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Phase 2a > Liver and GI (& GU!) > Flashcards

Liver and GI (& GU!) Flashcards

1
Q

Why does physiological neonatal jaundice occur?

A
  • foetal Hb broken down as it is replaced by adult Hb
  • liver metabolic pathways are immature and unable to conjugate bilirubin
  • bilirubin accumulates in the blood
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2
Q

What are some causes of unconjugated hyperbilirubinaemia?

A
  • haemolysis
  • impaired hepatic uptake
  • impaired conjugation
  • physiological newborn jaundice
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3
Q

What can cause impaired hepatic uptake of bilirubin?

A
  • drugs

- right heart failure causing hepatic venous congestion

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4
Q

What can cause impaired conjugation of bilirubin?

A
  • Gilbert’s syndrome - decreased UGT enzyme activity

- Crigler Najjar disease - mutation in UGT causing impairment or absence of the enzyme

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5
Q

Appearance of urine and stool in unconjugated hyperbilirubinaemia?

A
  • normal urine and stool
  • unconjugated bilirubin cannot be excreted via urine therefore urine not dark
  • stercobilin is not obstructed to stool is a normal colour
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6
Q

Appearance of urine and stool in conjugated hyperbilirubinaemia?

A
  • dark urine and pale stool
  • excessive conjugated bilirubin can be excreted in urine so urine is dark
  • obstruction of stercobilin / less bilirubin entering gut to become stercobilin (as it’s excreted in urine) causes pale stools
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7
Q

What is indicated by AST/ ALT to ALP ratio?

A
  • raised AST/ALT indicates hepatocellular disease

- raised ALP indicates cholestasis

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8
Q

What are some intra-hepatic causes of jaundice?

A
  • viruses
  • pregnancy
  • cirrhosis
  • alcohol
  • drugs
  • liver mets
  • metabolic syndromes
  • right heart failure
  • toxins
  • fungi
  • swelling
  • bile excretion abnormalities
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9
Q

What is the most common cause of peptic ulcers?

A

H. Pylori

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10
Q

Gram stain appearance of H. Pylori?

A

Gram negative.

Curved rods.

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11
Q

Treatment of H. Pylori?

A

Clarithromycin / metronidazole.
Amoxicillin.
PPI (omeprazole / lansoprazole).

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12
Q

What are some causes of peptic ulcers?

A
  • H. Pylori
  • increased stomach acid production
  • recurrent NSAID use
  • mucosa ischaemia
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13
Q

What are some risk factors for GORD?

A
  • obesity
  • hiatus hernia
  • smoking
  • pregnancy
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14
Q

What type of pain is characteristic of duodenal ulcers?

A

They cause pain several hours after eating and the pain gets better when eating.

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15
Q

Smoking and IBD?

A

Ulcerative colitis - protective.

Crohn’s - risk factor.

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16
Q

Risk factors for oesophageal cancer?

A
  • achalasia
  • alcohol
  • obesity
  • smoking
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17
Q

Where are the majority of colon cancers found?

A

Distal colon.

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18
Q

Causes of diverticulum (diverticulosis)?

A
  • low fibre diet
  • obesity
  • NSAIDs
  • smoking
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19
Q

What is shown on duodenal biopsy of a patient with coeliac disease?

A

Villous atrophy and crypt hyperplasia.

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20
Q

Causes of AKI?

A
  • acute tubular necrosis
  • hypovolaemia
  • nephrotoxins
    - prostate hyperplasia
  • sepsis
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21
Q

What is stage 1 CKD?

A

eGFR > 90 ml/min with evidence of tissue damage.

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22
Q

What is stage 2 CKD?

A

eGFR 60 - 89 ml/min.

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23
Q

What is stage 3a CKD?

A

eGFR 45 - 59 ml/min.

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24
Q

What is stage 3b CKD?

A

eGFR 30 - 44 ml/min.

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25
Q

What is stage 4 CKD?

A

eGFR 15 - 29 ml/min.

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26
Q

What is stage 5 CKD?

A

eGFR < 15 ml/min.

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27
Q

What are some risk factors for CKD?

A
  • diabetes
  • family history
  • old age
  • recurrent UTIs
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28
Q

Most common cause of pyelonephritis?

A

E. Coli

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29
Q

First-line treatment of lower UTI in pregnant women?

A

Nitrofurantoin

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30
Q

When should nitrafurantoin be avoided in pregnant women?

A

At term due to risk of neonatal haemolysis.

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31
Q

Which antibiotic is contraindicated for UTI treatment in pregnant women?

A

Trimethoprim - teratogenic effects.

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32
Q

Patient presenting with conjunctivitis, urethritis and arthritis?

A

Reiter’s syndrome (reactive arthritis).

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33
Q

Inheritance of polycystic kidney disease?

A

Autosomal dominant.

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34
Q

What are some complications of polycystic kidney disease?

A
  • cardiovascular disease
  • kidney stones
  • polycystic liver disease
  • subarachnoid haemorrhage (due to Berry aneurysms)
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35
Q

Are granulomas found in Crohn’s or UC?

A

Crohn’s

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36
Q

Are crypt abscesses found in Crohn’s or UC?

A

Crohn’s and UC

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37
Q

Are goblet cells depleted in Crohn’s or UC?

A

UC

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38
Q

Does Crohn’s or UC have a cobblestone appearance?

A

Crohn’s

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39
Q

What condition is likely if a patient has more difficulty swallowing solid food compared to liquids?

A

Achalasia

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40
Q

CXR findings in achalasia?

A

Very dilated oesophagus.

Small / absent gastric bubble.

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41
Q

Complication of achalasia?

A

Aspiration pneumonia.

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42
Q

Investigations for achalasia?

A
  • CXR

- barium swallow

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43
Q

Complications of coeliac disease?

A
  • osteoporosis

- dermatitis herpetiformis

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44
Q

How to distinguish between gastric and duodenal ulcers?

A
  • gastric ulcer pain is worse with eating

- duodenal ulcer pain is relieved by eating

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45
Q

What is haematochezia?

A

Blood in stool.

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46
Q

Risk factors for oesophageal cancer?

A
  • achalasia
  • barret’s oesophagus
  • corrosive oesophagitis
  • diverticulitis
  • oesophageal web
  • familial
  • GORD
  • hiatal hernia
  • alcohol & smoking
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47
Q

Viral cause of diarrhoea?

A
  • norovirus

- rotavirus

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48
Q

Bacterial cause of diarrhoea?

A
  • E. coli
  • Salmonella (non-typhoidal)
  • campylobacter
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49
Q

What is diverticulosis?

A

herniation of the mucosa and submucosa through the muscular layer of the colonic wall

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50
Q

What is the pathophysiology of diverticulosis?

A

Colonic smooth muscle over-activity.

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51
Q

What is diverticulitis?

A

Inflammation of diverticula, may be caused by infection.

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52
Q

Risk factors for diverticulosis / diverticulitis?

A
  • ageing
  • low fibre diet
  • obesity
  • smoking
  • sedentary lifestyle
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53
Q

How is diverticulitis managed?

A

Uncomplicated - oral antibiotics and liquid diet.

Complicated - IV antibiotics, abscess drainage, surgical resection.

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54
Q

When is surgery indicated in diverticulitis?

A
  • complicated disease
  • recurrent disease
  • immunocompromised
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55
Q

First line treatment of C. diff infection?

A

Vancomycin (125mg orally 4x per day for 10 days).

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56
Q

Most likely cause of bowel obstruction in a child?

A

Intussusception

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57
Q

What are some causes of mechanical bowel obstruction?

A
  • post-surgery adhesions
  • hernia
  • volvulus
  • intussusception
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58
Q

What are some causes of functional bowel obstruction?

A
  • post-operative ileus
  • appendicitis
  • peritonitis
  • hypothyroidism
  • hypokalaemia
  • hypercalcaemia
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59
Q

What is the difference between mesenteric ischaemia and ischaemic colitis?

A

Mesenteric ischaemia - narrowed / blocked arteries restrict blood flow to the small intestine.
Ischaemic colitis - temporary restriction of blood supply to the large intestine due to vasoconstriction or low pressure flow.

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60
Q

Risk factors for ischaemic colitis?

A
  • clotting abnormalities (e.g. factor V leiden)
  • high cholesterol
  • reduction of blood flow (heart failure, low BP)
  • previous abdominal surgery
  • heavy exercise
  • surgery involving the aorta
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61
Q

Causes of oesophageal varices?

A
  • liver cirrhosis
  • hepatitis
  • primary biliary cholangitis
  • parasitic infection (schistosomiasis)
  • thrombosis of portal / splenic veins
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62
Q

How is a Mallory-Weiss tear managed?

A
  • most self-resolve in a few days
  • endoscopic therapy (coagulation)
  • transfusions if Hb is low
  • surgical repair
  • PPI
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63
Q

What is indicated if AST > ALT with a 2:1 ratio?

A

Alcoholic liver disease

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64
Q

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

A

Terminal ileum

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65
Q

What do testicular seminomas secrete?

A

ALP

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66
Q

Which type of testicular cancer secretes alpha fetoprotein?

A

Endodermal yolk sac tumour

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67
Q

Drug with prognostic benefit in prostate cancer?

A

5-alpha reductase inhibitor (e.g. finasteride)

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68
Q

Which antibodies are memory antibodies?

A

IgG

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69
Q

What is Korsakoff’s syndrome?

A

Long-term irreversible complication of Wernicke’s encephalopathy.

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70
Q

What is diapedesis?

A

Leucocyte extravasation

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71
Q

What is Beck’s triad?

A

Cardiac tamponade:

  • muffled heart sounds
  • hypotension
  • raised JVP
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72
Q

What is acute cholecystitis?

A

Inflammation of the gallbladder, usually occurs when a gallstone completely obstructs the gallbladder neck or cystic duct. There may be infection of the gallbladder.

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73
Q

What is acalculous cholecystitis?

A

Obstruction of the cystic duct causing inflammation of the gallbladder, without gallstones.

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74
Q

Signs and symptoms of acute cholecystitis?

A
  • RUQ pain and tenderness
  • fever
  • nausea & vomiting
  • palpable gallbladder
  • Murphy’s sign
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75
Q

What is Murphy’s sign?

A

Pain on inspiration when the right subcostal area is palpated.

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76
Q

Where can pain be referred / radiate to in acute cholecystitis?

A
  • right shoulder (due to phrenic nerve irritation)

- around the right side to the back (intercostal nerve irritation)

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77
Q

First line investigation for cholecystitis?

A

Abdominal ultrasound

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78
Q

Investigations for cholecystitis?

A
  • abdominal ultrasound
  • MRCP (if ultrasound doesn’t detect the stone)
  • blood cultures
  • FBC (elevated WCC)
  • LFTs (generally normal)
  • serum lipase / amylase (exclude pancreatitis)
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79
Q

Management of acute cholecystitis?

A
  • analgesia
  • IV antibiotics
  • laparoscopic cholecystectomy
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80
Q

Complications of acute cholecystitis?`

A
  • gallbladder perforation
  • gangrenous cholecystitis
  • sepsis
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81
Q

What is meant by cholelithiasis?

A

Gallstone formation in the gallbladder or other parts of the biliary tree.

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82
Q

What is meant by choledocholithiasis?

A

Gallstones in the common bile duct.

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83
Q

What is biliary colic?

A

Intermittent RUQ pain caused by gallstones irritating the bile ducts (worse after eating, particularly fatty foods).

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84
Q

What do gallstones consist of?

A
  • 90% are cholesterol stones

- 10% are black / brown pigment stones

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85
Q

Risk factors for cholesterol gallstones?

A
  • female
  • increasing age
  • diabetes / metabolic syndrome
  • obesity
  • pregnancy
  • rapid weight loss / prolonged fasting
  • medications (e.g. oestrogen, GLP-1 analogues)
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86
Q

What causes black pigment stones?

A

High bilirubin / red cell turnover states - i.e. haemolytic anaemia.

