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Phase 2a > GI > Flashcards

GI Flashcards

1
Q

What are some causes of GORD?

A

Hiatus hernia, obesity, gastric acid hyper secretion, delayed gastric emptying, smoking, alcohol

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2
Q

How does GORD present?

A

Oesophagus - heartburn, belching, acid brash, water brash

Extra-oesophagus - nocturnal asthma, chronic cough, laryngitis, sinusitis

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3
Q

How is GORD diagnosed?

A

Endoscopy if dysphagia, 24h oesophageal pH monitoring

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4
Q

How is GORD managed?

A

Lifestyle - weight loss, smoking cessation, small, regular meals
Drugs - antacids
Surgery

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5
Q

What is a peptic ulcer?

A

A break in the inner lining of the stomach, first part of the small intestine or sometimes the lower oesphagus

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6
Q

Describe the pathology of peptic ulceration

A

Inflammation caused by the bacteria H. pylori, or erosion from stomach acids

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7
Q

How do peptic ulcers present?

A

Epigastric pain often related to hunger, specific foods or time of day, ‘heart burn’, tender epigastrium
Alarm symptoms - anaemia, weight loss, anorexia, haematemesis

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8
Q

How do gastric/duodenal ulcers present and get diagnosed?

A

Asymptomatic, epigastric pain, weight loss

Upper GI endoscopy, test for H.pylori

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9
Q

How are peptic ulcers managed?

A

Lifestyle: decrease alcohol and tobacco use
H.pylori eradication
Drugs to reduce acid - proton pump inhibitors
Stop taking drugs causing drug-induced ulcers

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10
Q

What are oesophago-gastric varices?

A

Submucosal venous dilatations secondary to high portal pressures.

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11
Q

What are the causes of oesophago-gastric varices?

A

Cirrhosis, thrombosis, parasitic infection

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12
Q

What are the risk factors for oesophago-gastric variceal bleeds?

A

High portal pressure, variceal size, advanced liver disease

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13
Q

How do oesophago-gastric varices present?

A

Only symptomatic if they bleed; vomit blood, bloody stools, light headedness, loss of consciousness in severe cases

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14
Q

How can oesophago-gastric varices be prevented?

A

Don’t drink alcohol, healthy diet and weight, reduce risk of hepatitis

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15
Q

How are oesophago-gastric varices managed?

A

Endoscopic banding or sclerotherapy

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16
Q

What is haematemesis?

A

Vomiting blood

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17
Q

What is melaena?

A

Black motions, often like tar, and has a characteristic smell of altered blood

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18
Q

What is a Mallory-Weiss tear?

A

A tear in the mucous membrane where the oesophagus meets the stomach

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19
Q

What are the symptoms of a Mallory-Weiss tear and how are they managed?

A

Persistent vomiting causes haematemesis via the tear.

Endoscopy to stop the bleeding

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20
Q

What is gastritis?

A

Inflammation of the lining of the stomach

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21
Q

What are the causes of gastritis?

A

Irritation due to excessive alcohol use, chronic vomiting, stress, or the use of certain medications such as aspirin.
Helicobacter pylori, bile reflux, infections caused by bacteria and viruses

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22
Q

What are the risk factors for gastritis?

A

Alcohol, NSAIDs, H.pylori, reflux hernia

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23
Q

How does gastritis present?

A

Epigastric pain, vomiting, indigestion, abdominal bloating

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24
Q

How is gastritis diagnosed?

A

Upper GI endoscopy, blood tests (anaemia/ H.pylori), faecal occult blood tests

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25
Q

How is gastritis managed?

A

H2 receptor antagonists, proton pump inhibitors, avoid hot and spicy foods

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26
Q

What is coeliac disease?

A

A disease in which the small intestine is hypersensitive to gluten, leading to difficulty in digesting food

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27
Q

Describe the pathology of coeliac disease

A

T-cell responses to gluten in the small bowel causes villous atrophy and malabsorption

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28
Q

How does coeliac disease present?

