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(SG) condensed phase 2a > Gastrointestinal / Liver > Flashcards

Gastrointestinal / Liver Flashcards

1
Q

Define Gastro-oesphageal reflux disease (GORD)

A

Prolonged or recurrent reflux of the gastic contents into the oesphagus.

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2
Q

Define Mallory-weiss tear

A

Mucosal lacerations in the upper GI tract

-> bleeding.

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3
Q

Define Oesophago-gastric varices

A

Dilated veins at the junction between the portal and systemic venous systems leading to variceal haemorrhage.

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4
Q

How does Gastro-oesphageal reflux disease (GORD) clinically present?

A

Heartburn, related to lying down and meals.

Odynophagia (painful swallowing) and regurgitation.

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5
Q

How does Mallory-weiss tear clinically present?

A

Bout of retching or vomiting

-> Haemetesis (vomiting blood).

Others: Syncope, light headedness, dizziness.

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6
Q

How does Oesophago-gastric varices clinically present?

A

Haematemesis (vomiting blood).

Liver disease.

Pallor.

Shock (low blood pressure / high heart rate).

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7
Q

Cause of Gastro-oesphageal reflux disease (GORD)

A

Smoking, alcohol, pregnancy, obesity, big meals.

Complication of a hiatus hernia.

Any reason for inadequate LOS function.

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8
Q

Cause of Mallory-weiss tear

A

Trauma from frequent cough, vomit, retching or even hiccuping.

RF: Excessive alcohol consumption.

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9
Q

Cause of Oesophago-gastric varices

A

Portal Hypertension.

Majority of patients with oesophageal varices have chronic liver disease.

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10
Q

Diagnostic test for Gastro-oesphageal reflux disease (GORD)

A

Endoscopy,

barium swallow.

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11
Q

Diagnostic test for Mallory-weiss tear

A

Endoscopy.

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12
Q

Diagnostic test for Oesophago-gastric varices

A

Endoscopy.

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13
Q

Treatment of Gastro-oesphageal reflux disease (GORD)

A

Lifestyle; weight loss, avoidance of excess alcohol, cessation of smoking.

Antacids (gaviscon, sodium bicarbonate) sufficient for mild.

Severe may require PPI (omeprazole).

H2 receptor antagonist (cimetidine)

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14
Q

Treatment of Mallory-weiss tear

A

Resuscitation.

Maintain airway, high flow oxygen, correct fluid losses. Identify comorbidities.

Tear tends to heal rapidly.

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15
Q

Treatment of Oesophago-gastric varices

A

Resuscitation.

Maintain airway.

Treat shock.

Vasoactive drugs, endoscopic band ligation and antibiotics (as prophylaxis).

Can obturate with glue like substance.

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16
Q

Complications of Gastro-oesphageal reflux disease (GORD)

A

Oesophageal stricture formation: worsening dysphagia.

Barrett’s Oesophagus: abnormal columnar epithelium replaces the squamous epithelium of the distal oesophageus.

Irreversible.

Can develop into oesophageal cancer.

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17
Q

Complications of Mallory-weiss tear

A

Hypovolaemic shock (and death).

Rebleeding.

MI.

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18
Q

Complications of Oesophago-gastric varices

A

70% chance of rebleeding.

Significant risk of death.

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19
Q

Define Peptic ulcer

A

Break in the GI mucosa in or adjacent to acid bearing area.

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20
Q

Define Gastritis

A

Inflammation of the gastric mucosa.

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21
Q

Define Gastropathy

A

Injury to the gastric mucosa with epithelial cell damage and regeneration.

Little to no inflammation.

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22
Q

Types of peptic ulcer

A

Gastric

Duodenal

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23
Q

Types of gastritis

A

Acute

Chronic

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24
Q

How does a peptic ulcer clinically present?

A

Burning epigastric pain.

Nausea, heartburn, and flatulence.

Occasionally painless haemorrhage.

Differences: Duodenal - more pain when the patient is hungry, and at night.

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25
Q

How does gastritis clinically present?

A

Usually asymptomatic.

Sometimes functional dyspepsia.

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26
Q

How does gastropathy clinically present?

A

Indigestion,

vomiting

and haemorrhage.

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27
Q

What is associated with H. pylori?

A

Peptic ulcers. 80-90% association.

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28
Q

Duodenal or gastric ulcer: which has higher prevalence of H. pylori association?

A

Duodenal associated with 95% of cases.

Gastric associated with 80% of cases.

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29
Q

What is acute gastritis associated with?

A

Associated with neutrophilic infiltration.

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30
Q

What is chronic gastritis associated with?

A

Associated with mononuclear cells

(lymphocytes, plasma cells and macrophages).

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31
Q

Causes of peptic ulcers

A

H. pylori and NSAIDs.

H. pylori: Increased gastric acid secretions.

Disruption of mucous protective layer.

Reduced duodenal bicarbonate production

NSAIDs: Reduced production of prostaglandins which provide mucosal protection in the upper GI.

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32
Q

Causes of gastritis

A

Most commonly: H. pylori infection.

Also possible; autoimmune gastritis (antibodies to parietal cells and intrinsic factor), viruses, duodeno-gastric reflux.

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33
Q

Cause of gastropathy

A

Most commonly: Use of NSAIDs.

Also possible; severe stress, high amounts of alcohol, CMV and herpes simplex infection.

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34
Q

Epidemiology of peptic ulcers

A

50% of all UGIB

Differences: Duodenal 2-3 times more common than gastric.

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35
Q

Diagnostic test for peptic ulcers

A

Testing for H. pylori: Carbon-13 urea breath test or stool antigen test.

Alternatively Endoscopy possible.

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36
Q

Diagnostic test for gastritis

A

Endoscopy: Can appear reddened, or normal.

Histological change; detected through biopsy.

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37
Q

Diagnostic test for gastropathy

A

Endoscopy: Erosions and subepithelial haemorrhage.

