Gastrointestinal Flashcards
(133 cards)
1
Q
What is malabsorption?
A
Failure to fully absorb nutrients, insufficient intake must be ruled out first.
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).
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).
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.
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.
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
19
Q
IRRITABLE BOWEL SYNDROME
What is the pathophysiology of IBS?
A
- Relapsing functional bowel disorder associated with a change in bowel habit.
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).
21
Q
IRRITABLE BOWEL SYNDROME
What is the epidemiology of IBS?
A
- 10-20% prevalence, age at onset ≤40y/o, F:M ≥ 2:1
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).
23
Q
IRRITABLE BOWEL SYNDROME
What are the differentials of IBS?
A
- Coeliac disease.
- IBD.
- Colorectal cancer.
- Lactos intolerance.
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.
25
IRRITABLE BOWEL SYNDROME
| What is the should IBS treatment focus on?
- Focus on symptomatic control, lifestyle/dietary measures + then cognitive therapy if needed.
26
```
IRRITABLE BOWEL SYNDROME
How can the following be treated in IBS...
i) Constipation?
ii) Diarrhoea?
iii) Colic/bloating?
```
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.
27
COELIAC DISEASE
| What is the pathophysiology of coeliac disease?
- 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.
28
COELIAC DISEASE
| What is the toxic portion of gluten? What part of the GI tract is usually affected?
- Alpha gliadin.
| - Duodenum
29
COELIAC DISEASE
| What is the epidemiology of coeliac disease?
- Peaks in infancy + adults in fifth decade.
- 1 in 100.
- Relative risk in first degree relatives = x6
30
COELIAC DISEASE
| What is the clinical presentation of coeliac disease?
- Diarrhoea.
- Weight loss.
- Abdominal pain.
- Bloating.
- Nausea + vomiting.
- Iron/B12/folate deficiency.
31
COELIAC DISEASE
| What are the complications with coeliac disease?
Increased risk of malignancy (lymphoma, gastric, oesophageal)...
- Incidence may be reduced by gluten-free diet.
Hyposplenism...
- Offer flu + pneumococcal vaccine.
Osteoporosis.
32
COELIAC DISEASE
| What are the investigations for coeliac disease?
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.
33
COELIAC DISEASE
| What is the treatment of coeliac disease?
Lifelong gluten-free diet + correction of any vitamin deficiencies.
34
GORD
| What is the pathophysiology of gastro-oesophageal reflux disease (GORD)?
- 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.
35
GORD
| What is the aetiology of GORD?
- Male gender.
- Hiatus hernia.
- Oesophageal dysmotility.
- Obesity, pregnancy (increaed abdominal pressure).
- Smoking, alcohol.
36
GORD
| What is the clinical presentation of GORD?
- Heartburn, belching, pain when swallowing, increased salivation.
- Chronic cough, nocturnal asthma (aspiration).
37
GORD
| What are the complications with GORD?
- Oesophagitis.
- Ulcer.
- Barrett's oesophagus (epithelium undergoes metaplasia from squamous to columnar epithelium + small amount progress to oesophageal cancer).
38
GORD
| What are the investigations for GORD?
Clinical.
| - Endoscopy, 24h oesophageal pH monitoring.
39
GORD
| What is the lifestyle advice for GORD?
- Weight loss, smoking cessation, reduce hot drinks + alcohol, eat small regular meals, reduce citrus fruit, avoid eating <3h before bed.
40
GORD
| What is the pharmacological treatment for GORD?
- Antacids like Gaviscon.
- PPIs like lansoprazole.
- H2 blockers like ranitidine.
- Avoid drugs affecting oesophageal motility (nitrates, anticholinergics) or that damage mucosa (NSAIDs, bisphosphonates).
41
OESOPHAGEAL CANCER
| What is the distribution + type of oesophageal cancer
```
Distribution...
- 20% upper, 50% middle, 30% lower.
Type...
- Squamous cell cancers proximal 2/3rds.
- Adenocarcinomas distal 1/3rd.
```
42
OESOPHAGEAL CANCER
| What are the aetiologies of oesophageal cancers?
Squamous cell carcinoma...
- Smoking, alcohol, poor diet.
Adenocarcinoma...
- Obesity, Barrett's oesophagus.
43
OESOPHAGEAL CANCER
| What is the clinical presentation for oesophageal cancer?
- Dysphagia.