A

Stinking stools, diarrhoea, abdominal pain, nausea and vomiting, aphthous ulcers, weight loss, fatigue, weakness

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29
Q

How is coeliac disease diagnosed?

A 
Antibodies: anti-transglutaminase - check IgA levels to exclude subclass deficiency 
Duodenal biopsy whilst gluten-containing diet - villous atrophy
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30
Q

How is coeliac disease managed?

A

Lifelong gluten-free diet
Limited consumption of oats may be tolerated in patients with mild disease.
Monitor response by symptoms and repeat serology

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31
Q

What are the complications of coeliac disease?

A

Anaemia, dermatitis herpetiformis, osteopenia/ osteoporosis

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32
Q

What is malabsorption?

A

The small intestine can’t absorb enough of certain nutrients and fluids. Malabsorption of protein fat and carbohydrate leads to weight loss and malnutrition

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33
Q

What causes malabsorption?

A

Coeliac disease, chronic pancreatitis, Crohn’s disease, pancreatic insufficiency, infection

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34
Q

How does malabsorption present?

A

Diarrhoea, weight loss, lethargy, bloating, anaemia, bleeding disorders, oedema, metabolic bone disease

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35
Q

How is malabsorption diagnosed?

A

FBC: low calcium, iron, B12 and folate
Lipid profile - coeliac tests
Stool - Sudan stain for fat globules

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36
Q

How is malabsorption managed?

A

Correction of nutritional deficiencies

Treatment of causative disease

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37
Q

What is inflammatory bowel disease?

A

A term used to describe ulcerative colitis and Crohn’s disease, which involve inflammation of the gut

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38
Q

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

A

Crohn’s disease favours the ileum but can occur anywhere along the intestinal tract, whereas UC only affects the colon

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39
Q

What are skip lesions?

A

Present in Crohn’s disease - unaffected bowel between areas of active disease

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40
Q

What causes Crohn’s disease?

A

An inappropriate immune response against the gut flora in a genetically susceptible individual

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41
Q

How does Crohn’s disease present?

A

Diarrhoea, abdominal pain, weight loss/failure to thrive, systemic symptoms

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42
Q

What are the signs for Crohn’s disease?

A

Bowel ulceration, abdominal tenderness, perianal abscess, anal strictures, clubbing, skin, joint and eye problems

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43
Q

How are Crohn’s and ulcerative colitis diagnosed?

A

Bloods, stool to exclude C.difficile, Campylobacter
Faecal calprotectin
Colonoscopy and biopsy

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44
Q

How is Crohn’s managed?

A

Quit smoking, optimise nutrition
Mild-moderate: prednisolone, surgery
Severe: admit for IV hydration/electrolyte replacement, consider need for blood transfusion

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45
Q

How does ulcerative colitis present?

A

Episodic/ chronic diarrhoea, crampy abdominal discomfort, bowel frequency relates to severity, urgency, systemic symptoms

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46
Q

What are the complications of ulcerative colitis?

A

Venous thromboembolism, colonic cancer

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47
Q

How is ulcerative colitis managed?

A

Mild: prednisolone, mesalamine for maintenance
Moderate: induce remission oral prednisolone
Severe: IV hydration/ electrolyte replacement

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48
Q

What is irritable bowel syndrome?

A

A mixed group of abdominal symptoms for which no organic cause can be found

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49
Q

How does IBS present?

A

Urgency, abdominal bloating/distension, worsening of symptoms after food, symptoms are chronic (>6 months), exacerbated by stress, menstruation or gastroenteritis

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50
Q

How is IBS diagnosed?

A

Bloods, coeliac screen, faecal calprotectin
Only diagnose IBS if recurrent abdominal pain is associated with at least 2 of;
relief by defecation, altered stool form, altered bowel frequency

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51
Q

How is IBS managed?

