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Phase 2a Resits > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is inflammatory bowel disease?

A
  • umbrella term for disease causing inflammation of the GI tract
  • associated with periods of remission and exacerbation
  • crohn’s and ulcerative colitis
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2
Q

Crohn’s vs UC: Crohn’s

A

NESTS

  • no blood or mucous (less common)
  • entire GI tract
  • skip lesions on endoscopy
  • terminal ileum most affected and transmural (full thickness) inflammation
  • smoking is a risk factor

also associated with weight loss, strictures and fistulas

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3
Q

Crohn’s vs UC: UC

A

CLOSEUP

  • continuous inflammation
  • limited to colon and rectum
  • only superficial mucosa affected
  • smoking is protective
  • excrete blood and mucus
  • use aminosalicyclates
  • primary sclerosing cholangitis
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4
Q

Presentation of inflammatory bowel disease

A
  • diarrhoea
  • abdominal pain
  • passing blood
  • weight loss
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5
Q

Testing for inflammatory bowel disease

A
  • routine bloods
  • CRP → inflammation and active disease
  • faecal calprotectin
  • DIAGNOSTIC = endoscopy (OGD/colonoscopy) with biopsy
  • imaging → complications
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6
Q

What is faecal calprotectin?

A
  • released by intestines when inflamed

- >90% sensitive and specific to IBD in adults

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7
Q

What does management of IBD involve?

A
  • inducing remission
  • maintaining remission
  • surgery
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8
Q

Inducing remission in Crohn’s

A
  1. steroids → oral prednisolone, IV hydrocortisone

- consider adding immunosuppressants

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9
Q

What immunosuppressants can be used in Crohn’s

A
  • azathioprine
  • mercaptopurine
  • methotrexate
  • infliximab
  • adalimumab
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10
Q

Maintaining remission in Crohn’s

A

based on risks, side effects, nature of the disease, patient’s wishes

  1. azathioprine, mercaptopurine

alternatives = rest of the immunosuppressants

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11
Q

Surgery in Crohn’s

A
  • if only distal ileum affected → surgical resection of area to prevent further flare ups
  • treat stricture and fistulas
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12
Q

Inducing remission in UC

A

mild to moderate

  1. aminosalicylates eg mesalazine
  2. corticosteroids eg prednisolone

severe

  1. IV corticosteroids eg hydrocortisone
  2. IV ciclosporin
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13
Q

Maintaining remission in UC

A
  • aminosalicylates
  • azathioprine
  • mercaptopurine
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14
Q

Surgery in UC

A
  • removal of colon and rectum → panproctocolectomy

- patient left with permanent ileostomy or ileo-anal anastomosis

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15
Q

What is IBS?

A
  • functional bowel disorder
  • no identifiable organic disease underlying symptoms
  • result of abnormal functioning of normal bowel
  • very common, more common if young/female
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16
Q

Symptoms of IBS

A

ABCDEF

  • abdominal pain
  • bloating
  • constipation
  • diarrhoea
  • eating makes it worse
  • fluctuating bowel habit
  • improved by opening bowels
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17
Q

Diagnostic criteria of IBS

A

diagnosis of exclusion

  • normal bloods
  • faecal calprotectin -ve
  • coeliac disease serology -ve
  • cancer not suspected/excluded
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18
Q

Management of IBS

A
  • general healthy diet and exercise advice
  1. loperamide for diarrhoea, linaclotide for constipation, antispasmodics for cramps
  2. tricyclic antidepressants
  3. SSRIs
    can also offer CBT
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19
Q

What is coeliac disease?

A
  • exposure to gluten = autoimmune reaction that causes inflammation in small bowel
  • usually develops in early childhood
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20
Q

Pathophysiology of coeliac disease

A
  1. auto-antibodies created in response to gluten
  2. target epithelial cells of the intestine → inflammation
  3. affects small bowel esp jejunum
  4. causes atrophy of intestinal villi and crypt hypertrophy
  5. malabsorption of nutrients → symptoms
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21
Q

Presentation of coeliac disease

A
  • often asymptomatic
  • failure to thrive in children
  • diarrhoea
  • fatigue
  • weight loss
  • mouth ulcers
  • anaemia secondary to iron, B12, folate deficiency
  • dermatitis herpetiformis
  • neurological symptoms (rare)
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22
Q

What is dermatitis herpetiformis?

