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2A > Liver & GI > Flashcards

Liver & GI Flashcards

1
Q

How long does hepatitis persist for to be deemed chronic?

A

6 months.

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2
Q

What are the simple stages that precede liver failure?

A

Hepatitis → fibrosis → compensated cirrhosis → decompensated cirrhosis (end stage liver failure)

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3
Q

Give 3 infective causes of acute hepatitis.

A

Hepatitis A to E infection.
EBV.
CMV.
Toxoplasmosis.

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4
Q

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

A

Alcohol.
Drugs.
Toxins.
Autoimmune.

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5
Q

Give 3 presentations of acute hepatitis.

A
  1. Malaise
  2. Nausea
  3. Anorexia
  4. Jaundice

Rarer:
1. Confusion
2. Bleeding
3. Liver pain

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6
Q

Give 3 infective causes of chronic hepatitis.

A

Hepatitis B (+/-D).
Hepatitis C.
Hepatitis E.

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7
Q

Give 3 presentations of chronic hepatitis

A
  1. Ascites
  2. Oedema
  3. Haematemesis (varices)
  4. Malaise
  5. anorexia
  6. wasting
  7. easy bruising
  8. itching
  9. hepatomegaly
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8
Q

Name 3 things that liver function tests measure.

A
  1. Serum bilirubin.
  2. Serum albumin.
  3. Pro-thrombin time.
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9
Q

What enzymes increase in the serum in hepatocellular liver disease?

A

Transaminases

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10
Q

What is jaundice

A

Raised serum bilirubin.
Can be prehepatic (unconjugated) ie haemolysis, Gilberts

Hepatic (conjugated) ie hepatitis: viral, drugs, immune, alcohol

Post-hepatic (conjugated) ie gallstone: bile duct, structure: malignant, ischaemic, inflammatory

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11
Q

Describe the urine, stools, itching, and liver 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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12
Q

Describe the urine, stools, itching, and liver in someone with post-hepatic jaundice?

A

Dark urine, stools may be pale. May be itching, abnormal LFT

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13
Q

Tests for jaundice?

A

Liver enzymes: very high AST/ALT suggests liver disease, some exceptions

Biliary obstruction: 90% have dilated intrahepatic bile ducts on ultra sound

Need further imaging:
CT
MRCP
ERCP

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14
Q

Where are most gallstones formed?

A

Gallbladder

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15
Q

What are gallstones made up of?

A

70% cholesterol
30% pigment
+/- calcium

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16
Q

Risk factors for gallstones

A

5F’s
Female, fat, fertile, forty, Fair

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17
Q

Gallstones in gallbladder vs bile duct

A

Cholecystitis in gallbladder but not bile duct

Obstructive jaundice seen in bile duct and sometimes in gallbladder

Cholangitis seen in bile duct but not gallbladder

Pancreatitis seen in bile duct but not gallbladder

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18
Q

Gallstones management

A

If symptomatic:
Gallbladder stones:
- laparoscopic cholecystectomy
- Bile acid dissolution therapy (<1/3 success)

Bile duct stones:
- ERCP with sphincterotomy and removal crushing stent placement

  • surgery (large stones)
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19
Q

What is isoniazid? What common side effect is there?

A

Isoniazid is commonly used to treat tuberculosis.

Common side effect: acute liver injury with jaundice

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20
Q

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

A

“What did you start recently?”
onset usually 1-12 weeks of starting

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21
Q

Name a drug that can cause drug induced liver injury.

A
  1. Augmentin.
  2. Flucloxacillin.
  3. Erythromycin.
  4. TB drugs.
  5. Acetaminophen
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22
Q

UK general practice DILI study: What drugs are found to be not involved in drug induced liver injury?

A
  • Low dose aspirin
  • NSAIDs other than Diclofenac
  • Beta blockers
  • HRT
  • ACE inhibitors
  • Thiazides
  • CCBs
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23
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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24
Q

Management of paracetamol induced fulminant hepatic failure?

A
  • N acetyl Cysteine (NAC)
  • Supportive to correct
    1. coagulation defects
    2. fluid electrolyte and acid base balance
    3. renal failure
    4. hypoglycaemia
    5. encephalopathy
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25
Q

What may indicate that paracetamol induced liver failure is severe?

A

Late presentation (NAC less effective >24 hours)

Acidosis (pH <7.3)

Prothrombin time >70 s

Serum creatinine > 300 umol/l

Consider emergency liver transplant: otherwise 80% mortality

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26
Q

What is ascites?

A

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

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27
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.
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28
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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29
Q

Ascites management?

A
  1. Restrict fluid and sodium
  2. Diuretics. - especially spironolactone +/- furosemide
  3. Drainage.
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30
Q

Stages of alcoholic liver disease?

A
  1. Drinking Alcohol leads to Steatosis (fatty liver, undamaged)
  2. Drinking more alcohol leads to inflammation
  3. Alcoholic hepatitis (with mallory bodies)
  4. Alcoholic Cirrhosis (micronodular)
  5. Hepatocellular carcinoma
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31
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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32
Q

What is non alcoholic steato-hepatitis (NASH)?

A

An advanced form of non-alcoholic fatty liver disease.

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33
Q

Give 3 causes of non-alcoholic fatty liver disease.

A
  1. Type 2 diabetes mellitus.
  2. Hypertension.
  3. Obesity.
  4. Hyperlipidaemia.
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34
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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35
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.
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36
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.
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37
Q

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

A

75%

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38
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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39
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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40
Q

What are the potential consequences of varices?

A

If they rupture ->haemorrhage.

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41
Q

What is the primary treatment for varices?

A

Endoscopic therapy - banding.

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42
Q

Why do patients with chronic liver disease ‘go off’?

A

Common causes:
1. Constipation
2. Drugs - sedatives, analgesics, NSAIDs, diuretics, ACE blockers
3. Gastrointestinal bleed
4. Infection
5. HYPO
6. Alcohol withdrawal

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43
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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44
Q

How can spontaneous bacterial peritonitis be diagnosed?

A

By looking for the presence of neutrophils in ascitic fluid.

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45
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.

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46
Q

Describe the treatment for spontaneous bacterial peritonitis.

A

Cefotaxime and metronidazole.

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47
Q

Causes of renal failure in liver disease

A

Drugs:
1. diuretics
2. NSAIDs
3. ACE inhibitors
4. Aminoglycosides

Infection
GI bleeding
Myoglobinuria
Renal tract obstruction

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48
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.

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49
Q

Bedside tests for encephalopathy

A

Serial 7’s
WORLD backwards
Animal counting in 1 minute
Draw 5 point star
Number connection test

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50
Q

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

A
  1. Ataxia.
  2. Opthalmoplegia.
  3. Confusion.
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51
Q

How can Wernicke’s encephalopathy be reversed?

A

Give IV thiamine.

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52
Q

What to do if a liver patient has ‘gone off’?

A
  1. ABC airways, breathing, circulation
  2. Look at chart - vital signs, O2, BM (glucose), drug chart
  3. Look at patient - focus of infection? Bleeding?
  4. Tests - FBC, U&E, blood cultures, ascitic fluid clotting, LFTs
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53
Q

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

A

IgG4.

