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Phase 2a > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Describe the epidemiology of small bowel obstructions (SBO)

A

Most common bowel obstruction (60-75%)

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2
Q

What are 4 causes of SBO?

A
  1. Adhesion (~60%) (due to previous abdo/pelvic surgery or abdo infection)
  2. Hernias (intestinal contents cannot pass through strangulated loop)
  3. Malignancy
  4. Crohn’s disease
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3
Q

Describe the pathophysiology of intestinal obstructions

A
  • Obstruction of bowel leads to distension above blockage due to build-up of fluid and contents
  • Causes increased pressure which pushes on the blood vessels within the bowel wall causing them to become compressed
  • Compressed vessels cannot supply blood resulting ischaemia and necrosis and eventually perforation
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4
Q

What are 3 signs of SBO?

A
  1. Abdominal distension
  2. Increased bowel sounds (tinkling)
  3. Tenderness (suggests strangulation/risk of perforation)
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5
Q

What are 3 symptoms of SBO?

A
  1. ‘Colicky’ pain higher in abdomen
  2. Profuse vomiting
  3. Constipation with no passage of gas (occurs later)
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6
Q

What are the investigations for patients with SBO?

A
  • Abdominal x-ray (1st line)
  • Examination of hernia orifices and rectum
  • FBC
  • Non contrast CT (gold standard - localises obstruction)
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7
Q

What does an abdominal x-ray look like in patients with SBO?

A
  • Central gas shadow that completely crosses lumen
  • No gas seen in large bowel
  • Distended loops proximal to obstruction
  • May see fluid levels within bowel
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8
Q

What is the treatment for intestinal obstructions?

A
  • Aggressive fluid resuscitation
  • Decompression of bowel (drip and suck, IV fluids with NG tube)
  • Analgesia and anti-emetics
  • Antibiotics
  • Laparotomy
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9
Q

Describe the epidemiology of large bowel obstructions (LBO)

A

LBO due to malignancy much more common in the EU/West than in Africa

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10
Q

What are 5 causes of LBO?

A
  1. Malignancy
  2. Volvulus (rotation/twisting of bowel on its mesenteric axis - commonly sigmoid colon)
  3. Diverticulitis
  4. Crohn’s disease
  5. Intussusception (bowel rolls inside of itself - almost exclusively in neonates/infants due to ‘softer’ bowels)
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11
Q

What are 3 signs of LBO?

A
  1. Abdominal distension (much more than SBO)
  2. Palpable mass e.g. hernia (most common in LIF)
  3. Normal bowel sounds initially and eventually silent
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12
Q

What are 3 symptoms of LBO?

A
  1. Abdominal pain in lower abdomen, especially LIF (more constant and diffuse than SBO)
  2. Vomiting
  3. Constipation with no passage of gas
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13
Q

What are the investigations for patients with LBO?

A
  • Abdominal x-ray (1st line)
  • Digital rectal exam (DRE)
  • FBC
  • CT (gold standard)
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14
Q

What does an abdominal x-ray look like in patients with LBO?

A
  • Peripheral gas shadows proximal to blockage
  • Caecum and ascending colon = distended
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15
Q

What does a digital rectal exam (DRE) look like in patients with LBO?

A
  • Empty rectum
  • Hard, compacted stools
  • Might be blood
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16
Q

What is a pseudo-obstruction?

A

Condition in which a patient has symptoms of intestinal obstruction but does not actually have anything blocking the intestines

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17
Q

What are 5 causes of pseudo-obstructions?

A
  1. Intra-abdo trauma
  2. Post-operative states e.g. paralytic ileus
  3. Intra-abdo sepsis
  4. Drugs e.g. opiates/antidepressants
  5. Electrolyte imbalances
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18
Q

How do pseudo-obstructions present?

A

Identically to SBO/LBO

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19
Q

What is the treatment for pseudo-obstruction?

A

Treat underlying cause

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20
Q

What is Crohn’s disease?

A

Intermittent chronic inflammation of the entire GI tract

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21
Q

Describe the epidemiology of Crohn’s disease

A
  • Presentation mostly in 20s-40s
  • Common in Northern European
  • Jewish people = most affected group
  • 400/100,000 in UK
  • Affects females more than males
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22
Q

What are 5 risk factors for Crohn’s disease?

A
  1. Smoking (2-4x greater risk)
  2. NSAIDs
  3. Jewish
  4. Female
  5. Family history
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23
Q

What are 4 causes of inflammatory bowel disease?

A
  1. Genetics (stronger association in Crohn’s than UC)
  2. Stress
  3. Depression
  4. Immune response
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24
Q

Describe the pathophysiology of Crohn’s disease

A
  • Transmural inflammation with granulomata
  • Occurs anywhere in the GI tract
  • Skip lesions
  • Deep ulcers and fissures (cobblestone appearance)
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25
Q

What are 3 signs of Crohn’s disease?

A
  1. Bowel ulceration
  2. Abdominal tenderness
  3. Abdominal mass
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26
Q

What are are 2 symptoms of Crohn’s disease (in the small bowel)?

A
  1. Weight loss
  2. Abdominal pain
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27
Q

What is a symptom of Crohn’s disease (in the terminal ileum)?

A

Right iliac fossa pain mimicking appendicitis

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28
Q

What are 2 symptoms of Crohn’s disease (in the colon)?

A
  1. Blood and mucous with diarrhoea
  2. Pain
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29
Q

What are 2 extra-intestinal symptoms of Crohn’s disease?

A
  1. Clubbing
  2. Oral aphthous ulcers
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30
Q

What are 6 investigations for inflammatory bowel disease?

A
  1. Sigmoidoscopy
  2. Colonoscopy with rectal biopsy (gold standard)
  3. Bloods (raised WCC/platelets/CRP/ESR)
  4. Stool samples
  5. Abdominal x-ray
  6. Faecal calprotectin = raised
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31
Q

What is the treatment for Crohn’s disease?

A
  • Stop smoking
  • Corticosteroids e.g. prednisolone (remission)
  • Anti-TNF antibodies e.g. infliximab, adalimumab (if no response to steroids)
  • Thiopurines e.g. azathioprine (maintain remission)
  • Surgery - resection/temporary ileostomy
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32
Q

What are 8 complications of Crohn’s disease?