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87
Q

What causes brown pigment stones?

A

Stasis and infection.

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88
Q

How do cholesterol stones form?

A
  • bile becomes supersaturated with cholesterol due to excessive amounts of cholesterol produced by the liver, compared with solubilising agents (bile salts and lethicin)
  • there is accelerated nucleation (crystallisation)
  • gallbladder hypomobility contributes to stone formation
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89
Q

Clinical manifestations of biliary colic?

A
  • severe colicky epigastric / RUQ pain
  • often triggered by meals (particularly fatty meals)
  • lasts 30 minutes - 8 hours
  • may be associated with nausea & vomiting
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90
Q

Investigations for biliary colic / gallstones?

A
  • abdominal ultrasound
  • LFTs (normal or elevated ALP/bilirubin if there is cholestasis)
  • MRCP (if common bile duct stones are suspected but have not been picked up on ultrasound)
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91
Q

Management of uncomplicated gallstone disease?

A
  • avoid fatty foods
  • analgesia
  • laparoscopic cholecystectomy if symptomatic
  • clear bile duct stones (ERCP / laparoscopic cholecystectomy)
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92
Q

Complications of gallstone disease?

A
  • biliary colic
  • acute cholecystitis
  • acute pancreatitis
  • acute cholangitis
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93
Q

What is ascending cholangitis?

A

Infection and inflammation of the biliary ducts - surgical emergency with high mortality from sepsis.

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94
Q

Most common infective organisms in ascending cholangitis?

A
  • E. coli
  • Klebsiella
  • Enterococcus
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95
Q

Causes of ascending cholangitis?

A
  • obstruction of the common bile duct

- infection introduced during ERCP

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96
Q

Risk factors for ascending cholangitis?

A
  • cholelithiasis
  • benign / malignant strictures
  • injury to the bile ducts (e.g. surgical, endoscopic, radiological)
  • history of primary sclerosing cholangitis
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97
Q

Pathophysiology of ascending cholangitis?

A
  • obstruction of the common bile duct leads to bacterial seeding and contamination of the biliary tree
  • sludge formation provides a growth medium for bacteria
  • bile duct pressure increases as the obstruction progresses, promoting extravasation of bacteria into the bloodstream
  • this leads to sepsis if untreated
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98
Q

Clinical manifestations of ascending cholangitis?

A
  • Charcot’s triad (jaundice, fever, RUQ pain)
  • pale stools
  • pruritus
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99
Q

Gold standard investigation for ascending cholangitis?

A

endoscopic retrograde cholangiopancreatography

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100
Q

Investigations for ascending cholangitis?

A
  • ERCP
  • abdominal ultrasound
  • FBC (raised WCC)
  • ABG (raised lactate, metabolic acidosis)
  • LFTs (raised ALP, bilirubin, and transaminases)
  • blood cultures
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101
Q

Differentials for ascending cholangitis?

A
  • acute cholecystitis
  • acute pancreatitis
  • acute appendicitis
  • acute pyelonephritis
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102
Q

Management of ascending cholangitis?

A
  • sepsis 6
  • ERCP for biliary decompression (with sphincterotomy / stent placement)
  • elective laparoscopic cholecystectomy in stabilised patients
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103
Q

What is the sepsis 6?

A

3 in, 3 out:

  • O2 to target saturations
  • IV fluids
  • IV antibiotics
  • blood cultures
  • serial lactates
  • monitor urine output
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104
Q

Complications of ascending cholangitis?

A
  • sepsis

- acute pancreatitis

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105
Q

What is primary biliary cholangitis?

A

Chronic autoimmune disease of the small intra-hepatic bile ducts. Obstruction of the bile ducts results in chronic inflammation and fibrosis.

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106
Q

Epidemiology of PBC?

A
  • peak incidence 45-60
  • affects females much more than males (10:1)
  • associated with other autoimmune conditions (rheumatoid arthritis, Sjogren’s)
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107
Q

Pathophysiology of PBC?

A
  • T lymphocyte-mediated damage to bile duct epithelial cells, with autoantibody involvement
  • cholestasis occurs as a result of autoimmune bile duct damage
  • this leads to bile acid retention, causing further liver damage and progressive loss of bile ducts
  • this results in liver fibrosis and eventually cirrhosis
  • bile acids, bilirubin, and cholesterol build up in the blood
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108
Q

Signs and symptoms of PBC?

A
  • pruritus
  • jaundice
  • xanthelasma (cholesterol deposits on eyelids)
  • xanthoma (cholesterol deposits on in)
  • GI disturbance
  • abdominal pain
  • pale stools
  • signs of liver cirrhosis
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109
Q

Investigations for PBC?

A
  • raised ALP
  • raised bilirubin and transaminases (later in disease course)
  • autoantibodies (AMA are most specific, ANA may also be seen)
  • liver biopsy (usually not required as raised ALP and presence of specific autoantibodies normally sufficient for diagnosis)
  • imaging (abdominal ultrasound / MRCP) to exclude bile duct lesion or PSC
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110
Q

Differentials for PBC?

A
  • obstructive bile duct lesion

- PSC

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111
Q

Management of PBC?

A
  • ursodeoxycholic acid (reduces intestinal cholesterol absorption)
  • obeticholic acid (bile acid analogue, decreases circulating bile acids)
  • cholestyramine (bile acid sequestrant, binds bile in the GI tract to prevent its absorption)
  • prednisolone / azathioprine
  • liver transplant
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112
Q

Complications of PBC?

A

Hepatocellular carcinoma

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113
Q

What is primary sclerosing cholangitis?

A

Intra- or extra-hepatic bile ducts become strictured and fibrotic, causing cholestasis. Chronic bile obstruction eventually leads to liver inflammation, fibrosis and cirrhosis.

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114
Q

Epidemiology of PSC?

A

affects males more than females

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115
Q

Cause of PSC?

A

Immune-mediated condition with a genetic component.

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116
Q

Risk factors for PSC?

A
  • male
  • history of IBD
  • first degree relative with PSC
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117
Q

Signs and symptoms of PSC?

A
  • pruritus
  • jaundice
  • RUQ pain
  • vitamin deficiency (ADEK)
  • hepatomegaly
  • signs of liver cirrhosis
  • fever
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118
Q

Investigations for PSC?

A
  • LFTs - elevated ALP (transaminases and bilirubin elevated as the disease progresses)
  • autoantibodies (ANA, ANCA)
  • MRCP (‘beads on a string’ appearance)
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119
Q

Management of PSC?

A
  • cholestyramine (bile acid sequestrant to relieve pruritus)
  • ERCP to dilate and stent strictures
  • liver transplant
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120
Q

Complications of PSC?

A
  • hepatocellular carcinoma
  • cholangiocarcinoma
  • cirrhosis and liver failure
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121
Q

What is acute pancreatitis?

A

Inflammation of the pancreas, presenting with rapid onset of inflammation (both local and systemic) and symptoms.

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122
Q

Most common causes of acute pancreatitis?

A
  • gallstones (50%)

- alcohol (25%)

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123
Q

Causes of acute pancreatitis?

A
  • idiopathic
  • gallstones
  • ethanol
  • trauma
  • steroids
  • mumps
  • autoimmune
  • scorpion venom
  • hyperlipidaemia
  • ERCP
  • drugs (azathioprine)
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124
Q

Pathophysiology of acute pancreatitis?

A
  • inflammation damages acinar cells, resulting in the release of digestive enzymes
  • this is due to abnormal intra-cellular calcium accumulation which activates intra-cellular proteases, releasing stored digestive enzymes
  • proteases cause autodigestion and lipases cause fatty necrosis
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125
Q

What causes acute lung injury in acute pancreatitis?

A

Systemic inflammation and the release of pancreatic proteases results in lung damage.

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126
Q

Signs and symptoms of acute pancreatitis?

A
  • severe epigastric pain
  • pain radiates to back
  • pain improves leaning forward
  • nausea & vomiting
  • anorexia
  • abdominal tenderness
  • hypovolaemia
  • pleural effusion
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127
Q

Signs of hypovolaemia?

A
  • hypotension
  • oliguria
  • dry mucous membranes
  • tachycardia
  • decreased skin turgor
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128
Q

Gold standard investigation for acute pancreatitis?

A

Serum amylase / lipase - greater than 3 times the upper limit of the normal range.

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129
Q

Investigations for acute pancreatitis?

A
  • serum amylase / lipase
  • FBC (elevated WCC and haematocrit)
  • CRP elevated
  • creatinine may be elevated
  • LFTs
  • CXR
  • abdominal ultrasound (gallstones)
  • CT abdomen (for complications)
  • ERCP / MRCP
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130
Q

Differentials for acute pancreatitis?

A
  • abdominal aortic aneurysm
  • ascending cholangitis
  • acute cholecystitis
  • MI
  • mesenteric ischaemia
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131
Q

Management of acute pancreatitis?

A
  • IV fluids
  • nil by mouth
  • analgesia
  • anti-emetics
  • ERCP / cholecystectomy for gallstones
  • IV antibiotics for infection
  • drain abscess
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132
Q

Complications (and likelihood) in acute pancreatitis?

A

High - acute renal failure.
Medium - sepsis / acute lung injury.
Low - chronic pancreatitis.

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133
Q

What is chronic pancreatitis?

A

Chronic inflammation in the pancreas, resulting in fibrosis and loss of pancreatic function.

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134
Q

What is the most common cause of chronic pancreatitis in adults?

A

Alcohol

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135
Q

What is the most common cause of chronic pancreatitis in children?

A

Cystic fibrosis

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136
Q

Risk factors for chronic pancreatitis?

A
  • alcohol
  • repeated episodes of acute pancreatitis
  • family history
  • coeliac disease
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137
Q

Signs and symptoms of chronic pancreatitis?

A
  • dull epigastric pain
  • pain worse around 30 minutes after eating
  • pain radiates to the back
  • steatorrhoea
  • weight loss and malnutrition
  • jaundice
  • nausea and vomiting
  • diabetes mellitus / glucose intolerance
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138
Q

Investigations for chronic pancreatitis?

A
  • CT / MRI abdomen - shows pancreatic calcifications, enlargement, and dilation of ducts
  • endoscopic ultrasound
  • secretin-enhanced MRCP - demonstates abnormal exocrine function
  • biopsy and histology - shows fibrosis, loss of acini
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139
Q

Management of chronic pancreatitis?

A
  • alcohol and smoking cessation
  • dietary supplementation
  • pancreatic enzyme replacement therapy
  • blood glucose monitoring
  • analgesia
  • ERCP for duct stenting and stricture dilatation
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140
Q

Complications of chronic pancreatitis?

A
  • exocrine insufficiency
  • diabetes mellitus
  • osteoporosis
  • pancreatic cancer
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141
Q

Pathophysiology of alcoholic liver disease?

A
  • ethanol is directly toxic to the liver, resulting in the development of steatosis due to altered lipid metabolism
  • steatosis initially develops in hepatocytes surrounding the central vein
  • there is progression to hepatitis with activation of Kupffer cells (and hepatic stellate cells )which induce inflammation
  • Mallory-Denk bodies are seen within hepatocytes
  • fibrosis and cirrhosis develop following deposition of extracellular matrix proteins by hepatic stellate cells
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142
Q

Signs and symptoms of alcoholic liver disease?

A
  • fatigue, malaise, nausea, anorexia
  • abdominal pain
  • jaundice
  • hepatomegaly
  • spider naevi
  • ascites
  • caput medusae
  • asterixis
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143
Q

What are caput medusae?

A

Engorged superficial epigastric veins.

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144
Q

Investigations for alcoholic liver disease?

A
  • LFTs (AST:ALT ratio >2 is strongly suggestive)
  • increased prothrombin time
  • liver ultrasound
  • CT/MRI abdomen
  • liver biopsy
  • endoscopy (assess for oesophageal varices)
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145
Q

Differentials for alcoholic liver disease?