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38
Q

Treatment of peptic ulcers

A

Avoid NSAIDs.

Cessation of smoking.

Eradication of H. pylori through antibiotics and PPI (triple therapy: clarithromycin, omeprazole, metronidazole).

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39
Q

Treatment of gastritis

A

Eradication of H. pylori

(triple therapy: clarithromycin, omeprazole, metronidazole).

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40
Q

Treatment of gastropathy

A

PPI with removal of causative agent.

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41
Q

Complications of peptic ulcers

A

Can cause Upper GI bleed.

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42
Q

Complications of gastritis

A

Peptic ulcer.

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43
Q

Complications of gastropathy

A

Peptic ulcer.

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44
Q

Sequelae of gastritis

A

Pernicious anaemia (if due to autoimmune attack of IF).

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45
Q

Define Cholangitis

A

Infection of the biliary tree.

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46
Q

Define Primary sclerosing cholangitis.

A

Chronic inflammation and fibrosis of the bile ducts.

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47
Q

How does Cholangitis clinically present?

A

Charcot’s triad:

Fever (with chills),

right upper quadrant pain,

jaundice (dark urine, pale stool, pruritus) in most patients.

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48
Q

How does Primary sclerosing cholangitis present.

A

May be asymptomatic.

Usually incidentally found after LFT.

Charcot’s triad:

Fever (with chills),

right upper quadrant pain

and jaundice (dark urine, stool, pruritus).

Hepatomegaly.

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49
Q

Primary sclerosing cholangitis - note

A

75% have association with ulcerative colitis.

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50
Q

Cause of Cholangitis

A

Generally caused by gallstones.

Other causes include infection (usually Klebsiella or E. coli.

Can be due to benign strictures or malignancy of the head of the pancreas.

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51
Q

Causes of Primary sclerosing cholangitis

A

Generally unknown.

Possibly genetic, lymphocyte recruitment, portal bacteraemia and bile salt toxicity.

Secondary: Can be secondary to infection, thrombosis or iatrogenic/trauma

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52
Q

Diagnostic tests for Cholangitis

A

FBC: Raised CRP (and ESR?) LFT: Raised ALP, AST, ALT

Ultrasound: Detect stone/stent/stricture

Blood culture: (if septic)

ERCP: Definitive.

Culturing and can remove blockage.

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53
Q

Diagnostic tests for Primary sclerosing cholangitis

A

Ultrasound: May show bile duct dilatation (not diagnostic)

ERCP: Can help, but invasive.

LFT: elevated ALP or GGT.

Serum transaminase levels can be normal to several times normal.

Serum albumin drops with progression.

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54
Q

Treatment of Cholangitis

A

Fluid resuscitation.

Antibiotic therapy.

Clear obstruction with ERCP.

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55
Q

Treatment of Primary sclerosing cholangitis

A

Usually manage symptoms of liver failure (eventual liver transplant).

ERCP can dilate some extra-hepatic strictures to slow progression.

High dose ursodeoxycholic acid can slow progression.

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56
Q

Complications of Cholangitis

A

Can lead to sepsis.

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57
Q

Complications of Primary sclerosing cholangitis

A

Eventual liver failure.

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58
Q

Sequelae of Primary sclerosing cholangitis

A

15% get cholangiocarcinoma.

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59
Q

Define Achalasia

A

Oesophageal aperistalsis

and failure of LOS to relax impairs oesophageal emptying.

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60
Q

Define Systemic Sclerosis (Scleroderma) (SSc)

A

Multisystem autoimmune disease.

Increased fibroblast activity

-> abnormal growth of connective tissue.

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61
Q

Types of Systemic Sclerosis (Scleroderma) (SSc)

A

Limited cutaneous (CREST syndrome).

Diffuse cutaneous.

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62
Q

How does Achalasia clinically present?

A

Onset at any age.

Long Hx of dysphagia for solids and liquids.

Retrosternal chest pain (not cardiac).

Weight loss.

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63
Q

How does limited cutaneous (CREST syndrome) - (type of Systemic Sclerosis (Scleroderma) (SSc)) clinically present?

A

Raynaud’s phenomenon.

Skin hardening in hands or face.

MSK: Joint pain and swelling.

CREST: Calcinosis Raynaud’s Esophageal dysmotility Sclerodactyly and Telangiectasia

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64
Q

How does Diffuse cutaneous - (type of Systemic Sclerosis (Scleroderma) (SSc)) clinically present?

A

As above (limited cutaneous (CREST syndrome) but more rapid and widespread onset in diffuse.

GI symptoms: Heartburn, reflux oesophagitis.

Delayed gastric emptying.

Pulmonary: Pulmonary fibrosis.

Pulmonary arterial hypertension.

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65
Q

Limited cutaneous (CREST syndrome) - (type of Systemic Sclerosis (Scleroderma) (SSc)) - note

A

70% of SSc.

Affects face, forearms and lower legs up to the knee.

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66
Q

Diffuse cutaneous - (type of Systemic Sclerosis (Scleroderma) (SSc)) - note

A

30% of SSc.

Also affects upper arms, thighs or trunk.

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67
Q

Cause of Achalasia

A

Unknown.

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68
Q

Cause of Systemic Sclerosis (Scleroderma) (SSc)

A

Uknown.

Likely a genetic component.

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69
Q

Diagnostic tests for Achalasia

A

Barium swallow: Aperistalsis and ‘beak deformity’ (oesophagus tapering to a point)

Oesophageal manometry: Demonstrates aperistalsis and failure of LOS to relax on swallowing.

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70
Q

Diagnostic test for Systemic Sclerosis (Scleroderma) (SSc)

A

Antinuclear antibodies: Positive in 90% but not specific.

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71
Q

Treatment of Achalasia

A

No cure.

Treat symptoms.

Surgical division of LOS and endoscopic balloon dilatation.

Nitrates where surgery is not an option.

Botox: Best for elderly (who can’t do surgery).

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72
Q

Treatment of Systemic Sclerosis (Scleroderma) (SSc)

A

No cure.