A

itchy blistering skin rash that typically appears on the abdomen

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23
Q

Diagnosis of coeliac

A
  1. raised anti-TTG
    - raised anti-EMA
    - total IgA levels → exclude IgA deficiency first
    - endoscopy and intestinal biopsy → crypt hypertrophy and villous atrophy
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24
Q

What auto-antibodies are created in response to gluten?

A
  • anti-tissue transglutaminase (anti-TTG)

- anti-endomysial (anti-EMA)

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25
Q

What conditions are associated with coeliac disease?

A
  • T1DM
  • thyroid disease
  • autoimmune hepatitis
  • PBC
  • PSC
  • Down’s syndrome
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26
Q

Complications of coeliac disease

A
  • vitamin deficiency
  • anaemia
  • osteoporosis
  • ulcerative jejunitis
  • non-hodgkin’s lymphoma
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27
Q

Treatment for coeliac diease

A

lifelong gluten free diet

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28
Q

What is GORD?

A
  • gastro-oesophageal reflux disease

- acid from stomach refluxes through the lower oesophageal sphincter and irritates lining of oesophagus

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29
Q

Why is the oesophagus more sensitive to stomach acid?

A

the epithelial lining is squamous

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30
Q

Presentation of GORD

A
  • dyspepsia
  • heartburn
  • acid regurgitation
  • retrosternal/epigastric pain
  • bloating
  • nocturnal cough
  • hoarse voice
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31
Q

Diagnosis of GORD

A
  • clinical diagnosis

- refer for endoscopy if red flags

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32
Q

When would you refer for an endoscopy?

A
  • dysphagia
  • > 55yrs
  • weight loss
  • upper abdominal pain/reflux
  • treatment resistant dyspepsia
  • N&V
  • anaemia
  • raised platelets
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33
Q

Management for GORD

A
  • lifestyle advice
  • acid neutralising medications → gaviscon, rennies
  • PPIs → reduce stomach acid eg omeprazole, lansoprazole
  • ranitidine = alternative to PPIs

surgery = laparascopic fundoplication → tie fundus of stomach around lower oesophagus → narrows lower oesophageal sphincter

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34
Q

What lifestyle advice would you suggest for GI problems?

A
  • reduce tea, coffee, alcohol
  • weight loss
  • avoid smoking
  • smaller, lighter meals
  • avoid heavy meals before bed time
  • stay upright after meals
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35
Q

What is a peptic ulcer?

A

ulceration of the mucosa of the stomach (gastric) or duodenum (duodenal)

duodenal are more common

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36
Q

Risk factors of peptic ulcers

A
  • h.pylori
  • NSAIDs/SSRIs/steroids
  • smoking

gastric → stress
duodenal → alcohol

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37
Q

Presentation of peptic ulcers

A

epigastric pain

  • gastric = worse on eating, relieved by antacids
  • duodenal = before meals and at night, relieved by eating/milk
  • N&V
  • dyspepsia
  • bleeding causing haematemesis, coffee ground vomiting, maelaena
  • iron deficiency anaemia
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38
Q

Diagnosis of peptic ulcers

A
  • h.pylori test → urease breath test

- endoscopy if red flags

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39
Q

Treatment for peptic ulcers

A
  • lifestyle modification
  • treat cause
  • high dose PPIs
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40
Q

Complications of peptic ulcer

A
  • haemorrhage
  • perforation
  • gastric outflow obstruction
  • malignancy
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41
Q

What is appendicitis?

A
  • inflammation of the appendix
  • peak incidence = 10-20
  • less common in young children and adults over 50
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42
Q

Pathophysiology of appendicitis

A
  1. pathogens can get trapped due to obstruction at the point where appendix meets bowel
  2. infection and inflammation
  3. may proceed to gangrene and rupture
  4. faecal contents and infective material are released into peritoneal cavity
  5. peritonitis → inflammation of peritoneal lining
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43
Q

Signs and symptoms of appendicitis

A

KEY FEATURE = abdominal pain

  • loss of appetite
  • N&V
  • low-grade fever
  • Rovsing’s sign → palpation of LIF causes pain in RIF
  • guarding on palpation
  • rebound tenderness in RIF
  • percussion tenderness
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44
Q

Describe abdominal pain in appendicitis

A
  • starts as central
  • moves down to RIF within first 24hrs
  • eventually becomes localised in RIF
  • on palpation → tenderness at McBurney’s point
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45
Q