A
  • non-alcoholic steatohepatitis
  • acute / chronic viral hepatitis
  • Wilson’s disease
  • autoimmune hepatitis
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146
Q

Management of alcoholic liver disease?

A
  • stop drinking alcohol
  • smoking cessation
  • liver transplant
  • corticosteroids for alcoholic hepatitis
  • treat complications
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147
Q

Complications of alcoholic liver disease?

A
  • ascites
  • hepatic encephalopathy
  • portal hypertension
  • oesophageal varices
  • hepatocellular carcinoma
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148
Q

Why does hepatic encephalopathy occur?

A

Decreased ammonia metabolism by the damaged liver results in build-up of ammonia in the blood.

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149
Q

Pathophysiology of portal hypertension?

A

Increased resistance in the liver as a result of fibrosis / cirrhosis, results in an increase in blood pressure in the portal vein.

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150
Q

Gold standard investigation for portal hypertension?

A

Pressure measurement - catheterisation via the internal jugular vein.

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151
Q

Investigations for portal hypertension?

A
  • catheterisation via internal jugular vein and blood pressure measurement
  • doppler ultrasound
  • upper GI endoscopy (for oesophageal varices)
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152
Q

Surgical intervention for portal hypertension?

A

TIPSS - transjugular intrahepatic portal systemic shunt.

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153
Q

Medication for prevention of varices bleeding?

A

Propanolol

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154
Q

Medication for ruptured varices?

A

Terlipressin (vasopressin analogue) causes vasoconstriction and slows bleeding.

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155
Q

Endoscopic intervention for oesophageal varices?

A
  • elastic band ligation

- injection scleropathy (to cause clotting)

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156
Q

What type of virus is hep A?

A

Single-stranded RNA virus.

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157
Q

How is hep A transmitted?

A

Faecal-oral (contaminated food and water).

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158
Q

Gold standard investigation for hep A?

A

IgM anti-hepatitis A serology.

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159
Q

How is hep A managed?

A
  • supportive care (analgesia)

- resolves in 1-3 months

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160
Q

Signs and symptoms of hep A?

A
  • nausea and vomiting
  • anorexia
  • jaundice
  • dark urine and pale stools
  • hepatomegaly
  • fever
  • RUQ pain
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161
Q

What type of virus is hep B?

A

DNA virus

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162
Q

How is hep B transmitted?

A

Contact with blood or bodily fluids (needle-sharing, sexual intercourse).

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163
Q

Clinical presentation of acute hep B?

A

70% of patients are asymptomatic.

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164
Q

Clinical presentation of chronic hep B?

A

Patients are asymptomatic until they develop chronic liver disease.

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165
Q

Signs and symptoms of hep B?

A
  • jaundice
  • hepatomegaly
  • fever
  • nausea and vomiting
  • fatigue
  • RUQ pain
  • signs of cirrhosis
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166
Q

What does serum hep B surface antigen indicate?

A

Active infection

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167
Q

What does serum hep B e antigen indicate?

A

Marker of viral replication, indicates high infectivity.

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168
Q

What does serum antibody to the hep B surface antigen indicate?

A
  • vaccination
  • previous infection
  • current infection (if other markers are also present)
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169
Q

What does serum antibody to the hep B core antigen indicate?

A

Past or current infection.

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170
Q

What does serum hep B DNA indicate?

A

Direct measure of viral load.

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171
Q

Management of hep B?

A
  • supportive care and antiviral therapy

- liver transplant

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172
Q

Complications of hep B?

A
  • hepatocellular carcinoma
  • liver cirrhosis
  • liver failure
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173
Q

Hep B prognosis?

A
  • over 95% achieve seroconversion without treatment within 2 months
  • some patients become chronic hep B carriers (viral DNA integrated into their own DNA)
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174
Q

What type of virus is hep C?

A

Single stranded RNA (positive-sense)

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175
Q

How is hep C transmitted?

A
  • IVDU
  • sexual transmission is uncommon
  • contaminated blood transfusion / medical equipment
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176
Q

Clinical manifestations of acute hep C?

A

Patients usually asymptomatic

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177
Q

Clinical manifestations of chronic hep C?

A
  • fatigue, myalgia, anorexia
  • jaundice
  • ascites
  • hepatic encephalopathy
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178
Q

Investigations for hep C?

A
  • hep C antibody (current / past infection)
  • hep C RNA PCR (current infection)
  • serum aminotransferases elevated
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179
Q

Management of hep C?

A
  • direct acting antiviral treatment for 8-12 weeks

- liver transplant

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180
Q

Prognosis for hep C?

A
  • some young, healthy patients develop an immune response that eradicates the virus
  • the majority of infected patients have chronic infection and progressive liver damage
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181
Q

What type of virus is hep D?

A

Single stranded RNA virus (negative sense).

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182
Q

How does hep D survive in the host?

A

Attaches itself to the hep B surface antigen.

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183
Q

What type of virus is hep E?

A

RNA virus

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184
Q

How is hep E transmitted?

A

Faecal-oral

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185
Q

Clinical manifestations of hep E?

A

Normally produces a mild illness that clears in a month without treatment.
Rare to progress to chronic hepatitis and liver failure.

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186
Q

What is autoimmune hepatitis?

A

Chronic inflammatory disease of the liver - characterised by the presence of circulating autoantibodies, inflammatory changes on liver histology, and response to immunosuppressive treatment.

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187
Q

Aetiology of autoimmune hepatitis?

A
  • genetic predisposition

- environmental triggering agents (viruses, drugs, etc)

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188
Q

HLA association with autoimmune hepatitis?

A

HLA-DR3 and HLA-DR4 are associated with type 1 AIH.

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189
Q

Pathophysiology of autoimmune hepatitis?

A

T-cell mediated response against hepatocytes, with auto-antibody involvement. This leads to chronic inflammation and liver fibrosis.

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190
Q

Signs and symptoms of AIH?

A
  • fatigue, malaise, anorexia
  • abdominal pain
  • hepatomegaly / splenomegaly
  • jaundice
  • encephalopathy
  • pruritus
  • fever
  • nausea
  • ascites
  • spider naevi
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191
Q

Investigations for AIH?

A
  • LFTs (greater increase in aminotransferases than ALP and bilirubin)
  • serum autoantibodies
  • serum immunoglobulin concentration
  • liver biopsy
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192
Q

What autoantibodies are present in AIH?

A
  • ANA
  • anti smooth muscle antibody
  • pANCA
  • anti soluble liver / pancreas antigens
  • anti liver-kidney microsome 1 antibody
  • anti liver cytosol antibody
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193
Q

Management of AIH?

A
  • corticosteroid (prednisolone)
  • plus immunosuppressant if necessary (azathioprine)
  • liver transplant
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194
Q

Complications of AIH?

A
  • steroid complications
  • hepatocellular carcinoma
  • liver failure
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195
Q

What is haemochromatosis?

A

Autosomal recessive iron storage disorder resulting in excessive total body iron, and iron deposition in tissues.

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196
Q

Aetiology of haemochromatosis?

A

Autosomal recessive mutation in the human haemochromatosis protein (HFE) on chromosome 6.

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197
Q

What does the human haemochromatosis protein do?

A

Regulates the expression of hepcidin.

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198
Q

Pathophysiology of haemochromatosis?

A
  • hepcidin expression is too low
  • hepcidin is a negative regulator of iron, so this results in ongoing duodenal absorption of iron despite adequate iron stores
  • there is also continued release of iron from macrophages (from erythrophagocytosis)
  • serum iron and transferrin saturation is high
  • this leads to iron accumulation in multiple organisms
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199
Q

Clinical presentation of haemochromatosis?

A

Usually presents after 40 (later in females due to iron loss from menstruation).

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200
Q

Signs and symptoms of haemochromatosis?

A
  • chronic fatigue
  • bronze / grey skin discolouration
  • joint pain
  • hypogonadism (impotence, loss of libido) and erectile dysfunction
  • memory and mood disturbance
  • hepatomegaly
  • diabetes mellitus
  • arrhythmias
  • congestive heart failure
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201
Q

Investigations to diagnose haemochromatosis?

A
  • serum ferritin elevated
  • total iron binding capacity reduced (fasting transferrin saturation)
  • genetic testing confirms Dx
  • LFTs may be normal
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202
Q

Investigations to assess iron deposition in haemochromatosis?

A
  • liver biopsy with Perl’s stain
  • fasting blood glucose
  • ECG and echocardiogram
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203
Q

Management of haemochromatosis?

A
  • phlebotomy

- manage complications

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204
Q

What are some complications of haemochromatosis?

A
  • type 1 diabetes
  • liver cirrhosis
  • hepatocellular carcinoma
  • infertility
  • congestive heart failure
  • bone loss
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205
Q

What is Wilson’s disease?

A

Autosomal recessive disease causing copper accumulation in tissues.

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206
Q

What is the genetic cause of Wilson’s disease?

A

Mutation in the ATP7B copper-binding protein on chromosome 13.

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207
Q

Pathophysiology of Wilson’s disease?

A
  • ATP7B normally produces a protein involved in the excretion of excess copper in the bile, where it is subsequently eliminated in the stool
  • faulty ATP7B production results in high levels of free copper, causing toxicity by oxidant damage
  • this leads to cell injury, inflammation, and death
  • excess copper is stored in the liver, which causes hepatitis and eventually fibrosis due to inflammation and cell injury
  • the basal ganglia and movement co-ordination areas of the brain are most sensitive to copper accumulation
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208
Q

Clinical manifestations of Wilson’s disease?

A

Patients present with either hepatic problems, or neurological / psychiatric problems.

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209
Q

What is the transport protein for copper?

A

Ceruloplasmin

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210
Q

Where is ceruloplasmin synthesised?

A

Liver

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211
Q

Hepatic manifestations of Wilson’s disease?

A
  • jaundice
  • RUQ tenderness
  • spider naevi
  • ascites
  • GI bleeding (varices)
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212
Q

Neurological manifestations of Wilson’s disease?

A
  • behavioural abnormalities
  • tremor
  • dysarthria
  • dysphagia
  • incoordination
  • ophthalmoplegia
  • dysdiadochokinesia
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213
Q

What is dysdiadochokinesia?

A

Slowness in alternating hands from prone to supine position.

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214
Q

What are Kayser-Fleischer rings?

A

Brown circles surrounding the iris. Seen in Wilson’s disease due to copper deposition.

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215
Q

Gold standard investigation for Wilson’s disease?

A

Liver biopsy

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216
Q

Investigations for Wilson’s disease?

A
  • liver biopsy
  • 24 hour urine copper
  • serum ceruloplasmin (low)
  • LFTs (raised transaminases and bilirubin, low albumin)
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217
Q

Management of Wilson’s disease?

A
  • trientine (copper chelator)
  • zinc (blocks copper absorption)
  • dietary restriction of liver and shellfish
  • liver transplant
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218
Q

What is the mechanism of action for trientine?

A

Copper chelator, enhances urinary excretion of copper.

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219
Q

Complications of Wilson’s disease?

A
  • liver failure

- oesophageal varices

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220
Q

What is alpha 1 antitrypsin deficiency?

A

Autosomal co-dominant disorder in which there is insufficient production of A1AT, resulting in lung and liver damage.

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221
Q

Genetic cause of A1AT deficiency?

A

Allele mutations in the SERPINA1 gene.

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222
Q

What is the inheritance pattern of A1AT deficiency?

A

Autosomal co-dominant.

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223
Q

Pathophysiology of A1AT deficiency?

A
  • A1AT is made in the liver, and nomally inhibits neutrophil elastase (enzyme that digests connective tissues)
  • deficiency results in lung damage because excess protease enzymes attack connective tissue
  • liver damage occurs because the abnormal A1AT protein becomes trapped and accumulates, leading to fibrosis over time
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224
Q

Signs and symptoms of A1AT?

A
  • productive cough
  • shortness of breath on exertion
  • hepatomegaly
  • ascites
  • hepatic encephalopathy
  • jaundice / scleral icterus
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225
Q

What are the lung manifestations of A1AT deficiency?

