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Phase 2a > GI + liver > Flashcards

GI + liver Flashcards

1
Q

What is gastritis?

A

gastric mucosal inflammation

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2
Q

What is the most common cause of acute non-erosive gastritis?

A

Helicobacter Pylori infection

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3
Q

What can cause erosive gastritis?

A

Chronic NSAID or alcohol use/misuse
Reflux of bile salts from pyloric dysfunction (e.g. gastric surgery)

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4
Q

Aetiology of gastritis

A

H.pylori infection
Chronic NSAID or alcohol use/misuse
Reflux of bile salts into stomach
Autoimmune disorders
Bacterial invasion of gastric wall

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5
Q

Risk factors for gastritis

A

Helicobacter pylori infection
non-steroidal anti-inflammatory drug (NSAID) use
alcohol use/toxic ingestions
previous gastric surgery
critically ill patients
autoimmune disease

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6
Q

Symptoms of gastritis

A

Dyspepsia
Nausea, vomiting
Loss of appetite
Epigastric discomfort

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7
Q

What investigations would be carried out for suspected gastritis?

A

H pylori urea breath test (first line)
H pylori faecal antigen test
FBC
endoscopy
gastric mucosal histology
serum vitamin B12

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8
Q

What are some differentials of gastritis?

A

Peptic ulcer disease (PUD)
Gastro-oesophageal reflux disease (GORD)
Non-ulcer dyspepsia
Gastric lymphoma
Gastric carcinoma

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9
Q

How would you treat gastritis caused by H.pylori?

A

PPI + 2 antibiotics

can also do PPI + bismuth + 2 antibiotics

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10
Q

How would you treat erosive gastritis

A

Reduce exposure, e.g. discontinue NSAIDS, limit alcohol

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11
Q

How would you treat gastritis caused by bile reflux?

A

rabeprazole or sucralfate

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12
Q

How would you manage autoimmune gastritis?

A

more at risk for b12 deficiency
check levels and if needed treat with IM cyanocobalamin

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13
Q

Complications of gastritis

A

Peptic ulcer
Gastric carcinoma
Achlorhydria (decreased/absent production of hydrochloric acid)
Vitamin b12 deficiency

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14
Q

What are the 2 main types of IBD?

A

Ulcerative colitis
Crohn’s

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15
Q

What is ulcerative colitis

A

type of IBD that involves chronic inflammation of the colonic mucosa
confined to colon + rectum
follows a relapsing + remitting course

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16
Q

What is peritonitis?

A

Inflammation of the peritoneum

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17
Q

What are the 2 main types of peritonitis?

A

Spontaneous bacterial peritonitis
Secondary peritonitis

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18
Q

What is ascites?

A

a pathological collection of fluid in the peritoneal cavity

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19
Q

What is the most common cause of ascites?

A

cirrhosis

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20
Q

What are some non-peritoneal causes of ascites?

A

Portal hypertension: cirrhosis, CHF, alcoholic liver disease, hepatitis
Hypo-albuminaemia: nephrotic syndrome
Other causes are ovarian tumours, surgical trauma

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21
Q

What are some peritoneal causes of ascites?

A

Infectious causes, e.g. TB
Malignancy
SLE

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22
Q

What is a more common cause of ascites? (non-peritoneal or peritoneal)

A

Non-peritoneal (portal hypertension)

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23
Q

What is portal hypertension?

A

Increased BP in the portal system
Portal pressure more than 5mmHg than pressure in IVC

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24
Q

What is the most common cause of portal hypertension?

A

Cirrhosis

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25
Q

How can you sample ascitic fluid to help find cause?

A

abdo paracentesis

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26
Q

What does the serum-ascitic albumin gradient compare?

A

compares albumin concentration in the ascitic fluid and the serum albumin concentration

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27
Q

What is a high SAAG and what does that suggest?

A

High SAAG ≥ 1.1g/dL
fluid is pushed out of circulation, causing increase of serum albumin, but ascitic albumin is lower
hydrostatic pressure imbalance, e.g. portal hypertension

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28
Q

What is ascites with a high SAAG usually caused by?

A

Portal hypertension
e.g. cirrhosis, CHF, budd-chiari syndrome

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29
Q

What is ascites with a low SAAG usually caused by?

A

Infections
Peritoneal malignancy
Pancreatitis
Nephrotic syndrome

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30
Q

How would you treat asicites with a high SAAG?

A

diuretics (spironolactone) + low salt diet
paracentesis with albumin infusion

main points: treat underlying cause, relieve symptoms, prevent complicat

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31
Q

How would you treat low SAAG ascites?

A

repeated paracentesis + treatment of underlying cause

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32
Q

What are the presentations of ascites?

A

Abdo distension
Fluid and shifting dullness on exam

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33
Q

Differentials of ascites

A

Hepatitis
Alcoholic liver disease
Congestive heart failure
Nephrotic syndrome
Pancreatitis

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34
Q

Clinical features of ascites

A

Abdominal distension
Abdominal discomfort
Weight gain
Shortness of breath
Reduced appetite

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35
Q

What is exudative ascites?

A

Protein concentration above 25 gm/l

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36
Q

What is transudative ascites?

A

Protein concentration below 25 gm/l

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37
Q

How can portal hypertension cause ascites?

(pathophysiology)

A
  • Endothelial cells lining blood vessels release more nitric oxide
  • Vasodilation, Bp drops, aldosterone released
  • Kidneys retain more sodium and water
  • Plasma volume increases and fluid is pushed into tissues and peritoneal cavity
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38
Q

How can portal hypertension cause oesophageal varices?

A

Venous blood accumulates in hepatic portal system
Blood backs up into systemic veins
Portal hypertension leads to formation of portosystemic shunts
In oesophagous

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39
Q

What is gastro-oesophageal reflux disease?

& epidemiology

A

reflux of gastritic contents through lower oesophagel sphincter into oesophagus causing irritation of the lining and symptoms

common condition affecting all ages groups

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40
Q

What are the risk factors for developing GORD?

A

Family hx of GORD
Hiatus hernia
Obesity
Smoking
NSIADs
Diet: caffeine, carbonated drinks, chocolate, citrus, spicy

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41
Q

What is the pathophysiology of GORD?

A

lower oesophageal sphincter relaxes more frequently and contents from stomach can reflux into the oesophagus.
The oesophageal lining is stratified squamous epithelium and is more irritated and damaged.
Scar tissue can form and lead to oesophageal stenosis
Barrett’s oesophagus can also occur

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42
Q

What is Barrett’s oesophagus?

occurs with chronic GORD

A

an oesophagus in which any portion of the normal distal squamous epithelial lining has been replaced by metaplastic columnar epithelium through metaplasia

increases risk of neoplastic (cancerous) changes

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43
Q

What are the main features of GORD?

A

Heartburn and acid regurgitation typically after meals
Relief with an antacid

diagnosis is made clinically

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44
Q

What are the extra-oesophageal symptoms of GORD?

A

Cough
laryngitis
asthma
dental erosion

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45
Q

How does reflux induced asthma occur?

A

chronic aspiration of reflux contents and vasovagal bronchoconstriction

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46
Q

What are the alarm symptoms in patients presenting with “GORD”?

A

anaemia,
dysphagia
haematemesis- vomiting fresh blood
melaena- black tarry stools from upper GI bleeding
persistent vomiting
involuntary weight loss

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47
Q

What are some possible differentials of GORD?

A

ACS
Stable angina
Functional heartburn or dyspepsia
Achalasia
Peptic ulcer disease
Eosinophilic oesophagitis
Malignancy
Laryngopharyngeal reflux
Non-acid reflux

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48
Q

How is GORD managed?

A

PPI: omeprazole 20mg once daily
Lifestyle changes

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49
Q

What are the possible complications of GORD?

A

oesophageal ulcer, haemorrhage, or perforation
oesophageal stricture
Barrett’s oesophagus
adenocarcinoma of the oesophagus

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50
Q

What is coeliac disease?

A

A systemic autoimmune disease triggered by dietary gluten peptides.

common, about 1 in 100

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51
Q

What common grains is gluten found in?

A

Wheat
Rye
Barley

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52
Q

What are the 3 autoantibodies present in coeliac disease?

A

Anti-tissue transglutaminase antibodies (anti-TTG)
Anti-endomysial antibodies (anti-EMA)
Anti-deamidated gliadin peptide antibodies (anti-DGP)

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53
Q

What is the pathophysiology of coeliac disease?

A

Gluten peptide triggers immune response and autoantibodies against tissue transglutaminase and anti-EMA

Autoantibodies cause inflammation particularly in the jejunum and cause atrophy of the villi, leading to malabsorption

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54
Q

What are the 2 major histocompatibility complex class-II molecules associated with coeliac disease?

A

HLA-DQ2
HLA-DQ8

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55
Q

What typically causes coeliac disease?

A

genetic predisposition (HLA-DQ2 and -DQ8) and environmental trigger

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56
Q

What are the symptoms of coeliac disease?

A

GI: diarrhoea, abdo discomfort, bloating
dermatitis herpetiformis
fatigue
weight loss
failure to thrive in kids

may be asymptomatic

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57
Q

Which patients should be screened for coeliac disease?

A

Autoimmune thyroid disease
Dermatitis herpetiformis
Irritable bowel syndrome
Type 1 diabetes
First-degree relatives (parents, siblings or children) with coeliac disease

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58
Q

What are some risk factors for coeliac disease?

A

family hx of coeliac disease
IgA deficiency
T1DM
autoimmune thyroid disease
Down’s syndrome
Turner’s syndrome

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59
Q

What investigations should be run for coeliac?

A

MUST CONTINUE EATING GLUTEN DURING TESTING
Quantitative IgA: normal/low
IgA tissue transglutaminase: raised
Small bowel histology: intra-epithelial lymphocytes, villous atrophy, and crypt hyperplasia

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60
Q

What’s the gold standard test for coeliac disease?

A

Small bowel histology: intra-epithelial lymphocytes, villous atrophy, and crypt hyperplasia

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61
Q

What’s the management for coeliac disease?