Treat symptoms.

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73
Q

Complications of Achalasia

A

Untreated

-> Inhalation of material in oesophagus

-> choking.

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74
Q

Complications of Systemic Sclerosis (Scleroderma) (SSc)

A

Malnutrition due to swallowing problems.

Obstruction in GI tract due to reduced motility.

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75
Q

Sequelae of Achalasia

A

Oesophageal cancer.

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76
Q

Define Coeliac disease

A

Immune mediated inflammatory condition provoked by gluten.

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77
Q

Define Ulcerative colitis

A

Continuous chronic inflammation of only the colon.

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78
Q

Define Crohn’s disease

A

Intermittent chronic inflammation of the entire GI tract.

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79
Q

How does Coeliac disease clinically present?

A

Range of possible symptoms, with onset at any age (two peaks; infancy and 5th decade).

Persistent GI symptoms.

Faltering growth.

Prolonged fatigue.

Unexplained weight loss.

Severe mouth ulcers.

Iron, B12 or folate deficiency (anaemia).

IBS.

FH of Coeliac.

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80
Q

How does Ulcerative colitis clinically present?

A

Recurrent diarrhoea, often with blood and mucus.

Some extragastrointestinal manifestations: arthralgia,

fatty liver,

and gall stones.

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81
Q

How does Crohn’s disease - clinically present?

A

Symptoms depend on the region affected.

Small bowel: Weight loss, abdominal pain.

Terminal ileum: Right iliac fossa pain mimicking appendicitis.

Colonic: Blood and mucus with diarrhoea, with pain.

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82
Q

What does DQ stand for?

A

DQ: “Dietary query”

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83
Q

What aids ulcerative colitis?

A

Smoking protects.

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84
Q

How does smoking impact Crohn’s?

A

Smoking damages.

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85
Q

Cause of Coeliac disease

A

Strong genetic association with HLA DQ2 and DQ8.

Attacks caused by the presence of gluten in the diet.

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86
Q

Cause of inflammatory bowel disease - Ulcerative colitis & Crohn’s disease

A

Genetics: Mild genetic link (Strong in Crohn’s).

Environmental: Stress and depression -> attacks.

Immune response: Effector T cells predominating over regulatory T cells

-> Pro-inflammatory cytokines (IL12, IL5, IL17 and interferon gamma)

-> Stimulate macrophages to produce Tumour Necrosis Factor Alpha, IL-1 and IL-6.

Neutrophils, mast cells and eosinophils are also activated.

All this causes a wide variety of inflammatory mediators -> Cell damage

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87
Q

Diagnostic test for Coeliac disease

A

Serology: IgA tissue transglutaminase antibodies have a very high sensitivity and specificity for Coeliacs.

Also endomysial antibodies.

Then, Distal Duodenal Biopsy: Histological changes.

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88
Q

Diagnostic test for inflammatory bowel disease - Ulcerative colitis & Crohn’s disease

A

Seek to distinguish between the two.

Sigmoidoscopy/rectal biopsy

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89
Q

Treatment of Coeliac disease

A

Gluten free diet.

Nutrituonal supplement as required.

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90
Q

Treatment of Ulcerative colitis

A

5-Aminosalicylic acid (mesalazine) - Drug of choice for remission and relapse prevention.

Surgical resection.

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91
Q

Treatment of Crohn’s disease

A

Stop smoking.

Corticosteroids induce remission (but don’t prevent relapse).

Thiopurines maintain remission (but have side effects)

Azathioprine.

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92
Q

Complications of Coeliac disease

A

Increased incidence of malignancy, reduced by gluten-free.

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93
Q

Complications of Ulcerative colitis

A

Psychosocial and sexual problems.

Frequent relapse.

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94
Q

Complications of Crohn’s disease

A

Bowel obstructions from strictures.

May cause short stature in children.

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95
Q

Sequelae of Ulcerative colitis

A

Colorectal cancer risk doubled.

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96
Q

Sequelae of Crohn’s disease

A

Osteoporosis

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97
Q

Define Ischaemic colitis

A

Lack of blood supply to the colon cause inflammation and injury.

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98
Q

Define Mesenteric ischaemia

A

Lack of blood supply to the colon.

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99
Q

Types of Mesenteric ischaemia

A

Acute.

Chronic.

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100
Q

How does Ischaemic colitis clinically present?

A

Abdominal pain and rectal bleeding.

Occasionally shock.

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101
Q

How does acute mesenteric ischaemia clinically present?

A

Moderate-severe- colicky/constant poorly localised pain,

out of proportional to physical findings.

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102
Q

How does chronic mesenteric ischaemia clinically present?

A

Moderate-severe- colicky/constant poorly localised post-prandial pain,

out of proportional to physical findings.

Fear of eating, nausea, vomiting or bowel irreguarity

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103
Q

What does mesenteric ischaemia refer to?

A

Umbrella term,

including embolus/thrombus,

non-occlusive mesenteric ischaemia.

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104
Q

Chronic mesenteric ischaemia refers to which arteries?

A

Can be all three major mesenteric arteries.

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105
Q

Cause of Ischaemic colitis

A

Usually underlying atherosclerosis and vessel occlusion.

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106
Q

Causes of Acute mesenteric ischaemia

A

Arterial thrombosis/embolus,

aortic dissection,

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107
Q

Cause of Chronic mesenteric ischaemia

A

Usually atherosclerosis.

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108
Q

Diagnostic test for Ischaemic colitis

A

Sigmoidoscopy shows normal, with some blood.

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109
Q

Diagnostic test for Acute mesenteric ischaemia

A

Angiography: Shows arterial blockage

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110
Q

Diagnostic test for Chronic mesenteric ischaemia

A

Ultrasound,

arteriography

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111
Q

Treatment of Ischaemic colitis

A

Treat symptoms.

Possible anticoagulants.

Surgery may be required for gangrene, perforation or stricture formation.

