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Phase 2a > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is malabsorption?

A

Failure to fully absorb nutrients, insufficient intake must be ruled out first.

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2
Q

What are the causes of malabsorption?

A
  • Defective intraluminal digestion (pancreatic insufficiency, defective bile secretion).
  • Insufficient absorptive area (coeliac + Crohn’s).
  • Lack of digestive enzymes (lactose intolerance).
  • Defective epithelial transport.
  • Lymphatic obstruction (lymphoma, TB).
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3
Q

CROHN’S DISEASE (IBD)

What is the pathophysiology of Crohn’s?

A

A chronic inflammatory disease characterised by transmural granulomatous inflammation affecting any part of the GI tract from mouth to anus (esp. terminal ileum) with skip lesions (patchy).

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4
Q

CROHN’S DISEASE (IBD)
What does Crohn’s disease look like…
i) Macroscopically?
ii) Microscopically?

A

i) Skip lesions, cobblestone appearance, thickened + narrowed.
ii) Transmural, non-caseating granulomas, goblet cells present.

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5
Q

CROHN’S DISEASE (IBD)

What is the aetiology of Crohn’s disease? What are the associations of Crohn’s?

A
  • An inappropriate immune response against gut flora in a genetically susceptible individual.
  • Smoking (x3-4 risk), female, stress + depression (relapses), mutation on NOD2 gene, chromosome 16.
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6
Q

CROHN’S DISEASE (IBD)

What are the symptoms of Crohn’s disease?

A

Often associated with region…

  • Small bowel = abdominal pain, weight loss.
  • Terminal ileum - RIF pain mimicking appendicitis.
  • Colonic = bloody diarrhoea, defecation pain.
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7
Q

CROHN’S DISEASE (IBD)

What are the signs of Crohn’s disease?

A
  • Bowel ulceration.
  • Abdominal tenderness/mass.
  • Perianal abscess/fistulae/skin tags.
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8
Q

CROHN’S DISEASE (IBD)

What are the complications with Crohn’s disease?

A
  • Malabsorption.
  • Fistula.
  • GI obstruction (fibrosis leading to contraction + subsequent obstruction).
  • GI perforation.
  • Anal fissures.
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9
Q

CROHN’S DISEASE (IBD)

What are the investigations for Crohn’s disease?

A

Bloods = FBC, U+E, LFTs, ESR/CRP.
Stool microscopy culture + sensitivity to rule out infection.
Colonoscopy + biopsy for histological examination.
CT enterography.

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10
Q

CROHN’S DISEASE (IBD)

What is the treatment for Crohn’s disease?

A

Lifestyle…
- Smoking cessation.
Corticosteroids like prednisolone induce remission.
Anti-TNF-alpha (adalimumab)
Methotexate to remain in remission.
Surgery if drug failure (resect affected areas).

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11
Q 
ULCERATIVE COLITIS (IBD)
What is the pathophysiology of ulcerative colitis?
A
  • Ulcerative colitis is a relapsing + remitting inflammatory disorder of the colonic mucosa, originating in the anus + continuously progressing proximally but never to the ileocaecal valve.
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12
Q

ULCERATIVE COLITIS (IBD)
What does ulcerative colitis look like…
i) Macroscopically?
ii) Microscopically?

A

i) Continuous inflammation, ulcers, psuedo-polyps.

ii) Mucosal inflammation, no granuloma, depleted goblet cells, increased crypt abscesses.

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13
Q 
ULCERATIVE COLITIS (IBD)
What is the aetiology of ulcerative colitis?
A
  • Inappropriate immune response against colonic flora in genetically susceptible individuals.
  • UC is 3-fold as common in non-smokers + may relapse on smoking cessation.
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14
Q 
ULCERATIVE COLITIS (IBD)
What are the symptoms of ulcerative colitis?
A
  • Episodic or recurrent diarrhoea (± blood or mucous).
  • Crampy abdominal discomfort (LLQ).
  • Bowel frequency relates to severity.
  • Systemically = fever, malaise, weight loss.
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15
Q 
ULCERATIVE COLITIS (IBD)
What are the signs of ulcerative colitis?
A
  • Tender, distended abdomen.
  • Fever.
  • Extra-intestinal signs = clubbing, erythema nodosum, ankylosing spondylitis.
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16
Q 
ULCERATIVE COLITIS (IBD)
What are the acute + chronic complications of ulcerative colitis?
A

Acute…
- Toxic dilatation of colon w/ risk of perforation, venous thromboembolism.
Chronic…
- Colonic cancer risk.