A
  1. Bowel obstructions from strictures
  2. Short stature in children
  3. Osteoporosis
  4. Malabsorption
  5. Toxic dilatation
  6. Bowel perforation
  7. Abscess/fistula formation
  8. Colorectal cancer
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33
Q

What is ulcerative colitis?

A

Continuous chronic inflammation of only the colon

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34
Q

Describe the epidemiology of ulcerative colitis

A
  • Higher incidence than Crohn’s
  • Presentation mostly in teens-20s
  • Common in Northern European
  • Jewish people = most affected group
  • 400/100,000 in UK
  • Incidence is 3x higher in non-smokers
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35
Q

What are 3 risk factors for ulcerative colitis?

A
  1. Family history
  2. NSAIDs
  3. Jewish
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36
Q

Describe the pathophysiology of ulcerative colitis

A
  • Mucosal inflammation only
  • No granulomata
  • Starts at rectum, can progress as far as the ileocecal valve
  • Circumferential and continuous inflammation (no skip lesions)
  • Ulcers and pseudo-polyps in severe disease
  • Crypt abscesses and depleted goblet cells
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37
Q

What are 5 signs of ulcerative colitis?

A
  1. 90% have PSC
  2. Tender, distended abdomen
    Extra-GI manifestations:
  3. Arthralgia
  4. Fatty liver
  5. Gallstone
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38
Q

What are 7 symptoms of ulcerative colitis?

A
  1. Malaise
  2. Fever
  3. Anorexia
  4. Weight loss
  5. Pain in LLQ
  6. Abdominal cramps/discomfort
  7. Recurrent diarrhoea often with blood and mucus
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39
Q

What is the treatment for ulcerative colitis?

A
  • Aminosalicylates e.g. mesalazine (intestinal anti-inflammatory - remission and relapse prevention)
  • Corticosteroids e.g. prednisolone (remission)
  • Thiopurines e.g. azathioprine and methotrexate (maintain remission)
  • Surgery - colectomy
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40
Q

What are 8 complications of ulcerative colitis?

A
  1. Psychosocial and sexual problems
  2. Frequent relapse
  3. Colorectal cancer (risk doubled)
  4. Blood loss
  5. Perforation
  6. Toxic dilatation
  7. Pyoderma gangrenosum (painful ulcers)
  8. Erythema nodosum (tender red bumps)
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41
Q

What is the acronym for remembering Crohn’s?

A

NESTS
N - no blood/mucus
E - entire GI tract
S - skip lesions
T - terminal ileum is most affected, transmural inflammation
S - smoking is a RF

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42
Q

What is the acronym for remembering ulcerative colitis?

A

CLOSE UP
C - continuous inflammation
L - limited to colon and rectum
O - only superficial mucosa affected
S - smoking is protective
E - excrete blood and mucus
U - use aminosalicylates
P - primary sclerosing cholangitis association

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43
Q

What is irritable bowel syndrome (IBS)?

A

Mixed group of abdominal symptoms with no organic cause

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44
Q

Describe the epidemiology of IBS

A
  • Age of onset under 40 years
  • More common in females
  • 1/5 in the Western World
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45
Q

What are 5 risk factors for IBS?

A
  1. GI infections
  2. Previous severe long-term diarrhoea
  3. Anxiety and depression
  4. Psychological stress/trauma/abuse
  5. Eating disorders
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46
Q

What are 4 pathophysiology theories of IBS?

A
  1. Disorders of intestinal motility
  2. Enhanced visceral perception
  3. Dysfunction of brain-gut axis
  4. Microbial dysbiosis (imbalance)
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47
Q

What are 7 differential diagnoses for IBS?

A
  1. Coeliac disease
  2. Lactose intolerance
  3. Bile acid malabsorption
  4. IBD
  5. Colorectal cancer
  6. GI infection
  7. Pancreatic insufficiency
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48
Q

What is the diagnosis criteria of IBS?

A

Abdominal pain/discomfort associated with 2+ of:
- Relieved by defecation
- Altered stool form
- Altered bowel frequency

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49
Q

What are 3 main symptoms of IBS?

A

ABC
- Abdominal pain/discomfort
- Bloating
- Change in bowel habit

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50
Q

What is the difference between IBS-C, IBS-D and IBS-M?

A

IBS-C = with constipation
IBS-D = with diarrhoea
IBS-M = mixed with alternating constipation and diarrhoea

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51
Q

What 4 things exacerbate symptoms of IBS?

A
  1. Stress
  2. Menstruation
  3. Gastroenteritis
  4. Food
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52
Q

What are 8 symptoms of IBS?

A
  1. Painful periods
  2. Bladder symptoms (frequency, urgency, nocturia, incomplete emptying)
  3. Back pain
  4. Joint hypermobility
  5. Fatigue
  6. Nausea
  7. Mucus in rectum/stool
  8. Hard/soft/mixed stool
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53
Q

What are 3 investigations for patients with IBS?

A
  1. Bloods
  2. Faecal calprotectin = raised
  3. Colonoscopy
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54
Q

What is the treatment for mild IBS?

A

Dietary modifications:
- Regular meals OR small frequent meals
- Plenty of fluids
- Avoid caffeinated, alcoholic, fizzy drinks
- Avoid fermentable oligosaccharides, disaccharides, monosaccharides and polyols

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55
Q

What is the treatment for moderate IBS?

A

Pharmacotherapy
- Antispasmodics (for pain/bloating) e.g. mebeverine, buscopan
- Loperamide (for diarrhoea) e.g. imodium
- Laxatives (for constipation) e.g. macrogol, docusate, sena

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56
Q

What are alternative laxative options for moderate IBS?

A
  • Linaclotide if 12 months constipation not relieved by 2 different max dose laxative classes
  • Prucalopride when all other laxatives fail
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57
Q

What is the treatment for IBS-C?

A

Soluble fibre:
- Dissolves in water
- Broken down by bacteria
- Soften stool
- E.g. barley, oats, beans, prunes, figs

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58
Q

What is the treatment for IBS-D?

A

AVOID soluble fibre:
- Makes diarrhoea worse
- Doesn’t dissolve in water
- Passes through gut unchanged
- Bulks up faeces
- Increases gut motility
- E.g. cereal, whole-wheat bread, lentils, apples, avacados

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59
Q

What is the treatment for IBS if ineffective?