What is McBurney’s point

A

1/3 of the distance from the anterior superior iliac spine to the umbilicus

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46
Q

Diagnosis of appendicitis

A
  • based on clinical presentation and raised inflammatory markers
  • GOLD STANDARD = CT → confirms diagnosis
  • US to exclude female pathology
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47
Q

Differential diagnoses for appendicitis

A
  • ectopic pregnancy
  • ovarian cysts
  • Meckel’s diverticulum = malformation of distal ileum
  • mesenteric adenitis
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48
Q

Management of appendicitis

A
  • appendicectomy

- laparoscopic preferred → less risks and faster recovery

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49
Q

Complications of appendidectomy

A
  • damage to other organs eg bowel, bladder

- removal of normal appendix

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50
Q

What is a diverticulum?

A
  • a pouch/pocket in the bowel wall
  • 0.5-1cm
  • diverticulosis = diverticula without inflammation or infection
  • diverticular disease = if patients have symptoms
  • diverticulitis = inflammation and infection of diverticula
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51
Q

Pathophysiology of diverticula

A
  • wall of LI contains a layer of circular muscle
  • weaker in areas penetrated by blood vessels
  • increased pressure can cause a gap to form
  • mucus herniates through muscle layer and forms diveritcula

do not form in the rectum

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52
Q

Diverticulosis

A
  • wear and tear of bowel
  • most commonly in sigmoid colon
  • diagnosis = colonoscopy or CT
  • treatment not needed if asymptomatic
  • high fibre diet, bulk-forming laxatives
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53
Q

Presentation of diverticulitis

A
  • pain and tenderness in LIF
  • fever
  • D,N&V
  • rectal bleeding
  • palpable abdominal mass
  • rasied inflammatory markers
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54
Q

Management of diverticulitis

A
  • oral co-amoxiclav (5 days)
  • analgesia (not NSAIDs or opiates)
  • clear liquids until symptoms improve

severe
- manage like acute abdomen/sepsis

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55
Q

Complications of diverticulitis

A
  • perforation
  • peritonitis
  • peridiverticular disease
  • large haemorrhage
  • fistula
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56
Q

What is acute gastritis?

A

acute inflammation of the stomach mucosa due to imbalance between mucus defence and acid

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57
Q

Pathophysiology of acute gastritis

A
  • stomach usually lined by HCO3, prostaglandins and mucus barrier → protects against stomach acid
  • acid damage → superficial inflammation and can given erosions
  • loss of superficial layer
  • progression to ulcer
  • loss of mucosal layer
58
Q

Risk factors for acute gastritis

A
  • alcohol
  • drugs → NSAIDs, steroids
  • hiatus hernia
59
Q

Symptoms of acute gastritis

A
  • epigastric pain/discomfort
  • vomiting
  • heartburn
60
Q

Management of acute gastritis

A
  • PPIs/H2 blockers

- decrease alcohol and tobacco

61
Q

What is chronic infective gastritis?

A
  • most common form of gastritis
  • caused by H.pylori → makes a urease enzyme
  • breaks down mucus defence
  • destroys protective layer
  • leads to chronic inflammation
62
Q

What can chronic inflammation lead to in gastritis?

A

increases risk of

  • gastric adenocarcinoma
  • MALT lymphoma
63
Q

Symptoms of chronic infective gastritis

A
  • epigastric pain

- peptic ulcer disease

64
Q

Tests for chronic infective gastritis

A
  1. breath test
  • stool antigen, serology
  • histology from biopsy, CLO test → pH
65
Q

Management for chronic infective gastritis

A

tripe therapy to kill H.pylori

  • PPI → lansoprazole
  • amoxicillin
  • clarithromycin
66
Q

What is chronic autoimmune gastritis?

A
  • occurs due to autoimmune destruction of gastric parietal cells
  • T cells make antibodies against parietal cells and/or IFs → stomach atrophy

main problem = lack of IF → B12 deficiency

67
Q

Symptoms of chronic autoimmune gastritis

A
  • megaloblastic/pernicious anaemia (lack of IF)
  • mild jaundice
  • diarrhoea
  • sore tongue
68
Q

Management of chronic autoimmune gastritis

A
  • B12 injections

- folic acid supplements

69
Q

What are oesophageal varices?