A

strict lifelong gluten-free diet
supplements for any deficiencies

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62
Q

What are some differentials for coeliac disease?

A

Crohn’s
Enteropathy
Non-coeliac gluten sensitivity

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63
Q

What are the possible complications of coeliac disease?

A

Osteoporosis/penia
Vitamin deficiencies
Malignancy, e.g. intestinal lymphoma

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64
Q

What’s the most common form of IBD?

A

Ulcerative colitis

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65
Q

What’s the aetiology for IBD?

A

Exact is unclear but a genetic predisposition + environmental trigger cause an abnormal inflammatory response to gut bacteria

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66
Q

Where does ulcerative colitis typically affect?

A

Begins distally at rectum
Can only affect rectum and colon
L sided affects up to splenic flexure
If whole colon is affected = pancolitis (extensive UC)

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67
Q

What are the risk factors for UC?

and what ages is it often diagnosed?

A

Family hx of IBD
HLA-B27 positive
Infection risking a relapse

peak around 20-40 but increasily diagnosed in the over 60s now

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68
Q

What is proctitis?

A

inflammation confined to the rectum

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69
Q

What is the cardinal feature of UC?

A

Bloody diarrhoea

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70
Q

What are the symptoms of UC?

A

BLOODY DIARRHOEA
Blood in stool/ rectal bleeding
feeling of incomplete defecation (tenesmus)
Increased stool frequency and urgency
Abdominal pain

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71
Q

What histological changes would be seen on a biopsy for UC?

A

Crypt abscess formation
Reduced goblet cells
Non-granulomatous

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72
Q

What would be visible on a colonscopy for UC?

A

Continuous inflammation (proximal from rectum)
Pseudopolyps
Superficial ulceration

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73
Q

What criteria is used to grade UC from mild to severe?

A

Truelove and Witts

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74
Q

What investigations and results would show for UC?

A

Stool culture: negative
Faecal calprotectin: elevated
Sigmoidoscopy/ileocolonoscopy + biopsy: crypt abscesses, non-granulomatous

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75
Q

What are the possible differentials for UC?

A

Crohn’s
IBS
Colitis
Diverticulitis

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76
Q

What is mild UC?

A

passage of ≤4 stools per day (with or without blood)
absence of any systemic illness
normal levels of inflammatory markers (ESR)

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77
Q

What is moderate UC?

A

passage of >4 stools per day
minimal signs of systemic toxicity

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78
Q

What is the classification for severe UC?

A

passage of ≥6 bloody stools daily + one of:
HR: 90+ bpm
temp 37.5ºC
Hb <10.5 g/dL
ESR of at least 30 mm/hour

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79
Q

What is the management for mild to severe UC?

A

Mild: Aminosalicylate: mesalazine
Moderate to severe: corticosteroid: prednisolone
Acute severe: IV hydrocortisone

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80
Q

What are some possible complications of UC?

A

Toxic megacolon
Perforation
Infection
Inflammatory pseudopolyps

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81
Q

What is Crohn’s disease?

what ages does it affect?

A

A type of IBD characterised by transmural inflammation of the GI tract

all ages, diagnosis peaks 15-30yrs

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82
Q

What happens in the GI tract in Crohn’s?

A

transmural inflammation (affecting all layers of the bowel) in the affected region of bowel, producing deep ulcers and fissures (cobblestoning)
Inflammation is not continuous, forming skip lesions throughout the bowel

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83
Q

What is the hallmark appearance of Crohn’s disease on biopsy/colonoscopy?

A

Cobblestoning
Non-caseating granulomas
Skip lesions
transmural ulcers

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84
Q

Where in the GI tract can Crohn’s affect?

A

Anywhere from mouth to anus
Terminal ileum and R colon often affected

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85
Q

What are some conditions associated with IBD?

A

Erythema nodosum
Pyoderma gangrenosum (rapidly enlarging, painful skin ulcers)
Enteropathic arthritis
Primary sclerosing cholangitis (particularly with UC)
Red eye conditions (e.g., episcleritis, scleritis and anterior uveitis)

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86
Q

What are some of the risk factors for Crohn’s?

A

white ethnicity and Ashkenazi Jewish ancestry
age 15-40 or 50-60 years
family history of CD
smoking

oral contraceptive pill + NSAIDs may also increase risk

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87
Q

How might Crohn’s disease present?

A

chronic diarrhoea
weight loss
R lower quadrant abdominal pain
Fever
Fatigue
Some blood in stool
extra-intestinal manifestations (e.g., erythema nodosum or pyoderma gangrenosum)
perianal lesions

episodic

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88
Q

What investigations should be run for suspected Crohn’s?

A

colonoscopy with ileoscopy and tissue biopsy
FBC
Comprehensive metabolic panel
Serum iron, b12, folate
Stool microscopy + culture: negative
CRP and ESR: raised

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89
Q

What are the differentials for Crohn’s disease?

A

UC
Colitis
Acute appendicitis
Diverticular disease
Colorectal cancer

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90
Q

What is the first line treatment of Crohn’s?

A

Inducing remission
- Oral prednisolone
- Enteral nutrition if concerns about corticosteroids, e.g. in kids
Maintaining remission
- Azathioprine

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91
Q

What are the possible complications of Crohn’s disease?

A

Intestinal obstruction
Malabsorption related, e.g. anaemia

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92
Q

What’s going wrong in IBS?

A

Disturbance in gut/brain interaction
Functional so no underlying disease causing symptoms

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93
Q

What are the 4 subtypes of IBS?

A

IBS with diarrhoea
IBS with constipation
Mixed IBS
Unspecified

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94
Q

What criteria is used to classify IBS and how does it define IBS?

A

Rome IV
presence of abdominal pain related to defecation, associated with a change in stool frequency and/or stool form

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95
Q

What are the risk factors for IBS?

A

Family hx of IBS
age <50 years
female sex
previous enteric infection
stress

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96
Q

How may IBS present?

A

Recurrent abdominal pain often relieved by defecation
Changes in bowel habits
Bloating
Flatulence
Urgency
Mucus with stools
Sensation of incomplete emptying

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97
Q

What investigations could be run to exclude differentials in IBS?

A
  • Full blood count for anaemia
  • Inflammatory markers (e.g., ESR and CRP)
  • Coeliac serology (e.g., anti-TTG antibodies)
  • Faecal calprotectin for IBD
  • CA125 for ovarian cancer
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98
Q

What are the differentials for IBS?

A

IBD
Colitis
Colon cancer
Coeliac disease
Bowel infection

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99
Q

What is required for an IBS diagnosis?

A

at least 6 months of abdo pain/discomfort with at least one of:
- Pain or discomfort relieved by opening the bowels
- Bowel habit abnormalities (more or less frequent)
- Stool abnormalities (e.g., watery, loose or hard)

and 2 of straining, bloating, worse after eating, passing mucus

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100
Q

How does the Rome IV criteria diagnosis IBS?

A

Recurrent abdominal pain, at least 1 day per week in the last 3 months and associated with 2+:
- Related to defecation
- Associated with a change in stool frequency
- Associated with a change in stool form

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101
Q

What are some dietary modifications that can be made in IBS?

A
  • Reduce caffeine, alcohol and fizzy drinks
  • Have regular meals
  • Drink lots of fluids
  • Low FODMAP diet
  • Adjust fibre intake depending on symptoms
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102
Q

What are the possible pharmacological treatments for IBS?

A

Diarrhoea: loperamide
Constipation: laxative
Pain or bloating: antispasmodics, e.g. dicycloverine

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103
Q

What is appendicitis and which age group has the highest incidence rate?

A

inflammation of the appendix
highest incidence rate in children and adolescents

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104
Q

How can appendicitis lead to peritonitis?

A

There is a single opening to the appendix that connects it to the bowel
Pathogens can get trapped where appendix meets bowel.
Leads to infection and inflammation.
Inflammation may proceed to gangrene and rupture
Faecal contents and infective material released into the peritoneal cavity
Peritonitis

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105
Q

What is the main cause of appendicitis?

A

Obstruction of the lumen of the appendix, via
- Faecolith (a hard mass of faecal matter)
- normal stool
- lymphoid hyperplasia

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106
Q

When should you suspect appendicitis?

A

Any patient with:
- Acute severe right iliac fossa pain
- Poorly localised central abdominal pain that becomes localised to the right lower quadrant
- Anorexia, nausea, and vomiting

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107
Q

What is the most common presentation of acute appendicitis?

A

poorly localised central abdominal pain that becomes localised to the right lower quadrant as inflammation progresses

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108
Q

How might acute appendicitis present?

A

poorly localised central abdominal pain that localises to R lower quadrant
Tenderness at McBurney’s point
Anorexia – almost always present
Nausea and vomiting
Loose stool or constipation

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109
Q

What investigations should be run for suspected appendicitis?

A

FBC: leukocytosis
CRP: elevated
CT or ultrasound

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110
Q

Possible differentials for appendicitis

A

Mesenteric adenitis
Viral gastroenteritis
Meckel’s diverticulitis
Crohn’s
Peptic ulcer disease
R sided ureteric stone
Ectopic pregnancy

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111
Q

What is the treatment for acute appendicitis?

A

Removal of the inflamed appendix (appendicectomy)

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112
Q

What are the main complications of appendicitis?

A

Perforation
Peritonitis

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113
Q

What is achalasia?

A

an oesophageal motor disorder characterised by a loss of oesophageal peristalsis and failure of the lower oesophageal sphincter to relax in response to swallowing

incidence increases with age, mean age 53

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114
Q

What causes achalasia?

A

progressive destruction of the ganglion cells in the myenteric plexus
possible triggers include infection, autoimmunity, and genetic factors

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115
Q

How does achalasia present?

A

dysphagia to solids and liquids, regurgitation, and retrosternal pain
slowly progressive over months to years

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116
Q

What investigations are done for achalasia?

A

endoscopy to exclude malignancy
barium swallow
high-resolution oesophageal manometry

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117
Q

What are some differentials for achalasia?