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54
Q

How is autoimmune chronic pancreatitis treated?

A

It is very steroid responsive.

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55
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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56
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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57
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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58
Q

Give 3 diseases associated with primary biliary cirrhosis.

A
  1. Thyroiditis.
  2. RA.
    3.Coeliac disease.
    Lung disease.
    (Other autoimmune diseases).
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59
Q

Give 5 symptoms of primary biliary cirrhosis.

A
  1. Itching.
  2. Fatigue.
  3. Dry eyes,
  4. Joint pains.
  5. Variceal bleeding.
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60
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.

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61
Q

Treatment of cholestatic itch

A

Cholestyramine
UDCA, antihistamines - little help
Rifampicin effective - occasionally damages liver

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62
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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63
Q

Give 3 symptoms of primary sclerosing cholangitis.

A
  1. Itching.
  2. Rigor.
  3. Pain.
  4. Jaundice.
    75% also have IBD.
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64
Q

What is biliary colic?

A

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

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65
Q

What can trigger biliary colic?

A

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

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66
Q

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

A

HFE gene

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67
Q

Haemochromatosis is a genetic disorder. How is it inherited?

A

Autosomal recessive

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68
Q

Describe the pathophysiology of haemochromatosis.

A

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

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69
Q

What protein is responsible for controlling iron absorption?

A

Hepcidin.

Levels of this protein are decreased in haemochromatosis.

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70
Q

How might you diagnose someone with haemochromatosis?

A

Raised ferritin.
HFE genotyping.
Liver biopsy.

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71
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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72
Q

What is Budd-Chiari syndrome?

A

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

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73
Q

How does normal flora discourage infection?

A
  1. Inhibiting overgrowth of endogenous pathogens
  2. Preventing colonisation by exogenous pathogens.
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74
Q

What is normal flora?

A

The community of microorganisms that live on another living organism without causing disease.

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75
Q

Name 3 things that can increase the risk of intraluminal infections?

A
  1. Less gastric acid (drugs such as PPIs)
  2. Broad spectrum antibiotics
  3. Raised gastric pH
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76
Q

Is C. Difficile Gram positive or negative?

A

Gram positive spore forming bacteria

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77
Q

How is C. diff treated?

A

Metronidazole or oral vancomycin. Sometimes can be treated by faecal transplant

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78
Q

Name a complication of C. diff

A

Pseudomembranous colitis

Recurrence rate is 25%
Faecal transplant to restore normal flora

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79
Q

List 3 infective causes of diarrhoea

A

Campylobacter
Salmonella
HIV
bacterial or amoebic dysentery
cholera

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80
Q

Bacterial causes of watery diarrhoea?

A

Bacteria:
Vibrio cholerae
E.Coli (ETEC)
Clostridium perfringens
Bacillus cereus
Staph. aureus

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81
Q

Viral causes of watery diarrhoea

A

Virus:
Rotavirus
Norovirus

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82
Q

Parasitic causes of watery diarrhoea?

A

Parasites:
Giardia
Cryptosporidium

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83
Q

Bacterial causes of bloody, mucoid diarrhoea? List 3

A

Shigella
E.Coli (EIEC, EHEC)
Salmonella enteritidis
V.parahaemolyticus
Clostridium difficile
Campylobacter jejuni

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84
Q

Parasitic causes of blood, mucoid diarrhoea?

A

Entamoeba histolytica

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85
Q

In the UK what is the major cause of diarrhoea?

A

50-70% of diarrhoea caused by viruses - rotavirus, norovirus

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86
Q

Define diarrhoea

A

Three or more loose or unformed stools a day

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87
Q

Give 3 causes of traveller’s diarrhoea.

A

Enterotoxigenic e.coli (30-70%)
Campylobacter (5-20%)
Shigella (5-20%)
Non-typhoidal Salmonella (5%)
V.parahaemolyticus (shellfish)
Viral (10-20%)
Protozoal (5-10% more chronic)
Cholera!

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88
Q

Which bacteria is the most common cause of traveller’s diarrhoea?

A

ETEC: enterotoxigenic E. coli

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89
Q

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

A

EHEC: EnteroHaemorrhagic

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90
Q

Which type of E. coli can cause dysentery like illness and is similar to Shigella?

A

EIEC: Enteroinvasive

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91
Q

Which E. colis’ are non invasive and cause watery diarrhoea due to adhesion to the luminal wall?

A

EPEC: EnteroPathogenic
EAEC: EnteroAggregative
DAEC: Diffusely Adherent

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92
Q

How would you describe cholera-related diarrhoea?

A

Profuse watery “rice water” diarrhoea up to 20L a day

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93
Q

How would you treat cholera infection?

A

Fluids and doxycycline

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94
Q

What is the gold standard for treating fluid loss as a result of acute diarrhoea?

A

Oral rehydration therapy

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95
Q

Name a helminth responsible for causing diarrhoeal infection.

A

Schistosomiasis.

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96
Q

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

A
  1. Microscopy
  2. Stool culture
  3. PCR
  4. Ova, cysts, parasites
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97
Q

List 3 red flags of Diarrhoea?

A

Dehydration
Electrolyte imbalance
Renal failure
Immunocompromise
Severe abdominal pain
Cancer risk factors
Over 50
Chronic diarrhoea
Weight loss
Blood in stool
FH cancer

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98
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.

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99
Q

How would you treat H. pylori infection?

A

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

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100
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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101
Q

Give 3 symptoms of acute cholecystitis.

A
  1. Gallbladder inflammation
  2. cystic duct obstruction by gall stones
  3. RUQ or epigastric pain
  4. fever
  5. leucocytosis
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102
Q

How can acute cholecystitis be diagnosed?

A

Ultrasound

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103
Q

Treatment of acute cholecystitis

A

Treatment: IV fluids, analgesia and antibiotics

Surgery: Cholecystectomy

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104
Q

What is ascending cholangitis?

A

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

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105
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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106
Q

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

A

Endoscopic retrograde cholangiopancreatography (ERCP)

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107
Q

Treatment of ascending cholangitis?

A

Prompt admission and IV antibiotics
ERCP
Cholecystectomy

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108
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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109
Q

Where would the pain be located in someone with a liver abscess?

A

RUQ

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110
Q

Name a bacteria that can cause liver abscess?

A

Faecal flora eg E.coli, Klebsiella spp

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111
Q

Name an amoeba that can cause liver abscesses?

A

Entamoeba histolytica

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112
Q

Hydatid that can cause liver abscesses?

A

Echinococcus granulosus (dog tapeworm)

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113
Q

What is peritonitis?

A

Inflammation of the peritoneum often due to infection.

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114
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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115
Q

Which bacteria causes enteric fever?

A

Salmonella (para)typhi

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116
Q

Where is the pain located in someone with enteric fever?

A

Generalised / R lower quadrant pain

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117
Q

Enteric fever symptoms

A

Generalised / R lower quadrant pain
High fever
“Relative bradycardia”
Headache and myalgia
Rose spots
Constipation/green diarrhoea

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118
Q

How is enteric fever diagnosed?