A

Bronchiectasis and emphysema.

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226
Q

Investigations for A1AT deficiency?

A
  • serum A1AT
  • genetic testing for A1AT gene
  • liver biopsy
  • CT chest
  • LFTs (elevated transaminases, ALP, and bilirubin)
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227
Q

Management of A1AT deficiency?

A
  • stop smoking
  • short / long acting bronchodilators
  • inhaled corticosteroids
  • pulmonary rehabilitation
  • lung transplant
  • liver transplant
  • manage hepatic complications
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228
Q

Complications of A1AT deficiency?

A

Hepatocellular carcinoma

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229
Q

Risk factors for hepatocellular carcinoma?

A
  • chronic hep B / C infection
  • alcoholic liver disease
  • non-alcoholic steatohepatitis
  • haemochromatosis
  • A1AT deficiency
  • PBC / PSC
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230
Q

How is hep B directly carcinogenic?

A

Causes methylation of the P16 gene, leading to hepatocellular carcinogenesis.

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231
Q

Signs and symptoms of hepatocellular carcinoma?

A
  • weight loss
  • anorexia
  • abdominal pain
  • nausea & vomiting
  • jaundice
  • pruritus
  • cirrhosis (ascites, spider naevi, caput medusae, varices, asterixis)
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232
Q

Investigations for HCC?

A
  • alpha fetoprotein
  • liver ultrasound
  • CT / MRI abdomen
  • liver biopsy
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233
Q

Is conventional chemotherapy / radiotherapy effective for HCC?

A

No, HCC is generally considered resistant to chemotherapy and radiotherapy.

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234
Q

Summary of HCC management?

A
  • surgical resection of individual tumours
  • liver transplant
  • kinase inhibitors
  • transcatheter arterial embolisation
  • radiofrequency ablation
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235
Q

What are kinase inhibitors?

A

Inhibit cancer cell proliferation (e.g. sorafenib).

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236
Q

What is Budd-Chiari syndrome?

A

Rare disorder characterised by narrowing and occlusion of hepatic veins.

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237
Q

Signs and symptoms of paracetamol overdose?

A
  • nausea & vomiting
  • RUQ pain
  • jaundice
  • hepatomegaly
  • altered consciousness level & asterixis (due to hepatic encephalopathy)
  • loin pain
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238
Q

What causes loin pain in paracetamol overdose?

A

AKI

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239
Q

Investigations for paracetamol overdose?

A
  • serum paracetamol
  • LFTs (raised transaminases)
  • serum creatinine elevated
  • ABG (lactic acidosis)
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240
Q

Blood glucose in paracetamol overdose?

A

Hypoglycaemia

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241
Q

Management of paracetamol overdose?

A
  • activated charcoal (within 1 hour)
  • acetylcysteine to prevent liver damage
  • refer to psychological support
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242
Q

First-line treatment for mild UC?

A

Aminosalicylate - e.g. mesalazine.

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243
Q

What is nephrolithiasis?

A

Calculi form in the renal pelvis before travelling down the ureters. They may be symptomatic until they irritate or become stuck in the ureters.

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244
Q

Where do renal stones commonly become stuck?

A

Vesico-ureteric junction

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245
Q

Most common type of renal stone?

A

Calcium based

  • calcium oxalate (more common)
  • calcium phosphate
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246
Q

Types of renal stone?

A
  • calcium oxalate / calcium phosphate
  • uric acid
  • struvite
  • cystine
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247
Q

Causes of struvite stones?

A

Produced by bacteria, associated with infection.

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248
Q

Causes of cystine stones?

A

Cystinuria - autosomal recessive disease.

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249
Q

What is a staghorn calculus?

A

Complex renal stone occupying the majority of the renal collecting system - associated with high risk of sepsis.

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250
Q

Most common cause of staghorn calculus?

A

Upper UTI - bacteria hydrolyse the urea in urine to ammonia, producing struvite.

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251
Q

Risk factors for renal stones?

A
  • UTI
  • obesity
  • excessive uric acid intake
  • dehydration
  • previous renal stones
  • hyperparathyroidism
  • anatomical urinary tract abnormalities
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252
Q

Signs and symptoms of renal colic?

A
  • acute severe spasmodic flank pain radiating to the ipsilateral groin
  • nausea and vomiting
  • urinary frequency / urgency
  • haematuria
  • costovertebral angle and flank tenderness
  • restlessness
  • fever (if infection)
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253
Q

What pain is characteristic of renal colic?

A

Acute severe spasmodic flank pain, radiating to the ipsilateral groin.

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254
Q

Investigations for renal stones?

A
  • urine dipstick (haematuria, nitrites & leucocytes if UTI)
  • non-contrast CT KUB (renal ultrasound in pregnant patients)
  • U&Es
  • X ray KUB - shows calcification
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255
Q

Differentials for renal stones?

A
  • acute appendicitis
  • ectopic pregnancy
  • ovarian cyst
  • bowel obstruction
256
Q

When is urgent intervention indicated in a patient with a renal stone?

A

Obstruction with or without infection.

257
Q

Urgent management of renal stone?

A
  • decompression (ureteric stent or percutaneous nephrostomy tube)
  • antibiotics for infection
  • stone removal after drainage complete and infection cleared
258
Q

Supportive care for renal stone?

A
  • analgesia (strong - e.g. diclofenac)
  • anti-emetic
  • hydration
259
Q

Management of renal stones without obstruction or infection?

A 
Stone less than 10mm - consider watchful waiting.
Stone greater than 10mm:
- tamsulosin
- shock wave lithotripsy
- ureteroscopy
- percutaneous nephrolithotomy
260
Q

Prevention of uric acid renal stones?

A

Oral alkalinisation therapy - potassium citrate.

261
Q

What is AKI?

A

An acute drop in kidney function leading to a rise in serum creatinine or a fall in urine output.

262
Q

NICE criteria for AKI?

A
  • creatinine rise > 25 micromol/L in 48 hours
  • creatinine rise > 50% from baseline in 7 days
  • urine output < 0.5 ml/kg/hour for > 6 hours
263
Q

Pre-renal causes of AKI?

A
  • hypovolaemia / haemorrhage
  • sepsis
  • third-spacing of fluid (acute pancreatitis)
  • heart failure
  • hepatorenal syndrome
  • renal artery stenosis
264
Q

Intrinsic causes of AKI?

A
  • acute tubular necrosis
  • rapidly progressive glomerulonephritis
  • interstitial nephritis
  • thrombosis
  • haemolytic uraemic syndrome
265
Q

Post-renal causes of AKI?

A
  • strictures
  • tumour
  • prostate hyperplasia
  • renal calculi
  • ascending UTI
  • urinary retention
266
Q

Risk factors for AKI?

A
  • underlying renal disease
  • sepsis
  • IV iodinated contrast
  • hypovolaemia
  • pancreatitis
  • renal stones
  • older age
  • nephrotoxic drugs
267
Q

Causes of acute tubular necrosis?

A
  • ischaemia
  • drug-induced
  • contrast-induced
268
Q

Pathophysiology of post-renal AKI?

A
  • obstruction increases intratubular pressure

- this causes tubular ischaemia and atropy

269
Q

Examples of nephrotoxic drugs?

A
  • ibuprofen
  • lithium
  • antibiotics (cefotaxime, gentamicin, vancomycin)
  • immunosuppressants (methotrexate, sulfasalazine)
  • ACE inhibitors and ARBs
270
Q

Investigations for AKI?

A
  • U&Es (hyperkalaemia)
  • serum creatinine
  • urine output
  • renal tract ultrasound for obstruction
271
Q

Management of AKI?

A

STOP AKI
- screen for and treat sepsis
- toxins - stop nephrotoxic drugs
- optimise volume status and BP
- prevent harm: treat underlying cause and complications (hyperkalaemia)
Emergency renal replacement therapy if not responding to treatment.

272
Q

What is CKD?

A

Reduction in kidney function present for more than 3 months.

273
Q

Units for GFR?

A

ml/min/1.73m^2

274
Q

Risk factors for CKD?

A
  • diabetes
  • hypertension
  • older age
  • glomerulonephritis
  • polycystic kidney disease
  • nephrotoxic drugs
  • obstructive uropathy
  • SLE
  • AKI
275
Q

How does CKD lead to bone disease?

A
  • kidney no longer activates vitamin D, leading to hypocalcaemia
  • hypocalcaemia stimulates increased PTH secretion, increasing bone resorption
  • bones become brittle and weak due to mineral loss
276
Q

How does CKD lead to hypertension?

A

Low rate of blood flow through the glomerulus results in increased renin secretion.

277
Q

Management of CKD?

A
  • treat underlying cause (diabetes, hypertension, glomerulonephritis)
  • reduce CVD risk - atorvastatin 20 mg
  • manage complications (vitamin D and iron supplementation)
  • dialysis and transplant
278
Q

Complications of CKD?

A
  • AKI
  • hypertension
  • cardiovascular disease
  • anaemia
  • bone disease
  • metabolic acidosis
  • arrhythmias (hyperkalaemia)
  • uraemic pericarditis
279
Q

What is renal cell carcinoma?

A

Adenocarcinoma arising from the kidney tubules, most common form of renal cancer.

280
Q

Most common subtype of RCC?

A

Clear cell renal carcinoma

281
Q

What is Wilms’ tumour?

A

Specific kidney tumour affecting young children.

282
Q

Risk factors for RCC?

A
  • smoking
  • obesity
  • hypertension
  • end-stage renal failure
  • von-hippel lindau
  • haemodialysis
283
Q

What is Von-Hippel Lindau?

A

Rare genetic multi-system disorder characterised by the development of benign tumours, with potential for malignant transformation.

284
Q

Signs and symptoms of RCC?

A
  • haematuria
  • loin pain
  • weight loss
  • fatigue
  • anorexia
  • night sweats
  • renal mass
285
Q

Local spread of RCC?

A

Within the renal fascia, renal vein, inferior vena cava.

286
Q

Common presentation of metastatic RCC?

A

Cannonball lung metastases

287
Q

Paraneoplastic syndromes associated with RCC?

A
  • polycythaemia (unregulated EPO)
  • hypercalcaemia (secretion of PTH mimicking hormone)
  • hypertension
  • Stauffer’s syndrome
288
Q

What is Stauffer’s syndrome?

A

Paraneoplastic syndrome seen in RCC. Causes abnormal LFTs without liver metastasis.

289
Q

First line investigation for RCC?

A

Abdominal / pelvic ultrasound.

290
Q

Gold-standard investigation for RCC staging?

A

CT thorax, abdomen, pelvis.

291
Q

Investigations for RCC?

A
  • abdominal / pelvic ultrasound
  • CT thorax, abdomen, pelvis
  • biopsy (or pathology post-resection)
  • FBC - increased haematocrit
  • LFT derangement
  • serum creatinine - elevated
  • urinalysis - haematuria / proteinuria
292
Q

Management of RCC?

A

Surgical resection (partial or radical nephrectomy).
Other options are arterial embolisation or radiofrequency ablation.
Chemotherapy / radiotherapy.

293
Q

Most common type of bladder cancer?

A

Transitional cell carcinoma

294
Q

Risk factors for bladder cancer?

A
  • smoking
  • increased age
  • aromatic amine exposure (dye and rubber industries)
  • pelvic irradiation
  • bladder stone (chronic inflammation)
295
Q

Clinical presentation of bladder cancer?

A

Painless haematuria

296
Q

Gold standard investigation for bladder cancer?

A

Cystoscopy and biopsy.

297
Q

Management of bladder cancer?

A
  • transurethral resection of bladder tumour
  • post-TURBT intravesical chemotherapy
  • radical cystectomy
  • intravesical BCG
  • chemotherapy / radiotherapy
298
Q

Most common type of prostate cancer?

A

Adenocarcinoma

299
Q

Risk factors for prostate cancer?

A
  • increasing age

- family history

300
Q

Local invasion of prostate cancer?

