?

A

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

296
Q

What can cause transudative ascites?

A

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

297
Q

Give 2 signs of ascites.

A
  1. Flank swelling.
  2. Dull to percuss and shifting dullness
  3. abdo distension
  4. jaundice
298
Q

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

A
  1. Ultrasound, CT or MRI

2. Ascitic tap.

299
Q

Describe the treatment for ascites.

A
  1. Restrict sodium.
  2. anti aldosterone Diuretics (spironolactone)
  3. Drainage.
  4. prophylactic Abx
300
Q

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

A

In the descending/sigmoid colon and rectum.

301
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.

302
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.
303
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.

304
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.
305
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.
306
Q

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

A
  1. Ataxia.
  2. Opthalmoplegia (extraocular muscle palsy)
  3. Confusion.
307
Q

How can Wernicke’s encephalopathy be reversed?

A

Give IV thiamine.

308
Q

What histological stain can be used for haemochromatosis?

A

Perl’s stain.

309
Q

Name 4 fat soluble vitamins.

A

A, D, E and K.

310
Q

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

A

Acute cholecystitis has an inflammatory component!

311
Q

What is the treatment for acute cholecystitis?

A
  • Bill by mouth (rest gall bladder)
  • IV fluids
  • IV Abx
  • IRCP (remove stones trapped in CBD)
  • Laparoscopic cholecystectomy (GB removal)
312
Q

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

A

Because there is a build up of bilirubin.

313
Q

Give 3 components of gallstones.

A
  1. Cholesterol.
  2. Bile pigment.
  3. Phospholipid.
314
Q

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

A

Ultrasound!

ERCP.

315
Q

Are most liver cancers primary or secondary?

A

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

316
Q

Where have most secondary liver cancers arisen from?

A
  1. The Gi tract.
  2. Breast.
  3. Bronchus.
317
Q

Describe the aetiology of HCC.

A

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

318
Q

Give 5 symptoms of HCC.

A
  1. Weight loss.
  2. Anorexia.
  3. Fever.
  4. Malaise.
  5. Ascites.
319
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.
320
Q

Describe the treatment for HCC.

A
  1. Surgical resection of solitary tumours.
  2. Liver transplant.
  3. Percutaneous ablation.
321
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.

322
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.

323
Q

Give 3 symptoms of haemochromatosis.

A
  1. Hepatomegaly.
  2. Cardiomegaly.
  3. Diabetes mellitus.
  4. Hyperpigmentation of skin.
  5. Lethargy.
324
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.
325
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.
326
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.

327
Q

Give 4 complications of liver failure.

A
  1. Hepatic encephalopathy.
  2. Abnormal bleeding.
  3. Jaundice.
  4. Ascites.
328
Q

Describe the treatment for liver failure.

A
  1. Nutrition.
  2. Supplements.
  3. Treat complications.
  4. Liver transplant.
329
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.

330
Q

Describe the treatment for spontaneous bacterial peritonitis.

A

Cefotaxime and metronidazole.

331
Q

Give 5 symptoms of ruptured varices.

A
  1. Haematemesis.
  2. Melaena.
  3. Abdominal pain.
  4. Dysphagia.
  5. Anaemia.
332
Q

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

A

They would have anti-HBVs IgG in their serum.

333
Q

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

A

Macrocytic anaemia.

334
Q

Name a protozoa that can cause amoebic liver abscess?

A

Entemoeba histolytica.

335
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.

336
Q

What is the treatment for entemoeba histolytica?

A

Metronidazole.

337
Q

What is the treatment for mild/moderate UC?

A

Mesalazine.

338
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.

339
Q

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

A

IV N-Acetyl-Cysteine.

340
Q

With which disease would you associate Reynold’s pentad?

A

Ascending cholangitis.

341
Q

Describe Reynold’s pentad.

A
  • Charcot’s triad (fever, RUQ pain and jaundice).
    • hypotension.
    • altered mental state.
342
Q

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

A

Gastric cancer.

343
Q

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

A

Duodenal ulcer.

344
Q

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

A

Pancreatitis or AAA.

345
Q

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

A

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

346
Q

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

A

Mallory bodies.

347
Q

What feature seen on liver biopsy is diagnostic of cirrhosis?

A

Nodular regeneration.

348
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.

349
Q

What is the treatment for Wilson’s disease.

A

Lifetime treatment with penicillamine.

350
Q

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

A
  1. High portal venous pressure.

2. Low serum albumin.

351
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.

352
Q

Why is morphine contraindicated in acute pancreatitis?

A

Morphine increases sphincter of Oddi pressure and so aggravates pancreatitis.

353
Q

What two enzymes, if raised, suggest pancreatitis?

A

LDH and AST.

354
Q

Where is folate absorbed?

A

In the jejunum.

355
Q

Where is vitamin B12 absorbed?

A

In the terminal ileum.

356
Q

Where is iron absorbed?

A

In the duodenum.

357
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.

358
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.
359
Q

What lymph nodes can oesophageal carcinoma commonly metastasise to?

A

Para-oesophageal lymph nodes.

360
Q

What hormone is responsible for the production of gastric acid?

A

Gastrin.

361
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.
362
Q

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

A

Hypoalbuminaemia.

363
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.
364
Q

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

A
  1. FBC.

2. ESR/CRP.

365
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.

366
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.

367
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.
368
Q

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

A
  1. NSAIDs.
  2. Diuretics.
  3. Steroids.
369
Q

What 2 products does haem break down in to?

A

Haem -> Fe2+ and biliverdin.

370
Q

What enzyme converts biliverdin to unconjugated bilirubin?

A

Biliverdin reductase.

371
Q

What is the function of glucuronosyltransferase?

A

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

372
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.

373
Q

What does conjugated bilirubin form?

A

Urobilinogen.

374
Q

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

A

Intestinal bacteria.

375
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.
376
Q

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

A

Crohn’s.

2a (12 decks)

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