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Hamzah's GI pathology > Hamzah's GI pathology > Flashcards

Hamzah's GI pathology Flashcards

1
Q

What is Crohn’s disease?

A

Chronic idiopathic inflammatory bowel disease characterised by transmural granulomatous inflammation`

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2
Q

Aetiology of Crohn’s disease

A

Unknown
CARD15 possible gene mutation
smoking increases risk
host immune response

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3
Q

Risk factors for Crohn’s disease

A

FH, smoking

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4
Q

Macroscopic pathology of Crohn’s disease

A
  • affects any part of GI tract
  • skip lesions - discontinuous GI involvement
  • Deep ulcers and fissures in mucosa – cobblestone appearance
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5
Q

Microscopic pathology of Crohn’s

A
  • Transmural inflammation – spans full depth of intestinal wall
  • Granulomas present in 50%
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6
Q

Epidemiology of Crohn’s

A
  • Usually presents in teenagers and people in their 20s

- 40 IBD patients / 100,000 patients (UK)

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7
Q

Symptoms of Crohn’s

A

Urgent diarrhoea, abdominal pain, weight loss, fever, malaise, anorexia

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8
Q

Signs of Crohn’s

A 
o	Abdominal tenderness/mass
o	Perianal skin tags/abscesses/fistulas
o	Aphthous ulcerations 
o	Clubbing
o	Skin, joint and eye problems
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9
Q

Complications of Crohn’s

A

Small bowel obstruction, fistulae, abscess formation, perforation, fatty liver, colon cancer, renal stones, malnutrition

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10
Q

Differential diagnosis of Crohn’s

A

UC, TB, carcinoid, amyloidosis, infective diarrhoea, IBS

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11
Q

Diagnostic tests for Crohn’s

A
  • Blood = FBC, ESR, CRP, U&es, LFT, INR, ferratin
  • Stool = MC&S to exclude C. diff, E. coli
  • Colonoscopy and rectal biopsy
  • Small bowel enema = identifies ileal disease
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12
Q

Treatment of mild attacks in Crohn’s

A

oral prednisolone, review in clinic (lower dose every few weeks if symptoms are improving)

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13
Q

Treatment of severe attacks in Crohn’s

A
  • IV steroids –> hydrocortisone
  • Treat rectal disease –> steroids
  • Metronidazole
  • blood transfusion
  • TNF-alpha inhibitors - infliximab can decrease disease activity
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14
Q

Treatment of perianal disorders

A
  • oral abx
  • immunosuppressants and infliximab
  • local surgery
    immunosuppressant - azathioprine
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15
Q

Surgery in Crohn’s

A

NOT CURATIVE

temporary ileostomy, resection of part of normal bowel

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16
Q

Why is bypass and patch surgery not done in Crohn’s?

A

widespread disease –> high risk of recurrence

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17
Q

What is UC?

A

A relapsing and remitting inflammatory bowel disease that is restricted to the large bowel mucosa.

Always involves the rectum and extends proximally

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18
Q

UC just rectum

A

proctitis

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19
Q

UC with left colon

A

left-sided colitis

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20
Q

UC entire colone

A

pancolitis

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21
Q

What does UC never pass?

A

ileo-cecal valve

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22
Q

Aetiology of UC

A
  • unknown

- abnormal mucosal response to luminal bacteria

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23
Q

Is smoking protective in UC

A

YES

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24
Q

Epidemiology of UC

A
  • Most cases present in individuals between the ages 15-30

- 3x as common in non-smokers

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25
Q

Risk factors for UC

A

history, ethnicity (White and Ashkenazi Jews)

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26
Q

Pathophysiology of UC

A
  • Pseudo polyps and hyperaemic/haemorrhagic granular colonic mucosa formed by inflammation
  • Punctate ulcers may extend deep into lamina propria
  • Different from Crohn’s disease as it is not a transmural disease. (UC=mucosal disease)
  • No skip lesions
  • Red mucosa – bleeds easily
  • No granulomata
  • Goblet cell depletion
  • Crypt abscesses
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27
Q

Symptoms of UC

A

o Episodic/chronic diarrhoea with blood/mucus
o Crampy abdominal discomfort
o Bowel frequency relates to severity (>6 motions = severe)
o Urgency/tenesmus = proctitis
o Systemic symptoms in attacks = fever, malaise, anorexia, weight loss

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28
Q

Signs of UC

A

o May be none
o Acute severe UC = fever, tachycardia, distended abdomen
o Extraintestinal signs = clubbing, aphthous oral ulcers, joint arthritis, fatty liver, amyloidosis

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29
Q

Differential diagnosis of UC

A

Crohn’s, laxative abuse, infective colitis, colonic polyps

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30
Q

DT for UC

A

Blood - FBC, U&E, ESR, CRP, LFT
Stool - MC&S (C. diff)
AXR - mucosal thickening, colonic dilatation
Erect CXR - perforation
Colonoscopy - allows biopsy - mucosal ulcers, crypt abscesses, goblet cell depletion

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31
Q

Complications of UC

A
  • perforation and bleeding
  • toxic megacolon venous thrombosis
  • colonic cancer
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32
Q

What is the goal for treatment in UC?