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17
Q 
ULCERATIVE COLITIS (IBD)
What are the investigations for ulcerative colitis?
A

Bloods = FBC, ESR/CRP, U+E, LFTs.
Stool microscopy culture + sensitivity to exclude infection.
Testing for pANCA antibody.
- Faecal calprotectin (non-invasive test for GI inflammation).
- CT abdomen.
- Flexible sigmoidoscopy + biopsy.

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18
Q 
ULCERATIVE COLITIS (IBD)
What are the treatments for ulcerative colitis?
A

Goals to induce then maintian disease remission.

  • 5-aminosalicylic acid like mesalazine.
  • Topical steroid foams.
  • Colectomy if failed medical therapy.
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19
Q

IRRITABLE BOWEL SYNDROME

What is the pathophysiology of IBS?

A
  • Relapsing functional bowel disorder associated with a change in bowel habit.
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20
Q

IRRITABLE BOWEL SYNDROME

What factors can contribute to IBS?

A
  • Psychological morbidity like trauma in early life, stress.
  • Abnormal gut motility.
  • Genetics.
  • Altered gut signalling (visceral hypersensitivity).
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21
Q

IRRITABLE BOWEL SYNDROME

What is the epidemiology of IBS?

A
  • 10-20% prevalence, age at onset ≤40y/o, F:M ≥ 2:1
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22
Q

IRRITABLE BOWEL SYNDROME

What are the symptoms of IBS?

A
  • Crampy abdominal pain.
  • Pain relieved by defaction/wind.
  • Altered stool form.
  • Altered bowel frequency (constipation/diarrhoea may alternate).
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23
Q

IRRITABLE BOWEL SYNDROME

What are the differentials of IBS?

A
  • Coeliac disease.
  • IBD.
  • Colorectal cancer.
  • Lactos intolerance.
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24
Q

IRRITABLE BOWEL SYNDROME

What are the investigations for IBS?

A

Clinical…
- Recurrent abdominal pain with ≥2 symptoms.
- Symptoms chronic >6m
- Symptoms exacerbated by stress, menstruation or gastroenteritis.
Exclude other causes…
- Bloods – FBC, U+E, LFT, ESR/CRP.
- Coeliac serology.

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25
Q

IRRITABLE BOWEL SYNDROME

What is the should IBS treatment focus on?

A
  • Focus on symptomatic control, lifestyle/dietary measures + then cognitive therapy if needed.
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26
Q 
IRRITABLE BOWEL SYNDROME
How can the following be treated in IBS...
i) Constipation?
ii) Diarrhoea?
iii) Colic/bloating?
A

i) Adequate water + fibre, physical activity, laxatives or self-administered anal irrigation if needed.
ii) Avoid alcohol, caffeine, identify trigger foods, bulking agent ± anti-motility agent (loperamide) after each loose stool.
iii) Loperamide.

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27
Q

COELIAC DISEASE

What is the pathophysiology of coeliac disease?

A
  • Gliadin is resistant to proteases in the small intestinal lumen + passes through a damaged epithelial barrier of the small intestine where it’s deaminated by tissue transglutaminase – increasing its immunogenicity.
  • Gliadin then interacts with antigen-presenting cells (MHCII) in the lamina propria via HLA-DQ2+8, activates gluten-sensitive T cells.
  • The resultant inflammatory cascade + release of mediators contribute to the villous atrophy + crypt hyperplasia.
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28
Q

COELIAC DISEASE

What is the toxic portion of gluten? What part of the GI tract is usually affected?

A
  • Alpha gliadin.

- Duodenum

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29
Q

COELIAC DISEASE

What is the epidemiology of coeliac disease?

A
  • Peaks in infancy + adults in fifth decade.
  • 1 in 100.
  • Relative risk in first degree relatives = x6
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30
Q

COELIAC DISEASE

What is the clinical presentation of coeliac disease?

A
  • Diarrhoea.
  • Weight loss.
  • Abdominal pain.
  • Bloating.
  • Nausea + vomiting.
  • Iron/B12/folate deficiency.
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31
Q

COELIAC DISEASE

What are the complications with coeliac disease?

