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Phase 2a > Gashtro 2 > Flashcards

Gashtro 2 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. Malignancy4. 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 distension2. 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 abdomen2. Profuse vomiting3. 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. Malignancy2. Volvulus (rotation/twisting of bowel on its mesenteric axis - commonly sigmoid colon)3. Diverticulitis4. Crohn’s disease5. 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. Vomiting3. 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 trauma2. Post-operative states e.g. paralytic ileus3. Intra-abdo sepsis4. Drugs e.g. opiates/antidepressants5. 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. NSAIDs3. Jewish4. Female5. 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. Stress3. Depression4. 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 ulceration2. Abdominal tenderness3. Abdominal mass
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26
Q

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

A
  1. Weight loss2. 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. Clubbing2. Oral aphthous ulcers
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30
Q

What are 6 investigations for inflammatory bowel disease?

A
  1. Sigmoidoscopy2. Colonoscopy with rectal biopsy (gold standard)3. Bloods (raised WCC/platelets/CRP/ESR)4. Stool samples5. Abdominal x-ray6. 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 strictures2. Short stature in children3. Osteoporosis4. Malabsorption5. Toxic dilatation6. Bowel perforation7. Abscess/fistula formation8. 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 history2. NSAIDs3. 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 PSC2. Tender, distended abdomenExtra-GI manifestations:3. Arthralgia4. Fatty liver5. Gallstone
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38
Q

What are 7 symptoms of ulcerative colitis?

A
  1. Malaise2. Fever3. Anorexia4. Weight loss5. Pain in LLQ6. Abdominal cramps/discomfort7. 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 problems2. Frequent relapse3. Colorectal cancer (risk doubled)4. Blood loss5. Perforation6. Toxic dilatation7. 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

NESTSN - no blood/mucusE - entire GI tractS - skip lesionsT - terminal ileum is most affected, transmural inflammationS - smoking is a RF

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42
Q

What is the acronym for remembering ulcerative colitis?

A

CLOSE UPC - continuous inflammationL - limited to colon and rectumO - only superficial mucosa affectedS - smoking is protectiveE - excrete blood and mucusU - use aminosalicylatesP - 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 infections2. Previous severe long-term diarrhoea3. Anxiety and depression4. Psychological stress/trauma/abuse5. Eating disorders
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46
Q

What are 4 pathophysiology theories of IBS?

A
  1. Disorders of intestinal motility2. Enhanced visceral perception3. Dysfunction of brain-gut axis4. Microbial dysbiosis (imbalance)
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47
Q

What are 7 differential diagnoses for IBS?

A
  1. Coeliac disease2. Lactose intolerance3. Bile acid malabsorption4. IBD5. Colorectal cancer6. GI infection7. 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 constipationIBS-D = with diarrhoeaIBS-M = mixed with alternating constipation and diarrhoea

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51
Q

What 4 things exacerbate symptoms of IBS?

A
  1. Stress2. Menstruation3. Gastroenteritis4. Food
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52
Q

What are 8 symptoms of IBS?

A
  1. Painful periods2. Bladder symptoms (frequency, urgency, nocturia, incomplete emptying)3. Back pain4. Joint hypermobility5. Fatigue6. Nausea7. Mucus in rectum/stool8. Hard/soft/mixed stool
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53
Q

What are 3 investigations for patients with IBS?

A
  1. Bloods2. Faecal calprotectin = raised3. 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 diseases2. 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. Malabsorption2. Steathorrhoea (increase in fat excretion in stools)3. Anaemia4. Failure to thrive (children)5. Osteomalacia
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66
Q

What are 9 symptoms of coeliac disease?

A
  1. Weight loss2. Fatigue and weakness3. Diarrhoea4. Abdominal pain5. Bloating6. Nausea/vomiting7. Aphthous ulcers8. Angular stomatitis9. 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. Anaemia2. Osteoporosis3. Hyposplenism4. Neuropathies5. 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 infection2. Autoimmune gastritis3. Viruses4. Duodeno-gastro reflux5. NSAIDs6. 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 infiltrationChronic = associated with mononuclear cells (lymphocytes, plasma cells, macrophages)

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79
Q

What are 7 symptoms of gastritis?

A

Usually asymptomatic1. Functional dyspepsia (indigestion)2. Upper abdominal pain3. Nausea and vomiting4. Loss of appetite5. Haematemesis6. Abdominal bloating7. 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 - MetronidazoleORH2 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 hernia2. Smoking3. Alcoholism4. Obesity5. 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 regurgitation4. Nocturnal asthma5. Chronic cough6. Laryngitis, sinusitis
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89
Q

What are 2 investigations for patients with GORD?

A
  1. Endoscopy2. 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. Smoking3. Drugs4. Stress
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97
Q

What are 4 risk factors for duodenal peptic ulcers?

A
  1. H. Pylori (95% association)2. Smoking3. Drugs4. 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 pain2. Nausea3. Heartburn4. Flatulence5. 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 antacidsDuodenal = 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 test2. H. Pylori stool antigen test3. 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 bleed2. Haemorrhage3. Perforation4. 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. Gastroenteritis3. Bulimia4. Chronic cough
108
Q

What are 3 risk factors for Mallory-Weiss Tears?

A
  1. Excessive alcohol consumption2. Male3. 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. Haematemesis2. Melaena (black coloured stool)Symptoms of hypovolaemic shock:3. Dizziness4. Light headedness5. Syncope
112
Q

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

A
  1. Endoscopy2. 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 shock2. Rebleeding3. 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 hypertension2. 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 Chiari2. RHF3. Constrictive pericarditis4. 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 disease2. Shock (low BP, high HR)3. Haematemesis (vomiting blood)4. Melaena5. Epigastric discomfort6. 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 rebleeding2. 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 liquids2. Retrosternal chest pain3. Weight loss4. Regurgitation
129
Q

What are 2 investigations for patients with achalasia?