A

induce and maintain remission

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33
Q

Treatment of mild UC

A
  • mild = less than 4 stools per day
  • 5-aminosalicylic acid
  • steroids - prednisolone (PR)
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34
Q

Treatment of moderate UC

A
  • moderate = 4-6 stools per day

- oral prednisolone and 5-aminosalicylic acid and twice daily steroid enemas

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35
Q

Treatment of severe UC

A
  • severe = more than 6 motions per day
  • hospital admission - nil by mouth, IV hydration
  • IV hydrocortisone
  • rectal steroids
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36
Q

What do you give when there is improvement in UC?

A

5-aminosalicylic acid and prednisolone

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37
Q

What do you give when there is no improvement in UC?

A

colectomy

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38
Q

Surgery in UC

A
  • proctocolectomy and terminal ileostomy

- colectomy with ileo-anal pouch

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39
Q

Drug for maintaining remission of UC for life

A

5ASA for life

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40
Q

What is IBS

A

a mixed group of abdominal symptoms for which no organic cause can be found

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41
Q

Aetiology of IBS

A

F:M = 2:1

Age at onset = <40 days

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42
Q

Diagnosis of IBS requires

A
  • pain/discomfort relieved by defecation
  • altered stool form/bowel frequency
  • urgency, incomplete defecation, abdominal bloating distension, mucus PR, worsening of symptoms after food
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43
Q

Other symptoms of IBS

A

nausea, bladder symptoms, back ache

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44
Q

What exacerbates IBS?

A

stress, menstruation, gastroenteritis

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45
Q

Signs of IBS

A

general abdominal tenderness / normal examination

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46
Q

Differential diagnosis of IBS

A

colon cancer, IBD, coeliac disease, gastroenteritis

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47
Q

Diagnostic tests for IBS

A
  • FBC, CRP, ESR, U&Es
  • Coeliac screen
  • Serum CA-125 to exclude ovarian cancer
  • Faecal calprotectin = marker of bowel inflammation, raised in IBD
  • Colonoscopy if over 60 and any marker of organic disease
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48
Q

Treatment of IBS

A
  • Healthy diet - fibre, lactose, fructose, fizzy drinks, caffeine
  • constipation - lactulose
  • diarrhoea - loperamide
  • for bloating - oral antispasmodics - mebeverine
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49
Q

What is coeliac disease?

A

An autoimmune disorder caused by an abnormal immune response to dietary gluten

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50
Q

What happens to the mucosa of the duodenum and jejunum in coeliac disease?

A

villous atrophy and malabsorption

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51
Q

What is gluten found in?

A

wheat, rye and barley

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52
Q

What triggers the immune response in coeliac disease?

A

Gliadin

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53
Q

Pathogenesis of coeliac disease

A
  • Associated with HLA class 2 molecules DQ2 (95% of cases) and DQ8
    o Alpha-gliadin peptide is the toxic portion of gluten
    o Alpha-gliadin is resistant to proteases in the small intestine lumen
    o It passes through the cell membrane by binding to transferrin receptors on enterocytes
    o Its deaminated by tissue transglutaminases and becomes negatively charged
    o This then binds to APCs in the lamina propria via HLA-Dq2
    o This activates gluten-sensitive T cells
    o Inflammatory cascade and mediator release leads to VILLOUS ATROPHY and CRYPT HYPERPLASIA
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54
Q

Epidemiology of coeliac disease

A
  • common in Irish

- peaks in infancy and 50-60 year olds

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55
Q

Symptoms of coeliac disease

A

50% = asymptomatic
children = failure to thrive, bloating, diarrheoa
o Diarrhoea, steatorrhea, abdominal pain, bloating, nausea/vomiting, weight loss, fatigue

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56
Q

Signs of coeliac disease

A
  • Dermatitis herpetiformis, osteomalacia, aphthous ulcers, angular stomatitis
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57
Q