A

Focus on controlling symptoms - lifestyle measures, then try BCT
Constipation - adequate water, fibre and physical activity
Diarrhoea - avoid sorbitol sweeteners, alcohol and caffeine
Colic/bloating - oral antispasmodics
Psychological symptoms - emphasise positive (sinister pathology excluded)

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52
Q

What is gastroenteritis?

A

Diarrhoea +/- vomiting due to enteric infection with viruses, bacteria or parasites

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53
Q

How do gastro-intestinal infections present?

A

Watery diarrhoea, cramps, nausea, vomiting, fever

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54
Q

How are gastro-intestinal infections diagnosed?

A

Clinical, stool sample - antigens in stool identify the toxin

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55
Q

How are gastro-intestinal infections managed?

A

Supportive, anti-motility agents, routine vaccination for rotavirus

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56
Q

Give 3 examples of organisms that can cause gastroenteritis

A

Norovirus, rotavirus, enterotoxigenic E.coli

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57
Q

How can traveller’s diarrhoea be prevented?

A

Boil water, cool thoroughly, peel fruit and vegetables. Avoid ice, salads and shellfish. Drink with a straw

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58
Q

How does traveller’s diarrhoea present?

A

E.coli: watery diarrhoea preceded by cramps and nausea
Giardia lamblia: upper GI symptoms e.g. bloating
Campylobacter jejuni and Shigella: colitis symptoms, urgency, cramps

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59
Q

How is traveller’s diarrhoea diagnosed?

A

3 or more unformed stools per day plus one of the following:

Abdominal pain, cramps, nausea, vomiting, dysentery

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60
Q

How is traveller’s diarrhoea managed?

A

Oral rehydration. Clear fluid or oral rehydration salts, anti motility agents, antibiotics

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61
Q

What are the different types of diarrhoea?

A

Acute: >3 episodes partially formed or watery stool/day for <14 d
Dysentery: infectious gastroenteritis with bloody diarrhoea
Persistent: Acutely starting diarrhoea lasting >14d
Traveller’s diarrhoea: starting during, or after foreign travel

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62
Q

What are some infective causes of diarrhoea?

A

Rotavirus/norovirus in UK, shigella, campylobacter, salmonella, S.aureus, E.coli, C.diff

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63
Q

Through what food can you contract campylobacter from?

A

Meat

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64
Q

Through what food can you contract bacillus cereus from?

A

Rice

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65
Q

Through what food can you contract salmonella from?

A

Poultry

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66
Q

Through what food can you contract norovirus from?

A

Shellfish

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67
Q

What are the diarrhoea red flags?

A

Dehydration, electrolyte imbalance, immune compromise, renal failure, severe abdominal pain

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68
Q

How is diarrhoea diagnosed?

A

Stool tests - toxin detection, blood tests - inflammatory markers, lower GI endoscopy

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69
Q

How is diarrhoea managed?

A

Treat. cause, oral rehydration, avoid antibiotics

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70
Q

What is Clostridium difficile?

A

Gram positive spore forming bacteria. The cause of pseudomembranous colitis

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71
Q

What antibiotics can cause clostridium difficile?

A

Clindamycin, Ciprofloxacin, Co-amoxiclav, Cephalosprosins

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72
Q

How does C. diff present?

A

Increased temperature, diarrhoea with systemic upset, high CRP, WCC and low albumin

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73
Q

How is C.diff detected?

A

Urgent testing of suspicious stool (characteristic smell)

Specific ELISA for toxins

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74
Q

How is C.diff treated?

A

Stop causative antibiotics, barrier nursing

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75
Q

How do oesophageal tumours present?

A

Dysphagia, weight loss, retrosternal chest pain

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76
Q

How are oesophageal tumours diagnosed?

A

Oesophagoscopy, endoscopic ultrasound, CT/ MRI for staging

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77
Q

How are oesophageal tumours managed?