A

Increased risk of malignancy (lymphoma, gastric, oesophageal)…
- Incidence may be reduced by gluten-free diet.
Hyposplenism…
- Offer flu + pneumococcal vaccine.
Osteoporosis.

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32
Q

COELIAC DISEASE

What are the investigations for coeliac disease?

A

Blood count…
- Mild anaemia, folate+iron deficiency may be present.
Serology, serum antibodies…
- Anti-transglutaminase + endomysial antibodies (IgA).
Endoscopy duodenal biopsy..
- While on gluten diet = subtotal villous atrophy, increased intra-epithelial WBCs, crypt hyperplasia.

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33
Q

COELIAC DISEASE

What is the treatment of coeliac disease?

A

Lifelong gluten-free diet + correction of any vitamin deficiencies.

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34
Q

GORD

What is the pathophysiology of gastro-oesophageal reflux disease (GORD)?

A
  • Reflux of gastric acid, pepsin, bile + duodenal contents back into oesophagus.
  • Transient lower oesophageal sphincter relaxation part of normal physiology but occur more frequent in patients with GORD allowing back-flow.
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35
Q

GORD

What is the aetiology of GORD?

A
  • Male gender.
  • Hiatus hernia.
  • Oesophageal dysmotility.
  • Obesity, pregnancy (increaed abdominal pressure).
  • Smoking, alcohol.
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36
Q

GORD

What is the clinical presentation of GORD?

A
  • Heartburn, belching, pain when swallowing, increased salivation.
  • Chronic cough, nocturnal asthma (aspiration).
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37
Q

GORD

What are the complications with GORD?

A
  • Oesophagitis.
  • Ulcer.
  • Barrett’s oesophagus (epithelium undergoes metaplasia from squamous to columnar epithelium + small amount progress to oesophageal cancer).
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38
Q

GORD

What are the investigations for GORD?

A

Clinical.

- Endoscopy, 24h oesophageal pH monitoring.

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39
Q

GORD

What is the lifestyle advice for GORD?

A
  • Weight loss, smoking cessation, reduce hot drinks + alcohol, eat small regular meals, reduce citrus fruit, avoid eating <3h before bed.
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40
Q

GORD

What is the pharmacological treatment for GORD?

A
  • Antacids like Gaviscon.
  • PPIs like lansoprazole.
  • H2 blockers like ranitidine.
  • Avoid drugs affecting oesophageal motility (nitrates, anticholinergics) or that damage mucosa (NSAIDs, bisphosphonates).
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41
Q

OESOPHAGEAL CANCER

What is the distribution + type of oesophageal cancer

A 
Distribution...
- 20% upper, 50% middle, 30% lower.
Type...
- Squamous cell cancers proximal 2/3rds.
- Adenocarcinomas distal 1/3rd.
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42
Q

OESOPHAGEAL CANCER

What are the aetiologies of oesophageal cancers?

A

Squamous cell carcinoma…
- Smoking, alcohol, poor diet.
Adenocarcinoma…
- Obesity, Barrett’s oesophagus.

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43
Q

OESOPHAGEAL CANCER

What is the clinical presentation for oesophageal cancer?

A
  • Dysphagia.
  • Weight loss.
  • Heart burn.
  • Signs from upper 1/3rd = hoarseness, cough.
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44
Q

OESOPHAGEAL CANCER

What are the investigations for oesophageal cancer?

A
  • Oesophago-gastro-duodenoscopy (OGD) with biopsy.

- CT/MRI for staging.

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45
Q

OESOPHAGEAL CANCER

What is the treatment for oesophageal cancer?

A
  • Surgical resection if possible.

- Chemo/radiotherapy if more advanced.

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46
Q

GASTRIC CANCER

What is the pathophysiology of gastric cancer?

A
  • Tumours most commonly occur in the antrum + are almost always adenocarcinomas.
  • They are localised ulcerated lesions with rolled edges or diffuse with extensive submucosal spread.
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47
Q

GASTRIC CANCER

What are the risk factors for gastric cancer?

A
  • Helicobacter pylori x2
  • Smoked foods, pickles.
  • Gastritis + pernicious anaemia.
  • Familial diffuse gastric cancer (mutation in CDH1).
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48
Q

GASTRIC CANCER

What are the symptoms of gastric cancer?