A

Oesophageal carcinoma
Reflux oesophagitis
Connective tissue disorders (e.g., systemic sclerosis)
Pseudoachalasia

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118
Q

What would be seen on oesophageal manometry for achalasia?

A

Absence of oesophageal peristalsis
Failure of relaxation of the lower oesophageal sphincter
High resting lower oesophageal sphincter tone

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119
Q

Management options for achalasia

A

no interventions that can restore oesophageal peristalsis
CCBs: nifedipine
Surgery: pneumatic dilatation

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120
Q

What is a peptic ulcer?

A

A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter, with depth to the submucosa

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121
Q

What are the 2 sites that can be affected by peptic ulcers?

A

mucosa of the stomach (gastric ulcer), most often on lesser curvature of stomach
proximal duodenum (duodenal ulcer)

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122
Q

What are the risk factors for peptic ulcer disease?

A

H.pylori infection
NSAID use
Smoking
Increasing age
Personal or family hx of peptic ulcers

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123
Q

How does H.pylori cause ulceration?

A

Survive in the stomach by creating an alkaline microenvironment
Induces an inflammatory response in the mucosa leading to ulceration

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124
Q

How can NSAIDs cause a peptic ulcer?

A

inhibiting COX and prostaglandin synthesis, resulting in a reduced secretion of glycoprotein, mucus, and
mucosa more susceptible to damage

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125
Q

What are the 2 main causes of peptic ulcers?

A

H.pylori
NSAIDs

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126
Q

What is acid secretion like in gastric or duodenal ulcers?

A

Gastric: normal to low
Duodenal: hypersecretion, often in response to H.pylori in stomach

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127
Q

What’s the typical presentation of a patient with a peptic ulcer?

A

chronic, upper abdominal pain related to eating a meal (dyspepsia)
epigastric tenderness
nausea and vomiting

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128
Q

What are the signs of an upper GI bleed?

A

Haematemesis (vomiting blood)
Coffee ground vomiting
Melaena (black, tarry stools)
Fall in haemoglobin on a full blood count

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129
Q

How is a peptic ulcer diagnosed?

A

Endoscopy
Urea breath test for H.pylori

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130
Q

What are the differentials for peptic ulcer disease?

A

GI cancer
GORD
Gastroparesis
Acute pancreatitis
Functional dyspepsia
Coeliac
IBS

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131
Q

What’s the management for peptic ulcer disease?

A

Treat underlying cause: stop NSAIDs, treat H.pylori infection with amoxicillin
PPIs: omeprazole, lansoprazole

repeat endoscopy 6 to 8 weeks after beginning treatment

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132
Q

What are the possible complications of peptic ulcers?

A

Penetration
Perforation
Gastric obstruction
Upper GI bleed

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133
Q

How can peptic ulcers be avoided in people who require NSAIDs?

A

Prescribe them with a PPI

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134
Q

What are the 3 types of ischaemic bowel disease?

A

acute mesenteric ischaemia
chronic mesenteric ischaemia
colonic ischaemia

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135
Q

What’s the arterial blood supply of the bowel?

A

Small intestine blood from: coeliac artery and superior mesenteric artery
Colon: SMA and inferior MA
Rectum: internal iliac artery

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136
Q

What typically causes ischaemic bowel?

A

embolism
thrombus
non-occlusive cause, e.g. hypoperfusion

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137
Q

How does acute mesenteric ischaemia present?

A

abdominal pain out of proportion to examination
nausea/vomiting
rectal bleeding
abdo bruit

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138
Q

What investigations should be done for ischaemic bowel?

A

CT scan with contrast
FBC: leukocytosis, anaemia
ABG + serum lactate: acidosis

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139
Q

What is diverticular disease?

A

any clinical state caused by symptoms pertaining to colonic diverticula

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140
Q

What are diverticula?

A

outpouchings of the bowel wall

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141
Q

How do diverticula form?

A

Bowel is surrounded by circular muscle.
Bowel is weakened in areas where blood vessels penetrate and over time.
Increased pressure inside the lumen over time, can cause a gap to form in these areas of the circular muscle.
Gaps allow the mucosa to herniate through the muscle layer and pouches to form (diverticula)

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142
Q

Why don’t diverticula form in the rectum?

A

it has an outer longitudinal muscle layer that completely surrounds the diameter of the rectum
adding extra support

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143
Q

What are some predisposing factors for diverticular disease?

A

low fibre
decreased physical activity
obesity
increased red meat consumption
smoking
excessive alcohol and caffeine intake
steroids
NSAIDs

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144
Q

How does diverticular disease present?

A

In left lower quadrant:
- guarding
- tenderness
- abdo pain

rectal bleeding
constipation
bloating

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145
Q

What are the symptoms of acute diverticulitis?

A

acute abdominal pain, sharp, localised in the left iliac fossa pain, worsened by movement.
Localised tenderness
decreased appetite
pyrexia
nausea

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146
Q

What would a CT for diverticulitis show?

A

thickening of the colonic wall
pericolonic fat stranding
abscesses
localised air bubbles or free air

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147
Q

What investigations should be run for suspected diverticular disease?

A

FBC: polymorphonuclear leukocytosis
U&E: uraemia and elevated creatinine
C-reactive protein: elevated
CT abdomen-pelvis scan

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148
Q

What are the differentials for diverticular disease?

A

IBD
Endometriosis
Colorectal cancer
UTI
Appendicitis

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149
Q

Example of an antispasmodic which helps abdo cramping

A

dicycloverine

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150
Q

How is diverticulosis treated?

A

increased fibre in the diet
bulk-forming laxatives if constipated

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151
Q

How is diverticulitis managed?

A

Uncomplicated diverticulitis: oral co-amoxiclav if unwell, analgesia (not NSAIDs), avoid solid food for a few days
Complicated diverticulitis: IV co-amoxiclav + fluids, low residue diet, surgery

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152
Q

What is the rule of 2s in Meckel’s diverticulum?

A

Present in 2% of the population
symptomatic in 2% of those with it
children are usually less than 2 years old
males are 2x as common as female
found approximately 2 feet proximal to the ileocaecal valve
it is 2 inches long or less
has 2 types of ectopic tissue (gastric and pancreatic)

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153
Q

What is the commonest congenital malformation of the small bowel?

A

Meckel’s diverticulum

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154
Q

What is meckel’s diverticulum?

A

congenital abnormality
the remnants of the vitello-intestinal duct

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155
Q

How might meckel’s diverticulum present?

A

GI bleeding
Small bowel obstruction
Abdo pain and cramps
Nausea and vomiting

asymptomatic in most patients

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156
Q

How might meckel’s diverticulum be diagnosed?

A

FBC
CT/ultrasound of abdomen
Meckel’s scan

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157
Q

What is the management of meckel’s diverticulum?

A

Asymptomatic no treatment
Symptomatic: surgical resection of the diverticulum

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158
Q

What is a mallory-weiss tear?

A

A superficial tear of the oesophageal mucosa in the region of the gastroesophageal junction and gastric cardia

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159
Q

What are the risk factors for a mallory-weiss tear?

A

condition predisposing to retching, vomiting, and/or straining
chronic cough
hiatal hernia
endoscopy or other instrumentation
heavy alcohol use

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160
Q

What are some typical causes of a MWT?

mallory-weiss tear

A

coughing
retching
vomiting
binge drinking

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161
Q

How does a MWT typically present?

A

small and self-limiting episodes of haematemesis after a bout of retching, vomiting, coughing, straining, or blunt trauma

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162
Q

What are the initial investigations for a suspected MWT?

A

Upper GI endoscopy
FBC

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163
Q

What are the differentials of a MWT?

A

Spontaneous oesophageal perforation (Boerhaave’s syndrome)
Cameron erosions
Peptic ulcer disease
Oesophageal varices

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164
Q

How is a MWT managed?

A

Resus and ensure haemodynamically stable
Mostly self-limiting so treatment is supportive

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165
Q

What’s meant by bowel obstruction?

A

a mechanical blockage of the bowel, whereby a structural pathology physically blocks the passage of intestinal contents

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166
Q

What are the risk factors for developing small bowel obstruction?

A

previous abdominal surgery
malrotation
Crohn’s disease
hernia
appendicitis

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167
Q

What can cause small bowel obstruction?

A

Previous surgery
Inguinal hernia with incarceration
Crohn’s disease
Intestinal malignancy
Appendicitis

adhesions

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168
Q

What are the symptoms of a bowel obstruction?

A

intermittent abdominal pain
distention
vomiting
nausea
constipation

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169
Q

What are the differential diagnoses for a small bowel obstruction?

A

Ileus
Infectious gastroenteritis
Large bowel obstruction
Intestinal pseudo-obstruction
Acute appendicitis
Acute pancreatitis

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170
Q

What does obstruction in the instestine cause?

A

Obstruction results in a build up of gas and faecal matter before the obstruction.
This causes back-pressure, resulting in vomiting and dilatation of the intestines proximal to the obstruction

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171
Q

How can a bowel obstruction lead to hypovolaemia and third spacing of fluid?

A

The GI tract secretes fluid that is later absorbed in the colon. Obstruction means fluid can’t be reabsorbed.
Fluid loss from the intravascular space into the GI tract.
This leads to hypovolaemia and shock.

The higher up the intestine the obstruction, the greater the fluid losses as there is less bowel over which the fluid can be reabsorbed

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172
Q

What are the big 3 causes of bowel obstruction?

A

Adhesions (small bowel)
Hernias (small bowel)
Malignancy (large bowel)

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173
Q

What is a closed-loop obstruction in the bowel?

A

two points of obstruction along the bowel
meaning that there is a middle section sandwiched between two points of obstruction

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174
Q

What are some possible complications of a bowel obstruction?

A

progression to intestinal necrosis, perforation, sepsis, and death
Short bowel syndrome in a SBO

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175
Q

What are some risk factors for large bowel obstruction?