A
  • dilated veins at sites of portosystemic anastomosis

- left gastric and inferior oesophageal veins

70
Q

Causes of oesophageal varices

A

pre-hepatic

  • portal vein thrombosis
  • portal vein obstruction

hepatic

  • cirrhosis
  • schistosomiasis

post hepatic

  • Budd Chiari
  • RHS HF
  • constructive pericarditis
  • compression
71
Q

Presentation of oesophageal varices

A
  • haematemesis and/or melena
  • epigastric discomfort
  • sudden collapse → haemodynamic instability
72
Q

Investigations for oesophageal varices

A
  1. urgent endoscopy
  2. FBC, U&E, clotting (INR) LFTs
  3. chest xray/ascitic tap
73
Q

Management of oesophageal varices

A
  • ABCDE
  • Rockall score

bleeding varices

  • terlipressin
  • prophylactic Abs → ciprofloaxcin
  • balloon tamponade
  • endoscopic banding
  • TIPS

bleeding prevention

  • beta blocker
  • endoscopic banding
  • cirrhosis = screening endoscopy
74
Q

What is a Rockall score?

A

prediction of rebleeding and mortality

75
Q

What is Barrett’s oesophagus?

A
  • metaplasia of lower oesophagus mucosa

- stratified squamous to columnar epithelium with goblet cells

76
Q

Risk factors for Barrett’s oesophagus

A
  • GORD
  • male
  • caucasian
  • family history
  • hiatus hernia
  • obesity
  • smoking
  • alcohol
77
Q

Presentation of Barrett’s oesophagus

A

classic history = middle aged caucasian male with long history GORD and dysphagia

78
Q

Investigations for Barrett’s oesophagus

A
  • oesophago-gastro-duodenoscopy

- biopsy

79
Q

Management of Barrett’s oesophagus

A
  • lifestyle changes
  • endoscopic surveillance with biopsies
  • high dose PPIs
  • dysplasia → endoscopic mucosal resection, radiofrequency ablation
  • severe = oesophagectomy
80
Q

What lifestyle changes are needed in Barrett’s oesophagus?

A
  • weight loss
  • smoking cessation
  • reduce alcohol
  • small regular meals
  • avoid hot drinks/alcohol/eating <3hrs before bed
  • avoid nitrates, anticholinergics, TCAs, NSAIDs, K+ salts, alendronate
81
Q

What is a Mallory Weiss tear?

A

haematemesis from tear in oesophageal mucosa

82
Q

Risk factors for Mallory Weiss tear

A
  • alcoholism
  • hyperemesis gravidarum
  • gastroenteritis
  • bulimia
  • chronic cough
83
Q

Presentation of Mallory Weiss tear

A
  • haematemesis
  • melena
  • symptoms of hypovolaemic shock
84
Q

Investigations for Mallory Weiss tear

A
  • Rockall score
  • FBC, U&E, coagulation studies
  • ECG, cardiac enzymes
85
Q

Management of Mallory Weiss tear

A

most resolve spontaneously

  • ABCDE
  • terlipressin and urgent endoscopy
  • Rockall score
  • inpatient observation
  • banding/clipping
  • adrenaline
  • thermocoagulation
86
Q

What is Boerhaave syndrome?

A
  • oesophageal rupture

Mackler triad

  • vomiting
  • chest pain
  • subcutaneous emphysema
87
Q

What are the two types of oesophageal cancer?

A

adenocarcinoma

  • more common in developed world
  • lower 1/3 → near GO junction

squamous

  • more common in developing world
  • upper 2/3
88
Q

Risk factors of adenocarcinoma

A
  • GORD
  • Barrett’s oesophagus
  • smoking
  • achalasia
  • obesity
89
Q

Risk factors for squamous oesophageal cancer

A
  • smoking
  • alcohol
  • achalasia
  • obesity
  • low fruit/veg/fibre/vitA,C
  • hot drinks
  • Plummer-Vinson syndrome
90
Q

Symptoms of oesophageal cancer

A
  • vomiting
  • progressive dysphagia
  • anorexia and weight loss
  • odynophagia
  • hoarseness
  • malaena
  • cough
91
Q

Typical presentation of oesophageal cancer

A

ALARMS

  • anaemia
  • loss of weight
  • anorexia
  • recent onset progressive symptoms
  • malaena/haematemesis
  • swallowing difficulties eg dysphagia
92
Q

Investigations for oesophageal cancer

A
  1. upper GI endoscopy and biopsy

- CT scan/endoscopic US → staging

93
Q

Management of oesophageal cancer

A
  • operable disease → surgical resection, adjuvant chemo

- palliation

94
Q

What are the two types of gastric cancer?