- Weight loss.
- Heart burn.
- Signs from upper 1/3rd = hoarseness, cough.
44
OESOPHAGEAL CANCER
| What are the investigations for oesophageal cancer?
- Oesophago-gastro-duodenoscopy (OGD) with biopsy.
| - CT/MRI for staging.
45
OESOPHAGEAL CANCER
| What is the treatment for oesophageal cancer?
- Surgical resection if possible.
| - Chemo/radiotherapy if more advanced.
46
GASTRIC CANCER
| What is the pathophysiology of gastric cancer?
- 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.
47
GASTRIC CANCER
| What are the risk factors for gastric cancer?
- Helicobacter pylori x2
- Smoked foods, pickles.
- Gastritis + pernicious anaemia.
- Familial diffuse gastric cancer (mutation in CDH1).
48
GASTRIC CANCER
| What are the symptoms of gastric cancer?
- Dyspepsia + dysphagia.
- Weight loss.
- Vomiting.
49
GASTRIC CANCER
| What are the signs of gastric cancer?
- Epigastric mass.
- Hepatomegaly.
- Jaundice.
- Ascites.
50
GASTRIC CANCER
| What are the investigations of gastric cancer?
- Gastroscopy with biopsy for diagnosis.
| - CT/MRI for staging.
51
GASTRIC CANCER
| What is the treatment of gastric cancer?
- Surgical resection (either full if early proximal or partial gastroscopy if early distal).
- Chemo/radiotherapy.
- B12 supplementation as reduced intrinsic factor.
52
COLORECTAL CANCER
| What is the pathophysiology of colorectal cancer?
- Often occur sporadically, spread via direct invasion through bowel wall.
53
COLORECTAL CANCER
| What is the aetiology + risk factors of colorectal cancer?
- Familial adenomatous polyposis.
- Hereditary nonpolyposis colorectal cancer.
- RF = red + processed meat, alcohol, smoking.
54
COLORECTAL CANCER
What is...
i) familial adenomatous polyposis?
ii) hereditary nonpolyposis colorectal cancer?
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
COLORECTAL CANCER
What is the clinical presentation of...
i) Left sided
ii) Right sided + caecum
colorectal cancers?
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
COLORECTAL CANCER
| What are the investigations for colorectal cancer?
- Colonscopy + biopsy.
- Faecal occult blood for screening.
- FBC = microcytic anaemia.
- CT/MRI for staging.
57
COLORECTAL CANCER
| What can prevent adenoma formation and what is the treatment for colorectal cancer?
- NSAIDs.
- Surgical resection.
Chemotherapy + palliative care if metastatic.
58
COLORECTAL CANCER
| What is the bowel cancer screening programme and its effect?
- Men + women aged 64–75y/o get a faecal occult test every 2 years.
- Improved bowel cancer survival by catching it early.
59
PEPTIC ULCERATION
| What is the pathophysiology of peptic ulceration?
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
PEPTIC ULCERATION
| What are the two types of ulceration and how frequently is Helicobacter pylori associated with them?
- Gastric (80%).
| - Duodenal (95%).
61
PEPTIC ULCERATION
| What is the aetiology of peptic ulceration?
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
PEPTIC ULCERATION
| What is the clinical presentation of peptic ulceration?
- Burning epigastric pain.
- Heartburn + nausea.
- Weight loss.
- Duodenal = more pain when patient hungry + at night, pain relieved after food.
- Gastric = worse while eating.
63
PEPTIC ULCERATION
| What are the investigations for peptic ulceration?
- Endoscopy + biopsy.
| - Testing for Helicobacter pylori = C13 urea breath test, stool antigen test.
64
PEPTIC ULCERATION
| What is the treatment for peptic ulceration?
- Lifestyle = stop smoking.
- H. pylori +ve = Clarithromycin, metronidazole, omeprazole (PPI).
- H. pylori -ve = stop NSAID, PPI (omeprazole), H2 blocker (rantidine).
65
APPENDICITIS
| What is the pathophysiology of appendicitis?
- Lumen of appendix becomes obstruction + this causes gut flora to invade the appendix wall making it become inflamed + infection.
66
APPENDICITIS
| What two things can occur in appendicitis?
- Liable to rupture, infected + faecal matter into peritoneal cavity > peritonitis.
- Omentum localises infection + forms appendix abscess which presents as tender mass.