A

Radical curative oesophagectomy, chemoradiotherapy, palliation aims to restore swallowing

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78
Q

How do gastric carcinomas present?

A

Non-specific, dyspepsia, weight loss, vomiting, dysphagia, anaemia

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79
Q

What are the signs of gastric carcinomas?

A

Epigastric mass, hepatomegaly, jaundice, ascites

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80
Q

How are gastric carcinomas diagnosed?

A

Gastroscopy, ulcer edge biopsies, CT/MRI for staging

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81
Q

How are gastric carcinomas managed?

A

Partial gastrectomy for distal tumours, total gastrectomy if proximal, combination chemo, surgical palliation

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82
Q

How do colorectal carcinomas present?

A

Depends on site
Left - bleeding, altered bowel habit, tenesmus, PR mass
Right - weight loss, low Hb, abdominal pain

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83
Q

How are colorectal carcinomas diagnosed?

A

FBC - microcytic anaemia, faecal occult blood, sigmoidoscopy, barium enema, liver USS

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84
Q

How are colorectal carcinomas staged?

A 
Dukes' criteria;
A - limited to muscular mucosae
B - extension through muscularis mucosae
C - involvement of regional lymph nodes
D - distant metastases
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85
Q

How are colorectal carcinomas managed?

A

Surgery, radiotherapy, chemotherapy

86
Q

How do liver tumours present?

A

Fever, malaise, anorexia, weight loss, RUQ pain

87
Q

What are the signs of liver tumours?

A

Hepatomegaly, signs of chronic liver disease, abdominal mass, bruit over liver

88
Q

How are liver tumours diagnosed?

A

Bloods - alpha-fetoprotein, US/CT to identify lesions, biopsy to find primary tumour

89
Q

How are hepatocellular carcinomas managed?

A

Resecting solitary tumours, liver transplant, percutaneous ablation

90
Q

How are biliary tree cancers (cholangiocarcinomas) managed?

A

Stenting of an obstructed extra hepatic biliary tree, percutaneously or via ERCP

91
Q

Name two benign liver tumours

A

Haemangiomas, adenomas

92
Q

What are the signs of a pancreatic carcinoma?

A

Jaundice, palpable gallbladder, epigastric mass, hepatomegaly, splenomegaly, ascites

93
Q

How is a pancreatic carcinoma diagnosed?

A

Blood - cholestatic jaundice

US/CT to show pancreatic mass

94
Q

How is a pancreatic carcinoma managed?

A

Surgery, laparoscopic excision, post-op chemotherapy, pain management with opiates

95
Q

What is intestinal obstruction?

A

Blockage to the lumen of the gut

96
Q

What is a volvulus?

A

A twist/rotation of segment of bowel

97
Q

What are abdominal adhesions?

A

Intestinal obstruction due to abdominal structures sticking together e.g. solid organs, omentum, abdominal wall

98
Q

How are intestinal obstructions classified?

A

According to the site, extent of luminal obstruction, according to mechanism, according to pathology

99
Q

What are the causes of small bowel obstruction?

A

Adhesions (previous surgery), hernia

Rarer - Crohn’s, malignant, volvulus

100
Q

What are the causes of large bowel obstruction?

A

Colon carcinoma, constipation, diverticular stricture, volvulus

101
Q

What is a sigmoid volvulus?

A

Occurs when the bowel twists on its mesentery, which can produce severe, rapid, strangulated obstruction

102
Q

How do intestinal obstructions present?

A

Anorexia, nausea, vomiting, distension, abdominal pain, altered bowel habits

103
Q

How are intestinal obstructions diagnosed?

A

X-rays

104
Q

How are intestinal obstructions managed?

A

IV fluids to rehydrate and correct electrolyte imbalance
Large bowel obstruction requires surgery
Strangulation needs emergency surgery

105
Q

What is a hernia?

A

The protrusion of a viscus part or part of a viscus through to defect of the walls of its containing cavity into an abnormal position

106
Q

What is an irreducible hernia?