A

Through blood culture and bone marrow aspiration

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119
Q

Complications of enteric fever

A

GI bleed
Perforation/peritonitis
Myocarditis
Abscesses

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120
Q

Which organs count as upper GI

A

Oesophagus
Stomach
Duodenum

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121
Q

A patient presents with melaena for 3 days. What could this mean?

A

Melaena refers to the dark black faeces - associated with upper gastrointestinal bleeding.

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122
Q

What is haematemesis?

A

When a person begins to vomit blood

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123
Q

What is coffee ground vomiting?

A

As the name suggests, vomit that looks like coffee grounds. Can be a sign of internal bleeding

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124
Q

Likely causes of GI bleeding?

A

Peptic ulcer= most common (50%)
Oesophageal varices
Mallory-Weiss syndrome
Gastric carcinoma (uncommon)

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125
Q

How to manage patients with GI bleeds?

A

A B C D E
Airway
- is airway compromised
Breathing
- work of breathing
- need oxygen?
Circulation
- HR, BP
- Bloods
- IV fluids/blood transfusion?
Disability
- AVPU/GCS
- pupils
- blood sugar
Exposure
- active melaena/haematemesis

Do not forget to keep the patient nil by mouth

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126
Q

Scoring system for upper GI bleeds

A

Glasgow Blatchford Score
Score >0 means patient require admission for inpatient endoscopy
Score 0 means patient can be discharged

Most accurate in identifying risk patients in need of transfusion

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127
Q

How would you differentiate between variceal bleeds and non-variceal bleeds?

A

Variceal bleed:
1. suspect in patients with a history of liver disease of alcohol excess
2. antibiotics and Terlipressin reduces mortality
3. Endoscopy within 12 hours

Non-variceal bleed:
1. suspect in patients with a history of peptic ulcers, using certain medications; NSAIDs, anticoagulation or antiplatelets.
2. Consider proton pump inhibitors.
3. Endoscopy within 24 hours.

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128
Q

What is most important when it comes to GI bleeding?

A

Initial assessment and management rather than endoscopy in most cases

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129
Q

In the UK how often do you see upper GI bleeding?

A

Nearly one presentation every 6 minutes
= very common medical emergency

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130
Q

Endoscopy: How would you treat non variceal bleeds?

A
  1. Heater probe to cauterize it
  2. Hemoclip
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131
Q

Endoscopy: How would you treat variceal bleeds?

A

Banding - to cut the blood supply and stop bleeding

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132
Q

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

A
  1. Blockage.
  2. Contraction.
  3. Pressure.
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133
Q

Intestinal obstruction: give 3 causes of blockage.

A
  1. Tumour.
  2. Diaphragm disease.
  3. Gallstones in ileum (rare)
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134
Q

Intestinal obstruction: what is thought to cause diaphragm disease?

A

NSAIDS.

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135
Q

Intestinal obstruction: give 3 causes of contraction.

A
  1. Inflammation.
    - Crohn’s disease
    - Diverticular disease
  2. Intramural tumours.
  3. Hirschprung’s disease.
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136
Q

Describe how Crohn’s disease can cause intestinal obstruction.

A

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

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137
Q

Describe how Diverticular disease can cause intestinal obstruction?

A

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

138
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.

139
Q

What is small bowel obstruction?

A

Mechanical blockage of the small intestine.

140
Q

Symptoms of bowel obstruction

A
  1. Pain
  2. Distension
  3. Vomiting
  4. Constipation
141
Q

Causes of bowel obstruction

A
  1. Compression
  2. Occlusion
  3. Lack of peristalsis
142
Q

Intestinal obstruction: give 3 causes of compression.

A
  1. Adhesions.
  2. Tumour
  3. Hernia
143
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.

144
Q

Intestinal obstruction: what causes adhesions?

A

Adhesions often form secondary to abdominal surgery.

145
Q

Intestinal obstruction: give 3 luminal causes.

A

Growth - tumour
Foreign body - (digested or gallstone)
Structure - inflammatory, malignant, scarring

146
Q

Intestinal obstruction: give 3 causes of lack of peristalsis

A

Drugs - opioids
Low electrolytes
Neurological
Severe illness / post operative

147
Q

Signs of bowel obstruction upon examination

A

Distention
Tympanic
Tender
Hernias
Bowel sounds
Scars
PR

148
Q

Consequences of bowel obstruction

A

Issues with:
Nutrition
GI viability
Gut barrier / translocation
Fluid loss

149
Q

Investigations for bowel obstruction

A

Bloods
- FBC
- U&E
- CRP
- Lactate

Imaging
- AXR vs CT

150
Q

Treatment for small bowel obstruction

A

Decompression
Fluid replacement
Electrolyte replacement
Nutrition
Stent
Surgery

151
Q

Give 2 common causes of large bowel obstruction.

A

Colorectal malignancy.
2. Volvulus (especially in the developing world).

152
Q

Give 5 symptoms of large bowel obstruction.

A

Tenesmus.
Constipation.
Abdominal discomfort.
Bloating.
Vomiting.
Weight loss.

153
Q

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

A

Digital rectal examination.
Sigmoidoscopy.
Plain X-ray.
CT scan.

154
Q

Describe the management for a large bowel obstruction.

A

Fast the patient.
Supplement O2.
IV fluids to replace losses and correct electrolyte imbalance.
Urinary catheterisation to monitor urine output.

155
Q

Give 3 consequences of untreated intestinal obstructions.

A

Ischaemia.
Necrosis.
Perforation.

156
Q

What cells normally line the oesophagus?

A

What cells normally line the oesophagus?

157
Q

What is Barrett’s oesophagus?

A

When squamous cells undergo metaplastic changes and become columnar cells.

158
Q

What can cause Barrett’s oesophagus?

A
  1. GORD.
  2. Obesity.
159
Q

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

A

GORD damages normal oesophageal squamous cells.
Glandular columnar epithelial cells replace squamous cells (metaplasia).
Continuing reflux leads to dysplastic oesophageal glandular epithelium.
Continuing reflux leads to neoplastic oesophageal glandular epithelium - adenocarcinoma.

160
Q

Give 5 symptoms of oesophageal carcinoma.

A

Dysphagia.
Odynophagia (painful swallowing).
People often present very late.
Vomiting.
Weight loss.
Anaemia.
GI bleed.
Reflux.

161
Q

Give 3 causes of squamous cell carcinoma.

A

Smoking.
Alcohol.
Poor diet

162
Q

What can cause oesophageal adenocarcinoma?

A

Barrett’s oesophagus

163
Q

What can cause oesophageal squamous carcinoma?

A

Smoking.
Alcohol.

164
Q

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

A
  1. Barium swallow.
  2. Endoscopy.
165
Q

Describe the 2 treatment options for oesophageal cancer.

A

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.

Medically unfit and metastases = palliative care. Stents can help with dysphagia.

166
Q

Give 3 causes of gastric cancer.

A

Pickles.
H.pylori infection.
Smoked foods.
Pernicious anaemia.

167
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.

168
Q

Give 3 signs of gastric cancer.

A

Weight loss.
Anaemia.
Vomiting blood.
Melaena.
Dyspepsia.

169
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.

170
Q

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

A

Endoscopy.
CT.
Laparoscopy.