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112
Q

Treatment of Acute mesenteric ischaemia

A

Initial resuscitation with IV.

Surgical: Angioplasty, embolectomy.

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113
Q

Treatment of Chronic mesenteric ischaemia

A

Surgical intervention.

Medical: In surgical contraindicated.

Nitrates and anticoagulant.

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114
Q

Complications of Ischaemic colitis

A

Gangrene,

perforation

or stricture formation.

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115
Q

Complications of Acute mesenteric ischaemia

A

Poor outcome;

with treatment 50-80% mortality.

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116
Q

Complications of Chronic mesenteric ischaemia

A

Colitis.

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117
Q

Define Haemorrhoids (Piles)

A

Enlarged vascular mucosal cushions in the anal canal

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118
Q

Define Anorectal abscess

A

Collection of pus in the anal or rectal region.

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119
Q

Types of Haemorrhoids (Piles)

A

Internal: Above dentate line.

External: Below dentate line.

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120
Q

How do internal haemorrhoids clinically present?

A

Painless unless strangulated (upper anal canal has no pain fibres)

1st degree: Do not prolapse.

2nd degree: Prolapse on straining, spontaneous reduction

3rd degree: Prolapse on straining, manual reduction

4th degree: Permanently prolapse, no reduction.

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121
Q

How do external haemorrhoids clinically present?

A

Painful and itchy.

Visible on external examination.

Can coexist with the above.

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122
Q

How does an anorectal abscess clinically present?

A

Painful, hardened tissue in the perianal area,

discharge of pus from the rectum,

a lump or nodule,

tenderness,

fever,

constipation.

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123
Q

Cause of Haemorrhoids (Piles)

A

Unknown.

Risk factors:

Constipation,

prolonged straining,

increased abdominal pressure (ascites),

heavy lifting.

124
Q

Cause of an anorectal abscess

A

Infection of an anal fissure.

125
Q

Epidemiology of Haemorrhoids (Piles)

A

Prevalence between 4% and 34%.

126
Q

Diagnostic test for Haemorrhoids (Piles)

A

DRE: Internal won’t be palpable.

Proctoscopy

127
Q

Diagnostic test for an anorectal abscess

A

DRE.

128
Q

Treatment of Haemorrhoids (Piles)

A

Increase fluid and fibre.

Pain relief.

Intervention: Rubber band ligation (tie a band around it and necrotise it)

Surgical: Haemorrhoidectomy.

129
Q

Treatment of an anorectal abscess

A

Surgical drainage.

Pain refief.

130
Q

Complications of Haemorrhoids (Piles)

A

Skin tags.

If internal strangulated;

ischaemia -> gangrene.

131
Q

Complications of an anorectal abscess

A

Fistula in ano: Approx. 40% lead to this.

A chronic, abnormal communication between the epithelialised surface of the anal canal and the perianal skin.

132
Q

Define Fissure-in-ano

A

Tear in the mucosa of the anal canal.

133
Q

Define Pilonidal sinus

A

Obstruction of natural hair follicles above the anus.

134
Q

Types of Fissure-in-ano

A

Primary: No apparent cause.

Secondary: Due to underlying condition.

135
Q

How does Fissure-in-ano clinically present?

A

Pain on defecation.

Bright red bood on defecation.

136
Q

How does Pilonidal sinus clinically present?

A

Small hole about 6cm above the anus.

Usually no symptoms until infected; then a pus fuilled abscess.

Infection can cause pain, redness and swelling.

137
Q

Cause of Fissure-in-ano

A

Constipation: A hard stool tears the anal mucosa

IBD: Ulceration as part of inflammation.

Rectal malignancy.

138
Q

Cause of Pilonidal sinus

A

Congenital.

139
Q

Diagnostic test for Fissure-in-ano

A

Clinical.

140
Q

Diagnostic test for Pilonidal sinus

A

Diagnose by observation.

141
Q

Treatment of Fissure-in-ano

A

Simple pain relief.

Warm baths.

142
Q

Treatment of Pilonidal sinus

A

Asymptomatic: Keep clean through hygiene.

Shave hair around area

Infected: Consider excision of the sinus tract and closure.

Skin flaps can be used to cover the defect.

143
Q

Complications of Fissure-in-ano

A

Depends on underlying pathology.

Possible anorectal abscess.

144
Q

Complications of Pilonidal sinus

A

Infection.

145
Q

Sequelae of Fissue-in-ano

A

Recurrence.

146
Q

Define irritable bowel syndrome

A

Relapsing functional bowel disorder associated with a change in bowel habit

-> No organic cause found.

147
Q

Define diverticular disease

A

Pouches of mucosa extrude through the colonicmuscular wall to form diverticula.

148
Q

Define appendicitis

A

Inflammation of the appendix.

149
Q

Types of irritable bowel syndrome

A

Hard,

soft

and mixed stool.

150
Q

How does irritable bowel syndrome clinically present?

A

Crampy abdominal pain relieved by defecation or wind,

altered bowel habit,

sensation of incomplete evacuation (tenesmus),

abdominal bloating and distension.

151
Q

How does diverticular disease clinically present?

A

Asymptomatic in 95% of cases.

Symptoms that do occur relate to luminal narrowing;

pain, constipation, bleeding or diverticulitis.

Severe cases; left iliac fossa pain, fever, nausea.

152
Q

How does appendicitis clinically present?

A

Pain: umbilicus -> right iliac fossa, tender with guarding

General: Nausea, localised tenderness,

diarrhoea/constipation, pyrexia

153
Q

Pathophysiology of irritable bowel syndrome

A

Broadly unknown.

No organic cause can be found.

154
Q

Cause of irritable bowel syndrome

A

No structural lesion.

Broadly unknown.

Associated with psychological stress.

155
Q

Cause of diverticular disease

A

Unknown.

Related to a low fibre diet

-> Increased intracolonic pressure

-> herniation at sites of weakness?