67
APPENDICITIS
| What is the aetiology of appendicits
- Faecolith = hard discreet mass of thickened faeces obstructs lumen.
68
APPENDICITIS
| What is the clinical presentation of appendicitis?
- Umbilical pain localises to RIF.
- Tenderness + guarding in RIF due to localised peritonitis.
- Pyrexia, vomiting, diarrhoea.
- Tender mass.
69
APPENDICITIS
| What are the investigations for appendicitis?
Bloods – WCC raised, CRP/ESR raised.
Ultrasound abdomen.
CT abdomen = gold standard.
70
APPENDICITIS
| What is the treatment for appendicitis?
- Surgical removal of appendix either open or laparoscopically.
- Appendix abscess needs antibiotics or drainage.
71
INTESTINAL OBSTRUCTION
| What is the pathophysiology of mechanical intestinal obstruction?
- Physical factor prevents movement of contents of the intestine through the tract.
- Causes backing up of GI tract + inability to empty (vomiting + constipation).
72
INTESTINAL OBSTRUCTION
| What is the pathophysiology of functional ('ileus') intestinal obstruction and when is it seen?
- Bowel ceases to function, no peristalsis causing impaction since contents no longer move along intestine.
- Post-operative, drugs like amitriptyline.
73
INTESTINAL OBSTRUCTION
| What is the pathophysiology of pseudo-obstruction?
- Resembles mechanical but no obstructing lesion.
74
INTESTINAL OBSTRUCTION
| What three factors can intestinal obstruction be due to?
- Blockage by tumour, diaphragm disease.
- Contraction by inflammation, intramural tumours, Hirschsprung's disease.
- Pressure (adhesions, volvulus, peritoneal tumour).
75
INTESTINAL OBSTRUCTION
| What is Hirschsprung's disease?
- Conenital condition where lack of nerves in bowel so motility affected > obstruction + gross dilatation.
76
INTESTINAL OBSTRUCTION
| What is the aetiology of small bowel obstruction?
- 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
INTESTINAL OBSTRUCTION
| What is the aetiology of small bowel obstructions in children?
- Appendicitis.
- Volvulus.
- Intussusception (part of intestine invaginates into another section of intestine, telescoping).
78
INTESTINAL OBSTRUCTION
| What is the aetiology of large bowel obstruction?
- Colonic carcinoma.
- Constipation.
- Volvulus (especially sigmoid colon).
79
INTESTINAL OBSTRUCTION
| What is midgut malrotation?
- 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
INTESTINAL OBSTRUCTION
| What are the cardinal features of intestinal obstruction?
```
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
INTESTINAL OBSTRUCTION
| What are the complications of intestinal obstruction?
- Ischaemia.
- Necrosis.
- Perforation>peritonitis.
82
INTESTINAL OBSTRUCTION
| What are the investigations for intestinal obstruction?
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
INTESTINAL OBSTRUCTION
| What are the treatments for small bowel obstruction?
May resolve conservatively.
- Fluids
- Bowel decompression.
- Anti-emetics.
84
INTESTINAL OBSTRUCTION
| What are the treatments for large bowel obstruction?
- Fluids.
- Sigmoidoscopy for decompression.
- Surgery (bypass, resect).
- Anti-emetics.
85
```
DIVERTICULAR DISEASE
What is...
i) a GI diverticulum?
ii) Diverticulosis?
iii) Diverticulitis?
iv) Diverticular disease?
```
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
DIVERTICULAR DISEASE
| What is the pathophysiology behind diverticular disease?
- High intraluminal pressure force the mucosa to herniate through the muscle layers of the gut at weak points adjacent to penetrating vessels.
87
DIVERTICULAR DISEASE
| What is high intraluminal pressure related to?
- Low fibre diet, old people.
88
DIVERTICULAR DISEASE
| What is the clinical presentation of diverticular disease?
Asymptomatic 95%.
- Luminal narrowing (pain, constipation, bleeding).
- LIF pain.
- Nausea + flatulence.
89
DIVERTICULAR DISEASE
| What is the major complication with diverticular disease and how does it occur? Where does it most commonly occur?
- Diverticulitis.
- Faeces can get trapped + obstruct diverticular leading to abscess formation + inflammation.
- Descending colon.
90
DIVERTICULAR DISEASE
| What are the signs of diverticulitis? What are the investigations? What is the treatment?