A
  • Dyspepsia + dysphagia.
  • Weight loss.
  • Vomiting.
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49
Q

GASTRIC CANCER

What are the signs of gastric cancer?

A
  • Epigastric mass.
  • Hepatomegaly.
  • Jaundice.
  • Ascites.
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50
Q

GASTRIC CANCER

What are the investigations of gastric cancer?

A
  • Gastroscopy with biopsy for diagnosis.

- CT/MRI for staging.

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51
Q

GASTRIC CANCER

What is the treatment of gastric cancer?

A
  • Surgical resection (either full if early proximal or partial gastroscopy if early distal).
  • Chemo/radiotherapy.
  • B12 supplementation as reduced intrinsic factor.
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52
Q

COLORECTAL CANCER

What is the pathophysiology of colorectal cancer?

A
  • Often occur sporadically, spread via direct invasion through bowel wall.
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53
Q

COLORECTAL CANCER

What is the aetiology + risk factors of colorectal cancer?

A
  • Familial adenomatous polyposis.
  • Hereditary nonpolyposis colorectal cancer.
  • RF = red + processed meat, alcohol, smoking.
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54
Q

COLORECTAL CANCER
What is…
i) familial adenomatous polyposis?
ii) hereditary nonpolyposis colorectal cancer?

A

i) APC gene mutation leading to >100 polyps developing with 100% lifetime risk of colorectal cancer, AD inheritance.
ii) No DNA repair proteins causing accelerated progression of adenoma to colorectal cancer, >50% develop after 40y/o.

55
Q

COLORECTAL CANCER
What is the clinical presentation of…
i) Left sided
ii) Right sided + caecum

colorectal cancers?

A

i) Rectal bleeding/mucous, altered bowel habit, intestinal obstruction, tenesmus (continual inclination to evacuate bowels).
ii) Weight loss, abdominal pain, decreased Hb (iron deficiency anaemia).

56
Q

COLORECTAL CANCER

What are the investigations for colorectal cancer?

A
  • Colonscopy + biopsy.
  • Faecal occult blood for screening.
  • FBC = microcytic anaemia.
  • CT/MRI for staging.
57
Q

COLORECTAL CANCER

What can prevent adenoma formation and what is the treatment for colorectal cancer?

A
  • NSAIDs.
  • Surgical resection.
    Chemotherapy + palliative care if metastatic.
58
Q

COLORECTAL CANCER

What is the bowel cancer screening programme and its effect?

A
  • Men + women aged 64–75y/o get a faecal occult test every 2 years.
  • Improved bowel cancer survival by catching it early.
59
Q

PEPTIC ULCERATION

What is the pathophysiology of peptic ulceration?

A

A reduction in protective prostaglandins or increase in gastric acid secretions causes acidic contents of stomach/duodenum to break down mucosa.
- Helicobacter pylori can infect mucosa following this damage + cause further damage through inflammation + proteases.

60
Q

PEPTIC ULCERATION

What are the two types of ulceration and how frequently is Helicobacter pylori associated with them?

A
  • Gastric (80%).

- Duodenal (95%).

61
Q

PEPTIC ULCERATION

What is the aetiology of peptic ulceration?

A

Prolonged NSAID use…
- Reduced production of prostaglandins which provide protection.
Helicobacter pylori infection…
- Increased gastric acid secretions, disruption of mucous protective layer + reduced duodenal bicarbonate production.
- Hyperacidity.

62
Q

PEPTIC ULCERATION

What is the clinical presentation of peptic ulceration?

A
  • Burning epigastric pain.
  • Heartburn + nausea.
  • Weight loss.
  • Duodenal = more pain when patient hungry + at night, pain relieved after food.
  • Gastric = worse while eating.
63
Q

PEPTIC ULCERATION

What are the investigations for peptic ulceration?

A
  • Endoscopy + biopsy.

- Testing for Helicobacter pylori = C13 urea breath test, stool antigen test.

64
Q

PEPTIC ULCERATION

What is the treatment for peptic ulceration?

A
  • Lifestyle = stop smoking.
  • H. pylori +ve = Clarithromycin, metronidazole, omeprazole (PPI).
  • H. pylori -ve = stop NSAID, PPI (omeprazole), H2 blocker (rantidine).
65
Q

APPENDICITIS

What is the pathophysiology of appendicitis?