A
  • seminal vesicles
  • peri-prostatic tissue
  • bladder neck
301
Q

Sites of metastasis of prostate cancer?

A
  • bone
  • liver
  • lungs
302
Q

Grading system of prostate cancer?

A

Gleason score

303
Q

Clinical manifestations of prostate cancer?

A
  • LUTS
  • erectile dysfunction
  • lethargy, anorexia, weight loss
  • haematuria
  • asymmetric, firm, nodular prostate on DRE
304
Q

What is PCA3?

A

Urinary marker of prostate cancer.

305
Q

Gold standard investigation for prostate cancer?

A

Prostate biopsy (guided by ultrasound / MRI).

306
Q

Differentials for prostate cancer?

A
  • benign prostatic hyperplasia

- chronic prostatitis

307
Q

What options are there to actively treat prostate cancer?

A
  • radical prostatectomy
  • radiotherapy
  • androgen deprivation therapy
  • brachytherapy (insertion of radioactive source into prostate)
308
Q

Risk factors for testicular cancer?

A
  • undescended testes
  • male infertility
  • family history
309
Q

Clinical presentation of testicular cancer?

A 
Usually painless lump on the testicle.
- non-tender
- hard
- irregular
- not fluctuant
- no transillumination
Gynaecomastia may be present.
310
Q

Investigation to confirm testicular cancer?

A

Scrotal ultrasound

311
Q

Which type of testicular cancer causes raised alpha fetoprotein?

A
  • teratoma

- yolk sac tumour

312
Q

Which type of testicular cancer causes raised beta-hCG?

A
  • seminoma

- choriocarcinoma

313
Q

Staging system for testicular cancer?

A

Royal Marsden

314
Q

Management of testicular cancer?

A
  • radical orchidectomy
  • chemotherapy
  • radiotherapy
315
Q

Long term treatment side effects of testicular cancer?

A
  • infertility
  • hypogonadism
  • secondary cancers
316
Q

Function of PSA?

A

Liquefies semen

317
Q

How does BPH present?

A

LUTS

  • urinary frequency
  • urinary urgency
  • urine retention
  • hesistancy
  • terminal dribbling
  • weak flow
  • incomplete empyting
318
Q

Investigations for BPH?

A
  • DRE

- serum PSA (normal)

319
Q

Management of BPH?

A
  1. tamsulosin (alpha blocker).

2. finasteride (5-alpha reductase inhibitor).

320
Q

What is a testicular varicocele?

A

Abnormal enlargement of testicular veins within the pampiniform plexus.

321
Q

Presentation of testicular varicocele?

A

‘Bag of worms’ appearance.

322
Q

Investigations for testicular varicocele?

A

Doppler ultrasound

323
Q

What side do varicoceles most commonly occur on?

A

Left side

324
Q

Management of testicular varicocele?

A
  • usually conservative

- surgical intervention if symptomatic

325
Q

What is a hydrocele?

A

Fluid in the tunica vaginalis causing scrotal swelling.

326
Q

Presentation of testicular hydrocele?

A
  • soft
  • non-tender
  • transluminous
327
Q

Management of hydrocele?

A

Conservative

328
Q

Testicular torsion vs epididymitis?

A

Prehn’s sign is positive in epididymitis, negative in testicular torsion.

329
Q

What is Prehn’s sign?

A

Relief of pain on elevation of the affected testicle.

330
Q

Management of epididymitis?

A

IM ceftriaxone and oral doxycycline.

331
Q

What is testicular torsion?

A

Rotation of the testicle around the spermatic cord. Without intervention, leads to ischaemia and loss of the testis.

332
Q

Clinical presentation of testicular torsion?

A
  • sudden severe pain in scrotum and lower abdomen on affected side
  • swelling, redness, tenderness of testicle
  • upward retraction of testicle
333
Q

Management of testicular torsion?

A

Immediate surgical detorsion.

334
Q

Most common cause of scrotal swelling?

A

Epididymal cyst (lump on posterior aspect of testicle) - self-resolves.

335
Q

Defining features of nephritic syndrome?

A
  • haematuria
  • oliguria
  • proteinuria (sub-nephrotic range)
  • hypertension (due to fluid overload)
336
Q

Causes of nephritic syndrome?

A
  • SLE
  • post streptococcal glomerulonephritis
  • small vessel vasculitis (granulomatosis with polyangiitis)
  • anti-GBM disease (Goodpasture’s)
  • IgA nephropathy
337
Q

Gold standard investigation for nephritic syndrome?

A

Kidney biopsy

338
Q

Management of nephritic syndrome?

A
  • treat underlying cause
  • blood pressure control (ACEi / ARB)
  • corticosteroids to reduce kidney damage
339
Q

Most common cause of nephritic syndrome in the UK?

A

IgA nephropathy

340
Q

What is IgA nephropathy?

A

Glomerulonephritis caused by IgA immune deposits in the mesangium.

341
Q

What is Henoch-Schonlein purpura?

A

IgA vasculitis

342
Q

Common presentation of IgA nephropathy?

A

Asymptomatic with microscopic haematuria.

343
Q

What is post-streptococcal glomerulonephritis?

A

Glomerulonephritis occuring 1-3 weeks after a beta haemolytic strep infection (strep pyogenes). Presents with nephritic syndrome.

344
Q

Pathophysiology of post-strep GN?

A

Immune complexes of streptococcal antigens, antibodies, and complement proteins get stuck in the glomeruli and cause inflammation.

345
Q

Blood markers for strep pyogenes infection?

A

Anti-streptolysin antibodies.

346
Q

What is haemolytic uraemic syndrome?

A

Thrombosis occurs in small vessels throughout the body, usually triggered by the shiga toxin.

347
Q

Classic triad of HUS?

A
  • haemolytic anaemia
  • AKI
  • thrombocytopenia
348
Q

Which pathogens produce the Shiga toxin?

A
  • E. coli

- shigella

349
Q

What causes haemolytic anaemia in HUS?

A

Shearing forces created by blood clots.

350
Q

What causes AKI in HUS?

A

Impaired blood flow through the kidney, due to blood clots.

351
Q

Typical clinical presentation of HUS?

A

Symptoms manifest around 5 days after gastroenteritis (with bloody diarrhoea).

  • oliguria
  • haematuria
  • abdominal pain
  • confusion (uraemia)
  • bruising
  • pallor
352
Q

Investigations for HUS?

A
  • FBC (anaemia and thrombocytopenia)
  • peripheral blood smear (schistocytes)
  • serum creatinine (elevated)
  • stool culture on sorbitol MacConkey (E. coli O157 does not ferment sorbitol)
  • PCR for shiga toxin from stool samples
353
Q

Management of HUS?

A

Supportive care:

  • anti-hypertensives
  • blood transfusions
  • haemodialysis
354
Q

What is Goodpasture’s syndrome?

A

Anti-GBM disease - a rare small vessel vasculitis. Anti-GBM antibodies target type IV collagen in the kidneys and lungs, leading to life-threatening glomerulonephritis or pulmonary haemorrhage.

355
Q

What is vasculitis?

A

Inflammation of blood vessels.

356
Q

Signs and symptoms of Goodpasture’s syndrome?

A
  • constitutional features (lethargy, anorexia, weight loss, myalgia / arthralgia)
  • renal manifestations (nephritic syndrome)
  • pulmonary manifestations: cough, dyspnoea, haemoptysis, pulmonary haemorrhage
357
Q

Investigations for Goodpasture’s syndrome?

A
  • serum anti-GBM antibodies
  • renal biopsy (crescentic glomerulonephritis)
  • CXR / CT chest
358
Q

Management of Goodpasture’s syndrome?

A
  • plasmapheresis
  • immunosuppression - steroids and cyclophosphamides
  • haemodialysis
  • supportive pulmonary measures (intubation and ventilation)
359
Q

What is rapidly-progressive glomerulonephritis?

A

GN often occuring secondary to Goodpasture’s syndrome.

360
Q

Clinical presentation of rapidly-progressive GN?

A

Very acute illness with rapid deterioration in renal function. Presents with nephritic syndrome.

361
Q

Investigations for rapidly-progressive glomerulonephritis?

A

Renal biopsy shows crescentic glomerulonephritis.

362
Q

Management of rapidly-progressive glomerulonephritis?

A
  • immunosuppression
  • plasmapheresis
  • haemodialysis
  • anti-hypertensives
363
Q

How does Henoch-Schonlein purpura present?

A
  • purpuric rash on legs
  • nephritic syndrome
  • joint pain (due to IgA deposition)
364
Q

How is Henoch-Schonlein purpura managed?

A
  • corticosteroids

- ACE inhibitor / ARB for hypertension control

365
Q

Why does nephrotic syndrome occur?

A

Problem with the glomerular filtration barrier, primarily involving the podocytes. This results in the classic triad of proteinuria, hypoalbuminaemia, and oedema.

366
Q

Nephrotic proteinuria?

A

> 3g per 24 hours.

367
Q

Primary causes of nephrotic syndrome?

A
  • minimal change disease
  • focal segmental glomerulosclerosis
  • membranous nephropathy
368
Q

Secondary causes of nephrotic syndrome?

A
  • diabetes
  • drugs
  • autoimmune
  • neoplasia
  • infection
369
Q

Signs and symptoms of nephrotic syndrome?

A
  • oedema

- frothy urine (due to proteinuria)

370
Q

Investigations for nephrotic syndrome?

A
  • urinalysis
  • 24 hour urinary protein (> 3 g/day)
  • urine protein:creatinine ratio
  • renal biopsy
  • U&Es
  • lipid profile (hyperlipidaemia)
371
Q

Why does hyperlipidaemia occur in nephrotic syndrome?

A

Loss of albumin increases cholesterol formation.

372
Q

Management of nephrotic syndrome?

A
  • fluid and salt restriction
  • loop diuretics (for oedema)
  • treat underlying cause
  • ACE inhibitor / ARB to reduce proteinuria
  • statin for hyperlipidaemia
373
Q

Complications of nephrotic syndrome?

A

Venous thromboembolism due to increased clotting factors.

374
Q

How is VTE managed in nephrotic syndrome?

A

Anticoagulation (e.g. LMWH)

375
Q

Causes of focal segmental glomerulosclerosis?

A

Primary FSGS, or secondary to severe obesity or reflux nephropathy.

376
Q

Pathophysiology of primary FSGS?

A
  • circulating factor damages podocytes, leading to podocyte foot process effacement
  • this causes them to spread out and reduces the effectiveness of the filtration barrier
377
Q

Management of FSGS?

A

Primary - immunosuppression with steroids.
Secondary - treat underlying cause.
Blood pressure control (ACE inhibitor).

378
Q

What is membranous nephropathy?

A

Glomerular basement membrane thickening in the absence of significant cellular proliferation, leading to nephrotic syndrome.

379
Q

What causes membranous nephropathy?

A

Can be primary or secondary to SLE, viral hepatitis, prostate cancer, NSAID use.

380
Q

Pathophysiology of primary membranous nephropathy?

A
  • autoimmune reaction against antigens in the filtration barrier, with autoantibody development and immune complex deposition
  • this leads to thickening of the glomerular basement membrane
381
Q

What antibodies are seen in primary membranous nephropathy?

A

Anti-phospholipase A2 receptor antibodies.

382
Q

Investigations for primary membranous nephropathy?

A
  • serum anti-phospholipase A2 receptor antibodies

- renal biopsy

383
Q

Management of membranous nephropathy?

A
  • blood pressure control (ACE inhibitor)
  • primary: immunosuppression
  • secondary: treat underlying cause
384
Q

What is minimal change disease?

A

Most common cause of nephrotic syndrome in children.

385
Q

Causes of minimal change disease?

A

Majority of cases are idiopathic, but drugs, infection, or malignancy may be causes.

386
Q

Pathophysiology of minimal change disease?

A

Immune dysfunction leads to the production of a permeability factor that disrupts the filtration barrier. This leads to the fusion of podocyte foot processes.

387
Q

Management of minimal change disease?