A

Colorectal adenoma or polyp
Malignancy
IBD
Diverticular disease
Hernia

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176
Q

What can cause large bowel obstruction?

A

Malignancy most common cause
Diverticular disease
Volvulus

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177
Q

What imaging should be used for a suspected bowel obstruction?

A

Contrast CT of abdomen and pelvis

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178
Q

How is bowel obstruction managed?

A

NG decompression
Emergency surgery

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179
Q

What is a pseudo-obstruction of the bowel?

A

dilatation of the colon due to an adynamic bowel, in the absence of mechanical obstruction

most commonly affects caecum and ascending colon

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180
Q

What are the 2 subtypes of oesophageal cancer?

A

Squamous cell carcinoma: upper and middle 1/3s
Adenocarcinoma: lower 1/3 of oesophagus develops from barrett’s oesophagus, more common in developed countries

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181
Q

Where does oesophageal cancer tend to metastasize to?

A

peri-oesophageal lymph nodes
liver
lungs

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182
Q

What are the risk factors for oesophageal cancer?

A

Male
Older age
Low socioeconomic status
Smoking
excessive alcohol use
GORD
Barrett’s oesophagus
obesity

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183
Q

What are the symptoms of oesophageal cancer?

A

Dysphagia
Pain when swallowing
Weight loss
Hiccups from phrenic nerve involvement

typically present quite late

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184
Q

What imaging may be done for suspected oesophageal cancer?

A

Upper GI endoscopy with biopsy
CT of chest and abdomen

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185
Q

What are the possible differentials for oesophageal cancer?

A

Benign stricture
Achalasia
Barrett’s oesophagus

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186
Q

What are the possible options for managing oesophageal cancer?

A

Chemoradiotherapy
Surgical resection

187
Q

What is the most common form of gastric cancer?

A

Adenocarcinoma from gastric mucosa

188
Q

What tumour suppressor gene can be lost in gastric cancer?

A

p53

189
Q

What investigation is done for possible gastric cancer?

A

Upper GI endoscopy with biopsy

190
Q

What are the risk factors for gastric cancer?

A

pernicious anaemia
Helicobacter pylori
N-nitroso compounds
Family hx
smoking

191
Q

What are the differentials for gastric cancer?

A

Peptic ulcer disease
Benign oesophageal stricture
Achalasia

192
Q

What’s the management for gastric cancer?

A

Surgical resection
Subtotal gastrectomy
Chemoradiotherapy

193
Q

What’s the most common type of colorectal cancer and where does it typically affect?

A

Adenocarcinoma
66% of colorectal cancers in colon

194
Q

What is familial adenomatous polyposis (associated with colorectal cancer)?

A
  • autosomal dominant condition involving malfunctioning of the tumour suppressor genes called adenomatous polyposis coli (APC)
  • results in many polyps (adenomas) developing along the large intestine
  • polyps can become cancerous
195
Q

What is hereditary nonpolyposis colorectal cancer (lynch syndrome)?

associated with colorectal cancer

A
  • autosomal dominant condition that results from mutations in DNA mismatch repair (MMR) genes
  • patients at higher risk of colorectal cancer
196
Q

What does colorectal cancer typically arise from?

A

dysplastic adenomatous polyps
inactivation of tumour suppressor genes

mostly sporadic but can be familial, e.g. FAP or Lynch

197
Q

What are common presenting symptoms of colorectal cancer?

A

Abdominal pain
change in bowel habit
rectal bleeding
anaemia

198
Q

What are signs of advanced disease in colorectal cancer?

A

Abdominal distension
weight loss
vomiting

199
Q

What are some of the risk factors for colorectal cancer?

A

increasing age
family history
APC mutation (from FAP)
Lynch syndrome
Polyposis
IBD
Obesity

200
Q

What investigations should be done for colorectal cancer?

A

faecal immunochemical test
colonoscopy

201
Q

What’s the mainstay of colorectal cancer treatment?

A

Surgical resection

202
Q

What can cause haematemesis?

A

Oesophageal varices
Peptic ulcer disease
MWT
Oesophagitis
GI cancer

203
Q

What are haemorrhoids?

A

enlarged anal vascular cushions

haemorrhoidal cushions are normal vascular structures

can be internal or external

204
Q

How does haemorrhoidal disease typically present?

A

painless rectal bleeding
sudden onset of perianal pain with a tender palpable perianal mass

205
Q

What typically causes haemorrhoids?

A

Excessive straining due to constipation or diarrhoea

206
Q

What are some of the risk factors for developing haemorrhoidal disease?

A

age between 45 and 65 years
history of constipation
pregnancy
presence of a space-occupying pelvic lesion

207
Q

What are the differentials for haemorrhoids?

A

Anal fissure
Anal fistula
Colorectal cancer
IBD
Rectal prolapse

208
Q

What are some ways of managing haemorrhoids?

A

Increase fibre intake
Short term topical corticosteroids
Rubber band ligation/ sclerotherapy

209
Q

What is an anal fissure?

A

a split in the skin of the distal anal canal characterised by pain on defecation and rectal bleeding

210
Q

How are anal fissures treated?

A

Conservative therapy: high fibre diet, adequate fluid intake, topical analgesics
Consider topical diltiazem

211
Q

What is a perianal fistula?

A

an abnormal connection between the anal canal and the perianal skin
often a complication of an anorectal abscess

managed surgically

212
Q

How does an anal fistulae present?

A

recurrent perianal abcesses
intermittent or continuous discharge onto the perineum

213
Q

What is an anorectal abscess?

A

an infection of the soft tissues around the anus

common in crohn’s

214
Q

What are the symptoms of an anorectal abscess?

A

Severe perianal pain and swelling
Fever
Chills
Urinary retention
Anal fistula may be present

diagnosed through hx and clinical exam

215
Q

What are the risk factors for an anorectal abscess?

A

anal fistula
Crohn’s disease
male sex

216
Q

What are the differentials for an anorectal abscess?

A

Pilonidal abscess
STI
Anal fissure

217
Q

How is an anorectal abscess treated?

A

Incision and drainage

218
Q

What is pilonidal disease?

A

An acquired disease in which hair follicles become inserted into the skin, creating a chronic sinus tract, usually in the natal cleft

Acute infection may lead to a pilonidal abscess, requiring surgical drainage

commonly affects men age 16-35

219
Q

What are the symptoms of pilonidal disease?

A

Sacrococcygeal
- Discharge
- Pain and swelling
- Sinus tracts

presence of hair containing cysts

220
Q

What is pseudomembranous colitis?

A

Infection of the colon caused by C.Diff
Characterised by inflammation of the colon and the formation of pseudomembranes

Occurs in patients whose normal bowel flora has been disrupted by recent antibiotic use

221
Q

How does C.Diff colitis typically present?

A

diarrhoea
abdominal pain
leukocytosis
hx of recent antibiotic use

can also have distension, tenderness and fever

222
Q

How might C.Diff colitis be diagnosed?

A

Stool sample
- Faecal occult blood test
- PCR

223
Q

How is C.Diff colitis treated?

A

discontinue the inciting antimicrobial agent and start therapy with oral fidaxomicin or vancomycin

224
Q

What is acute liver failure?

A

a rapid decline in hepatic function characterised by jaundice, coagulopathy (INR >1.5), and hepatic encephalopathy in patients with no evidence of prior liver disease

very rare

225
Q

What causes acute liver failure?

A

Paracetamol overdose
Drug-induced
Hepatitis A or B

226
Q

Which LFTs show damage to liver cells?

A

ALT and AST show parenchymal damage
ALP and GGT are for cholestatic damage

227
Q

What are the symptoms of acute liver failure?

A

Jaundice
Coagulopathy
abdominal pain
nausea
vomiting
malaise
signs of cerebral oedema

228
Q

What investigations should be done in acute liver failure and what would they show?

A

LFTs: hyperbilirubinaemia, elevated liver enzymes
PT/INR: elevated INR (>1.5)
Basic metabolic panel

229
Q

What are the differentials for acute liver failure?

A

Severe acute hepatitis
Cholestasis
Haemolysis

230
Q

How should patients be managed in acute liver failure?

A

ICU admission and consider possible transplant
Treat paracetamol overdose if that’s cause

231
Q

What are the possible complications of acute liver failure?

A

rapidly progressing hepatic encephalopathy
coagulopathy
infection
renal failure and haemodynamic changes
metabolic disorders
cerebral oedema
GI bleed

232
Q

What is chronic liver disease?

A

the result of repeated damage to the liver
progressive liver dysfunction for 6 months or more

233
Q

What can cause chronic liver disease?

A

Alcohol
Hepatitis
Alpha-1-antitrypsin deficiency
Wilson’s disease
Non-alcoholic fatty liver disease
Hepatocellular carcinoma
Toxins
Ischaemia
Budd-Chiari

234
Q

What are the signs and symptoms of chronic liver disease?

A

jaundice
ascites
encephalopathy
Caput medusa
Splenomegaly
Spider naevi
Palmar erythema

235
Q

What is the max paracetamol dose in adults over 24hours?

A

4g

236
Q

What are the different types of paracetamol overdose?

A

Acute: taken in less than 1 hour, context of self-harm
Staggered: excessive amounts over longer than an hour in context of self harm
Therapeutic: excessive dose taken with intent to treat pain

237
Q

What are some risk factors for paracetamol overdose?

A

hx of self-harm
hx of frequent/repeated use of medications for pain relief
glutathione deficiency
drugs that induce liver enzymes (cytochrome P450 inducers)
low bodyweight (<50 kg)

238
Q

What is the pathophysiology of a paracetamol overdose?

A

After ingestion, paracetamol metabolised
About 4% of a therapeutic dose is metabolised by cytochrome P450 enzymes, mainly CYP2E1, to a potentially toxic intermediate metabolite N-acetyl-p-benzoquinone imine (NAPQI)
When the production of NAPQI exceeds the capacity to detoxify it, the excess NAPQI binds to cellular components, causing mitochondrial injury and hepatocyte death

239
Q

What are the main symptoms of a paracetamol overdose?