Differential diagnosis of coeliac disease

A

IBD, IBS, lactose intolerance

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58
Q

Diagnostic tests for coeliac disease

A
  • Bloods – FBC, low Hb, mild anaemia, iron deficiency, folate deficiency (folate is absorbed in the ileum bound to intrinsic factor which is released by parietal cells)
  • IgA anti-transglutaminase (tTG) antibodies = highly sensitive
  • IgA endomysial (EMA) antibodies = less sensitive
  • Duodenal biopsy –> crypt hyperplasia, villous atrophy, inflammatory cells in lamina propria
  • DEXA scan
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59
Q

Treatment of coeliac disease

A

lifelong gluten free diet

  • eat rice, potatoes and oats
  • can be prescribed gluten free food
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60
Q

Complications of coeliac disease

A
  • Anaemia
  • Dermatitis herpetiformis
  • Osteoporosis
  • Increased risk of malignancy
  • Secondary lactose intolerance
  • Hyposplenism
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61
Q

What is GORD?

A

reflux of stomach contents causing symptoms

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62
Q

What can prolonged reflux cause?

A
  • oesophagitis
  • benign oesophageal strictures
  • Barrett’s oesophagus
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63
Q

Aetiology of GORD

A

LOS hypotension, hiatus hernia, loss of oesophageal peristaltic function, obesity, HCl hypersecretion

64
Q

Risk factors for GORD

A

Overeating, smoking, alcohol, pregnancy, surgery in achalasia, drugs – CCBs, BBs, tricyclic antidepressants=amitriptyline, H. pylori? (eradication may help symptoms)

65
Q

Pathophysiology of GORD

A
  • LOS tone is reduced and there are frequent transient LOS relaxations
  • Increased mucosal sensitivity to gastric acid
  • Reduced oesophageal clearance of acid
  • Delayed gastric emptying and prolonged post-prandial and nocturnal reflux also contribute
66
Q

Oesophageal presentation of GORD

A

o Heartburn –> burning, retrosternal discomfort after meals, lying down or straining, relieved by antacids
o Belching
o Acid brash – acid/bile regurgitation
o Water brash – massively increased salivation –> mouth fills with saliva
o Odynophagia (pain when swallowing)

67
Q

Extra-oesophageal presentation of GORD

A

o Nocturnal asthma
o Chronic cough
o Laryngitis – hoarseness, throat clearing
o Sinusitis

68
Q

Complications of GORD

A

oesophagitis, ulcers, benign stricture, iron deficiency, metaplasia (oesophageal cancer)

69
Q

Differential diagnosis of GORD

A

-Cardiac disease, sphincter of Oddi malfunction, duodenal/gastric ulcers or cancers, oesophageal spasm, oesophagitis from NSAIDs, herpes, Candida

70
Q

Diagnostic tests for GORD

A
  • Endoscopy if >55 with alarm symptoms (weight loss, anaemia, haematemesis)
  • Barium swallow –> may show hiatus hernia
  • 24hr oesophageal monitoring and oesophgeal manometry (motility study)
71
Q

Lifestyle treatment in GORD

A

weight loss, avoid excess alcohol, hot drinks and spicy food, smoking cessation, small regular meals, raise bed head

72
Q

Drug treatment in GORD

A
  • Antacids - sodium bicarbonate
  • Alginates - Gaviscon
  • PPIs- lansoprazole
  • H2 receptor antagonists - ranitidine
73
Q

Surgery in GORD

A

laparoscopic Nissen fundoplication - fundus is wrapped around lower oesophagus - increases resting LOS pressure

74
Q

What is an ulcer?

A

a breach in the mucosal surface

75
Q

where can peptic ulcers occur?

A

oesophagus, stomach or proximal duodenum

76
Q

What cells are in the fundus and gastric body?

A

parietal and chief cells

77
Q

What cells are predominantly found at the gastric antrum?

A

G cells - release gastrin when food enters the stomach

78
Q

Where are Brunner glands found?

A

duodenum - secrete mucus

79
Q

Aetiology of peptic ulcers

A
  • H. pylori infection
  • NSAIDs
  • Zollinger-Ellsion syndrome
80
Q

How does H. pylori cause peptic ulcers?

A

colonises gastric mucosa

  • releases adhesions - proteases –> damage mucosal wall
  • damage starts in gastric antrum
81
Q

How do NSAIDs cause peptic ulcers?

A
  • inhibit cyclooxygenase (helps synthesis inflammatory prostaglandins)
  • gastric mucosa becomes susceptible to damage
82
Q

How does Zollinger-Ellison syndrome cause peptic ulcers?

A
  • gastrinoma

- Neuroendocrine tumour which secretes abnormal amounts of gastrin –> excess HCl production

83
Q

Risk factors for duodenal ulcers

A

H. pylori, drugs (NSAIDs, steroids, SSRIs), smoking

84
Q

Risk factors for gastric ulcers

A

H. pylori, smoking, NSAIDs

85
Q

Where do gastric ulcers typically occur?