156
Q

Cause of appendicitis

A

Formation of a faecolith (hard discreet mass of inspissated faeces) that obstructs the lumen of the appendix.

157
Q

Diagnostic test for irritable bowel syndrome

A

NOT a diagnosis of exclusion.

Coeliac screen.

158
Q

Diagnostic test for diverticular disease

A

CT scan.

Possibly ultrasound.

159
Q

Diagnostic test for appendicitis

A

Inflammation markers (CRP, ESR, white cell count) raised but not specific.

CT is gold standard.

160
Q

Treatment of irritable bowel syndrome

A

Regular meals.

Lots of fluids.

Fibre depends on type; more with diarrhoea less with constipation.

Placebo has strong effect.

161
Q

Treatment of diverticular disease

A

Antibiotics.

Rarely; surgery for frequent attacks or complications.

162
Q

Treatment of appendicitis

A

Surgical removal, open or laparoscopically.

Appendix mass can be treated with IV fluids and antibiotics,

and later appendectomy.

163
Q

Complications of diverticular disease

A

Perforation,

fistula formation with bladder or vagina,

intestinal obstruction.

Bleeding can be massive.

164
Q

Complications of appendicitis

A

Peritonitis.

Appendix abscess.

165
Q

Sequelae of diverticular disease

A

Recurrence.

166
Q

Define pancreatitis

A

Inflammation of the pancreas

167
Q

Types of pancreatitis

A

Acute

Chronic

168
Q

How does acute pancreatitis clinically present?

A

Epigastric or upper abdominal pain radiating through to the back.

Nausea and vomiting.

Coma and multiple organ failure are possible, and may delay diagnosis.

Ecchymoses around umbilicus or in flanks suggeset necrotising.

169
Q

How does chronic pancreatitis clinically present?

A

Severe epigastric abdominal pain radiating through to the back.

Severe weight loss possible.

Diabetes and steatorrhoea (due to insulin and liapse deficiency).

Jaundice possible (due to obstruction of the CBD).

170
Q

How is chronic pancreatitis subtyped?

A

Subtyped into large and small duct pancreatitis, based on the duct affected.

Small tends not to be associated with calcification.

171
Q

Causes of acute pancreatitis (think acronym!)

A

Gallbladder disease and excess alcohol consumption.

I GET SMASHED:

Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Autoimmune
Scorpion Stings
Hyperlipidaemia
ERCP (Endoscopic retrograde cholangio pancreatography).
Drugs

172
Q

Causes of chronic pancreatitis

A

Typically excess alcohol consumption.

Also possibly hereditary,

autoimmune

or as a complication of cystic fibrosis.

173
Q

Diagnostic test for acute pancreatitis

A

Serum amylase: 3x more than normal.

Lipase levels rising more sensitive.

174
Q

Diagnostic test for chronic pancreatitis

A

Xray/CT: Displays calcification (not valid in small duct).

Secretin stimulation test: Detects if pancreatic exocrine function is damaged.

175
Q

Treatment of acute pancreatitis

A

Mild: Pain relief, IV fluids

Severe: IV antibiotics if necrotising, feed with enteral nutrition.

Monitor for complications.

176
Q

Treatment of chronic pancreatitis

A

Pain relief.

Cessate alcohol.

Replace pancreatic enzymes (aids functionality and pain by down regulating release of pancreatic enzymes)

Surgery: Local resection to aleviate duct dilatation/duct stones.

177
Q

Complications of acute pancreatitis

A

Pancreatic necrosis.

Pancreatic ascites.

Pancreatic abscess (may require surgery).

178
Q

Complications of chronic pancreatitis

A

Diabetes.

179
Q

Sequelae of acute pancreatitis

A

Recurrence.

180
Q

Sequelae of chronic pancreatitis

A

Pancreatic carcinoma.

181
Q

Define Cholangiocarcinoma

A

Cancer of the biliary tree (in or out of liver).

182
Q

Define gallstones

A

Stones block the biliary tract.

183
Q

Types of gallstones

A

Cholesterol

Pigment

184
Q

How does cholangiocarcinoma clinically present?

A

Fever,

malaise,

weight loss.

Right upper quadrant pain, jaunce (early).

Hepatomegaly, ascites.

185
Q

How do gallstones clinically present?

A

70% of stones are asymptomatic at the time of diagnosis.

Of symptomatics, most common is Biliary Colic (Right upper quadrant, sudden, nausea and vomiting),

caused by a gallstone impacting on the cystic duct or the ampulla of vater.

Second most common;

acute cholecystitis,

where distension of the GB -> necrosis and ischaemia.

186
Q

Cause of cholangiocarcinoma

A

Caused by flukes,

primary sclerosing cholangitis,

HBV,

HCV,

DM,

Caroli’s.

187
Q

Cause of cholesterol gallstones

A

Multifactorial.

Cholesterol supersaturation,

nucleation factors

and reduced gallbladder motility

188
Q

Causes of pigment gallstones

A

Chronic haemlysis (sphereocytosis and sickle cell),

in which bilirubin production is increased.

Also cirrhosis.

Possible as complication of cholecystectomy and with duct strictures.

189
Q

Diagnostic test for cholangiocarcinoma

A

Contrast MRI: optimal imaging for diagnosis

ECRP: can obtain samples for biopsy.

190
Q

Diagnostic test for gallstones

A

Ultrasound.

191
Q

Treatment of cholangiocarcinoma

A

Complete surgical resection.

Stent (or surgical bypass) to relieve symptoms.

192
Q

Treatment of gallstones

A

Nonsurgical: Pain relief.

IV antibiotics if necessary

Surgical: Laparoscopic cholecystectomy.

193
Q

Complications of gallstones

A

Jaundice: if biliary obstruction

Acute cholecystitis: Cystic duct impaction

Pancreatitis: Blocks pancreatic duct

Gallstone ileus: Occludes intestinal lumen

Empyema: Obstructed GB fills with pus

Cholangitis: Inflammation of the gallbladder as a result of bile duct blockage

194
Q

Define hepatitis

A

Inflammation of the liver as a result of direct viral infection.