A
  • Tricyclic antidepressants (dampens down gut severity) e.g. amitriptyline, nortriptyline
  • SSRIs
  • CBT
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60
Q

What is coeliac disease?

A

Inflammation of the mucosa of the upper small bowel in response to gluten

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61
Q

Describe the epidemiology of coeliac disease

A
  • ~1% of population in UK
  • Any age, peaks in infancy and 40-60 years
  • Familial link and risk
  • HLA-DQ2 and HLA-DQ8 association
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62
Q

What are 2 risk factors for coeliac disease?

A
  1. Other autoimmune diseases
  2. IgA deficiency
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63
Q

Describe the pathophysiology of coeliac disease

A
  • Autoimmune - T cell mediated
  • Intolerance to prolamin (in wheat, barley, rye, oats - component of gluten protein)
  • a-gliadin (type of prolamin) is resistant to digestion from protease enzymes (pepsin and chymotrypsin) in SI lumen
  • This passes through damaged epithelial walls into cells
  • Deaminated by transglutaminase
  • Interacts with APCs and activate gluten-sensitive CD4+ T cells
  • T cell produces pro inflammatory cytokines –> inflammatory cascade
  • Causes villous atrophy and crypt hyperplasia
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64
Q

What are the autoantibodies present in majority of coeliac patients?

A

Anti-TTG and anti-EMA (attack enzymes that repair damage in the body)

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65
Q

What are 5 signs of coeliac disease?

A
  1. Malabsorption
  2. Steathorrhoea (increase in fat excretion in stools)
  3. Anaemia
  4. Failure to thrive (children)
  5. Osteomalacia
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66
Q

What are 9 symptoms of coeliac disease?

A
  1. Weight loss
  2. Fatigue and weakness
  3. Diarrhoea
  4. Abdominal pain
  5. Bloating
  6. Nausea/vomiting
  7. Aphthous ulcers
  8. Angular stomatitis
  9. Dermatitis herpetiformis (raised red patch of skin)
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67
Q

What is the first line investigation for patients with coeliac disease?

A

Serum antibody testing:
- IgA tissue transglutaminase (TTG)
- IgA anti-EMA
- Total IgA
- Very high sensitivity and specificity

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68
Q

What is the gold standard investigation for patients with coeliac disease?

A

Duodenal biopsy
- Endoscopically
- +ve findings = villous atrophy, crypt hyperplasia, increased epithelial WBCs

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69
Q

What are other investigations for coeliac disease?

A
  • FBC (low Hb/folate/ferritin/B12)
  • Genetic testing (HLA-DQ2 and HLA-DQ8)
  • DEXA scan
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70
Q

What is the treatment for coeliac disease?

A
  • Lifelong gluten-free diet (avoid foods containing wheat, barley, rye, oats)
  • Correct vitamin deficiencies
  • Pneumococcal vaccine given (hyposplenism)
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71
Q

What are 5 complications of coeliac disease?

A
  1. Anaemia
  2. Osteoporosis
  3. Hyposplenism
  4. Neuropathies
  5. Increased risk of malignancy
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72
Q

Which malignancies do patients with coeliac disease have a higher risk of?

A
  1. T cell lymphoma (increased T cells in GI wall)
  2. Gastric, oesophageal, small bowel, colorectal cancer (increased cell turnover)
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73
Q

What is gastritis?

A

Inflammation of the stomach’s mucosal lining

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74
Q

What are 6 causes of gastritis?

A
  1. H. Pylori infection
  2. Autoimmune gastritis
  3. Viruses
  4. Duodeno-gastro reflux
  5. NSAIDs
  6. Stress
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75
Q

Describe the pathophysiology of gastritis

A
  • H. Pylori lives in the gastric mucus
  • Secretes urease which splits urea in the stomach into CO2 and ammonia
  • Ammonia + H+ = ammonium
  • Ammonium, proteases, phospholipases and vacuolating cytotoxin A damages gastric epithelium
  • This causes an inflammatory response reducing mucosal defence
  • This also causes increased acid secretion
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76
Q

Describe the pathophysiology of autoimmune gastritis

A
  • Affects the fundus and body of stomach
  • This leads to atrophic gastritis and loss of parietal cells with intrinsic factor deficiency
  • This results in pernicious anaemia
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77
Q

Describe the pathophysiology of gastritis due to aspirin/NSAIDs

A
  • Aspirin/NSAIDs inhibit prostaglandins via the inhibition of cyclo-oxygenase
  • This results in less mucus production
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78
Q

What is the difference between acute and chronic gastritis?

A

Acute = associated with neutrophilic infiltration
Chronic = associated with mononuclear cells (lymphocytes, plasma cells, macrophages)

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79
Q

What are 7 symptoms of gastritis?

A

Usually asymptomatic
1. Functional dyspepsia (indigestion)
2. Upper abdominal pain
3. Nausea and vomiting
4. Loss of appetite
5. Haematemesis
6. Abdominal bloating
7. Autoimmune pernicious anaemia

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80
Q

What are the investigations for patients with gastritis?

A
  • Endoscopy
  • Biopsy
  • H. Pylori urea breath test
  • H. Pylori stool antigen test
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81
Q

What is the treatment for gastritis?

A
  • Eradication of H. Pylori (triple therapy):
    • Clarithromycin
    • Omeprazole
    • Metronidazole
      OR
      H2 antagonists (to reduce acid release)
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82
Q

What is a complication of gastritis?

A

Peptic ulcer

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83
Q

What is gastro-oesophageal reflux disease (GORD)?

A

Prolonged or current reflux of the gastric contents through the lower oesophageal sphincter to the oesophagus

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84
Q

Describe the epidemiology of GORD

A

2-3 times more common in men

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85
Q

What are 5 causes of GORD?

A
  1. Complication of a hiatus hernia
  2. Smoking
  3. Alcoholism
  4. Obesity
  5. Pregnancy
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86
Q

Describe the pathophysiology of GORD

A
  • Increase in transient lower oesophageal sphincter relaxations (due to reduced tone of LOS)
  • This results in reflux of gastric contents (gastric acid, bile, pepsin etc.)
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87
Q

What is the normal epithelial lining of the oesophagus and stomach?