A

Nausea
Vomiting
Altered consciousness level

can show signs of an AKI or metabolic acidosis (in mixed overdose)

240
Q

What are the most common causes of cirrhosis?

A

alcohol-related liver disease
non-alcoholic fatty liver disease (NAFLD)
chronic viral hepatitis (B and C)

240
Q

What are the investigations for a paracetamol overdose?

A

serum paracetamol concentration
liver function tests
prothrombin time and INR
blood glucose (hypo indicates acute liver injury)

241
Q

How is a paracetamol overdose managed?

A

Immediate acetylcysteine
Activated charcoal if patient presents within an hour

242
Q

What is liver cirrhosis?

A

pathological end-stage of any chronic liver disease
characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules

243
Q

What metabolic disorders can result in cirrhosis?

A

NAFLD
haemochromatosis
Wilson’s disease
alpha-1 antitrypsin deficiency

244
Q

What can cause liver cirrhosis?

A

Viral hepatitis
Alcohol use
Metabolic: NAFLD, NA steatohepatitis, haemochromatosis, alpha 1 antitrypsin deficiency, Wilson’s
Drug induced, e.g. methotrexate
Autoimmune hepatitis
Venous outflow obstruction: e.g. Budd-Chiari, occlusion

245
Q

What is the pathophysiology of liver cirrhosis?

A

Insult causes inflammation and scarring, fibrosis
Nodules of scar tissue form + capillarisation of sinusoids
Increase in blood flow resistance leading to portal HTN

246
Q

What are some signs of cirrhosis?

A

Leukonychia – white nails
palmar erythema
spider naevi
jaundiced sclera
caput medusa
hepatosplenomegaly
distension
muscle wasting
peripheral oedema

247
Q

What disease scoring systems can be used for liver cirrhosis?

A

Child-Pugh-Turcotte (CPT)
Model of End-Stage Liver Disease (MELD)

248
Q

What investigations should be run for cirrhosis?

A

LFTs
Liver biopsy
PT
FBC + electrolytes

249
Q

What are the features of decompensated liver disease that may suggest transplantation is required?

A

A – Ascites
H – Hepatic encephalopathy
O – Oesophageal varices bleeding
Y – Yellow (jaundice)

250
Q

What are the general principles of management for liver cirrhosis?

A

Treat underlying cause
Manage and monitor complications
Liver transplant

251
Q

What are some possible complications of liver cirrhosis?

A

Ascites
Gastro-oesophageal varices
Bleeding and thrombosis
Hepatocellular carcinoma

252
Q

What are some pre-hepatic causes of portal htn?

A

portal or splenic vein thrombosis
AV malformation
splenomegaly

253
Q

What are some intra-hepatic causes of portal HTN?

A

cirrhosis (most common cause)
primary sclerosing cholangitis
schistosomiasis

254
Q

What are some post-hepatic causes of portal HTN?

A

IVC obstruction
R heart failure
Budd-Chiari syndrome

255
Q

What are the 3 stages of alcohol-related liver disease?

A
  • fatty liver (steatosis)
  • alcohol-related hepatitis (inflammation and necrosis)
  • alcohol-related cirrhosis
256
Q

What is the main cause of alcoholic liver disease?

A

chronic heavy alcohol ingestion

257
Q

What happens in alcoholic fatty liver?

stage of ARLD

A

Drinking leads to a build-up of fat in the liver
Reversible with abstinence.

258
Q

What happens in alcoholic hepatitis?

stage of ARLD

A

Drinking alcohol over a long period/ Binge drinking causes inflammation in the liver cells.
Mild alcoholic hepatitis is usually reversible with permanent abstinence

259
Q

What is binge drinking defined as in men and women?

A

6 or more units for women
8 or more for men
in a single session

260
Q

What are the 2 main pathways that alcohol is metabolised through in the liver?

A

alcohol dehydrogenase
cytochrome P-450 2E1

261
Q

In ARLD what is happening in the alcohol dehydrogenase pathway?

A

Alcohol dehydrogenase (hepatic enzyme) converts alcohol to acetaldehyde, which is then metabolised to acetate
Dehydrogenases convert NAD to NADH.
Excessive NADH in relation to NAD inhibits gluconeogenesis and increases fatty acid oxidation, which promotes fatty infiltration in the liver

262
Q

In ARLD, what is happening in the cP450-2E1 pathway of metabolism?

A

cP-450 2E1 pathway generates free radicals through the oxidation of NADPH to NADP.
Chronic alcohol use upregulates cytochrome P-450 2E1 and produces more free radicals

263
Q

What are symptoms of severe hepatocellular failure in advanced liver disease?

A

Abdominal distension and weight gain (ascites)
Confusion (hepatic encephalopathy)
Haematemesis or melaena (gastrointestinal bleeding)
Asterixis
Leg swelling.

264
Q

What questionnaires can be used to assess alcohol dependency?

A

AUDIT
CAGE

265
Q

What are some signs of portal HTN?

A

Ascites
Splenomegaly
Venous collateral circulations

266
Q

What are the risk factors for alcohol-related liver disease?

A

prolonged and heavy alcohol consumption
hepatitis C
female sex: develops more rapidly and at low drinking levels

267
Q

What are the signs and symptoms of ARLD?

A

Fatigue
Anorexia
Weight loss
Jaundice
Fever
Nausea and vomiting
Right upper quadrant abdominal discomfort.
Hepatomegaly
Caput medusae
Telangiectasia
Ascites

268
Q

What are some of the possible differentials for ARLD?

A

Hepatitis A,B,C, drug-induced, autoimmune
Cholecystitis
Hepatic vein thrombosis
Acute liver failure
Haemochromatosis
Wilson’s disease
Wernicke’s encephalopathy
Biliary obstruction

268
Q

What investigations should be done for ARLD and what might they show?

A

LFTs: most elevated
AST/ALT ratio: ratio >2, AST elevated higher
FBC: anaemia
Liver ultrasound
Increased PT

269
Q

What is the management of ARLD?

A

Alcohol abstinence
Nutrition supplementation
Weight reduction
Smoking cessation
Consider pred in severe alcohol-related hepatitis

270
Q

What are the complications of ARLD?

A

hepatic encephalopathy
portal hypertension
GI bleeding
coagulopathy
renal failure
hepatorenal syndrome

271
Q

How does alcoholic liver disease lead to wernicke’s encephalopathy?

A

Alcohol excess leads to thiamine (vitamin B1) deficiency as it’s poorly absorbed in the presence of alcohol
Thiamine deficiency leads to WE and Korsakoff syndrome.

272
Q

What is steatosis?

A

an accumulation of fat in the liver

273
Q

What is NAFLD?

A

evidence of steatotic liver disease in the absence of secondary causes of hepatic fat accumulation

274
Q

What are the stages of NAFLD?

A

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

275
Q

What are some of the metabolic comorbidities for NAFLD?

A

obesity, DM, HTN, dyslipidaemia, obstructive sleep apnoea, CVD, CKD

276
Q

What happens in NAFLD?

A

accumulation of excessive triglycerides in the liver
interferes with liver cell functioning

277
Q

What are the signs and symptoms of NAFLD?

A

Many patients asymptomatic
Hepatosplenomegaly
Fatigue
Malaise
Abdo pain

278
Q

What are the risk factors for NAFLD?

A

obesity
insulin resistance or diabetes
dyslipidaemia
hypertension
metabolic syndrome
rapid weight loss
medications, e.g. NSAIDs, corticosteroids
total parenteral nutrition

279
Q

How could NAFLD be diagnosed?

A

LFTs: elevated
FBC: anaemia
Abnormal metabolic panel
Liver biopsy: gold standard, but not used on every patient
exclusion of alcohol use as the cause
Enhance liver fibrosis test

280
Q

What are the differentials of NAFLD?

A

ARLD
Hepatitis
Metabolic liver disease
Primary biliary cholangitis
Primary sclerosing cholangitis

281
Q

What is the management of NAFLD?

A

Lifestyle modifications, e.g. weight loss, alcohol reduced, healthy diet, exercise
Consider pioglitazone + vitamin E

282
Q

What is jaundice?

A

the result of accumulation of bilirubin in the bloodstream and subsequent deposition in the skin, sclera, and mucous membranes

283
Q

When is bilirubin produced?

A

Breakdown of haem

284
Q

What are the different mechanisms of bilirubin?

A

from increased bilirubin production (prehepatic)
diseases that impair hepatocyte function (hepatocellular)
obstruction of the biliary system (cholestatic/ post-hepatic)

285
Q

What are the pre-hepatic causes of jaundice?

A
  • Excessive haemolysis, e.g. haemolytic anaemia, haemolytic drugs, blood transfusions, sickle cell, thalassaemia
  • impaired conjugation, e.g. gilberts
286
Q

What are some causes of hepatocellular jaundice?

A
  • Damaged hepatocytes, e.g. hepatitis + other infections, cirrhosis, hepatic carcinoma, toxins
  • Metabolic liver disease: Haemochromatosis, Wilson’s disease, Alpha 1 antitrypsin deficiency
287
Q

What are some causes of cholestatic/post-hepatic jaundice?

A

Something stopping bile flow, e.g. cholecystitis, pancreatic head carcinoma, cholangitis

288
Q

What investigations should be run for jaundice?

A

Serum LFTs with fractionation of bilirubin
PT/INR
FBC
Patient Hx: e.g is it painful

289
Q

What is Wernicke’s encephalopathy?

A

a neurological emergency resulting from thiamine deficiency

290
Q

Where is thiamine stored and how long do stores last?

A

a water-soluble vitamin stored predominantly in the liver
up to 18 days

291
Q

What’s the classic triad of presentation for wernicke’s encephalopathy?

not actually that common in patients, 10%

A

mental status changes
ophthalmoplegia
gait dysfunction

292
Q

What are some symptoms of WE?

A

Cognitive dysfunction
Ocular motor changes
Gait disturbances
Confusion
Altered level of consciousness

293
Q

What are important features of a Hx in suspected WE?