A

Prednisolone

388
Q

How many adult cases of nephrotic syndrome are caused by minimal change disease?

A

25%

389
Q

Microscopy appearance in minimal change disease?

A

Normal

390
Q

Most common cause of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis.

391
Q

Does nephritic or nephrotic syndrome impact GFR more?

A

Nephritic syndrome

392
Q

Where does bladder cancer spread?

A
  • iliac and para-aortic lymph nodes
  • liver
  • lungs
393
Q

What is a UTI?

A

Infection of any part of the urinary tract (kidney to urethra). Presents with characteristic symptoms and bacteriuria.

394
Q

What is an upper UTI?

A

Pyelonephritis

395
Q

What is a lower UTI?

A

Infection of the bladder / urethra.

396
Q

UTIs are considered uncomplicated in what group of patients?

A

Healthy, non-pregnant females.

397
Q

What factors complicate a UTI?

A
  • male
  • diabetes
  • infant < 3 months
  • catheters
  • pregnancy
398
Q

Most common cause of UTI?

A

E. coli

399
Q

Causes of UTI?

A
  • klebsiella pneumoniae
  • e. coli
  • enterococci
  • proteus mirabilis
  • staphylococcus saprophyticus
400
Q

Which organism commonly causes renal stone associated UTI?

A

Proteus mirabilis

401
Q

Which organism commonly causes catheter associated UTI?

A

Klebsiella pneumoniae

402
Q

Which organism commonly causes UTI in young women?

A

Staphylococcus saprophyticus

403
Q

Risk factors for UTI?

A
  • recent sexual intercourse
  • diabetes
  • history of UTIs
  • catheters
404
Q

Why are UTIs uncommon in men?

A
  • longer urethra
  • anti-microbial properties of prostatic secretions
  • drier periurethral area
405
Q

Typical signs and symptoms of UTI?

A
  • dysuria (burning pain)
  • increased urinary frequency
  • urgency
  • incontinence
406
Q

What signs and symptoms of UTI indicate pyelonephritis?

A
  • nausea & vomiting
  • fever
  • flank pain and costovertebral angle tenderness
  • pyuria
407
Q

Red flags for urosepsis?

A
  • haemodynamic instability (tachycardia and hypotension)
  • tachypnoea
  • changes to mental status
  • reduced urine output
  • pyrexia
408
Q

Investigations for UTI?

A
  • midstream urine MC&S
  • urine dipstick - leucocytes and nitrites, haematuria
  • U&Es (renal function may be impaired)
  • ultrasound - may show obstruction
409
Q

Antibiotic course length for females vs males in uncomplicated lower UTI?

A

Females - 3 days

Males - 7-14 days

410
Q

Antibiotics for lower UTI?

A

Trimethoprim / nitrofurantoin / cefalexin

411
Q

Antibiotics for uncomplicated pyelonephritis?

A

Oral ciprofloxacin (14 days)

412
Q

Empirical treatment for urosepsis?

A

Piperacillin / tazobactam

413
Q

Antibiotics for complicated cystitis / pyelonephritis?

A

IV co-amoxiclav

414
Q

Management of urosepsis?

A

3 in:

  • oxygen
  • antibiotics
  • fluids

3 out:

  • serial lactates
  • blood cultures
  • urine output
415
Q

What symptom indicates cystitis?

A

Suprapubic tenderness / discomfort.

416
Q

Most common cause of prostatitis?

A

E. coli

417
Q

How does acute bacterial prostatitis present?

A
  • very tender prostate on DRE
  • fever, chills, malaise
  • voiding symptoms (dysuria)
418
Q

Investigations for acute bacterial prostatitis?

A
  • urinalysis (haematuria, leucocytes)
  • midstream urine MC&S
  • blood cultures in febrile patients
419
Q

Management of acute bacterial prostatitis?

A

Ciprofloxacin (14 days).

420
Q

Most common bacterial STI?

A

Chlamydia (caused by chlamydia trachomatis).

421
Q

Second most common bacterial STI?

A

Gonorrhoea (caused by neisseria gonorrhoea).

422
Q

How does chlamydia present?

A

Males - testicular pain, dysuria.

Females - vaginal discharge, dysuria.

423
Q

How is chlamydia diagnosed?

A

Nucleic acid amplification testing.

424
Q

How is chlamydia managed?

A
  • 1g single oral dose of azithromycin OR

- 7 day course of doxycycline BD

425
Q

How does gonorrhoea present?

A

Males - dysuria, frequency, discharge.

Females - pelvic pain, dysuria, vaginal discharge.

426
Q

Investigations for gonorrhoea?

A
  • nucleic acid amplification testing

- swab of infected areas for microscopy and culture

427
Q

Treatment for gonorrhoea?

A

Single dose of IM ceftriaxone.

428
Q

First line investigation for renal stones?

A

KUB X ray

429
Q

Gold standard investigation for renal stones?

A

Non-contrast CT-KUB

430
Q

Common locations for renal stones?

A
  • vesico-ureteric junction
  • pelvic brim
  • pelvico-ureteric junction
431
Q

What is autosomal dominant polycystic kidney disease?

A

Common genetic disorder characterised by the development of multiple renal cysts and progressive renal impairment.

432
Q

What two gene mutations cause PKD?

A

PKD1 and PKD2

433
Q

Most common gene mutation of ADPKD?

A

PKD1

434
Q

Investigations for polycystic kidney disease?

A
  • ultrasound (multiple bilateral cysts)
  • LFTs
  • MR angiography for cerebral aneurysm screening
  • genetic testing
  • urine protein:creatinine ratio
435
Q

Management of PKD?

A
  • blood pressure control with ACE inhibitors
  • cyst decompression
  • nephrectomy
  • renal transplant if CKD
  • treat complications (infected cysts)
436
Q

Complications of PKD?

A
  • polycystic liver disease
  • pancreatic cysts
  • cerebral aneurysms
437
Q

Functions of the kidney?

A
  • EPO secretion
  • acid-base balance
  • waste product excretion
  • activation of vitamin D
  • regulation of BP (RAA system)
  • fluid volume balance
438
Q

Medical emergency most associated with acute kidney injury?

A

Hyperkalaemia

439
Q

2 week wait referral criteria for bladder cancer?

A

Over 45 with unexplained visible haematuria with no UTI / haematuria persists after resolution of UTI.

440
Q

How can you identify a true scrotal mass?

A

You can palpate above a true mass.

441
Q

Conditions associated with erectile dysfunction?

A
  • diabetes mellitus
  • hypertension
  • pelvic fracture
  • prostatectomy
  • liver disease
  • renal failure
442
Q

What is Crohn’s disease?

A

Inflammatory bowel disease involving the full thickness of the intestinal wall. Affects discrete parts of the GI tract, leaving normal areas in between (‘skip lesions’).

443
Q

Is Crohn’s autoimmune?

A

Not auto-immune, but immune-mediate. Caused by environmental trigger in genetically susceptible individuals.

444
Q

Risk factors for Crohn’s?

A
  • family history
  • genetics (NOD2 mutation)
  • smoking
  • infectious gastroenteritis
445
Q

Signs and symptoms of Crohn’s?

A
  • diarrhoea (may be bloody)
  • right lower quadrant pain (terminal ileum)
  • fatigue, malaise, weight loss, anorexia
  • aphthmous mouth ulcers
  • joint pains
  • inflammatory eye disease
446
Q

Gold standard investigation for Crohn’s?

A

Colonoscopy - take multiple samples for biopsy.

447
Q

Investigations for Crohn’s?

A
  • colonscopy and biopsy
  • upper GI endoscopy (if upper GI symptoms)
  • FBC (anaemia)
  • faecal calprotectin
448
Q

Differentials for Crohn’s?

A
  • ulcerative colitis
  • pseudomembranous colitis
  • diverticulitis
  • coeliac disease
  • IBS
449
Q

Management of Crohn’s?

A
  • corticosteroids / immunosuppressants (azathioprine) / anti-TNF agents
  • surgery for fissures and strictures
  • bowel resection
  • stop smoking
  • vitamin & mineral supplements
450
Q

Complications of Crohn’s?

A
  • intestinal strictures
  • GI haemorrhage
  • osteoporosis
  • GI dilatation and perforation
  • anaemia
  • bowel cancer
451
Q

What is ulcerative colitis?

A

Chronic inflammatory disease of the GI tract. Characterised by diffuse, continuous inflammation of the large bowel, limited to the mucosa. Affects the rectum with a variable length of colon involved proximally.

452
Q

Subtypes of UC?

A
  • proctitis
  • proctosigmoiditis
  • left-sided colitis
  • pancolitis
453
Q

Aetiology of UC?

A

Immune mediated disease, possibly initiated by inflammation in response to colonic bacteria.
Occurs in genetically susceptible people in response to environmental triggers.

454
Q

Risk factors for UC?

A
  • family history
  • non-smoker
  • NSAIDs
455
Q

What is seen on histology in UC?

A
  • crypt abscesses filled with granulocytes
  • continuous inflammation involving the intestinal mucosa
  • goblet cell depletion
456
Q

Signs and symptoms of UC?

A
  • persistent diarrhoea (may contain blood / mucus)
  • abdominal pain (usually left lower quadrant)
  • increased frequency of defecation
  • faecal urgency / incontinence
  • tenesmus
  • fatigue, malaise, anorexia, weight loss
  • pallor
  • aphthous mouth ulcers
  • eye / joint / skin involvement
457
Q

What is tenesmus?

A

Persistent painful urge to pass stool even when the rectum is empty.

458
Q

Extra-intestinal manifestations of UC?

A
  • arthritis
  • erythema nodosum
  • uveitis
  • primary sclerosing cholangitis
459
Q

Gold standard investigation for UC?

A

Colonoscopy (or flexible sigmoidoscopy) with biopsy.

460
Q

Investigations for UC?

A
  • colonoscopy with biopsy
  • stool microscopy & culture (negative)
  • FBC (anaemia)
  • faceal calprotectin
461
Q

Investigation for UC presenting with acute abdomen?

A

AXR - exclude toxic megacolon, bowel obstruction, perforation.

462
Q

Differentials for UC?

A
  • Crohn’s disease
  • pseudomembranous colitis
  • diverticulosis
  • coeliac disease
  • IBS
463
Q

Drugs for mild UC?

A

Aminosalicylates (mesalazine).

Second line - add corticosteroid.

464
Q

Drugs for moderate / severe UC?

A
  • systemic corticosteroids
  • methotrexate
  • anti-TNF agent
465
Q

When is surgery indicated in UC?

A
  • if pharmacological management of moderate / severe UC is ineffective
  • acute severe UC if IV corticosteroids are ineffective
  • acute severe UC with toxic megacolon / bowel perforation
466
Q

Complications of UC?

A
  • toxic megacolon
  • bowel obstruction
  • bowel perforation
  • anaemia
  • fistulas & strictures
  • colorectal cancer
  • PSC
467
Q

What is IBS?

A

Chronic functional bowel disorder characterised by abdominal pain and altered bowel habits.

468
Q

What meant by a functional GI disorder?

A

Disorder not associated with structural or biochemical abnormalities. Symptoms are thought to be the result of dysregulation between the gut and the brain.

469
Q

Risk factors for IBS?

A
  • female
  • young
  • stressful life events
  • anxiety / depression
470
Q

Signs and symptoms of IBS?

A
  • abdominal pain
  • diarrhoea (not nocturnal)
  • tenesmus
  • constipation
  • bloating & distention
  • nausea
471
Q

Criteria for IBS diagnosis?

A

Rome IV: recurrent abdominal pain occurring on average at least one day per week over the last 3 months (6 months since symptom onset).

  • pain related to defecation
  • associated with a change in stool frequency / form
472
Q

Investigations for IBS?

A

Investigations for exclusion:

  • faecal calprotectin
  • FBC
  • CRP
  • coeliac serology
  • endoscopy
473
Q

Differentials for IBS?

A
  • Crohn’s disease
  • ulcerative colitis
  • colorectal cancer
  • coeliac disease
474
Q

Management of IBS?