A
  1. intestinal/differentiated → more common

2. diffuse/undifferentiated

95
Q

Risk factors of intestinal gastric cancer

A
  • male
  • h.pylori
  • chronic gastritis
  • atrophic gastritis
  • older age
96
Q

Features of intestinal gastric cancer

A
  • histology → glandular
  • appearance →large, irregular
  • locations → antrum, lesser curvature
97
Q

Risk factors of diffuse gastric cancer

A
  • blood type A
  • genetic
  • younger age
98
Q

Features of diffuse gastric cancer

A

histology

  • poorly differentiated
  • signet ring cells

appearance

  • gastric linitis → submucosa invasion
  • no movement on barium swallow = progressed

location = anywhere esp cardia

99
Q

Red flags for upper GI cancer

A 
upper abdominal mass consistent with stomach cancer and:
- dysphagia of any age
- age 55+ and weight loss with:
upper abdominal pain or
reflux or
dyspepsia

2 week wait for endoscopy

100
Q

What symptoms qualify for non-urgent endoscopy?

A
  • haematemesis
  • treatment resistant dyspepsia
  • upper abdominal pain
  • anaemia
101
Q

Presentation of gastric cancer

A
  • often late presentation
  • anorexia
  • weight loss
  • anaemia
  • dysphagia
  • N&V
  • epigastric pain → better with antacids
  • paraneoplastic syndromes
  • metaplastic signs
102
Q

Investigations for gastric cancer

A
  • gastroscopy → 8-10 biopsies
  • endoscopic US → depth of invasion
  • CT/MRI/PET
103
Q

Management of gastric cancer

A
  • nutritional support → fruit/veg/folate/fibre
  • surgical resection
  • chemo
104
Q

Risk factors for colon cancer

A
  • family history
  • hereditary conditions → FAP
  • IBD
  • diet → high fat/red meat, low fibre/folate/Ca2+
  • DM
  • lifestyle
  • history of bowel/endometrial/breast/ovarian cancer
  • later first pregnancy/early menopause
105
Q

Symptoms of colon cancer

A

depends on location

  • pain
  • palpable mass
  • bleeding
  • change in bowel habit
  • weight loss
  • vomiting
  • obstruction
106
Q

Diagnosis of colon cancer

A

faecal occult blood test

  • > 50 and bowel habit change/iron deficient anaemia
  • > 60 and anaemia

colonoscopy and biopsy

flexible sigmoidoscopy/barium enema/CT colonoscopy

107
Q

Management of colon cancer

A
  • surgical resection
  • depends on site of cancer
  • normally anastomosis required
108
Q

What are the key hereditary causes of colon cancer?

A
  • familial adenomatous polyposis
  • hereditary nonpolyposis colorectal cancer
  • Lynch syndrome
109
Q

What are bowel obstructions?

A

an arrest on the onward propulsion of intestinal contents

110
Q

What are the types of bowel obstructions?

A
  • small bowel → most common
  • large bowel
  • psudeo
111
Q

Causes of SBO

A
  • adhesions → previous abdominal/pelvic surgery or previous abdominal infections
  • hernias
  • malignancy
  • Crohn’s
112
Q

Pathophysiology of SBO

A
  1. obstruction of bowel
  2. distention above blockage due to buildup of fluid and contents
  3. increased pressure → pushes on blood vessels in bowel wall
  4. vessels become compressed
  5. vessels cannot supply blood
  6. ischaemia, necrosis, perforation
113
Q

Clinical presentation of SBO

A
  • pain → initially colicky then diffuse, high in abdomen
  • profuse vomiting following pain (earlier than LBO)
  • less abdominal distention than LBO
  • tenderness = strangulation/risk of perforation
  • constipation = late in SBO
  • increased bowel sounds → tinkling
114
Q

Diagnosis of SBO

A
  1. abdominal xray → central gas shadows, distended loops, fluid levels
  • examination of hernia orifices and rectum
  • FBC

GOLD STANDARD = non-contrast CT → locates obstruction

115
Q

Management of SBO

A
  • aggressive fluid resuscitation
  • decompression of bowel
  • analgesia and anti-emetics
  • Abs
  • surgery to remove obstruction → laparotomy
116
Q

What is involved in decompression of the bowel?