A

Contents cannot be pushed back into place

107
Q

What is an obstructed hernia?

A

Bowel contents cannot pass - features of intestinal obstruction

108
Q

What is a strangulated hernia?

A

Ischaemia occurs - the patient requires urgent surgery

109
Q

What is incarceration?

A

Contents of the hernial sac are stuck inside by adhesions

110
Q

How do hernias present?

A

Lump and pain

111
Q

What are femoral hernias?

A

Bowel enters the femoral canal, presenting as a mass in the upper medial thigh or above the inguinal ligament where it points down the leg, unlike an inguinal hernia which points to the groin

112
Q

What are inguinal hernias?

A

Indirect hernias pass through the internal inguinal ring and through external inguinal ring
Direct hernias push their way directly forward through the posterior wall of the inguinal canal, into a defect in the abdominal wall

113
Q

What are the predisposing conditions for inguinal hernias?

A

Male sex, chronic cough, urinary obstruction, past abdominal surgery

114
Q

Which type of inguinal hernia can strangulate?

A

Indirect

115
Q

How are inguinal hernias repaired?

A

Lose weight and stop smoking, mesh techniques to reinforce posterior wall

116
Q

What is ischaemic colitis?

A

Inflammation and injury of the large intestine result from inadequate blood supply

117
Q

How does ischaemic colitis present?

A

Lower left-sided abdominal pain, bloody diarrhoea

118
Q

How is ischaemic colitis diagnosed?

A

CT may be helpful but lower GI endoscopy is gold-standard

119
Q

How is ischaemic colitis managed?

A

Treatment is usually conservative with fluid replacement and antibiotics
Gangrenous ischaemic colitis requires resection of the affected bowel and stoma formation

120
Q

What is mesenteric ischaemia?

A

Injury to the small intestine due to inadequate blood supply

121
Q

What causes acute mesenteric ischaemia?

A

Superior mesenteric artery thrombosis, mesenteric vein thrombosis, trauma, strangulation

122
Q

How does acute mesenteric ischaemia present?

A

Classical clinical triad - acute severe abdominal pain, no abdominal signs, rapid hypovolaemia
Pain is constant, central/around RIF

123
Q

How is acute mesenteric ischaemia diagnosed?

A

High Hb due to plasma loss, high WCC, abdominal X-ray shows a gases abdomen, laparotomy

124
Q

How is acute mesenteric ischaemia managed?

A

Resuscitation with fluid, antibiotics, LMW heparin (following complications)

125
Q

What are the life-threatening complications secondary to acute mesenteric ischaemia?

A

Septic peritonitis, progression to multi-organ failure

126
Q

What is the main cause of chronic mesenteric ischaemia?

A

A combination of a low-flow state with atheroma

127
Q

How does chronic mesenteric ischaemia present?

A

Severe, colicky abdominal pain, weight loss (painful to eat), upper abdominal bruit

128
Q

How is chronic mesenteric ischaemia diagnosed?

A

CT angiography and contrast-enhanced MR angiography

129
Q

How is chronic mesenteric ischaemia managed?

A

Surgery

Percutaneous transluminal angioplasty and stent insertion

130
Q

What is appendicitis?

A

Inflamed and painful appendix

131
Q

How does appendicitis present?

A

Classic periumbilical pain that moves to the right iliac fossa, fever, tachycardia

132
Q

What are differential diagnoses for abdominal pain?

A

Appendicitis, UTI, mesenteric adenines, diverticulitis/cholecystitis/cystitis, food poisoning, Crohn’s disease

133
Q

How is appendicitis diagnosed?

A

Blood tests reveal elevated CRP

CT has high diagnosis accuracy

134
Q

How is appendicitis managed?

A

Prompt appendicectomy, antibiotics

135
Q

What are the complications of appendicitis?