A
  • Lumen of appendix becomes obstruction + this causes gut flora to invade the appendix wall making it become inflamed + infection.
66
Q

APPENDICITIS

What two things can occur in appendicitis?

A
  • Liable to rupture, infected + faecal matter into peritoneal cavity > peritonitis.
  • Omentum localises infection + forms appendix abscess which presents as tender mass.
67
Q

APPENDICITIS

What is the aetiology of appendicits

A
  • Faecolith = hard discreet mass of thickened faeces obstructs lumen.
68
Q

APPENDICITIS

What is the clinical presentation of appendicitis?

A
  • Umbilical pain localises to RIF.
  • Tenderness + guarding in RIF due to localised peritonitis.
  • Pyrexia, vomiting, diarrhoea.
  • Tender mass.
69
Q

APPENDICITIS

What are the investigations for appendicitis?

A

Bloods – WCC raised, CRP/ESR raised.
Ultrasound abdomen.
CT abdomen = gold standard.

70
Q

APPENDICITIS

What is the treatment for appendicitis?

A
  • Surgical removal of appendix either open or laparoscopically.
  • Appendix abscess needs antibiotics or drainage.
71
Q

INTESTINAL OBSTRUCTION

What is the pathophysiology of mechanical intestinal obstruction?

A
  • Physical factor prevents movement of contents of the intestine through the tract.
  • Causes backing up of GI tract + inability to empty (vomiting + constipation).
72
Q

INTESTINAL OBSTRUCTION

What is the pathophysiology of functional (‘ileus’) intestinal obstruction and when is it seen?

A
  • Bowel ceases to function, no peristalsis causing impaction since contents no longer move along intestine.
  • Post-operative, drugs like amitriptyline.
73
Q

INTESTINAL OBSTRUCTION

What is the pathophysiology of pseudo-obstruction?

A
  • Resembles mechanical but no obstructing lesion.
74
Q

INTESTINAL OBSTRUCTION

What three factors can intestinal obstruction be due to?

A
  • Blockage by tumour, diaphragm disease.
  • Contraction by inflammation, intramural tumours, Hirschsprung’s disease.
  • Pressure (adhesions, volvulus, peritoneal tumour).
75
Q

INTESTINAL OBSTRUCTION

What is Hirschsprung’s disease?

A
  • Conenital condition where lack of nerves in bowel so motility affected > obstruction + gross dilatation.
76
Q

INTESTINAL OBSTRUCTION

What is the aetiology of small bowel obstruction?

A
  • Adhesions (post-abdominal surgery loops of bowel stick together, bowel pulled + distorted).
  • Volvulus (twist/rotation in bowel around its mesenteric attachment, closed loop obstruction > ?necrosis).
  • Hernias, Crohn’s, malignancy.
77
Q

INTESTINAL OBSTRUCTION

What is the aetiology of small bowel obstructions in children?

A
  • Appendicitis.
  • Volvulus.
  • Intussusception (part of intestine invaginates into another section of intestine, telescoping).
78
Q

INTESTINAL OBSTRUCTION

What is the aetiology of large bowel obstruction?

A
  • Colonic carcinoma.
  • Constipation.
  • Volvulus (especially sigmoid colon).
79
Q

INTESTINAL OBSTRUCTION

What is midgut malrotation?

A
  • Congenital issue where midgut rotates + becomes fixed to posterior abdominal wall.
  • Passage of faecal matter slow + obstructed causing backing up of GI tract.
  • Symptomatic if volvulus occurs.
80
Q

INTESTINAL OBSTRUCTION

What are the cardinal features of intestinal obstruction?

A 
Vomiting, bilious (green/yellow)...
- Early in small bowel.
- Late in large bowel.
Colicky abdominal pain.
Distention (more distal, more distention).
Absolute constipation (no faeces or flatulence)...
- Early in large bowel.
- Late in small bowel.
Active, 'tinkling' bowel sounds.
81
Q

INTESTINAL OBSTRUCTION

What are the complications of intestinal obstruction?

A
  • Ischaemia.
  • Necrosis.
  • Perforation>peritonitis.
82
Q

INTESTINAL OBSTRUCTION

What are the investigations for intestinal obstruction?

A

Bloods – FBC, U+E, lactate.
Digital rectal exmination or sigmoidoscopy in large bowel.
X-ray abdomen shows gas throughout bowel in functional.
- CT, ultrasound, MRI.