171
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.

172
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.

173
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.

174
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.

175
Q

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

A

In the descending/sigmoid colon and rectum.

176
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.

177
Q

Describe the progression from normal epithelium to colorectal cancer.

A

Normal epithelium.
Adenoma.
Colorectal adenocarcinoma.
Metastatic colorectal adenocarcinoma.

178
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.

179
Q

What is the treatment for metastatic colorectal adenocarcinoma?

A

Chemotherapy and palliative care.

180
Q

Give 5 risk factors for colorectal cancer.

A

Low fibre diet.
Diet high in red meat.
Alcohol.
Smoking.
A PMH of adenoma or ulcerative colitis.
A family history of colorectal cancer; FAP or HNPCC

181
Q

What can affect the clinical presentation of a colorectal cancer?

A

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

182
Q

How does familial adenomatous polyposis (FAP) cause colorectal cancer? (only counts for 1% of colorectal cancer)

A

Adenomatous polyposis coli (APC) complex can normally bind to beta catenin and break it down.

Mutation in the APC gene means that the APC protein cannot break down the beta catenin protein. Beta catenin translocate to nucleus binds to DNA and upregulates genes for epithelial proliferation and adenoma -> colorectal cancer

183
Q

How does hereditary nonpolyposis colorectal cancer HNPCC occur?

A

Abnormal DNA repair protein genes leads to no DNA repair protein produced, this leads to HNPCC.

184
Q

Reasons for identifying HNPCC cancers

A

Risk of further cancers in index patient and relatives
Possible implications for therapy
- tolerance of 5-FU etc
- do not recognise DNA damage
- apoptosis not activated

185
Q

Give 3 signs of rectal cancer.

A

PR bleeding.
Mucus.
Thin stools.
Tenesmus.

186
Q

Give 2 signs of a left sided/sigmoid cancer.

A

Change of bowel habit e.g. diarrhoea, constipation.
PR bleeding

187
Q

Give 3 signs of a right sided cancer.

A

Anaemia.
Mass.
Diarrhoea that doesn’t settle.

188
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.

189
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.

190
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.

191
Q

What is diarrhoea?

A

Frequent loose or watery stools,
> 3 times per day or more frequently than normal

192
Q

Non infective causes of diarrhoeal diseases (list 4)

A

Neoplasm
Inflammatory
Irritable bowel
Anatomical
Hormonal
Radiation
Chemical

193
Q

Infective causes of diarrhoeal diseases

A

Non-bloody
Bloody (Dysentery)

194
Q

Chain of infection

A

AGENT -> Mode of transmission -> Portal of entry -> HOST -> Person to person spread -> RESERVOIR -> Portal of exit

195
Q

27 year old student just returned from backpacking holiday around South Asia.
Presents with frequent bouts of diarrhoea, flatulence, nausea and abdominal discomfort.
Likely diagnosis?

A

Vibrio cholerae

196
Q

2 year old child presents with loose stools for 2 days. Miserable. Loss of appetite but drinking ok. No fever.
Attends nursery and playgroup.
Recently been to a petting zoo.
Likely diagnosis?

A

Animal contact -> likely Escherichia coli, Salmonella

197
Q

87 year old resident of a care home presents with confusion, altered consciousness, dehydration and a history of diarrhoea.
Likely diagnosis?

A

Norovirus, rotavirus

198
Q

When does norovirus usually occur?

A

In the winter

199
Q

Where does norovirus usually occur?

A

Hospitals
Care Homes
Schools
Cruise ships
Families

200
Q

36 year old man presents with bouts of low volume bloody stools.
He works in a take-away.
Likely diagnosis?

A

Shigella, Salmonella, E. coli,

201
Q

What bacteria cause food poisoning through toxin production?

A

bacillus cereus
clostridium perfringens

202
Q

A patient falls ill after 3-6 hrs of ingesting contaminated food. What is likely the culprit?

A

Toxin producing bacteria
eg bacillus cereus, clostridium perfringens

203
Q

A patient falls ill after 12-24 hrs of ingesting contaminated food. What is likely the culprit?

A

Viruses
eg norovirus, rotavirus

204
Q

A patient falls ill after 2-3 days of ingesting contaminated food. What is likely the culprit?

A

Bacteria
eg Salmonella, E. coli, Shigella

205
Q

84 year old patient at the Northern General Hospital presents with diarrhoea.
She is recovering from a surgical operation a few days ago.
Likely diagnosis?

A

Clostridium difficile

206
Q

What does Clostridium difficile cause in hospitalised patients?

A

Antibiotic-associated diarrhoea
Antibiotic-associated colitis
Pseudomembranous colitis

207
Q

Clostridium difficile prevention?

A

SIGHT
Suspect C diff as a cause of diarrhoea
Isolate the case
Gloves and aprons must be worn
Hand washing with soap and water
Test stool for toxin

208
Q

Clostridium difficile management

A

Control antibiotic usage
Esp. Ampicillin, amoxicillin & cephalosporins

Standard infection control procedures
- Surveillance & case finding
Any patient with diarrhoea
- Isolate
- Enteric precautions
- Test stool samples
- Environmental cleaning
- Treat cases with metronidazole or vancomycin

209
Q

Clostridium difficile investigation

A

Test stool samples for the toxin

Can also culture it (in order to identify which strain it is)

Tissue samples (histology) obtained at sigmoidoscopy

Don’t need to screen or treat asymptomatic carriers

210
Q

59 year old patient presents with altered bowel motions, increased frequency and mucous content.
Symptoms for the past 6 months.
Some weight loss and he reports nightsweats.
Likely diagnosis?

A

Bowel cancer

211
Q

Diarrhoeal Disease in Children

A

Frequent loose or watery stools,
> 3 times per day or more frequently than normal
most episodes are mild

Significant fluid loss can occur in children
if not replaced can lead to death
“What comes out must go in”

Wide range of causative organisms
Rotavirus contributes to 40% of hospital admissions
E. coli, Shigella, Campylobacter, Salmonella & Cryptosporidium

212
Q

Package of Prevention and Treatment Measures (WHO-UNICEF, 2004)

A

Prevention package
1. Rotavirus and measles vaccinations
2. Promote early & exclusive breastfeeding + Vitamin A supplementation
3. Promote hand washing with soap
4. Improved water supply quantity & quality, including treatment & safe storage of household water
5. Community-wide sanitation promotion.

Treatment package
1. Fluid Replacement to prevent dehydration
2. Zinc treatment

213
Q

Control Measures - Checklist for diarrhoea prevention (List 5)

A

Hand-washing with soap
Ensure availability of safe drinking water
Safe disposal of human waste
Breastfeeding of infants & young children
Safe handling and processing of food
Control of flies/vectors
Case management including exclusion
Vaccination

214
Q

At risk groups for diarrhoeal disease?

A

A – Persons of doubtful personal hygiene or with unsatisfactory hygiene facilities at home, work or school

B – Children who attend pre school or nursery

C – People whose work involves preparing or serving unwrapped/uncooked food

D – HCW/Social care staff working with vulnerable people

215
Q

Acute hepatitis symptoms?