A

Oesophagus = squamous (sensitive to effects of stomach acid)
Stomach = columnar (more protected against stomach acid)

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88
Q

What are 6 symptoms of GORD?

A
  1. Heartburn (related to lying down and meals)
  2. Odynophagia (pain when swallowing)
  3. Acid regurgitation
  4. Nocturnal asthma
  5. Chronic cough
  6. Laryngitis, sinusitis
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89
Q

What are 2 investigations for patients with GORD?

A
  1. Endoscopy
  2. Barium swallow
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90
Q

What is the treatment for GORD?

A
  • Smoking/alcohol cessation
  • Weight loss
  • Antacids
  • Proton pump inhibitors e.g. omeprazole
  • H2 receptor antagonist
  • Surgery to tighten the lower oesophageal sphincter (laparoscopic fundoplication)
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91
Q

What are 2 complications of GORD?

A
  1. Oesophageal stricture formation (worsening dysphagia)
  2. Barrett’s oesophagus (can develop into oesophageal cancer)
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92
Q

What is Barrett’s oesophagus?

A

Normal squamous epithelium of distal oesophagus is replaced by abnormal columnar epithelium

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93
Q

What is the treatment for Barrett’s oesophagus?

A
  • Proton pump inhibitors e.g. omeprazole
  • Radiofrequency ablation (burn epithelial cells so they regenerate as normal stratified squamous cells)
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94
Q

What is a peptic ulcer?

A

Break in the gastric or duodenal mucosa in or adjacent to acid bearing area

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95
Q

Describe the epidemiology of peptic ulcers

A

Duodenal peptic ulcers are 2-3 times more common than gastric

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96
Q

What are 4 risk factors for gastric peptic ulcers?

A
  1. H. Pylori (80% association)
  2. Smoking
  3. Drugs
  4. Stress
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97
Q

What are 4 risk factors for duodenal peptic ulcers?

A
  1. H. Pylori (95% association)
  2. Smoking
  3. Drugs
  4. Alcohol
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98
Q

Describe the pathophysiology of peptic ulcers due to H. Pylori

A
  • Increases gastric acid secretion
  • Disrupts mucous protective layer
  • Reduced duodenal bicarbonate production
  • Leads to acidic contents of the stomach/duodenum breaking down the mucosa
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99
Q

Describe the pathophysiology of peptic ulcers due to NSAIDs

A
  • Reduced production of prostaglandins (which provide mucosal protection)
  • Leads to acidic contents of the stomach/duodenum breaking down the mucosa
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100
Q

What are 5 symptoms of peptic ulcers?

A
  1. Burning epigastric pain
  2. Nausea
  3. Heartburn
  4. Flatulence
  5. Occasionally painless haemorrhage
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101
Q

What is the difference in burning epigastric pain between people with gastric peptic ulcers and duodenal peptic ulcers?

A

Gastric = worse on eating, relieved by antacids
Duodenal = worse when hungry/at night, relieved by eating/milk

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102
Q

What are 3 investigations for patients with peptic ulcers?

A
  1. H. Pylori urea breath test
  2. H. Pylori stool antigen test
  3. Endoscopy
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103
Q

What is the treatment for peptic ulcers?

A
  • Avoid NSAIDs
  • Smoking cessation
  • Eradication of H. Pylori (triple therapy):
    • Clarithromycin
    • Omeprazole
    • Metronidazole
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104
Q

What are 4 complications of peptic ulcers?

A
  1. Upper GI bleed
  2. Haemorrhage
  3. Perforation
  4. Gastric outflow obstruction
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105
Q

What is a Mallory-Weiss Tear?

A

Mucosal lacerations in the upper GI tract causing bleeding/haematemesis

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106
Q

Describe the epidemiology of Mallory-Weiss Tears

A
  • More common in males mainly between 20-50
  • 4-8% of all upper gastrointestinal bleeding
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107
Q

What are 4 causes of Mallory-Weiss Tears?

A
  1. Hyperemesis gravidarum (severe nausea/vomiting in pregnancy)
  2. Gastroenteritis
  3. Bulimia
  4. Chronic cough
108
Q

What are 3 risk factors for Mallory-Weiss Tears?

A
  1. Excessive alcohol consumption
  2. Male
  3. NSAID abuse
109
Q

Describe the pathophysiology of Mallory-Weiss Tears

A
  • Sudden increased intragastric pressure within non-distensible oesophagus can cause tearing of the mucosa
  • Blood is able to enter the oesophagus
110
Q

What is a sign of Mallory-Weiss Tears?

A

Postural hypotension

111
Q

What are 5 symptoms of Mallory-Weiss Tears?

A
  1. Haematemesis
  2. Melaena (black coloured stool)
    Symptoms of hypovolaemic shock:
  3. Dizziness
  4. Light headedness
  5. Syncope
112
Q

What are 3 investigations for patients with Mallory-Weiss Tears?

A
  1. Endoscopy
  2. Rockall score (assess blood level - <3 = low risk)
  3. FBC (haematocrit)
113
Q

What is the treatment for Mallory-Weiss Tears?

A
  • ABCDE
  • Tears/bleeds tend to heal rapidly (24 hours)
  • Surgery
114
Q

What are 3 complications of Mallory-Weiss Tears?

A
  1. Hypovolaemic shock
  2. Rebleeding
  3. MI
115
Q

What are oesophageal varices?

A

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

116
Q

Describe the epidemiology of oesophageal varices

A
  • 90% of patients with cirrhosis develop this over 10 years (but only a third bleed)
  • 10-20% of all upper GI bleeding
117
Q

What are 2 pre-hepatic causes of oesophageal varices?

A
  1. Portal hypertension
  2. Portal vein thrombosis/obstruction
118
Q

What are 2 hepatic causes of oesophageal varices?

A
  1. Chronic liver disease (cirrhosis)
  2. Schistosomiasis
119
Q

What are 4 post hepatic causes of oesophageal varices?

A
  1. Budd Chiari
  2. RHF
  3. Constrictive pericarditis
  4. Compression
120
Q

Describe the pathophysiology of oesophageal varices

A
  • High pressure in portal vein
  • Vessels are thin and not meant to transport higher pressure blood
  • This causes damage and can lead to bleeding from the varices into the oesophagus
  • Rupture –> haematemesis –> blood digested –> melaena
121
Q

Describe 6 clinical presentations of oesophageal varices

A
  1. Liver disease
  2. Shock (low BP, high HR)
  3. Haematemesis (vomiting blood)
  4. Melaena
  5. Epigastric discomfort
  6. Pallor
122
Q

What is the investigation for oesophageal varices?