195
Q

Types of hepatitis

A

Hepatitis A, B, C

196
Q

How does Hep A clinically present?

A

Incubation period of 28 days.

Nausea, anorexia and distaste for cigarettes.

After 2 weeks, jaundice, with dark urine and pale stool.

Sometimes hepatomegaly.

197
Q

How does Hep B clinically present?

A

Flu-like symptoms.

Fever.

Jaundice in 10% of younger, and 50% of adults.

198
Q

How does Hep C clinically present?

A

Incubation period of 6-9 weeks.

Often asymptomatic in acute infection.

Chronic infection may present with malaise, weakness and anorexia.

199
Q

How is Hep A spread?

A

Spread by faecal-oral route.

Associated with shellfish.

200
Q

How is Hep B spread?

A

Parenteral route.

Infected blood or bodily fluids.

Mostly intercourse, or vertical transmission.

201
Q

How is Hep C spread?

A

Blood borne.

Mostly transmitted by poorly sterilised instruments/shared needles.

202
Q

Diagnostic test for Hep A

A

Blood: ALT rises

IgM: Antibody to HAV.

203
Q

Diagnostic test for Hep B

A

Blood: ALT rises.

HBsAg,

HBcAb,

HBsAb,

IgM HBcAb.

204
Q

Diagnostic test for Hep C

A

Liver enzymes: rise.

Antibodies to HCV.

205
Q

Treatment of Hep A

A

Prevention: Vaccine.

Treatment: Treat symptoms.

Avoid alcohol.

206
Q

Treatment of Hep B

A

Avoid unprotected sex and alcohol.

Treatment: treat symptoms.

Fulminant hepatitis: Antivirals.

207
Q

Treatment of Hep C

A

Antivirals: Weekly subcut peginterferon alfa-2a and daily oral ribavirin

Information: Advice on not sharing needles

208
Q

Complications of Hep A

A

Fulminant hepatic failure (rare).

209
Q

Complications of Hep B

A

Liver failure.

210
Q

Complications of Hep C

A

Hepatocellular carcinoma (if cirrhosis was found).

211
Q

Define alcoholic liver disease

A

Chronic liver disease caused by excess of alcohol.

212
Q

Define liver failure

A

Loss of the liver’s ability to regenerate or repair.

213
Q

Types of liver failure

A

Fulminant hepatic failure.

Late-onset hepatic failure.

Chronic decompensated hepatic failure.

214
Q

How does alcoholic liver disease clinically present?

A

Fatty liver: Usually no symptoms.

Possible hepatomegaly on examination.

Alcoholic hepatitis: Rapid onset jaundice.

Nauesea, anorexia, enecphalopathy, fever and ascites.

Alcoholic cirrhosis: May be asymptomatic.

Usually present with complications of cirrhosis.

Spider naevei are a classic.

215
Q

How does liver failure clinically present?

A

Hepatic encephalopathy, abnormal bleeding, ascites, jaundice.

Mental state shows drowsiness and confusion, due to cerebral oedema.

216
Q

When does fulminant hepatic failure occur?

A

Within 8 weeks of onset of underlying illness.

217
Q

When does late-onset hepatic failure occur?

A

8-26 week since onset of underlying illness.

218
Q

What is the latent period for chronic dgcompensated hepatic failure?

A

> 6 months

219
Q

What are the 3 main pathological lesions with ALD?

A

Fatty liver, hepatitis and cirrhosis.

220
Q

Causes of alcoholic liver disease

A

Excessive consumption of alcohol.

Exact mechanism is unknown, beyond identifying alcohol as a hepatoxin.

Some genetic predisposition.

221
Q

Causes of liver failure

A

Various.

Toxins: Alcohol, paracetamol poisoning

Infections: Viral hepatitis, Epstein-Barr virus, CMV

Neoplastic: Hepatocellular carcinoma

Metabolic: Wilson’s, A1AT deficiency, Haemochromatosis

Others: Acute fatty liver of pregnancy, ischaemia, autoimmune liver disease

222
Q

Epidemiology of alcoholic liver disease

A

Most common cause of chronic liver disease in western world.

Usually presents in men in 40-50s.

223
Q

Epidemiology of liver failure

(what is the most common cause in acute?)

A

1/100,000.

Paracetamol poisoning most common cause in acute.

224
Q

Diagnostic test for alcoholic liver disease

A

Liver biochem: AST and ALT rise (disproportionately AST)

Bloods: Elevated MCV.

225
Q

Diagnostic test for liver failure

A

Raised bilirubin.

Glucose low (no glucogenesis).

226
Q

Treatment of alcoholic liver disease

A

Lifelong abstinence from alcohol.

Corticosteroids to control inflammation if there is no renal failure.

227
Q

Treatment of liver failure

A

Liver transplantation in severe cases.

228
Q

Complications of alcoholic liver disease

A

Untreated: Liver failure.

229
Q

Complications of liver failure

A

Infection.

Haemorrhage.

230
Q

Define Hepatocellular carcinoma

A

Cancer of the hepatocyte.

231
Q

Define Haemochromatosis

A

Deficiency of the iron regulatory hormone hepcidin

-> Iron overload.

232
Q

Define Wilson’s Disease

A

Disorder of copper metabolism

-> Copper build up in the liver.

233
Q

Types of haemochromatosis

A

HFE mutations:

C282Y and H63D.

234
Q

How does Hepatocellular carcinoma clinically present?

A

Fever, malaise, weight loss.

Right upper quadrant pain, jaunce (late).

Hepatomegaly, ascites.

235
Q

How does haemochromatosis clinically present?

A

Often asymptomatic until later stages.

Usually presents between 40-60.

Fatigue, weakness, arthopathy, heart problems.

Advanced disease: Bronzing of the skin, diabetes, hepatomegaly, arthropathy.

236
Q

How does Wilson’s disease clinically present?