A
  • dietary changes (low FODMAP diet, avoid lactose / gluten, avoid excaerbating foods)
  • laxatives / loperamide
  • CBT
  • tricyclic antidepressants
475
Q

What is functional dyspepsia?

A

Functional GI disorder, characterised by:

  • bothersome post-prandial fullness
  • bothersome early satiation
  • bothersome epigastric pain / burning
476
Q

Management of functional dyspepsia?

A

After failure of PPI trial - tricyclic antidepressant / psychotherapy.

477
Q

What is coeliac disease?

A

Systemic autoimmune disease condition triggered by dietary gluten peptides, causing inflammation and damage to the small intestine.

478
Q

Genetic associations in coeliac disease?

A
  • HLA-DQ2

- HLA-DQ8

479
Q

Example of a prolamin?

A

Gliadin

480
Q

Pathophysiology of coeliac diease?

A
  • gliadin enters the lamina propria, where it is deaminated by tissue transglutaminase
  • deaminated gliadin is more immunogenic, and it binds to antigen-presenting immune cells
  • T helper cells are activated and secrete pro-inflammatory cytokines, and activate B cells
  • B cells produce auto-antibodies (anti-tTG and anti-endomysial)
  • immune system activation leads to chronic inflammation and damage, resulting in intra-epithelial lymphocyte activation, villous atrophy, and crypt hyperplasia
481
Q

Signs and symptoms of coeliac disease?

A
  • weight loss
  • fatigue
  • loose stools
  • steatorrhoea
  • mouth ulcers & angular stomatitis
  • anaemia
  • dermatitis herpetiformis
482
Q

Features of dermatitis herpetiformis?

A

Blistering, itchy rash on extensor surfaces.

483
Q

Gold standard investigation for coeliac disease?

A

Small bowel endoscopy with biopsy (multiple samples from both the duodenal bulb and distal duodenum).

484
Q

Histological findings in coeliac disease?

A
  • intra-epithelial lymphocytes
  • villous atrophy
  • crypt hyperplasia
485
Q

Investigations for coeliac disease?

A
  • elevated IgA-tTG
  • anti-endomysial antibodies
  • skin biopsy shows granular IgA deposits in dermatitis herpetiformis
  • FBC (anaemia)
  • HLA typing
486
Q

Management of coeliac disease?

A
  • gluten-free diet

- steroids & immunomodulatory drugs if refractory coeliac disease

487
Q

How is dermatitis herpetiformis treated?

A

Dapsone (oral sulphonamide antibiotic) and topical steroid cream.

488
Q

What is GORD?

A

Reflux of stomach contents into the oesophagus, characterised by symptoms of heartburn and acid regurgitation.

489
Q

Risk factors for GORD?

A
  • high BMI
  • smoking
  • pregnancy
  • hiatus hernia
490
Q

Pathophysiology of GORD?

A

Inappropriate relaxation of the lower oesophageal sphincter, allowing stomach contents to wash back into the oesophagus. Acidity of stomach contents results in damage to the oesophageal epithelium over time.

491
Q

Signs and symptoms of GORD?

A
  • heartburn
  • regurgitation
  • dyspepsia
  • cough
  • hoarse voice
  • dysphagia
  • nausea and vomiting
492
Q

Investigations for GORD?

A
  • pH monitoring via nasal tube

- gastroscopy (may be normal or show oesophagitis, Barrett’s oesophagus)

493
Q

Pharmacological management of GORD?

A
  • PPIs
  • histamine receptor antagonists
  • antacids
494
Q

How do PPIs work?

A

Inhibit H+/K+ ATPase in parietal cells, preventing gastric acid production.

495
Q

Example of histamine receptor antagonist?

A

Ranitidine

496
Q

What is erosive oesophagitis?

A

Inflammation caused by reflux of stomach contents into the oesophagus, resulting in ulcer formation, bleeding, and peptic strictures.

497
Q

What is Barrett’s oesophagus?

A

Metaplasia in the cells of the lower portion of the oesophagus - stratified squamous epithelium replaced by simple columnar epithelium with goblet cells.

498
Q

What cancer is Barrett’s oesophagus associated with?

A

Oesophageal adenocarcinoma

499
Q

Risk factors for Barrett’s oesophagus?

A
  • GORD
  • smoking
  • obesity
  • male
  • older age
  • hiatus hernia
500
Q

Investigation for Barrett’s oesophagus?

A

Endoscopy with tissue biopsy.

501
Q

Management of Barrett’s oesophagus?

A
  • PPIs
  • stop NSAIDs
  • weight loss
  • reduce alcohol intake
  • smoking cessation
  • Nissen fundoplication
  • regular endoscopies to monitor progression
502
Q

What is a Nissen fundoplication?

A

Fundus of stomach is wrapped and stapled around the lower oesophagus - used to treat GORD / Barrett’s oesophagus.

503
Q

What are the two main types of oesophageal cancer?

A
  • squamous cell carcinoma

- adenocarcinoma

504
Q

Most common type of oesophageal cancer in the UK?

A

Adenocarcinoma

505
Q

Risk factors for oesophageal cancer?

A
  • older age
  • radiotherapy
  • smoking
  • obesity
  • Barrett’s oesophagus
  • GORD
506
Q

Where does squamous cell carcinoma most commonly occur?

A

Middle third of the oesophagus.

507
Q

Where does adenocarcinoma of the oesophagus most commonly occur?

A

Distal third of the oesophagus.

508
Q

Signs and symptoms of oesophageal cancer?

A
  • weight loss
  • dysphagia
  • persistent indigestion / heartburn
  • retrosternal pain
  • food regurgitation
  • persistent cough
  • hoarse voice
  • haematemesis
  • dark stool
509
Q

Investigations for oesophageal cancer?

A
  • endoscopy and biopsy
  • CT
  • PET-CT
510
Q

Management of oesophageal cancer?

A
  • chemotherapy
  • radiotherapy
  • endoscopic mucosal resection
  • oesophagectomy
  • oesophageal stent
511
Q

Stomach cancer typical type?

A

Adenocarcinoma

512
Q

Most common histological type of stomach cancer?

A

Intestinal (also has better prognosis than diffuse).

513
Q

Anatomical classification of stomach cancer?

A

Distal - antrum / pylorus.

Proximal - cardia.

514
Q

What type of stomach cancer is more associated with H. pylori infection?

A

Distal

515
Q

Which type of stomach cancer is commonly seen in countries with high incidence?

A

Distal (proximal more likely in countries with low incidence).

516
Q

Risk factors for stomach cancer?

A
  • smoking
  • high salt intake
  • low fruit and vegetable intake
  • H. pylori infection
  • EBV
  • family history
517
Q

How does H. pylori increase risk of stomach cancer?

A

Causes inflammation, and secretes CagA into host cells (oncogenic protein).

518
Q

Signs and symptoms of stomach cancer?

A
  • anorexia, lethargy, weight loss, malaise
  • dyspepsia
  • nausea and vomiting
  • haematemesis
  • melaena
  • early satiety and post-prandial fullness (due to obstruction)
  • lymphadenopathy (Virchow node)
  • Sister Mary Joseph nodule
519
Q

Paraneoplastic syndromes associated with stomach cancer?

A
  • acanthosis nigricans (skin hyperpigmentation)
  • dermatomyositis
  • erythma gyratum repens (ring-shaped appearance, involves limbs and trunk)
520
Q

Gold standard investigation for stomach cancer?

A

Gastroscopy and biopsy.

521
Q

Common sites of metastasis of stomach cancer?

A
  • liver
  • lung
  • peritoneum
  • bone
522
Q

Management of stomach cancer?

A
  • resection (endoscopic submucosal dissection / gastrectomy)
  • chemotherapy (adjunct or primary treatment for non-operable cancer)
  • trastuzumab
523
Q

Which immunological therapy can be used to treat stomach cancer?

A

Trastuzumab (herceptin)

524
Q

Risk factors for bowel cancer?

A
  • family history
  • familial adenomatous polyposis
  • hereditary nonpolyposis colorectal cancer
  • IBD
  • increased age
  • diet (low fibre, high red / processed meat intake)
  • obesity
  • smoking & alcohol
  • sedentary lifestyle
525
Q

Two hereditary risk factors for bowel cancer?

A
  • familial adenomatous polyposis

- hereditary nonpolyposis colorectal cancer

526
Q

What is familial adenomatous polyposis?

A
  • autosomal dominant
  • malfunctioning of tumour suppressor genes results in development of adenomas along the colon
  • adenomas have the potential to become cancerous
527
Q

What is hereditary nonpolyposis colorectal cancer?

A
  • autosomal dominant
  • increases risk of a number of cancers
  • does not cause adenomas, tumours develop in isolation
528
Q

Red flags for bowel cancer?

A
  • change in bowel habit (diarrhoea)
  • unexplained weight loss
  • rectal bleeding
  • unexplained abdominal pain
  • IDA
  • abdominal / rectal mass
529
Q

Acute presentation of bowel cancer?

A

Bowel obstruction - vomiting, abdominal pain, absolute constipation.

530
Q

Screening for bowel cancer?

A

FIT tests (faecal immunochemical tests).

531
Q

What do FIT tests detect?

A

Human Hb in stool (to detect bleeding).

532
Q

Investigations for bowel cancer?

A
  • colonoscopy and biopsy
  • CT colonography
  • CT chest, abdomen, pelvis
  • serum CEA (carcinoembryonic antigen)
533
Q

Gold standard investigation for bowel cancer?

A

Colonoscopy and biopsy.

534
Q

Tumour marker for bowel cancer?

A

CEA (carcinoembryonic antigen).

535
Q

Management of bowel cancer?

A
  • surgical resection (with end-to-end anastomosis or stoma)
  • chemotherapy
  • radiotherapy
536
Q

Complications of bowel resection?

A
  • nerve damage
  • bladder / ureter / bowel damage
  • post-operative ileus
  • failure of anastomosis
  • incisional hernia
  • intra-abdominal adhesions
537
Q

What is Hartmann’s procedure?

A

Proctosigmoidectomy with creation of Hartmann’s pouch (sealed remnant of rectum). Remaining colon is redirected to a colostomy. May be reversed later/

538
Q

What is peptic ulcer disease?

A

The development of gastric and duodenal ulcers - characterised by dyspepsia, abdominal discomfort, and nausea.

539
Q

Erosion vs ulcer?

A

Erosion - superficial or partial break within the epithelium or mucosal surface.
Ulcer - deep break through the full thickness of the epithelium or mucosal surface.

540
Q

Causes of PUD?

A
  • H. pylori (95% duodenal ulcers, 70-80% gastric ulcers).
  • drugs (NSAIDs, corticosteroids)
  • alcohol
  • Zollinger-Ellison syndrome
  • malignancy
541
Q

What is Zollinger-Ellison syndrome?

A

Hyper-secreting gastrinoma in the pancreas leads to hypergastrinaemia. This leads to peptic ulcer development.

542
Q

How do NSAIDs cause ulcers?

A
  • inhibition of COX-1 enzymes

- COX-1 enzymes have a protective effect on the gastric mucosa

543
Q

H. pylori microscopy?

A

Gram negative, spiral-shaped bacterium with flagella.

544
Q

What area of the stomach does H. pylori predominantly colonise?

A

Antrum

545
Q

How does H. pylori lead to ulcer formation?

A
  • urease (converts urea into water and ammonia) buffers gastric acid and raises pH
  • H. pylori bind strongly to the gastric epithelium and secrete effector molecules into host cells via their type IV secretion system (CagA and VacA - disrupt tight junctions and induce apoptosis)
546
Q

Signs and symptoms of peptic ulcers?

A
  • epigastric pain
  • dyspepsia
  • heartburn
  • distention and bloating
  • upper GI bleed (haematemesis, melaena)
547
Q

Complications of peptic ulcers?

A
  • upper GI haemorrhage
  • perforation
  • gastric outlet obstruction
548
Q

Presentation of GI perforation (peptic ulcer disease)?