A

Upper GI endoscopy

123
Q

What is the medicinal treatment for oesophageal varices?

A
  • Resuscitation/maintain airway
  • Beta blocker (to reduce CO and portal pressure)
  • Nitrate (to reduce portal pressure)
124
Q

What is the surgical treatment for oesophageal varices?

A
  • Band ligation
  • Trans jugular intrahepatic portosystemic shunt (TIPSS)
125
Q

What are 2 complications of oesophageal varices?

A
  1. 70% chance of rebleeding
  2. Significant risk of death
126
Q

What is achalasia?

A

Oesophageal aperistalsis and failure of LOS to relax impairing oesophageal emptying

127
Q

Describe the pathophysiology of achalasia

A
  • Decreased ganglionic cells in the nerve plexus of the oesophageal wall
  • Degeneration of vagus nerve
  • Causes failure of small muscle relaxation
128
Q

What are 4 symptoms of achalasia?

A
  1. Long history of dysphagia for solids and liquids
  2. Retrosternal chest pain
  3. Weight loss
  4. Regurgitation
129
Q

What are 2 investigations for patients with achalasia?

A
  1. Barium swallow
  2. Oesophageal manometry
130
Q

What is the treatment for achalasia?

A
  • No cure
  • Treat symptoms
  • Surgical division of LOS and endoscopic balloon dilatation
  • Nitrates or botox (if surgery not an option)
131
Q

What are 2 complications of achalasia?

A
  1. Untreated –> inhalation of material in oesophagus –> choking
  2. Oesophageal cancer
132
Q

What is ischaemic colitis?

A

Lack of blood supply to the colon causing inflammation and injury

133
Q

Describe the epidemiology of ischaemic colitis

A
  • More common in elderly
  • Related to underlying atherosclerosis and vessel occlusion
134
Q

What are 5 causes of ischaemic colitis?

A
  1. Atherosclerosis
  2. Thrombosis
  3. Emboli
  4. Decreased cardiac output and arrythmias
  5. Vasculitis
135
Q

What are 3 risk factors for ischaemic colitis?

A
  1. Contraceptive pill
  2. Vasculitis
  3. Thrombophilia
136
Q

Describe the pathophysiology of ischaemic colitis

A
  • Occlusion of a branch of the superior mesenteric artery or inferior mesenteric artery
  • = reduced blood flow (watershed area) to areas of the colon (usually splenic flexure and caecum)
137
Q

What are 3 symptoms of ischaemic colitis?

A
  1. LLQ abdominal pain
  2. Rectal bleeding (blood diarrhoea)
  3. Occasionally shock
138
Q

What are 4 investigations for patients with ischaemic colitis?

A
  1. Colonoscopy and biopsy (GOLD STANDARD)
  2. CT/MRI angiography
  3. Stool analysis
  4. Ultrasound and abdominal CT
139
Q

What is the treatment for ischaemic colitis?

A
  • Treat symptoms
  • Fluid replacement
  • Antibiotics (to reduce infection risks)
  • Possible anticoagulants
  • Surgery may be required for complications
140
Q

What are 3 complications of ischaemic colitis?

A
  1. Gangrene
  2. Perforation
  3. Stricture formation
141
Q

What is acute mesenteric ischaemia?

A

Lack of blood supply to the small intestine

142
Q

Describe the epidemiology of acute mesenteric ischaemia

A

> 50 years

143
Q

What are 6 causes of acute mesenteric ischaemia?

A
  1. Superior mesenteric artery thrombosis
  2. Superior mesenteric artery embolism (due to AF)
  3. Mesenteric vein thrombosis
  4. Aortic dissection
  5. Hypotension
  6. Vasopressive drugs
144
Q

What is a risk factor for acute mesenteric ischaemia?

A

Atrial fibrillation

145
Q

Describe the pathophysiology of acute mesenteric ischaemia

A
  • Rapid blockage in blood flow through the superior mesenteric artery
  • Prolonged ischaemia to the bowel will result in necrosis of bowel tissue and perforation
146
Q

What is a sign of acute mesenteric ischaemia?

A

Rapid hypovolaemic shock

147
Q

What is the main symptom of acute mesenteric ischaemia?

A

Acute, severe, non-specific abdominal pain

148
Q

What are 4 investigations for patients with acute mesenteric ischaemia?

A
  1. Contrast CT/MRI angiography
  2. Abdominal x-ray (to rule out bowel obstruction)
  3. Laparoscopy
  4. Bloods (metabolic acidosis, raised lactate)
149
Q

What is the treatment for acute mesenteric ischaemia?

A
  • Fluid resuscitation
  • Antibiotics e.g. metronidazole, gentamicin
  • IV heparin (to reduce clotting)
  • Surgery (remove necrotic bowel OR remove/bypass thrombus in blood vessel)
150
Q

What are 3 complications and the mortality rate for acute mesenteric ischaemia?

A
  1. Shock
  2. Sepsis
  3. Peritonitis
    Poor outcome with treatment = 50-80% mortality
151
Q

What is chronic mesenteric ischaemia?

A

Lack of blood supply to the small intestine (a.k.a intestinal angina)

152
Q

Describe the epidemiology of chronic mesenteric ischaemia

A

Average presentation of 60

153
Q

What is the main cause of chronic mesenteric ischaemia?

A

Atherosclerosis

154
Q

What are 5 risk factors for chronic mesenteric ischaemia?

A

Same usual CVD risk factors:
1. Increased age
2. Family history
3. Smoking
4. Hypertension
5. Hypercholesterolaemia

155
Q

Describe the pathophysiology of chronic mesenteric ischaemia

A
  • Narrowing of mesenteric blood vessels via atherosclerosis
  • Can be all three major mesenteric arteries (coeliac, superior mesenteric, inferior mesenteric)
156
Q

What is a sign of chronic mesenteric ischaemia?

A

Abdominal bruit upon auscultation

157
Q

What are 2 symptoms of chronic mesenteric ischaemia?