A
  • alcohol dependence
  • poor dietary intake
  • vomiting, diarrhoea
  • fever
  • co-existing conditions
  • immunodeficiency
  • recent abdominal surgery
294
Q

What are the risk factors for WE?

A

alcohol dependence
AIDS
cancer and treatment with chemotherapeutic agents
malnutrition
history of gastrointestinal surgery

295
Q

What investigations should be done for WE?

A

Therapeutic trial of thiamine
finger-prick glucose
FBC + electrolytes
renal function
LFTs
serum ammonia
blood alcohol level
blood thiamine and its metabolites

296
Q

What are some differentials for WE?

A

Alcohol intoxication
Alcohol withdrawal
Encephalitis

297
Q

How should WE be treated?

A

IV thiamine ASAP

298
Q

What is Korsakoff’s psychosis?

a complication of WE

A

disproportionate impairment of recent memory relative to other cognitive domains

299
Q

What are some of the complications of WE?

A

ataxia and varying degrees of ophthalmoparesis
seizures
Korsakoff’s psychosis
hearing loss

if not treated early, permanent brain injury

300
Q

What is haemochromatosis?

A

An autosomal recessive condition causing a build-up of iron levels in the body

301
Q

When does haemochromatosis typically present?

A

usually presents after age 40 when the iron overload becomes symptomatic
It presents later in females due to menstruation

302
Q

What normally causes haemochromatosis?

A

mutations in the HFE gene on chromosome 6

303
Q

What’s a common marker for haemochromatosis?

A

elevated transferrin saturation

304
Q

What are the cardinal symptoms of haemochromatosis?

A

lethargy
fatigue
loss of libido
skin bronzing

305
Q

How is haemochromatosis managed?

A

Venesection (regularly removing blood to remove excess iron – initially weekly)
avoid iron-fortified foods or iron-containing supplements

306
Q

What is Gilbert syndrome?

A

a genetic syndrome of mild unconjugated hyperbilirubinaemia
<102 micromol/L (<6 mg/dL)

307
Q

What goes wrong in Gilbert syndrome?

A

Decreased UDPGT activity leads to decreased conjugation of unconjugated bilirubin
bilirubin clearance is reduced by 60%.

308
Q

How does Gilbert syndrome typically present?

A

usually asymptomatic, with mild jaundice seen during times of fasting or physiological stress

309
Q

Does Gilbert syndrome require treatment?

A

No treatment is needed since there is no liver injury or progression to end-stage liver disease

310
Q

What features are typically present for a diagnosis of Gilbert syndrome?

A
  • Asymptomatic healthy patient with mild unconjugated hyperbilirubinaemia (<68.4 micromol/L [<4 mg/dL])
  • No evidence of haemolysis
  • Normal serum transaminases and alkaline phosphatase levels
  • Exclusion of medications that cause hyperbilirubinaemia
311
Q

What is Wilson’s disease?

A

an autosomal recessive genetic condition resulting in the excessive accumulation of copper in the body tissues, particularly in the liver

312
Q

What causes Wilson’s disease?

A

Autosomal recessive mutations in the ATP7B gene on chromosome 13

313
Q

What is going wrong in Wilson’s disease?

A

ATP7B facilitates trans-membrane transport of copper within hepatocytes
Mutation leads to decreased copper excretion from the liver and copper overload in hepatocytes.
When hepatic storage capacity is exceeded, copper is released into the circulation and deposited in other organs

314
Q

How can Wilson’s disease manifest?

A

liver disease (with jaundice, and possibly ascites and oedema)
neurological movement disorder (with tremor, dystonia, rigidity)

315
Q

What is seen in the eye in Wilson’s disease?

A

Kayser-Fleischer rings surrounding iris

316
Q

What investigations should be done for Wilson’s disease?

A
  • 24-hour urine copper measurement
  • ophthalmological slit-lamp examination for Kayser-Fleischer (KF) rings
  • serum ceruloplasmin levels
  • abnormal lfts
317
Q

How is Wilson’s disease managed?

A

Copper chelation: Penicillamine, trientine
Zinc acetate
Restriction of copper in diet

318
Q

What is alpha-1 antitrypsin (AAT) deficiency?

A

an autosomal codominant genetic disorder
Allele mutations cause ineffective activity of alpha-1 antitrypsin, the enzyme responsible for neutralising neutrophil elastase

319
Q

How does AAT deficiency affect liver?

A

Alpha-1 antitrypsin is produced in the liver.
Abnormal mutant version of the protein is made that gets trapped and builds up inside the liver cells (hepatocytes).
These mutant proteins are toxic to the hepatocytes, causing inflammation. Progresses to fibrosis, cirrhosis and potentially hepatocellular carcinoma

320
Q

How does AAT deficiency affect lungs?

A

In the lungs, the lack of a normal, functioning AAT protein leads to excess protease enzymes attacking the connective tissues.
Leads to bronchiectasis and emphysema.

Alpha-1 antitrypsin is a protease inhibitor

321
Q

What causes AAT deficiency?

A

decreased circulating plasma levels of AAT
due to the inheritance of variant alleles of the SERPINA1 gene

322
Q

How might AAT manifest?

A

Panacinar emphysema and associated obstructive lung disease
hepatitis and jaundice
bronchiectasis

323
Q

What investigations would be done for AAT deficiency and what would the results show?

A

plasma AAT level: low
pulmonary function testing: reduced FEV1
Chest XR/CT: emphysematous changes
LFTs: elevated

324
Q

What are the differentials for AAT deficiency?

A

Asthma
COPD
Bronchiectasis
Viral hepatitis
Alcohol-related liver disease

325
Q

What is the basic management for AAT deficiency?

A

Stop smoking
Standard management for manifestations, e.g. COPD or liver disease

326
Q

What is spontaneous bacterial peritonitis?

A

an infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition

327
Q

Who is SB peritonitis most commonly seen in?

A

most commonly seen in patients with end-stage liver disease

328
Q

What causes SB peritonitis?

A

(almost always) Monomicrobial infection of the ascitic fluid

329
Q

What’s the most common pathogen causing SB peritonitis?

A

E.Coli

gram negative more common than positive

330
Q

What are the symptoms of SB peritonitis?

A

Signs of ascites
abdominal pain
fever
vomiting
altered mental status
GI bleeding

331
Q

What investigations should be done for SB peritonitis?

A

diagnostic paracentesis: ascitic fluid absolute neutrophil count >250 cells/mm³, fluid culture
FBC: leukocytosis
Blood culture

332
Q

What’s the treatment for SB peritonitis?

A

Abx: IV 3rd-gen cephalosporin (e.g., cefotaxime, ceftriaxone), 5-7 days

333
Q

What are the possible complications of SB peritonitis?

A

Sepsis
Tense ascites
Renal failure

333
Q

What is cholestasis?

A

blockage to the flow of bile

334
Q

What is biliary colic?

A

intermittent right upper quadrant pain caused by gallstones irritating bile ducts

335
Q

What is cholelithiasis?

A

Cholelithiasis is the presence of solid concretions (stones) in the gallbladder

336
Q

What is choledocholithiasis?

A

Gallstones exit into the bile ducts

337
Q

When do symptoms occur in gallstones?

A

if a stone obstructs the cystic, bile, or pancreatic duct

338
Q

What are the risk factors for gallstones?

A

increasing age
female sex
obesity, diabetes, and metabolic syndrome
family hx
gene mutations
pregnancy/exogenous oestrogen
NAFLD
prolonged fasting/rapid weight loss

4 Fs: Female, fat, forty, fertile

339
Q

Why do gallstones form and what are the main types?

A

Gallstones form as a result of supersaturation of the bile.
Cholesterol stones (85-90%)
Pigment stones (15%)
Mixed stones – comprised of both cholesterol and bile pigments

340
Q

What are the main risk factors for cholesterol gallstones forming?

A

obesity, poor diet, rapid weight loss after weight loss surgery
female, oestrogen
other meds: octreotide, ceftriaxone

341
Q

How does biliary pain present?

gallstones causing obstruction to a duct

A

right upper quadrant or epigastric pain
Radiates to the right back or shoulder
Responds to analgesia
Typically occurs approximately 1 hour after eating, often in the evening, accompanied by nausea
Becomes increasingly intense and then stabilises
Typically lasts for at least 15-30 minutes, up to several hours

342
Q

What investigations are done for gallstones?

A

LFTs
Ultrasounds

343
Q

What are the management options for gallstones?

A

Analgesia: e.g. paracetamol or diclofenac
Elective cholecystectomy

344
Q

What are some complications of gallstones?

A

Acute cholecystitis
Acute cholangitis
Obstructive jaundice (if the stone blocks the ducts)
Pancreatitis

345
Q

What is acute cholecystitis?

A

acute gallbladder inflammation
major complication of cholelithiasis (gallstones)

346
Q

Who does cholecystitis tend to affect?

A

patients with gallstones, at least 90% of patients with cholecystitis have gallstones

347
Q

What normally causes acute cholecystitis?

A

caused by complete cystic duct obstruction usually due to an impacted gallstone
stops gallbladder from draining

348
Q

What is acalculous cholecystitis?

A

dysfunction in gallbladder emptying is caused by something other than gallstones
Gallbladder is not being stimulated by food to regularly empty, resulting in a build-up of pressure

349
Q

How do gallstones cause acute cholecystitis?

A

Fixed obstruction of gallstones into the gallbladder neck or cystic duct causes bile to become trapped in gallbladder
Irritation and pressure increases in gallbladder.
Stimulates prostaglandin synthesis and inflammatory response
Can result in secondary bacterial infection leading to necrosis and gallbladder perforation

350
Q

What are some signs/symptoms of acute cholecystitis?

A

Upper R quadrant pain and tenderness
Murphy’s sign
Fever
Nausea/vomiting

351
Q

What would be seen on an abdo ultrasound for acute cholecystitis?