A

Perforation, appendix mass (inflamed appendix covered with omentum), appendix abscess (appendix mass enlarges)

136
Q

How are gallstones managed?

A

Cholecystectomy, bile acid dissolution therapy, ERCP with removal/crushing/stent placement

137
Q

What complications are associated with stones in the gallbladder/cystic duct?

A

Biliary colic, acute and chronic cholecystitis, carcinoma

138
Q

What does bile consist of?

A

Cholesterol, bile pigments, phospholipids

139
Q

How do gallstones present?

A

Biliary pain, obstructive jaundice
Gallbladder - cholecystitis
Bile Duct - cholangitis, pancreatitis

140
Q

What is biliary colic and how is it diagnosed and treated?

A

Gallstones are symptomatic with cystic duct obstruction, RUQ pain radiating to back
Diagnosis - urinalysis, CXR
Treatment - analgesia, cholecystectomy

141
Q

What is acute cholecystitis and how is it diagnosed and treated?

A

Follows stone impaction in the neck of gallbladder, causing RUQ pain, vomiting, fever
Diagnosis - high WCC, US (shrunken gallbladder)
Treatment - Pain relief, antibiotics, nil by mouth

142
Q

What is chronic cholecystitis and how is it diagnosed and treated?

A

Chronic inflammation with abdominal discomfort, distention, nausea, flatulence
Diagnosis - US to image stones
Treatment - cholecystectomy

143
Q

What are the causes of acute pancreatitis?

A

GET SMASHED - gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion venom etc

144
Q

How does acute pancreatitis present?

A

Gradual or sudden severe epigastric or central abdominal pain. vomiting. pain radiates to back, sitting forward may relieve

145
Q

What are the signs of acute pancreatitis?

A

High heart rate, fever, jaundice, shock, rigid abdomen with local/general tenderness

146
Q

How is acute pancreatitis diagnosed?

A

Raised serum amylase - excreted renally so renal failure will increase levels
Serum lipase rises earlier and falls later
CT to assess severity

147
Q

How is acute pancreatitis managed?

A

Nil by mouth, analgesia, ERCP and gallstone removal

148
Q

What are the complications of acute pancreatitis?

A

Shock, renal failure, sepsis, pancreatic necrosis, thrombosis in splenic arteries causing bowel necrosis

149
Q

What is the difference between acute and chronic pancreatitis?

A

Chronic pancreatitis is chronic inflammation which leads to irreversibly low pancreatic function

150
Q

Describe the pathology of chronic pancreatitis

A

Chronic inflammation in the pancreas leads to the replacement of functional pancreatic tissue by fibrous scar tissue

151
Q

What are the causes of chronic pancreatitis?

A

Alcohol, smoking, autoimmune, pancreatic duct obstruction

152
Q

How does chronic pancreatitis present?

A

Persistent upper abdominal pain and weight loss, radiates to back and is relieved by sitting forward. steatorrhea and diabetes mellitus

153
Q

How is chronic pancreatitis diagnosed?

A

Ultrasound and CT scan - pancreatic calcifications confirm the diagnosis

154
Q

How is chronic pancreatitis managed?

A

Analgesia and fat-soluble vitamins, surgery - pancreatectomy for unremitting pain
Diet - no alcohol, low fat

155
Q

What are the complications of chronic pancreatitis?

A

Diabetes, biliary obstruction, local arterial aneurysm, gastric varices

156
Q

How does acute viral hepatitis present?

A

Can be asymptomatic, malaise, GI upset, abdominal pain, jaundice

157
Q

What are the causes of viral hepatitis?

A

Hepatitis A,B,C,D,E virus, herpes virus
Non-viral: spirochetes, mycobacteria
Non-infection: alcohol, toxins, autoimmune

158
Q

How does chronic viral hepatitis present?

A

Can be asymptomatic, signs of chronic liver disease (Dupuytren’s contracture, spider naevi)

159
Q

Who are the at risk groups for hepatitis B?