A
  1. Central colicky abdominal pain after eating
  2. Weight loss
158
Q

What is the investigation for patients with chronic mesenteric ischaemia?

A

CT angiography

159
Q

What is the treatment for chronic mesenteric ischaemia?

A
  • Reduce modifiable risk factors e.g. smoking cessation
  • Surgery (revascularisation)
  • Nitrates and anticoagulants (if surgery is contraindicated)
160
Q

What is appendicitis?

A

Inflammation of the appendix

161
Q

What are 5 causes of appendicitis?

A

Obstruction within appendix due to:
1. Faecoliths (mass of compacted faeces)
2. Bezoars/foreign bodies
3. Trauma
4. Intestinal worms
5. Lymphoid hyperplasia

162
Q

Describe the pathophysiology of appendicitis

A
  • Obstruction of appendix
  • = invasion of gut organisms into appendix wall
  • = inflammation, necrosis and eventually perforation
163
Q

What are 3 signs of appendicitis?

A
  1. Guarding
  2. Tender mass in RIF
  3. Peritonism (infection of inner lining of abdomen)
164
Q

What are 4 symptoms of appendicitis regarding pain?

A
  1. Early pain/discomfort around umbilicus that migrates to the RIF
  2. Severe, localised pain at McBurney’s point
  3. Rosving’s sign (RLQ pain elicited by pressure applied to LLQ)
  4. Moving/coughing causes pain
165
Q

What are 3 symptoms of appendicitis (not pain)?

A
  1. Anorexia
  2. Pyrexia (fever)
  3. Nausea and vomiting
166
Q

What are 4 investigations for appendicitis?

A
  1. Bloods (raised WCC/ESR/CRP)
  2. Ultrasound
  3. CT (GOLD STANDARD)
  4. Pregnancy test and urinalysis (to exclude pregnancy/UTI)
167
Q

What is the treatment for appendicitis?

A
  • Appendicectomy (GOLD STANDARD)
  • IV antibiotics and fluids both pre- and post-operatively e.g. metronidazole, cefuroxime
168
Q

What are 6 complications of appendicitis?

A
  1. Perforation
  2. Appendix mass (small bowel and omentum adhere to appendix)
  3. Appendiceal abscess
  4. Adhesions
  5. Pelvic inflammatory disease
  6. Peritonitis
169
Q

What is a diverticulum (diverticula pl.)?

A

An out pouch/pocket of gut mucosa in the bowel wall (usually range from 0.5-1cm)

170
Q

What is diverticulosis?

A

Presence of diverticula without inflammation or infection

171
Q

What is diverticular disease?

A

Diverticulosis with patients experiencing symptoms

172
Q

What is diverticulitis?

A

Inflammation and infection of diverticula

173
Q

Describe the epidemiology of diverticular diseases

A
  • Very common >50years
  • Two types = true and false
174
Q

What are 5 risk factors for diverticular diseases?

A
  1. Low fibre diet
  2. Obesity
  3. Age >40
  4. Smoking
  5. NSAIDs
175
Q

Describe the pathophysiology of diverticular diseases

A
  • Blood vessels penetrate circular muscle in the wall of the large intestine
  • When there is increased pressure in the lumens over time, gaps form
  • Mucosa herniates through the muscle layer and forms pouches (diverticula)
  • This mostly occurs in areas not covered by teniae coli (sigmoid and descending colon)
  • This can become inflamed (diverticulitis)
176
Q

What is the difference between true and false diverticular diseases?

A

True = all 3 layers of gut
False = does not include muscularis layer therefore are thin walled (typically colonic diverticula)

177
Q

What are 2 signs of diverticulitis?

A
  1. Tachycardia
  2. Palpable LIF mass
178
Q

What are 3 symptoms of diverticular disease?

A
  1. Lower left abdominal pain
  2. Constipation
  3. Rectal bleeding
179
Q

What are 5 symptoms of diverticulitis?

A
  1. LIF pain with tenderness
  2. Constipation/diarrhoea
  3. Nausea and vomiting
  4. Rectal bleeding
  5. Fever
180
Q

What are 4 investigations for patients with diverticular diseases?

A
  1. CT
  2. Colonoscopy
  3. Bloods (raised WCC/ESR/CRP)
  4. CXR/AXR
181
Q

What is the treatment for diverticular disease?

A
  • High fibre diet
  • Fluids +/- laxatives
  • Surgery
182
Q

What is the treatment for diverticulitis?

A
  • Oral/IV antibiotics e.g. ciprofloxacin, metronidazole
  • Analgesia and liquid diet +/- fluid resuscitation
  • Surgical resection (rare)
183
Q

What are 6 complications of diverticulitis?

A
  1. Perforation
  2. Peritonitis
  3. Peridiverticular abscess
  4. Large haemorrhage
  5. Fistula
  6. Ileus/obstruction
184
Q

What is Meckel’s Diverticulum?

A

Congenital malformation of distal ileum caused by an incomplete obstruction of the vitelline duct

185
Q

Describe the epidemiology of Meckel’s Diverticulum

A
  • 2-3% of the population
  • Most common in 2 year olds
186
Q

Describe the pathophysiology of Meckel’s Diverticulum

A
  • True diverticula (all 3 layers of small intestines)
  • Out pouch/pocket of gut mucosa in bowel wall
187
Q

What is a symptom of Meckel’s Diverticulum?

A

Usually asymptomatic
- Painless bleeding due to ulcer caused by heterotopic gastric tissue

188
Q

What is the investigation for patients with Meckel’s Diverticulum?

A

Nuclear medicine scan

189
Q

What is the treatment for Meckel’s Diverticulum?

A

Removal if found incidentally during other abdominal operations

190
Q

What are 3 complications of Meckel’s Diverticulum?

A
  1. Rupture
  2. Volvulus (intestine twists around itself)
  3. Intussusception (part of intestine slides into adjacent part)
191
Q

What is diarrhoea?

A

Abnormal passage of loose/liquid stool more than 3 times daily

192
Q

What are the 3 main causes of diarrhoea?

A
  1. Virus (majority)
  2. Bacteria
  3. Parasites
193
Q

What are 2 viral causes of diarrhoea?

A
  1. Rotavirus (children)
  2. Norovirus (adults)
194
Q

What are 5 bacterial causes of diarrhoea?