A

Symptoms:
None or non-specific, e.g. malaise, lethargy, myalgia
Gastrointestinal upset, abdominal pain
Jaundice + pale stools / dark urine

216
Q

Acute hepatitis signs?

A

Signs:
Tender hepatomegaly ± jaundice
± signs of fulminant hepatitis (acute liver failure), e.g. bleeding, ascites, encephalopathy

217
Q

Acute hepatitis bloods?

A

Bloods:
Raised transaminases (ALT/AST&raquo_space; GGT/ALP) ± raised bilirubin

218
Q

Causes of acute hepatitis? (infection and non-infection)

A

Infection

Viral:
Hepatitis A, B ± D, C & E
Human herpes viruses, e.g. HSV, VZV, CMV, EBV
Other, e.g. influenza, SARS-CoV-2

Non-viral:
Spirochaetes, e.g. leptospirosis, syphilis
Mycobacteria, e.g. M. tuberculosis
Bacteria, e.g. bartonella
Parasites, e.g. toxoplasma

Non-infection

Drugs
Alcohol
Other toxins / poisoning
Non-alcoholic fatty liver disease
Pregnancy
Autoimmune hepatitis
Hereditary metabolic causes

219
Q

Patient with chronic hepatitis signs and symptoms?

A

Can be asymptomatic or have non-specific symptoms only

May have signs of chronic liver disease:
clubbing, palmar erythema, Dupuytren’s contracture, spider naevi, etc.

Transaminases (ALT/AST) can be normal

Compensated: liver function maintained
Decompensated: coagulopathy (↑PT, INR); jaundice (↑bilirubin); low albumin; ascites (± bacterial peritonitis); encephalopathy
Other complications: hepatocellular carcinoma (HCC); portal hypertension (varices, bleeding)

220
Q

Causes of chronic hepatitis (infectious and non-infectious?)

A

Infection:
Viral
Hepatitis B ± D, C (& E)

Non-infection:
Drugs
Alcohol
Other toxins / poisoning
Non-alcoholic fatty liver disease
Autoimmune hepatitis
Hereditary metabolic causes

221
Q

Hepatitis A transmission?

A

Faeco-oral transmission
Contaminated food & water
Linkage to access to safe drinking water & socioeconomic indicators

High income countries:
Travel
Sex (MSM)
Injecting drug use

222
Q

Hepatitis A incubation period?

A

Short incubation period: 15 to 50 days (usually 14 to 28 days)

223
Q

Hepatitis A symptoms?

A

Usually symptomatic in adults:
Pre-icteric phase: constitutional symptoms + abdominal pain
Icteric phase (few days to 1 week after pre-icteric phase)
Rarely fulminant hepatitis / acute liver failure (0.35%)

224
Q

Hepatitis A immunity after infection?

A

100% immunity after infection

225
Q

Hepatitis A serological response

A

In acute phase: anti-HAV IgM, then later on will develop anti-HAV IgG

226
Q

Hepatitis A: Management

A

Supportive

  1. Monitor liver function (INR, albumin, bilirubin, etc.)
  2. Acute liver failure (“fulminant hepatitis”) in <1%
    - liaise with hepatology / liver transplant centre
  3. Management of close contacts (vaccine)
  4. Primary prevention: vaccination
    e.g. travellers, MSMs, PWIDs
227
Q

Hepatitis E transmission?

A

4 genotypes
Faeco-oral transmission:
G1 & 2: contaminated food & water
G3 & 4: undercooked meat (mammalian zoonotic reservoir, including pigs)
Blood and organ transplant recipients

228
Q

Which type of Hepatitis E can lead to chronic infection?

A

G3 & 4

229
Q

Hepatitis E symptoms?

A

> 95% cases asymptomatic

Usually self-limiting acute hepatitis
fulminant hepatitis 3.3%
increased risk in pregnancy with GT1/2, especially 2nd and 3rd trimesters
occasional acute-on-chronic liver failure (high mortality)

Extra-hepatic manifestations, e.g. neurological

Risk of chronic infection (GT3/4 only) in immunosuppressed patients
e.g. transplant recipients, HIV patients
rapid progression to cirrhosis

230
Q

Hepatitis E: Management

A

Acute infection:
Supportive
Monitor for fulminant hepatitis / acute-on-chronic liver failure:
Liaise with hepatology / liver transplant centre
Consider ribavirin

Chronic infection (persistent HEV RNA > 6 months):
Reverse immunosuppression (if possible)
If HEV RNA persists, treat with ribavirin ≥ 3 months (2nd line: pegylated interferon-α)

231
Q

Hepatitis E serological response?

A

Acute phase: anti-HEV IgM, then anti-HEV IgG
Anti-HEV IgG gives some immunity but not 100% unlike Anti-HAV IgG

HEV RNA test used instead, as serology test unreliable in immunosuppressed patients

232
Q

Hepatitis E prevention?

A

Prevention:
Avoid eating undercooked meats (especially if immunocompromised)
Screening of blood donors
Vaccine available in China only (HEV 239 (Hecolin®) against HEV genotype 1

233
Q

Hepatitis B ± D transmission?

A

Blood-borne virus

Transmission via blood and body fluids:
Mother-to-child***
Household contact
Blood products
Iatrogenic
Occupational
Sexual
Injecting drug use

234
Q

Hepatitis B natural history (immunocompetent adults)

A

Acute HBV infection (95% spontaneous resolution) -> Chronic HBV infection -> Cirrhosis -> Decompensated cirrhosis + Hepatocellular carcinoma

235
Q

How does hepatitis B natural history differ in adults vs neonates and infants?

A

Only 10% spontaneous resolution in neonates and infants. 90% chance that it will progress to chronic HBV infection

236
Q

Hepatitis B serological response

A

Acute phase: Anti-HB core IgM
Anti-HB core IgG develops later on
If hepatitis B surface antigen present, it means that there is current HBV infection

237
Q

Acute Hepatitis B incubation period?

A

Incubation period: 30 to 180 days (mean 75 days)

238
Q

Acute Hepatitis B management

A

Supportive management
Monitor liver function (INR, albumin, bilirubin, etc.)
Rarely fulminant hepatitic failure: 0.1 to 0.5%
Oral nucleos(t)ide analogue (tenofovir, entecavir)
Liaise with hepatology / liver transplant centre
Management of close contacts (HBV vaccine if non-immune)

239
Q

Hepatitis B clearance

A

95% of adults will clear Hepatitis B
Will develop core and surface anti-HB antibodies

If develop chronic Hepatitis B
Will not develop anti-HB surface antibodies and Hepatitis B surface antigens will remain

240
Q

Chronic hepatitis B treatment

A

Treatment option 1: pegylated interferon-α 2a
Treatment option 2: oral nucleos(t)ide analogues
Inhibit viral replication
HBV DNA polymerase
One tablet once a day
High barrier to resistance
Minimal side effects
Renal monitoring (TDF)
May be required lifelong

241
Q

What two phases of chronic hepatitis B would you treat?