83
Q

INTESTINAL OBSTRUCTION

What are the treatments for small bowel obstruction?

A

May resolve conservatively.

  • Fluids
  • Bowel decompression.
  • Anti-emetics.
84
Q

INTESTINAL OBSTRUCTION

What are the treatments for large bowel obstruction?

A
  • Fluids.
  • Sigmoidoscopy for decompression.
  • Surgery (bypass, resect).
  • Anti-emetics.
85
Q 
DIVERTICULAR DISEASE
What is...
i) a GI diverticulum?
ii) Diverticulosis?
iii) Diverticulitis?
iv) Diverticular disease?
A

i) Outpouching of the gut wall, usually at site of perforating arteries.
ii) Presence of diverticula.
iii) Inflammation of a diverticulum.
iv) Implies symptomatic diverticula.

86
Q

DIVERTICULAR DISEASE

What is the pathophysiology behind diverticular disease?

A
  • High intraluminal pressure force the mucosa to herniate through the muscle layers of the gut at weak points adjacent to penetrating vessels.
87
Q

DIVERTICULAR DISEASE

What is high intraluminal pressure related to?

A
  • Low fibre diet, old people.
88
Q

DIVERTICULAR DISEASE

What is the clinical presentation of diverticular disease?

A

Asymptomatic 95%.

  • Luminal narrowing (pain, constipation, bleeding).
  • LIF pain.
  • Nausea + flatulence.
89
Q

DIVERTICULAR DISEASE

What is the major complication with diverticular disease and how does it occur? Where does it most commonly occur?

A
  • Diverticulitis.
  • Faeces can get trapped + obstruct diverticular leading to abscess formation + inflammation.
  • Descending colon.
90
Q

DIVERTICULAR DISEASE

What are the signs of diverticulitis? What are the investigations? What is the treatment?

A
  • Pain in LIF, fever, tachycardia, intestinal obstruction.
  • Bloods, FBC with increased WCC, ESR/CRP, tender colon ± localised/generalised peritonitis.
  • Mild = bowel rest (fluids only) ± Abx), analgesia or surgery if peritonitis.
91
Q

DIVERTICULAR DISEASE

What are the investigations for diverticular disease?

A
  • Incidental finding at colonscopy.

- CT scan abdomen.

92
Q

DIVERTICULAR DISEASE

What is the treatment for diverticular disease?

A
  • Acute attacks with Abx.
  • Loperamide
  • Surgery for frequent attacks.
93
Q

GASTRITIS

What is the pathophysiology of gastritis?

A
  • Local inflammatory response to a trigger often causing an increase in gastric acid secretions causing further inflammation.
94
Q

GASTRITIS

What is the aetiology of gastritis? What are the risk factors?

A
  • Helicobacter pylori commonly.
  • Autoimmune gastritis, viruses, duodenogastric reflux.
  • Alcohol, NSAIDs, granulomas.
95
Q

GASTRITIS

What is the clinical presentation + investigations of gastritis?

A
  • Asymptomatic, ?epigastric pain, ?vomiting.
    Upper GI endoscopy with gastric mucosal biopsy…
    Acute = neutrophilic infiltration.
    Chronic = mononuclear cells (lymphocytes, plasma cells, macrophages).
96
Q

GASTRITIS

What is the treatment for Helicobacter pylori associated gastritis?

A
  • Clarithromycin.
  • Metronidazole.
  • Omeprazole.
97
Q

ISCHAEMIC COLITIS

What is the pathophysiology of ischaemic colitis?

A

Lack of blood flow via inferior mesenteric artery to areas of colon, usually splenic flexure + caecum, ranges from mild ischaemia to gangrenous colitis.

98
Q

ISCHAEMIC COLITIS

What is the aetiology of ischaemic colitis?

A

Underlying atherosclerosis + vessel occlusion…
- Elderly.
Combined oral contraceptive, thrombophilia, vasculitis…
- Younger.

99
Q

ISCHAEMIC COLITIS

What is the clinical presentation, investigations and treatment for ischaemic colitis?

A
  • LLQ pain, rectal bleeding, ?shock.
  • Sigmoidoscopy is normal but blood present.
  • Symptomatic relief, ?anticoagulants, fluid replacement w/ Abx, surgery if gangrene/perforation/strictures.
100
Q

MESENTERIC ISCHAEMIA

What is the pathophysiology of mesenteric ischaemia?