A
  1. Clostridium difficile (C. diff)
  2. Campylobacter jejuni (C. jejuni)
  3. E. Coli
  4. Salmonella
  5. Shigella
195
Q

Which 3 bacterial infections are associated with bloody diarrhoea?

A
  1. E. Coli
  2. Salmonella
  3. Shigella
196
Q

What are 3 parasitic causes of diarrhoea?

A
  1. Giardia lamblia
  2. Entamoeba histolytica
  3. Cryptosporidium
197
Q

What is the difference between acute and chronic diarrhoea?

A

Acute = <2 weeks
Chronic = >2 weeks

198
Q

What is the treatment for diarrhoea?

A

Usually self limiting
- Treat underlying cause (bacterial diarrhoea = metronidazole)
- Oral rehydration therapy
- Anti-emetics e.g. metoclopramide
- Anti-motility agents e.g. loperamide

199
Q

Describe the pathophysiology of Helicobacter Pylori

A
  • Bacteria that lives in the gastric mucosa
  • Secretes urease which splits urea into CO2 and ammonia
  • Ammonia + H+ –> ammonium
  • Ammonium, proteases, phospholipases and vacuolating cytotoxin A = all damage gastric epithelium (disrupt mucous protective layer)
  • Gastric acid secretion increased (gastrin release, reduced duodenal bicarb production etc.)
200
Q

What are the investigations for patients with Helicobacter Pylori?

A
  • H. Pylori urea breath test
  • H. Pylori stool antigen test
201
Q

What is the treatment for Helicobacter Pylori?

A

Triple therapy:
- Clarithromycin
- Omeprazole
- Metronidazole

202
Q

Describe the epidemiology of colorectal cancer

A
  • 4th most prevalent cancer in UK
  • Most common in rectum and sigmoid colon (left side of colon)
203
Q

What are 8 risk factors for colorectal cancer?

A
  1. Family history
  2. Genetics
  3. IBD
  4. Increasing age
  5. Diet high in red/processed meat and low in fibre
  6. Obesity/sedentary lifestyle
  7. Smoking
  8. Alcohol
204
Q

What are the 2 genetic risk factors for colorectal cancer?

A
  1. Familial adenomatous polyposis (FAP)
  2. Hereditary nonpolyposis colorectal cancer (HNPCC) a.k.a Lynch syndrome
205
Q

What is familial adenomatous polyposis?

A
  • Autosomal dominant
  • Malfunctioning of tumour suppressor gene (APC)
  • = lots of adenomas develop along large intestine
206
Q

What is hereditary nonpolyposis colorectal cancer a.k.a Lynch syndrome?

A
  • Autosomal dominant
  • Mutations in DNA mismatch repair genes
207
Q

What are the 6 red flags for colorectal cancer?

A
  1. Change in bowel (usually looser/more frequent)
  2. Unexplained weight loss
  3. Rectal bleeding (left side)
  4. Unexplained abdominal pain
  5. Iron deficiency anaemia (right side)
  6. Abdominal/rectal mass on examination
208
Q

What are 3 other symptoms of colorectal cancer?

A

Obstruction:
1. Vomiting
2. Abdominal pain
3. Absolute constipation

209
Q

What are the 2 main investigations for patients with colorectal cancer?

A
  1. Faecal immunochemical test (FIT)
  2. Colonoscopy with biopsy
210
Q

What are 4 other investigations for patients with colorectal cancer?

A
  1. Sigmoidoscopy
  2. CT colonography
  3. Staging CT scan (CT TAP)
  4. Carcinoembryonic antigen (CEA) tumour marker blood test (used for predicting relapse)
211
Q

Describe TNM classification

A

T - tumour
- TX = unable to assess size
- T1 = submucosa involvement
- T2 = involvement of muscularis propria
- T3 = involvement of subserosa and serosa
- T4 = spread through serosa (4a), reached other tissues/organs (4b)
N - nodes
- NX - unable to assess nodes
- N0 = no nodal spread
- N1 = spread to 1-3 nodes
- N2 = spread to more than 3 nodes
M - metastasis
- M0 = no metastasis
- M1 = metastasis

212
Q

What is the treatment for colorectal cancer?

A
  • Surgical resection
  • Chemotherapy
  • Radiotherapy
  • Palliative care
213
Q

What are 3 complications of colorectal cancer?

A
  1. General surgery complications
  2. Low anterior resection syndrome
  3. Local invasion and distant metastases often to liver and lung
214
Q

What is low anterior resection syndrome?

A

May occur after resection of a portion of bowel from the rectum, with anastomosis between the colon and rectum
Causes:
- Increased urgency/frequency of bowel movements
- Faecal incontinence
- Difficulty controlling flatulence

215
Q

What are 6 risk factors for gastric cancer?

A
  1. Male
  2. H. Pylori
  3. Chronic/atrophic gastritis
  4. Genetics
  5. Smoking
  6. Pernicious anaemia
216
Q

Describe the pathophysiology of gastric cancer

A
  • 90% are adenocarcinomas
  • Most involve pylorus
217
Q

What are 3 signs of gastric cancer?

A
  1. Epigastric mass
  2. Hepatomegaly
  3. Troisier’s sign (enlarged left supraclavicular nodes)
218
Q

What are 6 symptoms of gastric cancer?

A
  1. Epigastric pain
  2. Dyspepsia/dysphagia
  3. Nausea/vomiting/diarrhoea
  4. Weight loss/anorexia
  5. Anaemia
  6. Jaundice
219
Q

What are 2 investigations for patients with gastric cancer?

A
  1. Gastroscopy with biopsy
  2. CT/MRI to stage cancer
220
Q

What is the treatment for gastric cancer?

A
  • Gastrectomy (partial/total) with perioperative chemo
  • Nutritional support
221
Q

What are 3 risk factors for squamous oesophageal cancer?

A
  1. Smoking
  2. Alcohol
  3. Nitrous amines (barbecue food, tobacco)
222
Q

What are 2 risk factors for adenocarcinoma oesophageal cancer?

A
  1. Barrett’s oesophagus
  2. Obesity
223
Q

What are 5 symptoms of late oesophageal cancer?