A

Pericholecystic fluid
Distended gallbladder
Thickened gallbladder wall (>3 mm)
Gallstones
Positive sonographic Murphy’s sign

352
Q

What can be used to visualise the biliary tree in more detail if a common bile duct stone is suspected but not seen on an ultrasound?

A

magnetic resonance cholangiopancreatography

353
Q

What are some differentials for acute cholecystitis?

A

Acute cholangitis
Chronic cholecystitis
Peptic ulcer disease
Acute pancreatitis
Sickle cell crises
Appendicitis
Right lower lobe pneumonia

354
Q

What’s the management of acute cholecystitis?

A

Nil by mouth
IV fluids
Antibiotics (as per local guidelines)
Cholecystectomy

355
Q

What is gallbladder empyema? And how is it treated?

A

infected tissue and pus collecting in the gallbladder
IV Abx + either gallbladder drain or removal

356
Q

What are some complications of acute cholecystitis?

A

Sepsis
Gallbladder empyema
Gangrenous gallbladder
Perforation

357
Q

How does acute cholangitis lead to sepsis?

A

As the obstruction progresses, the bile duct pressure increases.
Forms a pressure gradient that promotes extravasation of bacteria into the bloodstream.
If not recognised and treated, this will lead to sepsis

358
Q

What is acute cholangitis?

A

infection and inflammation of the biliary tree, most commonly caused by obstruction of common bile duct

359
Q

What are the main causes of acute cholangitis?

A

cholelithiasis leading to choledocholithiasis and biliary obstruction
Iatrogenic biliary duct injury, i.e. surgical injury
Sclerosing cholangitis

360
Q

What’s the epidemiology of acute cholangitis?

A

relatively uncommon, presenting as a complication in less than 10% of patients admitted to hospital with cholelithiasis
average age 50-60 years

361
Q

What are the most common organisms causing acute cholangitis?

A

Escherichia coli
Klebsiella species
Enterococcus species

362
Q

What are the 3 main features of acute cholangitis? (Charcot’s triad)

A

Right upper quadrant pain
Fever
Jaundice

363
Q

How does acute cholangitis occur?

A

Obstruction leads to bile stasis and bile sludge, bacterial seeding
Bacteria can breed in bile sludge and travel from duodenum up biliary tree

364
Q

What are the risk factors for acute cholangitis?

A

Gallstones
Over 50
After endoscopic retrograde cholangiopancreatography
Stricture
Hx of sclerosing cholangitis

365
Q

What symptoms may be present in acute cholangitis?

A

Charcot’s triad: Right upper quadrant pain, Fever, Jaundice
Pale stool
Pruritus
Altered mental status
Hypotension

366
Q

What investigations should be done for acute cholangitis?

A

FBC: raised WBC
LFTs: raised ALP + transaminases
CRP: raised
Blood cultures
Transabdominal ultrasound: dilated bile duct
ERCP, often done following an MRCP

367
Q

How is acute cholangitis managed?

A

Broad spectrum IV Abx
IV fluids
Biliary decompression via ERCP

368
Q

What is primary biliary cholangitis?

A

Chronic, autoimmune condition where the immune system attacks the small intrahepatic bile ducts, causing bile duct damage and loss

369
Q

What’s the pathophysiology of primary biliary cholangitis?

A

Reduced immune tolerance
inflammation and damage to the epithelial cells of the small intrahepatic bile ducts
Over time, this can lead to obstruction of bile flow through these ducts and cholestasis
The back-pressure of bile and disease process ultimately lead to liver fibrosis, cirrhosis and failure

370
Q

What patient population is most commonly affected by primary biliary cholangitis?

A

females, 9:1 f:m ration
middle age, peaks at 40

371
Q

What is the aeitology of primary biliary cholangitis?

A

Autoimmune disease, with characteristic antimitochondrial antibody

372
Q

What are some signs and symptoms of primary biliary cholangitis?

A

Xanthoma and xanthelasma (cholesterol deposits)
Hepatomegaly
Signs of liver cirrhosis and portal hypertension
Fatigue, sleep disturbance
Pruritus (itching)
Gastrointestinal symptoms and abdominal pain
Jaundice
Pale, greasy stools
Dark urine
Dry eyes and mouth

often asymptomatic and detected in LFTs

373
Q

What is the diagnostic cirteria for primary biliary cholangitis?

A

LFTs: ALP and GGT elevated
Autoantibody profile: antimitochondrial antibody
Liver biopsy: bile duct lesions, granuloma formation

374
Q

How is primary biliary cholangitis treated?

A

ursodeoxycholic acid: hydrophilic bile acid that protects cholangiocytes, makes bile less harmful

Obeticholic acid (where UDCA is inadequate or not tolerated

375
Q

What are some complications of primary biliary cholangitis?

A

Hypercholesterolaemia
Cirrhosis and portal HTN

376
Q

What is primary sclerosing cholangitis?

A

a chronic progressive cholestatic liver disease, characterised by inflammation and fibrosis of the intrahepatic and/or extrahepatic bile ducts, resulting in diffuse, multi-focal stricture formation

causing continued destruction of the bile ducts

377
Q

What is the epidemiology of primary sclerosing cholangitis?

A

relatively rare
typically presents between 25 and 45 years, median age of 36-39 at diagnosis
Many patients with PSC have associated IBD (typically UC)
Affects men more than women

378
Q

What is the aetiology of primary sclerosing cholangitis?

A

Not completely clear but gen + environment
Genetic predisposition: HLA-B2/D3

379
Q

What are the risk factors for PSC?

A

male sex
inflammatory bowel disease (IBD)
first degree relative with PSC

380
Q

What are the symptoms of PSC?

A

Fatigue
Fever
Itching
Non-specific upper abdo pain
Jaundice
Fat-soluble vitamin deficiency

can just present with cirrhosis

Most commonly asymptomatic and found incidentally

381
Q

What investigations would be done for PSC?

A

LFTs: elevated
Autoantibodies: anti-smooth muscle, anti-nuclear, p-ANCA
MRCP: bile duct strictures looking like beads on a string

382
Q

How is PSC managed?

A

No definitive treatment found
- general lifestyle changes (including maintaining a healthy diet and weight, and limiting alcohol use)
- colestyramine for pruritus relief
- liver transplants in end stage, recurrence of PSC still a risk

383
Q

What is acute pancreatitis?

A

acute inflammation of the pancreas

rapid symptom onset

384
Q

What are the causes of acute pancreatitis?

I GET SMASHED

A

Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Microbiological (mumps, hepatitis, tb)
Autoimmune pancreatitis
Scorpion sting
Hyperlipidaemia + hypercal
ERCP + emboli
Drugs + thiazide diuretics (furosemide), opiated, VPA

385
Q

How do gallstones cause acute pancreatitis?

A

gallstones trapped at the end of the biliary system, blocking the flow of bile and pancreatic juice into the duodenum.

Bile refluxes into the pancreatic duct and prevents pancreatic juice from being secreted, results in inflammation in the pancreas

more common in women + older patients

386
Q

How does alcohol cause acute pancreatitis?

A

directly toxic to pancreatic cells, resulting in inflammation

more common in men + younger patients

387
Q

What are the risk factors for acute pancreatitis?

A

middle-aged women
young- to middle-aged men
gallstones
alcohol
hypertriglyceridaemia
use of causative drugs
endoscopic retrograde cholangiopancreatography (ERCP)

388
Q

What’s the diagnostic criteria for acute pancreatitis?

A

Upper abdominal pain (epigastric or left upper quadrant)
Elevated serum lipase or amylase (>3 times upper limit of normal)
Characteristic findings on abdominal imaging (CT, MRCP, ultrasound).

2/3 present

389
Q

How does acute pancreatitis typically present?

A

severe, constant upper abdominal pain, usually sudden in onset and often radiating to the back - with associated nausea/vomiting

390
Q

What investigations would be done for acute pancreatitis?

A

Serum lipase/amylase: >3 times the upper limit of the normal range
FBC: leukocytosis
CRP: elevated
Urea: elevated
LFTs: elevated ALT

391
Q

What’s the criteria for the glasgow score assessing severity of acute pancreatitis?

A

P – Pa02 < 8 KPa
A – Age > 55
N – Neutrophils (WBC > 15)
C – Calcium < 2
R – uRea >16
E – Enzymes (LDH > 600 or AST/ALT >200)
A – Albumin < 32
S – Sugar (Glucose >10)

0-1 – mild , 2 – moderate, 3+ – severe pancreatitis

1 point for each

392
Q

What’s the management for acute pancreatitis?

A

IV fluid resus
Oral feeding as soon as can be tolerated
ERCP for gallstones

393
Q

What are some possible complications of acute pancreatitis?

A

Necrosis of the pancreas
Infection in a necrotic area
Abscess formation
Acute peripancreatic fluid collections
Chronic pancreatitis
Sepsis
Acute renal failure (hypovolaemia)

394
Q

What’s the prognosis for acute pancreatitis?

A

80% have mild disease and will improve within 3 to 7 days of conservative management.
The overall mortality rate is low (approximately 5%) but this rises to 25% to 30% in severe acute pancreatitis

395
Q

What is chronic pancreatitis?

A

chronic inflammation in the pancreas.

396
Q

What can cause chronic pancreatitis?

who does it affect?

A

Chronic alcohol ingestion (>75%)
Idiopathic, hereditary

men twice as much as women, middle aged-older patients

397
Q

What are the typical features of chronic pancreatitis?

A

epigastric abdominal pain radiating to the back
steatorrhoea
malnutrition
diabetes mellitus

398
Q

What imaging should be done for chronic pancreatitis?

A

CT/MRI: pancreatic enlargement

399
Q

How is chronic pancreatitis managed?

A

Alcohol and smoking cessation
Dietary advice and supplementation (i.e. fat soluble vitamins ADEK)
Analgesia
Pancreatic enzyme replacement therapy

400
Q

What are some complications of chronic pancreatitis?

A

pancreatic exocrine insufficiency
diabetes mellitus
pancreatic calcifications
pancreatic duct obstruction
opiate addiction

401
Q

What is hepatic encephalopathy?