A

IV drug abusers and their sexual partners, health workers, haemophiliacs, sexually promiscuous

160
Q

How is hepatitis A treated?

A

Supportive, monitor liver function

161
Q

How is hepatitis B treated?

A

Avoid alcohol, immunise sexual contacts, antivirals, supportive

162
Q

What is cirrhosis?

A

Cirrhosis implies irreversible liver damage

163
Q

Describe the histology of cirrhosis

A

There is loss of normal hepatic architecture with bridging fibrosis and nodular regeneration

164
Q

What are the causes of cirrhosis?

A

Toxins (ALD), infections HBV/HCV), autoimmune, metabolic (NAFLD), and metabolic liver failure causes

165
Q

How does cirrhosis present?

A

Leukonychia (white nails with lunulae), palmar erythema, hyper dynamic circulation, hepatomegaly

166
Q

What are the complications of portal hypertension?

A

Ascites, splenomegaly, portosystemic shunt including oesophageal varices

167
Q

How is cirrhosis diagnosed?

A

Blood: increased bilirubin, low albumin and WCC
Liver US: small liver/ hepatomegaly/ splenomegaly
MRI: caudate lobe size

168
Q

How is cirrhosis managed?

A

Good nutrition is vital, alcohol abstinence

Transplant

169
Q

What is primary biliary cholangitis?

A

Primary biliary cirrhosis - autoimmune disease of the liver. Results from a slow, progressive destruction of the small bile ducts of the liver, causing bile and other toxins to build up in the liver

170
Q

Describe the pathology of primary biliary cholangitis

A

Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation causing cholestasis

171
Q

What causes primary biliary cholangitis?

A

Unknown environmental triggers and a genetic predisposition leading to loss of immune tolerance to self-mitochondrial proteins

172
Q

How does primary biliary cholangitis present?

A

Often asymptomatic and diagnosed incidentally

Lethargy, sleepiness, pruritus, jaundice, skin pigmentation, hepatosplenomegaly

173
Q

How is primary biliary cholangitis diagnosed?

A

Blood: high bilirubin and low albumin
US: excludes extra hepatic cholestasis

174
Q

How is primary biliary cholangitis managed?

A

Cholestyramine for symptomatic patients, fat-soluble vitamin prophylaxis
Liver transplant at end-stage disease

175
Q

What is alcoholic liver disease?

A

Liver disease due to excessive alcohol consumption, including fatty liver, alcoholic hepatitis, and chronic hepatitis with liver fibrosis or cirrhosis

176
Q

What are the 3 pathological stages of alcoholic liver disease?

A
  1. Steatosis 2. Alcoholic steatohepatitis (ASH) 3. Cirrhosis
177
Q

How does steatosis occur?

A

Alcohol metabolism in the liver generates high levels of NADH which stimulates fatty acid synthesis and production of triglycerides, leading to steatosis

178
Q

How does ASH occur and lead to cirrhosis?

A

Oxidative stress from metabolism of alcohol leads to hepatocyte injury and necro-inflammatory activity.
Ongoing, this causes liver fibrosis which may progress to cirrhosis

179
Q

How does alcoholic liver disease present?

A

Steatosis and mild ASH are usually asymptomatic

Severe - malaise, fever, jaundice

180
Q

What organs are affected by alcoholic liver disease and how?

A

Liver - fatty liver/ alcoholic hepatitis/ cirrhosis
CNS - self neglect, decreased memory function
Gut - obesity, peptic ulcers
Heart - arrhythmias, high BP

181
Q

How is alcoholic liver disease diagnosed?

A

Blood: high WCC, low platelets, high MCV, high urea

182
Q

How is alcoholic liver disease managed?

A

Alcohol withdrawal, acamprosate may help intense anxiety, insomnia and craving after alcohol withdrawal

183
Q

What are the metabolic causes of liver failure?