A

The immune reactive phase and immune escape phase

242
Q

Hepatitis B: Prevention (List 4)

A
  1. Antenatal screening (HBsAg testing) of pregnant mothers
    HBV vaccination administered to baby at birth and at 1, 2, 3, 4* and 12 months
    HBIG given to baby at birth if mother e-antigen positive and/or has high HBV DNA levels or baby birth weight <1.5kg
    tenofovir given to mother in pregnancy if high HBV DNA levels
  2. Universal childhood immunisation
    UK since 1st August 2017: hexavalent vaccine* at 8, 12 and 16 weeks
  3. Immunisation of healthcare workers + other risk groups (e.g. MSMs, PWIDs)
  4. Screening ± immunisation of sexual and household contacts
  5. Barrier contraception, PrEP (Tenofovir/Emtricitabine)
  6. Universal screening of blood products
  7. Sterile equipment and universal precautions in healthcare
243
Q

Hepatitis D transmission?

A

Blood-borne virus

Transmission via blood and body fluids:
Mother-to-child
Household contact
Blood products
Iatrogenic
Occupational
Sexual
Injecting drug use

244
Q

Hepatitis D test?

A

Test: Hepatitis D antibody: if positive, test HDV RNA

245
Q

Hepatitis D treatment

A

Treat: pegylated inteferon-α 48 weeks; buleviritide (Hepcludex®)(pending NICE)

246
Q

Hepatitis C transmission?

A

Blood-borne virus

Transmission via blood and body fluids:
Mother-to-child
Household contact
Blood products
Iatrogenic
Occupational
Sexual (MSM)
Injecting drug use***
Tattoos, piercings, etc.

247
Q

Hepatitis C natural history (immunocompetent adults)

A

Acute HCV infection (30% spontaneous resolution) -> Chronic HCV infection -> Cirrhosis -> Decompensated cirrhosis + Hepatocellular carcinoma

248
Q

Hepatitis C testing

A

HCV antibody* -> Reflex testing of
positive samples -> HCV RNA -> Reflex testing of positive samples -> HCV genotype

RNA testing is important as it allows you to see whether there is a current infection

249
Q

Hepatitis C treatment

A

Directly-acting antiviral (DAA) therapy

Glecaprevir/Pibrentasvir (Maviret®)
Elbasvir/Grazoprevir (Zepatier®)

250
Q

Hepatitis C: Prevention (List 5)

A

No vaccine
Previous infection does not confer immunity: can be re-infected
Screening blood products (in UK since 1991)
Universal precautions handling bodily fluids
Sterile medical equipment + safe disposal
Opiate addiction treatment (OAT), e.g. methadone, buprenorphine
Provision of sterile injecting equipment
Treatment and cure of “transmitters”, e.g. active PWIDs
Safe sex, e.g. condoms

251
Q

Mr JB is a 24 year old man who initially presented to primary care with diarrhoea for 6 months. He has announced that he was allergic to gluten and blood tests were performed in primary care:
FBC: Hb 95 ↓
UE: Normal
LFT: Normal
IgA: Normal
IgA tTG: 69 (0-7) ↑

Seeing these results, what further procedure should be undertaken?

A

gastroscopy - remove tissue for biopsy
Villous atrophy indicates indicates celiac disease

252
Q

What is coeliac disease?

A

An autoimmune enteropathy caused by ingestion of gluten

253
Q

Which gene is linked with coeliac disease?

A

HLA type

254
Q

Coeliac disease management (list 3)

A

Gluten free diet - strict and lifelong
Dietitian review
Bone density assessment
Coeliac UK information
Prescription for gluten free foods - variable dependent upon location
Immunisations

255
Q

Risks of coeliac patients not going for a gluten free diet? (List 4)

A

Enteropathy associated T-cell lymphoma
Small bowel adenocarcinoma
Vitamin deficiencies
Osteoporosis
Hyposplenism
Malnutrition
Depression
Delayed puberty
Anaemia
Iron deficiency

256
Q

What conditions are commonly associated with coeliac disease?

A

Dermatitis herpetiformis (v common)
T1DM
Hashimoto’s thyroiditis

257
Q

Name 6 things that can break down the mucin layer in the stomach and cause gastritis.

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

How would you treat gastritis caused by mucosal ischaemia?

A
  1. reverse the mucosal ischaemia
  2. reduce the acid - H2 blocker/proton pump inhibitor
259
Q

How would you treat gastritis caused by aspirin/NSAIDS?

A

Enteric coated aspirin

260
Q

How would you treat gastritis caused by Helicobacter infection?

A

Antibiotics

261
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.
262
Q

Malabsorption: what can cause defective intra-luminal digestion?

A
  1. Pancreatic insufficiency due to pancreatitis, CF.
  2. Defective bile secretion due to biliary obstruction or ileal resection.
  3. Bacterial overgrowth.
263
Q

Malabsorption: what can cause insufficient absorptive area?

A
  1. Coeliac disease.
  2. Crohn’s disease.
  3. Extensive parasitisation.
  4. Small intestinal resection.
264
Q

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

A
  1. Lactose intolerance - disaccharide enzyme deficiency.
  2. Bacterial overgrowth - brush border damage
265
Q

Malabsorption: what can cause defective epithelial transport.

A
  1. Abetalipoproteinemia
  2. Primary bile acid malabsorption - mutations in bile acid transporter protein
266
Q

Malabsorption: What can cause lymphatic obstruction?

A
  1. Lymphoma
  2. Tuberculosis
267
Q

Which hormone causes the release of bile into the small intestine?

A

Cholecystokinin

268
Q

List 4 conditions associated with bile stones

A
  1. Biliary colic
  2. Gallstone ileus
  3. Cholecystitis
  4. Choledocholithiasis
  5. Cholangitis
  6. Mirrizzi syndrome
  7. Pancreatitis
269
Q

Gallstones: signs and symptoms of someone who has biliary colic?

A
  • post prandial colicky pain , worse with fats, right upper quadrant/epigastrium
  • nausea/vomiting
270
Q

Gallstones: signs and symptoms of someone who has cholecystitis?

A
  • constant pain
  • fever, rigors
271
Q

Gallstones: signs and symptoms of someone who has choledocholithiasis?

A

Jaundice

272
Q

Gallstones: signs and symptoms of someone who has cholangitis?

A
  • Jaundice
  • Fever > 39 °C
273
Q

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

A

Ultrasound!
Bloods: FBC, LFT, Coag, U+E, Amylase/lipase
ERCP
MRCP

274
Q

What is Mirizzi’s syndrome?

A

Obstruction of the common bile duct by external compression from multiple or a single large impacted gallstone in the Hartman’s pouch.

275
Q

Causes of pancreatitis

A

IGETSMASHED

I - Idiopathic
G - Gallstones
E - Ethanol
T - Trauma
S - Steroid use
M - Mumps
A - Autoimmune
S - Scorpions
H - Hypertriglyceridaemia/calcaemia
E - ERCP
D - Drugs

276
Q

Pancreatitis symptoms and signs

A
  • Severe central pain going to back
  • Nausea and vomiting
  • Fever
  • Oliguria
  • Jaundice
  • Cullen’s and Grey turners
277
Q

Complications of pancreatitis?