A
  • IV fluids with nasogastric tube

- always try before surgery

117
Q

Causes of LBO

A
  • malignancy
  • volvulus
  • diverticulitis
  • Crohn’s
  • intussusception
118
Q

What is volvulus?

A
  • rotation/twisting of bowel on mesenteric axis

- commonly in sigmoid colon

119
Q

What is intussusception

A
  • bowel roles inside of itself

- almost only in neonates/infants → softer bowels

120
Q

Clinical presentation of LBO

A
  • abdominal pain → more constant and diffuse than SBO, lower abdomen
  • more abdominal distention than SBO
  • palpable mass eg hernia
  • vomiting → later than SBO
  • constipation → earlier than SBO
  • normal bowel sounds then louder then silent
121
Q

Diagnosis of LBO

A
  1. abdominal xray
  • FBC
  • digital rectal exam → empty rectum, hard/compacted stools, blood

GOLD STANDARD = CT

122
Q

What can be seen on an abdominal xray in LBO?

A
  • peripheral gas shadows proximal to blockage

- caecum and ascending colon distended

123
Q

Management of LBO

A

same as SBO

124
Q

What are psuedo-bowel obstructions?

A
  • identical presentation to SBO or LBO → depends on location

- entire bowel can be obstructed → both presentations

125
Q

Causes of psuedo-bowel obstructions

A
  • intra-abdominal trauma-
  • post-op states eg paralytic ileus
  • intra-abdominal sepsis
  • drugs eg opiates, antidepressants
  • electrolyte imbalances
126
Q

Treatment of pseudo-bowel obstructions

A

treat underlying cause

127
Q

What are the two types of diarrhoea?

A
  • acute → <2 weeks

- chronic → >2 weeks

128
Q

Causes of diarrhoea

A

viral → majority

  • children = rotavirus
  • adults = norovirus

bacterial

  • campylobacter jejuni
  • bloody diarrhoea
    • e.coli
    • salmonella
    • shigella

parasitic
- giardia lamblia

129
Q

Management of diarrhoea

A
  • treat underlying cause → bacterial = metronidazole
  • oral rehydration therapy
  • anti-emetics agents eg metoclopramide
  • anti-motility agents eg loperamide

self-limiting

130
Q

What are the 3 main types of ischaemic bowel disease?

A
  • acute mesenteric ischaemia → SB
  • chronic mesenteric ischaemia → SB
  • ischaemic colitis → LB
131
Q

What areas are most susceptible to ischaemia?

A

watershed areas

  • splenic flexure
  • caecum
132
Q

Causes of AMI

A
  • SMA thrombosis
  • SMA embolism due to AF
  • mesenteric vein thrombosis
  • non-occlusive disease → poor blood flow/CO
133
Q

Presentation of AMI

A

classic triad

  • acute, severe abdominal pain → constant, central
  • no abdominal signs on exam
  • rapid hypovolaemia → shock

AF and sever abdominal pain = AMI

134
Q

Diagnosis of AMI

A

blood

  • high Hb
  • metabolic acidosis

abdominal xray → rule out obstruction

laparoscopy → visualise necrosis

CT/MRI angiography → visualise blockages in arteries

135
Q

Management of AMI

A
  • fluid resuscitation
  • Abs → metronidazole, gentamicin
  • IV heparin
  • surgery → remove necrotic bowel
136
Q

Complications of AMI

A
  • sepsis

- peritonitis

137
Q

Chronic mesenteric ischaemia

A
  • very similar to AMI
  • symptoms on a lower level, persist for much longer
  • abdominal angina
138
Q

Causes of IC

A
  • thrombosis, emboli
  • low flow states → low CO, arrhythmias
  • surgery
  • vasculitis
  • coagulation disorders
  • the pill
  • idiopathic
139
Q

Presentation of IC

A
  • sudden onset LIF pain
  • passage of bright red blood
  • signs of hypovolaemic shock
140
Q

Diagnosis of IC

A
  • urgent CT → rule out perforation
  • flexible sigmoidoscopy with biopsy
  • barium enema

GOLD STANDARD = colonoscopy with biopsy

  • after recovery
  • exclude strictures at site, confirm mucosal healing
141
Q

Management of IC

A
  • most patients fine with symptomatic treatment
  • fluid replacement
  • Abs
142
Q

Gangrenous IC

A
  • peritonitis and hypovolaemic shock

- surgery

Phase 2a Resits (10 decks)

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