A

Wilson’s disease, hereditary haemochromatosis, alpha1-antitrypsin deficiency

184
Q

What is Wilson’s disease?

A

An inherited disorder of copper metabolism, leading to the accumulation of toxic levels of copper in the liver and brain

185
Q

How does Wilson’s disease present?

A

Most present in childhood with chronic liver disease
Kayser-Fleischer (KF) rings - Copper in iris
CNS signs: tremor, dysarthria, dysphagia

186
Q

How is Wilson’s disease diagnosed?

A

Urine: 24h copper excretion is high
High LFT, serum copper <11micromol/L
Slit lamp exam: KF rings seen in iris

187
Q

How is Wilson’s disease managed?

A

Diet: avoid foods with high copper content, drugs - lifelong penicillamine, liver transplant in severe liver failure

188
Q

What is hereditary haemochromatosis?

A

An inherited disorder characterised by increased intestinal absorption of iron, leading to iron overload in multiple organs, particularly the liver

189
Q

What is alpha1- antitrypsin deficiency?

A

An inherited disorder affecting the lungs (emphysema) and the liver (cirrhosis)

190
Q

What is ascites?

A

Effusion and accumulation of serous fluid (protein-containing) in the abdominal cavity

191
Q

How is ascites classified?

A

Stage 1 - detectable only after USS
Stage 2 - easily detectable but small volume
Stage 3 - obvious, not tense ascites
Stage 4 - tense ascites

192
Q

What causes ascites?

A

Cirrhosis, malignancy, heart failure, TB, pancreatitis

193
Q

How is ascites managed?

A

Treat underlying cause, diuretics, salt and fluid restriction

194
Q

What causes peritonitis?

A

Cholecystitis, pancreatitis, appendicitis, diverticulitis

195
Q

How does peritonitis present?

A

Abdominal pain, diarrhoea, swelling, prostration, shock, tenderness

196
Q

How is peritonitis diagnosed?

A

US/CT scan, raised WCC

197
Q

How is peritonitis managed?

A

Surgery - patch hole/remove organ/wash out infection

Intensive care, support of kidneys, nutrition

198
Q

What is a diverticulum?

A

An out pouching of the gut wall, usually at sites of entry of perforation arteries

199
Q

What is diverticulitis?

A

Refers to inflammation of a diverticulum

200
Q

Describe the pathology of diverticular disease

A

Firm stools require higher intraluminal pressures to propel, and higher pressure forces pouches of the colonic mucosa through an anatomical weak point in the mucosa layer where blood vessels pass through to supply the mucosal layer

201
Q

How does diverticular disease present?

A

Intermittent abdominal pain, altered bowel habit

Acute inflammation in a diverticulum presents with severe left iliac fossa pain

202
Q

How is diverticular disease diagnosed?

A

Diverticula are a common incidental finding at colonoscopy, CT abdomen - identify extent of disease

203
Q

How is diverticular disease managed?

A

Try antispasmodics, surgical resection

204
Q

How is diverticulitis managed?

A

Mild attacks treated at home with bowel rest (liquids only) and antibiotics

205
Q

What are haemorrhoids?

A

Abnormally dilated and prolapsed anal cushions. Thought to be due to disruption of the normal suspensory mechanisms caused by chronic straining at stool

206
Q

What are anal tags?

A

Polypoid projections of the anal mucosa and submucosa

207
Q

What are anal fissures?

A

A tear in the mucosa of the lower anal canal which is most always located posteriorly in the midline

208
Q

What is an anorectal abscess?

A

A collection of pus within deep perianal tissue. It is a complication of infection within a deep anal gland

209
Q

What is an anorectal fistula?

A

An abnormal epithelial-line tract connecting the anal canal to the perianal skin. Usually the result of infection in an anal gland

210
Q

What is ascending cholangitis and what is it caused by?

A

Inflammation of the bile duct.

Bacteria such as E.coli, Klebsiella

Phase 2a (16 decks)

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