A
  1. Barium swallow2. 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 –> choking2. 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. Atherosclerosis2. Thrombosis3. Emboli4. Decreased cardiac output and arrythmias5. Vasculitis
135
Q

What are 3 risk factors for ischaemic colitis?

A
  1. Contraceptive pill2. Vasculitis3. 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 pain2. 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 angiography3. Stool analysis4. 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. Gangrene2. Perforation3. 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 thrombosis2. Superior mesenteric artery embolism (due to AF)3. Mesenteric vein thrombosis4. Aortic dissection5. Hypotension6. 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 angiography2. Abdominal x-ray (to rule out bowel obstruction)3. Laparoscopy4. 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. Shock2. Sepsis3. PeritonitisPoor 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 age2. Family history3. Smoking4. Hypertension5. 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 eating2. 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 bodies3. Trauma4. Intestinal worms5. 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. Guarding2. Tender mass in RIF3. 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 RIF2. Severe, localised pain at McBurney’s point3. 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. Anorexia2. Pyrexia (fever)3. Nausea and vomiting
166
Q

What are 4 investigations for appendicitis?

A
  1. Bloods (raised WCC/ESR/CRP)2. Ultrasound3. 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. Perforation2. Appendix mass (small bowel and omentum adhere to appendix)3. Appendiceal abscess4. Adhesions5. Pelvic inflammatory disease6. 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 diet2. Obesity3. Age >404. 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 gutFalse = does not include muscularis layer therefore are thin walled (typically colonic diverticula)

177
Q

What are 2 signs of diverticulitis?

A
  1. Tachycardia2. Palpable LIF mass
178
Q

What are 3 symptoms of diverticular disease?

A
  1. Lower left abdominal pain2. Constipation3. Rectal bleeding
179
Q

What are 5 symptoms of diverticulitis?

A
  1. LIF pain with tenderness2. Constipation/diarrhoea3. Nausea and vomiting4. Rectal bleeding5. Fever
180
Q

What are 4 investigations for patients with diverticular diseases?

A
  1. CT2. Colonoscopy3. 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. Perforation2. Peritonitis3. Peridiverticular abscess4. Large haemorrhage5. Fistula6. 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. Rupture2. 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. Bacteria3. 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. Coli4. Salmonella5. Shigella
195
Q

Which 3 bacterial infections are associated with bloody diarrhoea?

A
  1. E. Coli2. Salmonella3. Shigella
196
Q

What are 3 parasitic causes of diarrhoea?

A
  1. Giardia lamblia2. Entamoeba histolytica3. Cryptosporidium
197
Q

What is the difference between acute and chronic diarrhoea?

A

Acute = <2 weeksChronic = >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 history2. Genetics3. IBD4. Increasing age5. Diet high in red/processed meat and low in fibre6. Obesity/sedentary lifestyle7. Smoking8. 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 loss3. Rectal bleeding (left side)4. Unexplained abdominal pain5. Iron deficiency anaemia (right side)6. Abdominal/rectal mass on examination
208
Q

What are 3 other symptoms of colorectal cancer?

A

Obstruction:1. Vomiting2. Abdominal pain3. 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. Sigmoidoscopy2. CT colonography3. 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 nodesM - 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 complications2. Low anterior resection syndrome3. 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 rectumCauses:- Increased urgency/frequency of bowel movements- Faecal incontinence- Difficulty controlling flatulence

215
Q

What are 6 risk factors for gastric cancer?

A
  1. Male2. H. Pylori3. Chronic/atrophic gastritis4. Genetics5. Smoking6. 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 mass2. Hepatomegaly3. Troisier’s sign (enlarged left supraclavicular nodes)
218
Q

What are 6 symptoms of gastric cancer?

A
  1. Epigastric pain2. Dyspepsia/dysphagia3. Nausea/vomiting/diarrhoea4. Weight loss/anorexia5. Anaemia6. Jaundice
219
Q

What are 2 investigations for patients with gastric cancer?

A
  1. Gastroscopy with biopsy2. 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. Smoking2. Alcohol3. Nitrous amines (barbecue food, tobacco)
222
Q

What are 2 risk factors for adenocarcinoma oesophageal cancer?

A
  1. Barrett’s oesophagus2. Obesity
223
Q

What are 5 symptoms of late oesophageal cancer?

A
  1. Dysphagia2. Weight loss3. Heartburn4. Haematemesis5. Hoarse voice
224
Q

What are 2 investigations for patients with oesophageal cancer?

A
  1. Oesophagoscopy with biopsy2. 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. Constipation2. Prolonged straining3. 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 lineExternal = below dentate line

237
Q

What are the clinical presentations for haemorrhoids (piles)?

A

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

238
Q

How are internal haemorrhoids (piles) classified?

A

1st degree = no prolapse2nd degree = prolapse on straining, spontaneous reduction3rd degree = prolapse on straining, manual reduction4th 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 discharge2. 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 mucosa2. IBD = ulceration as part of inflammation3. 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 defecation2. 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. Recurrence2. 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. Diabetes2. STI3. Immunocompromised4. IBD5. 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 area2. Discharge of pus from rectum3. Lump/nodules4. Tenderness5. Fever6. 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 abscess2. Pain3. Redness4. 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 areaInfected = excision of sinus tract and closure (skin flap used to cover defect)

Phase 2a (29 decks)

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