A

Lack of blood flow via superior + inferior mesenteric arteries to areas of colon, usually splenic flexure + caecum.

101
Q

MESENTERIC ISCHAEMIA

What is the aetiology of mesenteric ischaemia?

A
  • SMA thrombosis/embolism.
  • Mesenteric vein thrombosis.
  • Strangulation (volvulus).
102
Q

MESENTERIC ISCHAEMIA

What is the acute + chronic triad of mesenteric ischaemia?

A 
Acute = acute severe abdominal pain, no/minimal abdominal signs, rapid hypovolaemia > shock.
Chronic = severe, colicky post-prandial abdominal pain, weight loss (Eating hurts), upper abdominal bruit ± rectal bleeding, nausea + vomiting.
103
Q

MESENTERIC ISCHAEMIA

What are the investigations for acute + chronic mesenteric ischaemia?

A

Acute…
- CT scan may show signs of ischaemia.
- CT angiography shows arterial blockage.
Chronic…
- CT angiography + contrast-enhanced MR angiography.

104
Q

MESENTERIC ISCHAEMIA

What is the treatment for acute + chronic mesenteric ischaemia?

A

Acute…
- Fluids, LMWH, surgery to remove dead bowel.
Chronic…
- Surgical stent insertion.

105
Q

UPPER GI BLEEDING

What are the two types of upper GI bleeding?

A
  • Mallory-Weiss tear.

- Oesophago-gastric varices.

106
Q

UPPER GI BLEEDING

What is the pathophysiology of Mallory-Weiss tear?

A
  • Sudden increased intragastric pressure within the non-distensible lower oesophagus can cause tearing of mucosa where blood enters oesophagus.
107
Q

UPPER GI BLEEDING

What is the pathophysiology of oesophago-gastric varices?

A
  • Liver disease leads to high pressure in portal veins + so blood is diverted into collaterals at junction between portal/systemic venous systems (like gastro-oesophageal junction), causing them to distend (varices).
  • Causes damage + bleeding from varices into the oesophagus.
108
Q

UPPER GI BLEEDING

What is the aetiology of Mallory-Weiss tear + oesophago-gastric varices?

A
  • Trauma from frequent cough, vomit, hiccups, excessive alcohol consumption (RF).
  • Portal hypertension (majority w/ chronic liver disease).
109
Q

UPPER GI BLEEDING

What is the clinical presentation of Mallory-Weiss tear + oesophago-gastric varices?

A
  • Bout of retching/vomiting ± blood, syncope.

- Vomiting blood, liver disease, pallor, shock.

110
Q

UPPER GI BLEEDING

What are the complications, investigations and treatment of upper GI bleeding?

A
  • Hypovolaemic shock, death + re-bleeding.
  • Endoscopy.
  • Resuscitation, treat shock (vasoactive drugs), endoscopic band ligation + Abx.
111
Q

HIATUS HERNIA

What is a sliding hiatus hernia and the consequence of this?

A
  • Gastro-oesophageal junction + part of stomach ‘slides up’ the chest via the hiatus so that it lies above diaphragm.
  • Acid reflux often happens as lower oesophageal sphincter becomes less competent.
112
Q

HIATUS HERNIA

What is a rolling/para-oesophageal hiatus?

A
  • Part of fundus of stomach prolapses through the hiatus alongside oesophagus.
  • Reflux uncommon as gastro-oesophageal junction intact.
113
Q

HIATUS HERNIA

What is the clinical presentation of hiatus herniae?

A
  • 50/yo, obese women.

- 50% symptomatic GORD – dyspepsia, dysphagia.

114
Q

HIATUS HERNIA

What are the investigations + treatments for hiatus hernia?

A
  • Barium swallow confirms diagnosis, upper GI endoscopy to visualise mucosa.
  • Lose weight, treat reflux symptoms, surgically treat to prevent strangulation.
115
Q

ABDOMINAL HERNIAS

What is a hernia?

A
  • The protrusion of an organ or part of an organ through a defect of the walls of its containing cavity into an abnormal position.
116
Q 
ABDOMINAL HERNIAS
Define...
i) irreducible.
ii) obstructed.
iii) strangulated.
iv) incarceration
A

i) contents cannot be pushed back into place.
ii) bowel contents cannot pass.
iii) ischaemia occurs > urgent surgery.
iv) contents of hernial sac stuck inside by adhesions.