- 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
DIVERTICULAR DISEASE
| What are the investigations for diverticular disease?
- Incidental finding at colonscopy.
| - CT scan abdomen.
92
DIVERTICULAR DISEASE
| What is the treatment for diverticular disease?
- Acute attacks with Abx.
- Loperamide
- Surgery for frequent attacks.
93
GASTRITIS
| What is the pathophysiology of gastritis?
- Local inflammatory response to a trigger often causing an increase in gastric acid secretions causing further inflammation.
94
GASTRITIS
| What is the aetiology of gastritis? What are the risk factors?
- Helicobacter pylori commonly.
- Autoimmune gastritis, viruses, duodenogastric reflux.
- Alcohol, NSAIDs, granulomas.
95
GASTRITIS
| What is the clinical presentation + investigations of gastritis?
- Asymptomatic, ?epigastric pain, ?vomiting.
Upper GI endoscopy with gastric mucosal biopsy...
Acute = neutrophilic infiltration.
Chronic = mononuclear cells (lymphocytes, plasma cells, macrophages).
96
GASTRITIS
| What is the treatment for Helicobacter pylori associated gastritis?
- Clarithromycin.
- Metronidazole.
- Omeprazole.
97
ISCHAEMIC COLITIS
| What is the pathophysiology of ischaemic colitis?
Lack of blood flow via inferior mesenteric artery to areas of colon, usually splenic flexure + caecum, ranges from mild ischaemia to gangrenous colitis.
98
ISCHAEMIC COLITIS
| What is the aetiology of ischaemic colitis?
Underlying atherosclerosis + vessel occlusion...
- Elderly.
Combined oral contraceptive, thrombophilia, vasculitis...
- Younger.
99
ISCHAEMIC COLITIS
| What is the clinical presentation, investigations and treatment for ischaemic colitis?
- LLQ pain, rectal bleeding, ?shock.
- Sigmoidoscopy is normal but blood present.
- Symptomatic relief, ?anticoagulants, fluid replacement w/ Abx, surgery if gangrene/perforation/strictures.
100
MESENTERIC ISCHAEMIA
| What is the pathophysiology of mesenteric ischaemia?
Lack of blood flow via superior + inferior mesenteric arteries to areas of colon, usually splenic flexure + caecum.
101
MESENTERIC ISCHAEMIA
| What is the aetiology of mesenteric ischaemia?
- SMA thrombosis/embolism.
- Mesenteric vein thrombosis.
- Strangulation (volvulus).
102
MESENTERIC ISCHAEMIA
| What is the acute + chronic triad of mesenteric ischaemia?
```
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
MESENTERIC ISCHAEMIA
| What are the investigations for acute + chronic mesenteric ischaemia?
Acute...
- CT scan may show signs of ischaemia.
- CT angiography shows arterial blockage.
Chronic...
- CT angiography + contrast-enhanced MR angiography.
104
MESENTERIC ISCHAEMIA
| What is the treatment for acute + chronic mesenteric ischaemia?
Acute...
- Fluids, LMWH, surgery to remove dead bowel.
Chronic...
- Surgical stent insertion.
105
UPPER GI BLEEDING
| What are the two types of upper GI bleeding?
- Mallory-Weiss tear.
| - Oesophago-gastric varices.
106
UPPER GI BLEEDING
| What is the pathophysiology of Mallory-Weiss tear?
- Sudden increased intragastric pressure within the non-distensible lower oesophagus can cause tearing of mucosa where blood enters oesophagus.
107
UPPER GI BLEEDING
| What is the pathophysiology of oesophago-gastric varices?
- 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
UPPER GI BLEEDING
| What is the aetiology of Mallory-Weiss tear + oesophago-gastric varices?
- Trauma from frequent cough, vomit, hiccups, excessive alcohol consumption (RF).
- Portal hypertension (majority w/ chronic liver disease).
109
UPPER GI BLEEDING
| What is the clinical presentation of Mallory-Weiss tear + oesophago-gastric varices?
- Bout of retching/vomiting ± blood, syncope.
| - Vomiting blood, liver disease, pallor, shock.
110
UPPER GI BLEEDING
| What are the complications, investigations and treatment of upper GI bleeding?
- Hypovolaemic shock, death + re-bleeding.
- Endoscopy.
- Resuscitation, treat shock (vasoactive drugs), endoscopic band ligation + Abx.