A
  • acute severe abdominal pain and tenderness
  • abdominal guarding
  • features of shock
549
Q

Presentation of gastric outlet obstruction?

A
  • nausea & vomiting
  • upper abdominal pain and tenderness
  • early satiety
  • distention
  • succussion splash
550
Q

Gold standard for diagnosis of PUD?

A

Upper GI endoscopy and biopsy

551
Q

Investigations for PUD?

A
  • upper GI endoscopy and biopsy
  • FBC (anaemia)
  • ECG (exclude cardiac pathology)
  • H. pylori testing
552
Q

What are some tests for H. pylori?

A
  • urea breath test
  • serum IgG against H. pylori
  • stool antigen test
  • histology & culture from biopsy
553
Q

Management of non H. pylori-associated PUD?

A

4-8 weeks PPI treatment.

554
Q

Management of H. pylori-associated PUD?

A

Eradication therapy - 7 day course:

  • PPI
  • amoxicillin
  • clarithromycin / metronidazole
555
Q

Causes of appendicitis?

A
  • faecolith (hard collection of stool)
  • lymphoid hyperplasia
  • fibrous stricture
  • carcinoid tumour
556
Q

Pathophysiology of appendicitis?

A
  • obstruction of lumen causes stasis and bacterial overgrowth
  • increase in intra-luminal pressure causes peri-umbilical pain
  • increased pressure causes venous and lymphatic congestion, and eventually compromises arterial blood supply to the appendix
  • results in gangrene, perforation and generalised peritonitis
557
Q

What is Rovsing’s sign?

A

Pain in the right iliac fossa on palpation of the left. Indicates appendicitis.

558
Q

Investigations for appendicitis?

A
  • pregnancy test
  • abdominal ultrasound
  • contrast-enhanced abdominal CT / abdominal MRI in pregnant women
559
Q

Differentials for appendicitis?

A
  • intussusception
  • peptic ulcer disease
  • ectopic pregnancy
  • ovarian torsion
  • cholecystitis
560
Q

Management of appendicitis?

A
  • pre-operative antibiotics (co-amoxiclav)
  • laparoscopic appendicectomy
  • temporary drain insertion in some cases
561
Q

What is the Rockall score?

A

Gives the risk of adverse outcomes following upper GI bleeding.

562
Q

What is achalasia?

A

Oesophageal motility disorder characterised by oesophageal aperistalsis and insufficient lower oesophageal sphincter relaxation in response to swallowing.

563
Q

Named signs seen in acute appendicitis?

A
  • Rovsing
  • psoas
  • obturator
564
Q

Gold standard for appendicitis?

A

CT scan

565
Q

Risk factors for hernia?

A
  • muscle weakness (abdominal wall surgery)
  • older age
  • pregnancy
  • increased intra-abdominal pressure (cough, constipation, weight lifting)
566
Q

Management of reducible vs non-reducible hernia?

A

Reducible - watch and wait.

Non-reducible - surgery.

567
Q

Complications of hernia?

A
  • bowel obstruction

- strangulation hernia (compression of blood supply)

568
Q

Sliding vs paraoesophageal hiatus hernia?

A

Sliding - stomach moves upwards and slides over the oesophagus.
Paraoesophageal - stomach moves upwards alongside the oesophagus.

569
Q

Diagnosis of hiatal hernia?

A

Barium swallow.

570
Q

Direct vs indirect inguinal hernia?

A

Direct - via defect in the posterior wall of the inguinal canal.
Indirect - via inguinal ring.

571
Q

Is a femoral hernia more common in females or males?

A

Females

572
Q

What is an anal fissure?

A

Small tear in the skin of the distal anal canal, caused by passage of hard stool.

573
Q

Symptoms of anal fissure?

A
  • severe pain during defecation
  • bright red blood
  • constipation
  • may be itchy
574
Q

Management of anal fissure?

A
  • stool softeners
  • leave to heal
  • sphincterectomy is gold standard
575
Q

What is a perianal abscess?

A

Infection in anal gland.

576
Q

Risk factors for perianal abscess?

A
  • immunosuppression
  • IBD
  • diabetes
577
Q

Symptoms of perianal abscess?

A
  • fever and chills
  • constant anal pain
  • pus in stool
578
Q

Management of perianal abscess?

A

Surgical removal and drainage.

579
Q

Signs of an anal fistula?

A
  • visible fistula
  • blood
  • pus
580
Q

Treatment of anal fistula?

A
  • drain infection

- surgical repair

581
Q

What are haemorrhoids?

A

Bulging veins in anus.

582
Q

Risk factors for haemorrhoids?

A
  • constipation

- increased abdominal pressure

583
Q

Investigation for haemorrhoids?

A

Endoscopy - DRE not helpful.

584
Q

Symptoms of haemorrhoids?

A
  • bulging pain in anus
  • feeling of incomplete emptying
  • itchy
  • bleeding
585
Q

Treatment of haemorrhoids?

A

Gold standard is rubber band ligation. Also stool softeners.

586
Q

Symptoms of pseudomembranous colitis?

A
  • watery diarrhoea
  • fever
  • dehydration
587
Q

Investigations for C. diff infection?

A

Stool sample MC&S

588
Q

What is Meckel’s diverticulum?

A

Congenital outpouching of all three layers of the small bowel, highly vascular so causes bleeding.

589
Q

Blood marker for ovarian cancer?

A

CA-125

590
Q

Blood marker for pancreatic cancer?

A

CA 19-9

591
Q

What is Zenker’s diverticulum?

A

Pharyngeal pouch

592
Q

Signs and symptoms of pharyngeal pouch?

A
  • dysphagia
  • halitosis
  • regurgitation of undigested food
  • hoarseness
  • chronic cough
593
Q

What does mesenteric ischaemia affect?

A

Small bowel

594
Q

What is a Mallory Weiss tear?

A

Haematemesis from tear in the oesophageal mucosa.

595
Q

Causes of Mallory Weiss tear?

A
  • bulimia
  • alcoholism
  • hyperemesis gravidarum
  • chronic cough
  • gastroenteritis
596
Q

Management of Mallory Weiss tear?

A
  • terlipressin
  • banding / clipping
  • thermocoagulation
597
Q

Investigations for Mallory Weiss tear?

A
  • Rockall score
  • ECG
  • endoscopy
598
Q

What is Boerhaave syndrome?

A

Oesophageal rupture.

Characterised by vomiting, chest pain and subcutaneous emphysema.

599
Q

What is Mackler’s triad?

A

Vomiting, chest pain, subcutaneous emphysema - oesophageal rupture.

600
Q

What is gastritis?

A

Inflammation of the stomach mucosa.

601
Q

Causes of gastritis?

A
  • autoimmune
  • H. pylori
  • bile reflux
  • NSAIDs
  • stress
602
Q

Presentation of gastritis?

A
  • epigastric pain
  • nausea and vomiting
  • dyspepsia
603
Q

Investigations for gastritis?

A
  • H. pylori testing

- endoscopy and biopsy

604
Q

Management of gastritis?

A
  • treat underlying cause

- H. pylori eradication

605
Q

Cause of Meckel’s diverticulum?

A

Incomplete obliteration of the vitelline duct.

606
Q

Complications of Meckel’s diverticulum?

A
  • intussusception
  • volvulus
  • hernia
607
Q

Rule of 2s for Meckel’s diverticulum?

A
  • 2 years old
  • 2 ft from ileocaecal valve
  • 2 inches long
  • 2% of the population
608
Q

Where are diverticula most likely to occur?

A

Sigmoid colon (smallest luminal diameter and highest pressure).

609
Q

Presentation of diverticulitis?

A
  • LIF pain and tenderness
  • LIF mass
  • constipation
  • tachycardia
  • fever
  • nausea
610
Q

Investigations for diverticulitis?

A

Bloods - raised WCC, ESR & CRP.

Imaging - CXR, AXR, CT

611
Q

Imaging findings in diverticulitis?

A
  • pneumoperitoneum
  • dilated bowel loops
  • obstruction
  • abscess
612
Q

Causes of peritonitis?

A
  • bacterial infection of ascitic fluid
  • bowel perforation
  • pelvic inflammatory disease
  • peritoneal dialysis infection
  • gall bladder perforation
  • appendicitis
613
Q

Management of diverticulitis?

A
  • antibiotics (oral / IV ciprofloxacin or metronidazole)
  • analgesia
  • liquid diet
  • surgical resection in rare cases
614
Q

Histological appearance of intestinal type stomach cancer?

A

Glandular

615
Q

Histological appearance of diffuse type stomach cancer?

A

Poorly differentiated, signet ring cells.

616
Q

2 week wait criteria for stomach cancer?

A

Upper abdominal mass AND

  • dysphagia (any age)
  • over 55 with weight loss and upper abdominal pain / reflux / dyspepsia
617
Q

Top 3 sites for bowel cancer?

A
  1. rectum
  2. sigmoid colon
  3. descending colon
618
Q

Staging system for colon cancer?

A

Dukes’

619
Q

Dukes’ Stage A

A

Cancer confined to the submucosa.

620
Q

Dukes’ Stage B

A

Invasion through muscularis without lymph node involvement.

621
Q

Dukes’ Stage C

A

Invasion through muscularis with lymph node involvement.

622
Q

Dukes’ Stage D

A

Distant metastasis

623
Q

Causes of mechanical small bowel obstruction?

A
  • surgical adhesions
  • tumour
  • strangulated hernia
  • volvulus
  • intussusception
  • inflammatory strictures
  • gallstone ileus
624
Q

Causes of mechanical large bowel obstruction?

A
  • volvulus (sigmoid)
  • tumour
  • diverticular disease
  • strictures
625
Q

Clinical presentation of bowel obstruction?

A
  • abdominal pain
  • nausea and vomiting (early in SBO, late in LBO)
  • constipation (early in LBO, late in SBO)
  • distention
  • tinkling bowel sounds / absent bowel sounds
  • resonant percussion
626
Q

Conservative management of bowel obstruction?

A
  • decompression with NG tube aspiration
  • IV fluids
  • antibiotics
627
Q

Surgical management of bowel obstruction?

A
  • endoscopic decompression of volvulus

- bowel resection (with anastomosis or stoma formation)

628
Q

In diverticulosis, are the diverticula true or false?

A

False - acquired diverticula only involve outpouching of the mucosa and submucosa, not all three layers.
True diverticula are congenital.

629
Q

Investigations for diverticulosis?

A
  • colonoscopy

- barium enema

630
Q

What are the watershed areas in the bowel?

A
  • splenic flexure

- rectosigmoid junction

631
Q

Cause of acute vs chronic mesenteric ischaemia?

A

Acute - embolus, low perfusion (heart failure), thrombus.

Chronic - atherosclerosis.

632
Q

Signs and symptoms of intestinal ischaemia?

A
  • abdominal pain disproportionate to examination findings (widespread as ischaemia progresses)
  • nausea & vomiting
  • diarrhoea
  • rectal bleeding
  • abdominal distention (later in presentation)
633
Q

Risk factors for intestinal ischaemia?

A
  • atherosclerosis
  • age
  • smoking
  • AF
  • hypercoagulability
  • chronic organ failure
634
Q

Investigations for intestinal ischaemia?

A
  • FBC (leucocytosis)
  • ABG (elevated lactate)
  • CT with IV contrast (oedematous bowel, progressing to pneumatosis)
  • CT angiography
635
Q

Management of intestinal ischaemia?

A

Supportive care - IV fluids, oxygen, analgesia, antibiotics, blood transfusion.
Interventions - endovascular thrombectomy, exploratory laparascopy, bypass, excision of necrotic bowel.
Treat underlying cause of low perfusion.

636
Q

Complications of intestinal ischaemia?

A
  • bowel necrosis

- bowel perforation

637
Q

Why are patients with chronic liver disease more prone to infection?

A

Reticulo-endothelial dysfunction.

Phase 2a (10 decks)

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