A

Difficult to diagnose.

Onset usually in 20-30s.

Hepatic: Acute liver failure. Chronic hepatitis.

Psychological: Behavioural problems common, might lead to diagnosis.

Eyes: Kayser-Fleischer ring (bronze ring on the cornea), usually on examination with a slit lamp.

Also sunflower cataracts, also with slit lamp.

237
Q

Cause of Hepatocellular carcinoma

A

Hepatitis B and C,

aflatoxin, alcohol,

haemochromatosis,

cirrhosis and anabolic steroids.

238
Q

Cause of haemochromatosis

A

Often hereditary in autosomal recessive pattern of HFE gene (responsible for regulating iron uptake).

Can not be genetic or not be associated with HFE, but rarely.

239
Q

Cause of Wilson’s Disease

A

Mutation in ATP7B; over 500 identified.

Autosomal recessive.

240
Q

Diagnostic test for Hepatocellular carcinoma

A

CT and biopsy.

241
Q

Diagnostic test for haemochromatosis

A

Screening not advised; penetrance very low.

Consider genetic analysis in unexplained chronic liver disease.

Total Iron Binding capacity reduced, serum iron raised.

LFTs can be normal.

242
Q

Diagnostic test for Wilson’s Disease

A

Slit lamp analysis of eyes to detect Kayser-Fleischer rings.

Low serum caeruloplasmin.

243
Q

Treatment of Hepatocellular carcinoma

A

Surgery to resect individual tumours.

Liver transplant if multiple.

244
Q

Treatment of haemochromatosis

A

Phlebotomy; removing 400-500ml of blood every 2 weeks.

Tends to require insulin.

245
Q

Treatment of Wilson’s Disease

A

Avoid alcohol.

Prevent intestinal copper absorption: Chelation agents such as Zinc (lifelong).

Hepatic: About 5% of patients who presented with liver failure will need a transplant.

Neuro: Deep brain stimulation.

246
Q

Complications of haemochromatosis

A

Liver fibrosis, failure, cirrhosis and hepatocellular carcinoma.

Diabetes in there is deposition in the pancreas.

247
Q

Complications of Wilson’s Disease

A

Cirrhosis -> Liver failure.

Fatal if untreated.

248
Q

Define Alpha-1-antitrypsin deficiency

A

Deficiency of serine protease inhibitor alpha-1-antitrypsin.

249
Q

Define Volvulus

A

Complete twisting of a loop of intestine around its mesenteric attachment site.

250
Q

Define Midgut malrotation

A

Twisting of the entire midgut about the axis of the superior mesenteric artery.

251
Q

Types of volvulus

A

Stomach,

small intestine,

caecum,

transverse colon

and sigmoid colon.

252
Q

How does Alpha-1-antitrypsin deficiency clinically present?

A

Lung: presents between 30-50 (smokers earlier).

COPD like symptoms, early onset emphysema.

Liver: Not always present.

Neonates may present jaundice and hepatitis.

Possibly cirrhosis and liver failure.

253
Q

How does Volvulus clinically present?

A

Rapid onset and bilious vomiting.

Possible palpable abdominal mass.

Ischaemia can lead to acute abdomen pain, abdominal distension and peritonitis.

Blood may pass per rectum.

254
Q

How does Midgut malrotation clinically present?

A

Can be asymptomatic.

Intermittent intestinal obstruction.

If a volvulus develops, the obstruction will be complete.

Bilious vomiting (green/yellow vomit).

Failure to thrive, anorexia, constipation and bloody stool.

Older children: Recurrent abdominal pain, cyclical vomiting.

255
Q

Cause of Alpha-1-antitrypsin deficiency

A

Mutation in the SERPINA1 gene.

Autosomal recessive.

Relatively low penetrance.

Many possible mutations.

256
Q

Cause of a Volvulus

A

Tends to develop in long-standing constipation with large,

elongated, relatively atonic colon (particularly in sigmoid).

257
Q

Cause of Midgut malrotation

A

Congenital.

At the fourth week of gestation, the GI tract is a straight tube in the abdomen.

In the next 8 weeks, the midgut rotates and becomes fixed to the posterior abdominal wall.

Arrest of development at any stage narrows the mesenteric base and impairs fixation.

This creates high risk of volvulus.

258
Q

Epidemiology of Volvulus

A

More common in the elderly.

Rare in infants and children (when not associated with a malrotation).

259
Q

Epidemiology of Midgut malrotation

A

1/500 live births.

90% are diagnosed within the first year of life.

260
Q

Diagnostic test for Alpha-1-antitrypsin deficiency

A

Serum levels of A1AT.

261
Q

Diagnostic test for Volvulus

A

Plain abdominal X ray.

262
Q

Diagnostic test for Midgut malrotation

A

Contrast studies:

Duodenojejunal junction is misplaced; either at or to the right of the midline.

263
Q

Treatment of Alpha-1-antitrypsin deficiency

A

Lung: As COPD; cessate smoking, corticosteroids, bronchodilators, treat infection.

Liver: Cessate drinking. In liver failure, possibly transplant.

264
Q

Treatment of Voluvulus

A

(Sigmoid) Decompression: Sigmoidoscope is passed into the loop, and a flatus tube alongside it.

This produces a rush of liquid faeces and flatus and relief.

Surgery: Resection may be required in frequent recurrence.

265
Q

Treatment of Midgut malrotation

A

Surgery: Volvulus is a devastating complication, so corrected even in asymptomatic.

266
Q

Complications of Alpha-1-antitrypsin deficiency

A

Variable prognosis.

Untreated -> Liver failure.

267
Q

Complications of Volvulus

A

Recurrence.

If untreated: Perforation and faecal peritonitis (life-threatening).

268
Q

Complications of Midgut malrotation

A

Volvulus can develop,

leading to complete bowel obstruction,

and potentially a rupture -> Life-threatening peritonitis.

269
Q

Define Intestinal obstruction

A

Passage through the intestine is obstructed.