A

Auto digestion
- Haemorrhage
- Pseudoaneurysm
- Portal thrombosis
- Necrosis
- Infected necrosis
- Pseudocyst

Systemic inflammatory response system
- ARDS
- MOF

278
Q

Pancreatitis treatment?

A
  1. ANALGESIA!
  2. Catheterise and ABC approach for shock patients.
  3. Drainage of oedematous fluid collections.
  4. Antibiotics.
  5. Nutrition.
  6. Bowel rest.
279
Q

Give 2 potential complications of acute pancreatitis.

A
  1. Systemic inflammatory response syndrome.
  2. Multiple organ dysfunction.
280
Q

What is chronic pancreatitis?

A

Chronic inflammation of the pancreas leads to irreversible damage.

281
Q

What is the difference between ulcerative colitis and Crohn’s disease? Distribution

A

UC: continuous, starts distally from the rectum and extends proximally (pancolitis), only affects large bowel

CD: Patchy, anywhere from mouth to rectum, common in terminal ileum and right colon

282
Q

What is the difference between ulcerative colitis and Crohn’s disease? Mucosal inflammation

A

UC: superficial, continuous, denuded

CD: Transmural, patchy

283
Q

What is the difference between ulcerative colitis and Crohn’s disease? Histology

A

UC: cryptitis, crypt abscess

CD: 50-70% granulomas

284
Q

What is the difference between ulcerative colitis and Crohn’s disease? Fistula

A

UC: /

CD: Perianal, enteric

285
Q

What causes IBD?

A

Abnormal inflammatory response to gut bacteria in genetically susceptible individuals

286
Q

Management of ulcerative colitis?

A
  • Resuscitate
  • Prophylactic LMWH **
  • IV steroids (hydrocortisone 100mg 4x a day) **
  • Monitor BM
  • Stool cultures: exclude infections **
  • Stool chart
  • AXR
  • Flexible sigmoidoscopy
287
Q

Which criteria is used to assess ulcerative colitis?

A

Truelove and Witts criteria

288
Q

What type of medication is infliximab and ciclosporin?
What do they act on?

A

Anti-TNF Monoclonal antibodies used to treat IBD

Acts on transmembrane insoluble TNF and prevents them from binding to TNF receptors, reducing inflammation

289
Q

What surgery is done on patients with UC?

A

Subtotal colectomy.
- colon removed
- end ileostomy
- rectum remains

290
Q

Management of Crohn’s disease?

A
  • Resuscitate
  • Prophylactic LMWH**
  • IV steroids (hydrocortisone 100mg 4x a day) **
  • Monitor BM
  • Stool cultures: exclude infections**
  • Stool chart
  • AXR/MRE/CT AP
  • Triage: gastroenterology ward
291
Q

What surgery is done on patients with CD?

A

Right hemicolectomy
- remove diseased small bowel
- remove right side of colon

292
Q

What are Functional Gastrointestinal Disorders (FGIDs)?

A

Chronic GI symptoms in the absence of organic disease to explain the symptoms.

293
Q

What are the 2 most common FGIDs?

A

IBS (bowel)
Functional dyspepsia (stomach)

294
Q

What GI symptoms are associated with FGIDs?

A
  • Visceral hypersensitivity
  • Motility disturbances
  • Altered mucosal & immune
    function
  • Altered CNS processing
  • Altered gut microbiota
295
Q

IBS symptoms

A
  • Chronic frequent abdominal pain
  • Altered bowel habit
  • Bloating commonly associated
296
Q

Differential diagnosis for IBS?

A
  1. IBD
  2. Coeliac disease
  3. Chronic GI infections ie Giardiasis
  4. Colorectal cancer
  5. Ovarian cancer
297
Q

Endoscopies cannot be carried out for everyone with FGIDs why?

A
  • IBS and functional dyspepsia are very common
  • Endoscopies are invasive with appreciable risks
  • The diagnostic yield of serious pathology is low
  • Limit to those with alarm
    features
298
Q

When might you carry out further investigations for patients presenting with FGID symptoms?

A

Alarm features!
* Age >45 years
* Short history of symptoms
* Documented unintentional weight loss
* Nocturnal symptoms
* Family history of GI cancer/IBD
* GI Bleeding
* Palpable abdominal mass or lymphadenopathy
* Evidence of iron deficiency anaemia on blood
testing
* Evidence of inflammation on blood/stool testing

299
Q

What steps would you take to diagnose someone with functional dyspepsia?

A
  • Characteristics symptoms – chronic upper GI symptoms
  • Exclusion of organic pathology
    – History
    – Examination
    – 1st line investigations
    FBC,CRP, LFT, coeliac serology
    Stool Helicobacter pylori
    – 2nd line investigations in a subset with alarm features
    e.g.Upper GI endoscopy (OGD), Ultrasound abdomen
    CT scan (if suspect cancer)
300
Q

What steps would you take to diagnose someone with IBS?

A
  • Characteristics symptoms – chronic lower GI symptoms
  • Exclusion of organic pathology
    – History
    – Examination
    – 1st line investigations
    FBC,CRP, coeliac serology
    Stool faecal calprotectin
    Stool M,C & S
    Ca-125 in women (if appropriate)
    – 2nd line investigations in those with alarm features
    e.g. Lower GI endoscopy (Colonoscopy), CT scan (if suspect cancer
301
Q

What useful test can be used to differentiate between IBD and IBS?

A

Faecal calprotectin - sensitive marker that indicates GI inflammation = IBD

302
Q

What is the largest Cavity in the human body ?

A

Peritoneal Cavity

303
Q

Which organs are retroperitoneal organs?

A

SAD PUCKER:
S = Suprarenal (adrenal) Glands.
A = Aorta/IVC.
D =Duodenum (except the proximal 2cm, the duodenal cap)
P = Pancreas (except the tail)
U = Ureters.
C = Colon (ascending and descending parts)
K= Kidneys.
E = (O)esophagus.

304
Q

Function of Peritoneum normally

A

In health:
Visceral lubrication
Fluid & particulate absorption

305
Q

Function of peritoneum in disease

A

Pain perception.
Inflammatory and immune responses
Fibrinolytic activity

306
Q

Among the visceral and parietal peritoneum, which one is more sensitive to pain?

A

Parietal peritoneum - mores sensitive to pain

307
Q

What is peritonitis

A

Inflammation of peritoneum

308
Q

How can peritonitis be classified?