A
  1. Dysphagia
  2. Weight loss
  3. Heartburn
  4. Haematemesis
  5. Hoarse voice
224
Q

What are 2 investigations for patients with oesophageal cancer?

A
  1. Oesophagoscopy with biopsy
  2. CT/MRI to stage cancer
225
Q

What is the treatment for oesophageal cancer?

A

Oesophagectomy with perioperative chemo

226
Q

What is pseudomembranous colitis?

A

Swelling/inflammation of the large intestine due to a bacterial/viral infection

227
Q

What is the main cause of pseudomembranous colitis?

A

Overgrowth of clotridioides difficile bacteria induced with antibiotic use

228
Q

What is another less common cause of pseudomembranous colitis?

A

Cytomegalovirus (CMV) infection

229
Q

What is Clostridioides/Clostridium difficile a.k.a C. diff?

A

Gram +ve spore forming bacteria

230
Q

Describe the pathophysiology of pseudomembranous colitis

A
  • Antibiotic use kills normal gut flora allowing C. diff to over grow
  • This causes inflammation of the colon
  • Highly infectious
231
Q

What are 2 symptoms of pseudomembranous colitis?

A
  1. Severe diarrhoea –> dehydration (MAIN)
  2. CMV –> owl’s eye appearance of inclusion bodies
232
Q

What is the treatment for pseudomembranous colitis?

A

Stop using antibiotics and take vancomycin instead (antibiotic likely to be effective against C. diff)

233
Q

What are haemorrhoids (piles)?

A

Enlarged vascular mucosal cushions in the anal canal

234
Q

What are 4 risk factors for haemorrhoids (piles)?

A
  1. Constipation
  2. Prolonged straining
  3. Increased abdominal pressure (ascites)
  4. Heavy lifting
235
Q

Describe the pathophysiology of haemorrhoids (piles)

A
  • Vascular mucosal cushions function to maintain anal continence
  • When they enlarge, the vessels are brought close to abrasion and can bleed into the anus
236
Q

What is the difference between internal and external haemorrhoids (piles)?

A

Internal = above dentate line
External = below dentate line

237
Q

What are the clinical presentations for haemorrhoids (piles)?

A

Internal = painless unless strangulated
External = painful, itchy and visible on external examination

238
Q

How are internal haemorrhoids (piles) classified?

A

1st degree = no prolapse
2nd degree = prolapse on straining, spontaneous reduction
3rd degree = prolapse on straining, manual reduction
4th degree = permanently prolapse, no reduction

239
Q

What are the investigations for patients with haemorrhoids (piles)?

A
  • Digital rectal examination
  • Proctoscopy
240
Q

What is the treatment for haemorrhoids (piles)?

A
  • Increase fluids and fibre
  • Pain relief
  • Rubber band ligation
  • Haemorrhoidectomy
241
Q

What are 3 complications of haemorrhoids (piles)?

A
  • Skin tags
  • Strangulation (internal)
  • Gangrene (external)
242
Q

What is an anal fistula?

A

Abnormal ‘passage’ between inside of anus and elsewhere, commonly subcutaneous skin

243
Q

What are 2 symptoms of anal fistulae?

A
  1. Bloody/mucus discharge
  2. Pain
244
Q

What is the treatment for anal fistulae?

A
  • Surgical removal/drainage
  • Antibiotics if infected
245
Q

What is an anal fissure?

A

Tear in the mucosa of the anal canal

246
Q

What are 3 causes of anal fissures?

A
  1. Constipation = hard stool can tear anal mucosa
  2. IBD = ulceration as part of inflammation
  3. Rectal malignancy
247
Q

Describe the pathophysiology of anal fissures

A
  • Blood vessels of anal mucosa are very close to the surface
  • Lesions can cause bleeding under the pressure of defecation
248
Q

What are 2 symptoms of anal fissures?

A
  1. Pain on defecation
  2. Bright red blood on defecation
249
Q

What is the treatment for anal fissures?

A
  • Pain releief
  • Increase fibre and fluids
250
Q

What are 2 complications of anal fissures?

A
  1. Recurrence
  2. Anorectal/perianal abscess
251
Q

What is a perianal/anorectal abscess?

A

Collection of pus in anal/rectal region

252
Q

What is the cause of perianal/anorectal abscesses?

A

Infection of an anal fissure

253
Q

What are 5 risk factors for perianal/anorectal abscesses?

A
  1. Diabetes
  2. STI
  3. Immunocompromised
  4. IBD
  5. Male
254
Q

Describe the pathophysiology of perianal/anorectal abscesses

A
  • Infection of one of the anal sinuses
  • Leads to inflammation
  • Causes formation of abscess
255
Q

What are 6 clinical presentations of perianal/anorectal abscesses?

A
  1. Painful, hardened tissue in perianal area
  2. Discharge of pus from rectum
  3. Lump/nodules
  4. Tenderness
  5. Fever
  6. Constipation
256
Q

What is the investigation for perianal/anorectal abscesses?

A

Digital rectal examination (DRE)

257
Q

What is the treatment for perianal/anorectal abscesses?

A
  • Surgical drainage
  • Pain relief
258
Q

What is a complication of perianal/anorectal abscesses?

A

Anal fistula (40%)

259
Q

What is a pilonidal sinus/abscess?

A

Obstruction of natural hair follicles above the anus (congenital)

260
Q

Describe the epidemiology of pilonidal sinuses/abscesses

A
  • 10:1 male to female ratio
  • More common in Caucasian people
261
Q

What are 3 risk factors for pilonidal sinuses/abscesses?

A
  • Male
  • Obese
  • Caucasian
262
Q

What is the clinical presentation of non infected pilonidal sinuses/abscesses?

A
  • Small hole about 6cm above anus
  • No symptoms
263
Q

What are 4 extra clinical presentations of infected pilonidal sinuses/abscesses?

A
  1. Pus filled abscess
  2. Pain
  3. Redness
  4. Swelling
264
Q

Describe the pathophysiology of pilonidal sinuses/abscesses

A

Ingrowth of hair excites a foreign body reaction and causes abscess with foul smelling discharge

265
Q

What is the treatment for pilonidal sinuses/abscesses?

A

Asymptomatic = keep clean and shave hair around area
Infected = excision of sinus tract and closure (skin flap used to cover defect)

Phase 2a (29 decks)

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