117
Q

ABDOMINAL HERNIAS

What are the two types of inguinal hernias?

A
  • Direct = protrudes directly through a weakness in posterior wall of inguinal canal, medial to inferior epigastric vessels.
  • Indirect = protrudes through internal inguinal ring, lateral to inferior epigastric vessels.
118
Q

ABDOMINAL HERNIAS

Why are men more susceptible to inguinal hernias?

A

After the testicles descend through canal after birth, the canal doesn’t always close properly causing weakness.

119
Q

ABDOMINAL HERNIAS

What is the clinical presentation, investigations + treatment of inguinal hernias?

A
  • Swelling in groin (?lifting), increase in swelling on cough, indirect more prone to cause scrotal pain.
  • Utrasound abdomen.
  • Surgical repair (can incarcerate/strangulate).
120
Q

ABDOMINAL HERNIAS

What is a femoral hernia? How can this be differentiated from inguinal hernia? What is the treatment?

A
  • Bowel enters femoral canal, mass in upper medial thigh or above inguinal ligament.
  • Hernia points down leg, not groin.
  • Treatment via surgical repair as likely to be irreducible + strangulate.
121
Q

ABDOMINAL HERNIAS

What is an incisional hernia?

A
  • Follows breakdown of muscle closure after surgery.

- Repair hard if obese.

122
Q

HAEMORRHOIDS

What is the pathophysiology of haemorrhoids?

A
  • Vascular cushions protrude through a tight anus, become more congested + hypertrophy occurs to protrude again + more readily, they may strangulate.
123
Q

HAEMORRHOIDS

What are the risk factors for haemorrhoids?

A
  • Constipation, prolonged straining, ascites.
124
Q

HAEMORRHOIDS

What is the clinical presentation of haemorrhoids?

A
  • Bright red rectal bleeding, coating stools.

- Mucous discharge.

125
Q

HAEMORRHOIDS

What is the investigations + treatment for haemorrhoids?

A
  • Rectal examination.
  • Increase fluid + fibre, ± topical analgesics.
  • Rubber band ligation or surgical excision.
126
Q

PILONIDAL SINUS

What is the pathophysiology of pilonidal sinus?

A
  • Obstruction of natal cleft hair follicles (6cm above anus).
  • Ingrowing hair excites foreign body reaction.
127
Q

PILONIDAL SINUS

What is the aetiology, clinical presentation, investigations + treatment of pilonidal sinus?

A
  • Congeital, obese, M:F = 10:1
  • Abscesses w/ foul smelling discharge, inflammation.
  • Clinical.
  • Keep hygienic, shave hair around area, excision of sinus tract.
128
Q

ANAL FISTULAE

What is the pathophysiology of anal fistulae?

A
  • Blockage o deep intramuscular gland ducts predisposes to formation of abscesses which discharge to form fistula.
129
Q

ANAL FISTULAE

What is the clinical presentation, investigation + treatment of anal fistulae?

A
  • Pain, anal discharge.
  • MRI to exclude sepsis, Crohn’s, endoanal USS.
  • Fistulotomy + excision.
130
Q

ANAL FISSURE

What is the pathophysiology + aetiology of anal fissure?

A
  • Painful tear in squamous lining of lower anal canal.

- Hard faeces, spasm of inferior rectal artery > ischaemia + difficulty healing.

131
Q

ANAL FISSURE

What is the clinical presentation, investigations + treatment for anal fissure?

A
  • Extreme pain, especially on defecation, bleeding.
  • History, perianal inspection.
  • Increased fluids + fibre, lidocaine ointment.
132
Q

PERIANAL ABSCESS

What is the pathophysiology, clinical presentation, investigations + treatment of perianal abscess?

A
  • Infection of one of anal sinuses > inflammation + abscess.
  • Painful swellings, discharge.
  • Endoanal USS.
  • Surgical excision + drainage w/ Abx.
133
Q

BOWEL CANCER

What is the Duke’s cancer staging system?

A
  • Dukes’ A = invasion but not through bowel wall.
  • Dukes’ B = invasion through bowel wall penetrating muscle layer but not lymph nodes.
  • Dukes’ C = lymph node involvement.
  • Dukes’ D = widespread mets.

Phase 2a (12 decks)

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