A

Onset:
- Acute: sudden onset
- Chronic: gradual onset

Source of origin:
- Primary: no source
- Secondary: bowel perforation, appendicitis

309
Q

Peritonitis causes (list 5)

A
  1. Bacterial, gastrointestinal and non-gastrointestinal
  2. Chemical, e.g. bile, barium
  3. Traumatic, e.g. operative handling
  4. Ischaemia, e.g. strangulated bowel, vascular occlusion
  5. Miscellaneous, e.g. familial Mediterranean fever
310
Q

Paths to Peritoneal Infection (list 4)

A
  1. Gastrointestinal perforation, e.g. perforated ulcer, appendix, diverticulum
  2. Transmural translocation (no perforation), e.g. pancreatitis, ischaemic bowel, primary bacterial peritonitis
  3. Exogenous contamination, e.g. drains, open surgery, trauma, peritoneal dialysis
  4. Female genital tract infection, e.g. pelvic inflammatory disease
  5. Haematogenous spread (rare), e.g. septicaemia
311
Q

Microorganisms in peritonitis (list 4)

A

Gastrointestinal source
- Escherichia coli
- Streptococci I —Enterococci
- Bacteroides spp. I —Clostridium spp.
- Klebsiella pneumoniae

Other sources
- Chlamydia trachomatis I Neisseria gonorrhoeae
- Haemolytic streptococci I—Staphylococci I—
Streptococcus pneumoniae
- Mycobacterium tuberculosis and other species
- Fungal infections

312
Q

Signs and symptoms of localised peritonitis

A
  • Pain
  • Nausea and vomiting
  • Fever
  • Tachycardia
  • Localised guarding
  • Rebound tenderness
  • Shoulder tip pain ( subphrenic)
  • Tender rectal and / or vaginal examination (pelvic peritonitis).
313
Q

Signs and symptoms of diffuse (generalised) peritonitis - early

A
  • Abdominal pain ( worse by moving or breathing)
  • Tenderness
  • Generalised guarding
  • Infrequent bowel sounds àcease ( paralytic ileus)
  • Fever
  • Tachycardia
314
Q

Signs and symptoms of diffuse (generalised) peritonitis - late

A
  • Generalised rigidity
  • Distension
  • Absent bowel sounds
  • Circulatory failure
  • Thready irregular pulse
  • (Hippocratic face)
  • Loss of consciousness
315
Q

Investigations for suspected peritonitis

A
  1. Urine dipstix for urinary tract infection.
  2. ECG if diagnostic doubt (as to cause of abdominal pain) or cardiac history.
  3. Bloods I U&Es I Full blood count (WCC)
  4. Serum amylase (acute pancreatitis/ others like perf DU)
  5. Group and save.
316
Q

Management of peritonitis

A
  1. Correction of Fluid Loss & Circulating Volume
  2. Antibiotics
  3. Urinary Catheterisation I Gastric Decompression
  4. Analgesics

Surgical treatment of cause when appropriate

317
Q

What is ascites?

A

Effusion and accumulation of serous fluid in the peritoneal cavity

318
Q

How is ascites classified?

A

Stage 1 detectable only after careful examination / Ultrasound scan (Mild)
Stage 2 easily detectable but of relatively small volume.
Stage 3 obvious, not tense ascites. (moderate)
Stage 4 tense ascites. (Large)

319
Q

What can cause exudative ascites?

A

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

320
Q

What can cause transudative ascites?

A

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

321
Q

Give 2 signs of ascites.

A
  1. Flank swelling.
  2. Dull to percuss and shifting dullness.
322
Q

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

A
  1. Ultrasound.
  2. Ascitic tap.
323
Q

Describe the treatment for ascites.

A

Restrict sodium.
Diuretics.
Drainage.

324
Q

Duke’s staging system: Duke’s A

A

Dukes’ A
The cancer is in the inner lining of the bowel. Or it is slightly growing into the muscle layer.

325
Q

Duke’s staging system: Duke’s B

A

The cancer has grown through the muscle layer of the bowel.

326
Q

Duke’s staging system: Duke’s C

A

The cancer has spread to at least 1 lymph node close to the bowel.

327
Q

Duke’s staging system: Duke’s D

A

Advanced bowel cancer
The cancer has spread to another part of
the body, such as the liver, lungs or bones.

328
Q

A 19 year old woman presents with abdominal pain and loose stool. Which of the following features suggest that she has irritable bowel syndrome?

A: Anaemia
B: Nocturnal diarrhoea
C: Abdominal pain relieved by defecation
D: Weight loss
E: Blood in stool

A

C: Abdominal pain relieved by defecation

329
Q

A 35 year old woman with a 6 month history of epigastric pain and fullness after meals. No history of weight loss or vomiting. She is a non smoker and does not drink alcohol. She was treated with PPI with no benefit. Upper GI endoscopy was normal including biopsies. What is the most likely diagnosis?

A

Functional dyspepsia

330
Q

What is the SAFE level of alcohol consumption?

A

0!
14 units is the advised units of alcohol that you shouldn’t exceed per week

331
Q

A 25 year old man presents to the hospital with abdominal pain and diarrhoea. CT scan shows inflammation in the transverse colon and terminal ileum. What is the most likely diagnosis?

A

Crohn’s disease

332
Q

A 71 year old man was admitted to hospital with pneumonia. He was treated with a week of Augmentin (Co-amoxiclav) for his pneumonia. On day 7 of his admission, he started having diarrhoea 10 times a day without any blood. He feels unwell and dehydrated. What is the likely organism responsible for his diarrhoea?

A

Clostridium difficile - commonly linked with antibiotic use. No blood.

333
Q

52 year old woman was referred by GP with fatigue and deranged LFTs (raised ALT and ALP). Normal ultrasound liver. Hepatitis screen negative, antimitochondrial antibodies +ve. What is the most likely diagnosis?

A

Primary biliary cholangitis.
(if you see antimitochondrial antibodies in question will almost ALWAYS be PBC)

334
Q

A 45 year old man with known alcohol related liver cirrhosis presents to hospital with 5 day history of black stools. He is apyrexial, oriented but jaundiced. Blood shows new anaemia and raised urea. Which treatment is likely to reduce his mortality risk?

  1. tranexamic acid
  2. omeprazole
  3. co-amoxiclav
  4. metoclopramide
  5. iron infusion
A
  1. co-amoxiclav
    Patient likely to have varices
    - bloody stool
    - liver cirrhosis

Best drug to give to patient would be Terlipressin which stops GI bleed. Co-amoxiclav is an antibiotic which prevents bacteria -> sepsis (thus reducing mortality risk)

335
Q

40 year old man was admitted to the hospital with a fever and abdominal pain. He drinks 50 units of alcohol per week. On examination he is jaundiced and having tremors, and his abdomen is soft but distended and slightly tender. What is the most likely diagnosis?

A

50 units of alcohol per week -> liver cirrhosis
Likely spontaneous bacterial peritonitis

336
Q

A 32 year old woman complains of a 6 month history of bloating and diarrhoea. What is the most likely diagnosis if her villi is flat upon histology?

A

Celiac disease

337
Q

a 75 year old man presents with pain in RUQ with rigors and fever. On examination he has RUQ tenderness but negative Murphy’s sign. Blood tests show high CRP and bilirubin. What is the next most appropriate test?

A

abdominal ultrasound

338
Q

What might RUQ pain indicate?

A

Just RUQ pain -> symptomatic gallstone
RUQ pain + fever -> acute cholecystitis
RUQ pain + jaundice -> common bile duct stone
RUQ pain + jaundice + fever -> ascending cholangitis

339
Q

A 43 year old man with a history of renal transplant presented with deranged LFTs after eating raw pork meat while on holiday. What is the most likely cause of his deranged LFTs?

A

Hepatitis E

340
Q

Dysplasia vs metaplasia?

A

Dysplasia: Morphological changes seen in cells in the progression to becoming cancer

Metaplasia: The change in differentiation of a cell from one fully-differentiated cell type to another

2A (7 decks)

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