270
Q

Types of Intestinal obstruction

A

Mechanical.

Functional (‘ileus’).

271
Q

How does mechanical intestinal obstruction clinically present?

A

Colicky abdominal pain,

associated with vomiting (earlier with small bowel)

and absolute constipation (earlier with large bowel).

Distension and tinkling bowel sounds.

272
Q

How does functional intestinal obstruction clinically present?

A

Pain often not present, and bowel sounds reduced.

Constipation and vomiting.

273
Q

How can you subdivide mechanical intestinal obstruction?

A

Subdivides into small and large bowel obstruction depending on the location of the blockage.

274
Q

Pathophysiology of mechanical intestinal obstruction

A

Depending on the aetiology,

a physical factor is preventing the movement of contents of the intestine through the tract.

This then causes backing up of the GI tract and an inability to empty

-> vomiting and constipation.

275
Q

Pathophysiology of functional intestinal obstruction

A

Bowel ceases to function and there is no peristalsis.

This causes impaction since contents no longer move along the intestine.

276
Q

Cause of mechanical intestinal obstruction

A

Small: Adhesions, strangulated hernia or volvulus.

Possible malignancy.

Most commonly: intra-abdominal adhesions from operations.

Intussusception.

Large: Most often colorectal malignancies.

277
Q

Cause of functional intestinal obstruction

A

Most often post-operative to peritonitis, or any major abdominal surgery.

Associated with opiate treatment.

Possible; nerves or muscles are damaged.

278
Q

Epidemiology of mechanical intestinal obstruction

A

Small more common.

279
Q

Diagnostic test for mechanical intestinal obstruction

A

Abdo X-ray.

280
Q

Diagnostic test for functional intestinal obstruction

A

Xray: Gas seen throughout the bowel.

281
Q

Treatment of mechanical intestinal obstruction

A

Conservative; fluid replacement and intestinal decompression.

Surgery: Resection possible, usually done in large bowel.

If as a result of malignancy: Corticosteroids, opioids and anti-emetics.

282
Q

Treatment of functional intestinal obstruction

A

Conservative; fluid replacement and intestinal decompression.

283
Q

Complications of mechanical intestinal obstruction

A

Carcinoma that causes obstruction is usually already advanced and metastatic.

284
Q

Define Oesophageal cancer

A

Cancer of the oesophagus.

285
Q

Define Gastric cancer

A

Cancer of the stomach.

286
Q

Types of oesophageal cancer

A

Squamous.

Adenocarcinoma.

287
Q

How does Oesophageal cancer clinically present?

A

Early: No symptoms

Late: Dysphagia,

weight loss,

heartburn,

haematemesis.

Hoarse voice.

288
Q

How does Gastric cancer clinically present?

A

Nonspecific: Dyspepsia, weight loss, vomiting, dysphagia and anaemia.

Signs: Epigastric mass, hepatomegaly, jaundice, Troisier’s sign (enlarged left supraclavicular node (Virchow’s node)).

289
Q

How does Colorectal cancer (CRC) clinically present?

A

Most are left side of colon: rectal bleeding, increasing symptoms of intestinal obstruction (bowel habit, colicky pain).

Right side + ceacum: iron deficiency anaemia, mass in right iliac fossa.

Non-specific symptoms.

290
Q

Pathophysiology of squamous oesophageal cancer

A

Tends to be locatated in the proximal 2/3rds of the oesophagus.

Can locally cause pressure recurrent laryngeal nerve.

291
Q

Pathophysiology of adenocarcinoma (oesophageal cancer)

A

Tends to be located in the distal 1/3rd of the oesophagus.

Can locally cause pressure recurrent laryngeal nerve.

292
Q

Pathophysiology of gastric cancer

A

90% are adenocarcinomas.

Most involve the pylorus.

293
Q

Pathophysiology of colorectal cancer (CRC)

A

Adenomatous polyps develop over time, though benign they can become malignant through activation of oncogenes and inactivation of tumour suppressor genes.

> no. of polyps >chance of malignancy.

5% due to genetic syndromes:

HNPCC: accelerated progression of adenoma to CRC, >50% develop CRC after 40.

FAP: APC gene,

> 100 polyps develop in teenage years,

100% lifetime risk of CRC.

(Both have increased risk of extracolonic malignancy).

294
Q

Cause of squamous oesophageal cancer

A

Smoking,

alcohol,

nitrous amines (barbeque food, tobacco).

295
Q

Cause of adenocarcinoma (oesophageal cancer)

A

Barrett’s oesophagus,

obesity.

296
Q

Cause of gastric cancer

A

H. pylori can double the risk.

Smoking is a risk factor.

Gastritis and pernicious anaemia.

297
Q

Cause of colorectal cancer (CRC)

A

Age,

family history,

western diet.

298
Q

Epidemiology of adenocarcinoma (oesophageal cancer)

A

Obese people.

299
Q

Epidemiology of colorectal cancer (CRC)

A

Mean diagnosis age 60-65.

3rd most common, 2nd biggest killer cancer.

300
Q

Diagnostic test for oesophageal cancers

A

Oesophagoscopy with biopsy.

CT/MRI to stage cancer.

301
Q

Diagnostic test for gastric cancer

A

Gastroscopy with biopsy.

CT/MRI to stage cancer.

302
Q

Diagnostic test for colorectal cancer (CRC)

A

DRE, colonoscopy with biopsy.

Faecal occult blood test for screening only.

303
Q

Treatment of oesophageal cancers

A

Oesophagectomy with perioperative chemo.

304
Q

Treatment of gastric cancer

A

Gastrectomy (partial or total) with perioperative chemo.

305
Q

Treatment of colorectal cancer (CRC)

A

Surgery, ideally with end to end anastomosis, alt. colostomy.

Adjuvant chemo.

Palliation.

306
Q

Complications of colorectal cancer (CRC)

A

Local invasion and distant metastases, often liver and lung.

(SG) condensed phase 2a (9 decks)

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