A

brain dysfunction caused by advanced liver insufficiency and/or portosystemic shunt

402
Q

What causes hepatic encephalopathy?

A

build-up of neurotoxic substances that affect the brain, i.e. ammonia

often as a result of cirrhosis, excessive nitrogen load, benzos, SBP or hyponatraemia/kalaemia

403
Q

What is the pathophysiology of hepatic encephalopathy?

A

hepatocytes are less capable of metabolising waste product + shunts may have formed so ammonia bypasses liver
Blood containing nitrogenous compounds (ammonia) moves into IVC
Ammonia crosses BBB and leads to increased glutamine and oncotic pressure in astrocytes, swelling of astrocytes

404
Q

What are type A,B,C of hepatic encephalopathy?

A

Type A: HE associated with acute liver failure
Type B: HE associated predominantly with portosystemic bypass or shunting
Type C: HE associated with cirrhosis

405
Q

What are the risk factors for hepatic encephalopathy?

A

hypovolaemia
GI bleeding
constipation
excessive protein intake
hypokalaemia, hyponatraemia
metabolic alkalosis
hypoxia
sedative or opioid use
hepatic or portal vein thrombosis

406
Q

What are the symptoms of hepatic encephalopathy?

A

Mood, sleep and motor disturbances
positive Babinski in later stages
manifestations of underlying liver disease (ascites, jaundice)

407
Q

What would be seen on investigations of hepatic encephalopathy?

A

Diagnosed in presence of liver disease
Serum ammonia: elevated

408
Q

What’s the management of hepatic encephalopathy?

A

Lactulose (aiming for 2-3 soft stools daily)
Abx (e.g., rifaximin) to reduce the number of intestinal bacteria producing ammonia
Nutritional support

409
Q

What is hepatitis?

A

inflammation of the liver

410
Q

Which forms of viral hepatitis are RNA/DNA viruses?

A

A,C,D,E are RNA
B is DNA

411
Q

What is the most common liver infection?

A

Hep B

412
Q

How are the different forms of viral hepatitis transmitted?

A

A: faecal-oral route, not associated with chronic liver disease
B: blood/ bodily fluids
C: blood
D: attaches itself to the HBsAg and cannot survive without (hep b)
E: faecal-oral route

413
Q

Which viral hepatitis can cause acute/chronic disease?

A

A: acute
B: acute and chronic
C: acute and chronic
D: acute and chronic
E: mostly acute and self-limiting, can be chronic immunosuppressed

all viral hep are notifiable

414
Q

How does viral hepatitis present?

A

Abdominal pain (RUQ)
Hepatosplenomegaly
Fatigue
Flu-like illness
Pruritus (itching)
Muscle and joint aches
Nausea and vomiting
Jaundice

415
Q

What would LFTs show for viral hepatitis?

hepatitic picture

A

high transaminases (AST and ALT) with proportionally less of a rise in ALP
high bilirubin

416
Q

What viral markers are present for hepatitis B?

A

Surface antigen (HBsAg) – active infection
E antigen (HBeAg) – a marker of viral replication and implies high infectivity
Core antibodies (HBcAb) – implies past or current infection
Surface antibody (HBsAb) – implies vaccination or past or current infection
Hepatitis B virus DNA (HBV DNA) – a direct count of the viral load

417
Q

Which antigen is present for Hepatitis A?

A

IgM antibodies to HAV

418
Q

How is hep C diagnosed?

A

HCV antibody test
HCV RNA testing

419
Q

What are some of the complications of Hep B and C?

A

B: cirrhosis, hepatocellular carcinoma
C: rheumatological complications, cirrhosis, hepatocellular carcinoma

420
Q

Why is Hep D often linked with Hep B?

A

attaches itself to the HBsAg and cannot survive without this protein
increases severity and complications

421
Q

How is hepatitis D diagnosed?

A

Anti-HDV antibodies + HDV RNA
presence of HBV

422
Q

How is hep A treated?

A

supportive, mild analgesia

423
Q

How is hep C treated?

A

direct-acting antiviral therapy, e.g. sofosbuvir/velpatasvir

424
Q

How is hep b treated?

A

supportive care, antiviral therapy in chronic

425
Q

How is hep D treated?

A

supportive
liver transplant if liver failure occurs
peginterferon alfa and/or bulevirtide in chronic

426
Q

How is hepatitis E diagnosed?

A

serum antibody to HEV
HEV RNA

427
Q

Who can be more affected by Hep E?

A

Can cause acute liver failure in pregancy or become chronic in immunosuppressed

428
Q

Which viral hepatitis’ have vaccines?

A

A: vaccine, post-exposure prophylaxis
B: vaccine
C: no vaccine
D: no vaccine but hep b vaccine is protective
E: no vaccine

429
Q

When do hernias occur?

A

weak point in a cavity wall (usually affecting the muscle or fascia)
Body organ (e.g., bowel) normally be contained within that cavity to pass through the cavity wall

430
Q

How does an abdo hernia typically present?

A

A soft lump protruding from the abdominal wall
The lump may be reducible
The lump may protrude on coughing or standing
Aching, pulling or dragging sensation

431
Q

What’s a femoral hernia?

A

herniation of the abdominal contents through the femoral canal

432
Q

What’s a hiatus hernia?

and risk factors

A

protrusion of intra-abdominal contents into the thoracic cavity through an enlarged oesophageal hiatus of the diaphragm

obesity, increased age, increased intra-abdo pressure

433
Q

What’s an umbilical hernia and who does it typically affect?

A

hernias occur around the umbilicus due to a defect in the muscles around umbilicus
Neonates, closes by age 4-5 without treatment normally

434
Q

How can you differentiate between an indirect and direct hernia?

A

When an indirect hernia is reduced and pressure is applied to the deep inguinal ring, the hernia will remain reduced

435
Q

What are the inguinal hernias?

A

Inguinal:
- Indirect: hernia sac comes through the internal (deep) inguinal ring
- Direct: hernia protrudes directly through the abdominal wall

436
Q

What are incisional hernias?

A

hernias occur at the site of an incision from previous surgery

437
Q

How can diarrhoea be defined?

A

3 or more loose stools across a day
Stools that are more frequent than what is normal for the individual lasting <14 days
Stool weight greater than 200 g/day

438
Q

How is diarrhoea classifed based on duration?

A

Acute (≤14 days)
Persistent (>14 days)
Chronic (>4 weeks)

439
Q

What is primary liver cancer?

A

Cancer that starts in the liver
Main one is hepatocellular carcinoma

440
Q

What is secondary liver cancer?

A

Secondary liver cancer originates outside the liver and metastasises to the liver

441
Q

What are the main risk factors for primary liver cancer?

A

Liver cirrhosis caused by:
* Alcohol-related liver disease
* Non-alcoholic fatty liver disease (NAFLD)
* Hepatitis B
* Hepatitis C
* Rarer causes (e.g., primary sclerosing cholangitis)

442
Q

How is liver cancer screened for?

A

Ultrasound
Alpha-fetoprotein

every 6 months for liver cirrhosis patients

443
Q

What investigations are done for liver cancer?

A

Alpha-fetoprotein (tumour marker for hepatocellular carcinoma)
Liver ultrasound is the first-line imaging investigation
CT and MRI scans are used for further assessment and staging of the cancer
Biopsy is used for histology

444
Q

What are the symptoms of liver cancer?

A

Weight loss
Abdominal pain
Anorexia
Nausea and vomiting
Jaundice
Pruritus
Upper abdominal mass on palpation

445
Q

What are the management options for hepatocellular carcinoma?

A

Surgical resection or transplant
Radiofrequency or microwave ablation
Transarterial chemoembolisation (TACE)
Radiotherapy
Targeted drugs (e.g., kinase inhibitors and monoclonal antibodies)

446
Q

What are some criteria for a liver transplant?

A

Cancer isolated to liver
Alcohol free for 6 months

447
Q

What is a cholangiocarcinoma?

A

a type of cancer that originates in the bile ducts.
majority are adenocarcinomas

448
Q

What is the most common site for a cholangiocarcinoma?

A

perihilar region, where the right and left hepatic ducts have joined to become the common hepatic duct

449
Q

What is the tumour marker for cholangiocarcinoma?

A

CA19-9

450
Q

What are the symptoms of obstructive jaundice?

A

Pale stools
Dark urine
Generalised itching

451
Q

What are the majority of pancreatic cancers and where are they found?

A

adenocarcinomas found in head of pancreas

452
Q

Where do pancreatic cancers tend to metastasise to?

A

tend to spread and metastasise early, particularly to the liver, then to the peritoneum, lungs and bones

453
Q

What does Courvoisier’s law state?

A

palpable gallbladder along with jaundice is unlikely to be gallstones

pancreatic cancer or cholangiocarcinoma

454
Q

What is Trousseau’s sign of malignancy?

A

migratory thrombophlebitis as a sign of malignancy, particularly pancreatic adenocarcinoma.
Thrombophlebitis is where blood vessels become inflamed with an associated blood clot (thrombus) in that area.

455
Q

How does pancreatic cancer typically present?

A

Painless obstructive jaundice
Non-specific upper abdominal or back pain
Unintentional weight loss
Palpable mass in the epigastric region
Change in bowel habit
Nausea or vomiting
New-onset diabetes or worsening of type 2 diabetes

456
Q

What investigations can be done for pancreatic cancer?

A

CT thorax, abdomen and pelvis
CA 19-9 tumour marker
MRCP and ERCP
Biopsy

457
Q

What is the main differential for pancreatic cancer?

A

cholangiocarcinoma

458
Q

What are the management options for pancreatic cancer?

A

Surgery (Whipple)
Stent to relieve symptoms
Chemo and radiotherapy (palliative)

459
Q

What are oesophageal varices?

A

dilations of the porto-systemic anastomoses

460
Q

What typically causes oesophageal varices?

A

portal hypertension secondary to liver cirrhosis
most commonly ARLD

461
Q
A

Phase 2a (14 decks)

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