111
HIATUS HERNIA
| What is a sliding hiatus hernia and the consequence of this?
- 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
HIATUS HERNIA
| What is a rolling/para-oesophageal hiatus?
- Part of fundus of stomach prolapses through the hiatus alongside oesophagus.
- Reflux uncommon as gastro-oesophageal junction intact.
113
HIATUS HERNIA
| What is the clinical presentation of hiatus herniae?
- 50/yo, obese women.
| - 50% symptomatic GORD – dyspepsia, dysphagia.
114
HIATUS HERNIA
| What are the investigations + treatments for hiatus hernia?
- Barium swallow confirms diagnosis, upper GI endoscopy to visualise mucosa.
- Lose weight, treat reflux symptoms, surgically treat to prevent strangulation.
115
ABDOMINAL HERNIAS
| What is a hernia?
- 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
```
ABDOMINAL HERNIAS
Define...
i) irreducible.
ii) obstructed.
iii) strangulated.
iv) incarceration
```
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
ABDOMINAL HERNIAS
| What are the two types of inguinal hernias?
- 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
ABDOMINAL HERNIAS
| Why are men more susceptible to inguinal hernias?
After the testicles descend through canal after birth, the canal doesn't always close properly causing weakness.
119
ABDOMINAL HERNIAS
| What is the clinical presentation, investigations + treatment of inguinal hernias?
- Swelling in groin (?lifting), increase in swelling on cough, indirect more prone to cause scrotal pain.
- Utrasound abdomen.
- Surgical repair (can incarcerate/strangulate).
120
ABDOMINAL HERNIAS
| What is a femoral hernia? How can this be differentiated from inguinal hernia? What is the treatment?
- 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
ABDOMINAL HERNIAS
| What is an incisional hernia?
- Follows breakdown of muscle closure after surgery.
| - Repair hard if obese.
122
HAEMORRHOIDS
| What is the pathophysiology of haemorrhoids?
- Vascular cushions protrude through a tight anus, become more congested + hypertrophy occurs to protrude again + more readily, they may strangulate.
123
HAEMORRHOIDS
| What are the risk factors for haemorrhoids?
- Constipation, prolonged straining, ascites.
124
HAEMORRHOIDS
| What is the clinical presentation of haemorrhoids?
- Bright red rectal bleeding, coating stools.
| - Mucous discharge.
125
HAEMORRHOIDS
| What is the investigations + treatment for haemorrhoids?
- Rectal examination.
- Increase fluid + fibre, ± topical analgesics.
- Rubber band ligation or surgical excision.
126
PILONIDAL SINUS
| What is the pathophysiology of pilonidal sinus?
- Obstruction of natal cleft hair follicles (6cm above anus).
- Ingrowing hair excites foreign body reaction.
127
PILONIDAL SINUS
| What is the aetiology, clinical presentation, investigations + treatment of pilonidal sinus?
- Congeital, obese, M:F = 10:1
- Abscesses w/ foul smelling discharge, inflammation.
- Clinical.
- Keep hygienic, shave hair around area, excision of sinus tract.
128
ANAL FISTULAE
| What is the pathophysiology of anal fistulae?
- Blockage o deep intramuscular gland ducts predisposes to formation of abscesses which discharge to form fistula.
129
ANAL FISTULAE
| What is the clinical presentation, investigation + treatment of anal fistulae?
- Pain, anal discharge.
- MRI to exclude sepsis, Crohn's, endoanal USS.
- Fistulotomy + excision.
130
ANAL FISSURE
| What is the pathophysiology + aetiology of anal fissure?
- Painful tear in squamous lining of lower anal canal.
| - Hard faeces, spasm of inferior rectal artery > ischaemia + difficulty healing.
131
ANAL FISSURE
| What is the clinical presentation, investigations + treatment for anal fissure?
- Extreme pain, especially on defecation, bleeding.
- History, perianal inspection.
- Increased fluids + fibre, lidocaine ointment.
132
PERIANAL ABSCESS
| What is the pathophysiology, clinical presentation, investigations + treatment of perianal abscess?
- Infection of one of anal sinuses > inflammation + abscess.
- Painful swellings, discharge.
- Endoanal USS.
- Surgical excision + drainage w/ Abx.
133
BOWEL CANCER
| What is the Duke's cancer staging system?
- 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.