A

lesser curvature of the stomach

86
Q

Where do duodenal ulcers typically occur?

A

just after the pyloric sphincter and Brunner gland hypertrophy is present

87
Q

Clinical presentation of peptic ulcers

A
  • Gastric ulcer - pain increases when eating –> weight loss
  • Duodenal ulcer - pain decreases when eating –> weight gain
  • epigastric pain often relieved by antacids
  • bloating
  • fullness after meals
  • heartburn - retrosternal pain and reflux
  • tender epigastrium
88
Q

ALARM symptoms

A 
Anaemia (iron deficiency)
weight loss
anorexia
progressive symptoms
haematemesis
swallowing difficulty
89
Q

Differential diagnosis of dyspepsia (indigestion)

A

GORD, gastric malignancy, duodenitis, gastritis

90
Q

Diagnostic tests for peptic ulcers

A
  • <55 –> non-invasive H. pylori tests = 13C-urea breath test, stool antigen test
  • Upper GI endoscopy and biopsy (centre and edge of ulcer to establish if benign or malignant)
  • barium meal –> detect gastric outlet obstruction
91
Q

H. pylori positive treatment of peptic ulcers

A

clarithromycin, amoxicillin and PPI

- Eradication confirmed with stool test/breath sample

92
Q

H. pylori negative treatment of peptic ulcers

A

stop NSAIDs, steroids

Treat with PPIs

93
Q

Complications of peptic ulcers

A
  • bleeding - can erode into left gastric artery or gastroduodenal artery
  • perforation - duodenal ulcers can perforate and lead to air under diaphragm –> referred pain at right shoulder
  • gastric outflow obstruction - duodenal ulcers near pyloric sphincter can cause scarring and obstruction of gastric emptying
  • malignancy
94
Q

What is appendicitis?

A

inflammation of the appendix

95
Q

What is the highest incidence of appendicitis?

A

between 10-20 year olds - most common GI surgical emergency

96
Q

Aetiology of appendicitis

A
  • Faecolith - stone made of faeces
  • lymphoid hyperplasia
  • filarial worms
97
Q

Risk factors for appendicitis

A

FH, more common in males

98
Q

Differential diagnosis of appendicitis

A

UTI, cystitis, Crohn’s disease, perforated ulcer, diverticulitis, cholecystitis

99
Q

Pathogenesis of appendicitis

A
  • Gut microorganisms (E. coli) invade the appendix wall after lumen obstruction
  • Appendix keeps secreting mucus –> increases the psi within the appendix and it enlarges and irritates visceral nerve fibres and blood vessels, This leads to ischaemia of the appendix wall and the appendix can no longer secrete mucus –> microorganisms can now invade the appendix wall
100
Q

Clinical presentation of appendicitis

A
  • Periumbilical pain that moves to right iliac fossa
  • Anorexia
  • Constipation (but diarrhoea can occur)
  • General signs = tachycardia, fever, furred tongue, coughing hurts, foetor and flushing, shallow breathing
  • RIF signs = guarding, rebound and percussion tenderness, PR painful on right
101
Q

Diagnostic tests for appendicitis

A
  • Rovsing’s sign = pain greater in RIF than LIF when LIF is pressed
  • Psoas sign = pain on extending hip
  • Cope sign = pain on flexion and internal rotation of right hip
  • Blood tests = neutrophil leucocytosis, elevated CRP
  • Appendix is not always visualised with US
  • CT
102
Q

Treatment of appendicitis

A
  • prompt appendectomy
  • antibiotics - piperacillin and tazobactam
  • laparoscopy can be used (high xp surgeon needed)
103
Q

complications of appendicitis

A
  • perforation
  • appendix mass
  • appendix abscess –> drain
104
Q

M:F ratio of oesophageal cancer

A

5:1

105
Q

Risk factors for oesophageal cancer

A

Diet, excess alcohol, smoking, achalasia, obesity, low vitamin A and vitamin C, nitrosamine exposure, reflux oesophagitis

106
Q

Sites of oesophageal cancer

A
  • 20% = upper part
  • 50% = middle
  • 30% = lower
  • May be squamous cell (proximal) or adenocarcinomas (distal)
107
Q

Clinical presentation of oesophageal cancer

A
  • Dysphagia –> progressive (initially solids, then liquids)
  • Weight loss
  • Retrosternal chest pain
  • Upper 1/3 of oesophagus = hoarseness and cough
108
Q

Differential diagnosis of oesophageal cancer

A

Oesophagitis, diffuse oesophageal spasm, achalasia, benign oesophageal stricture

109
Q

DT for oesophageal cancer

A
  • Oesophagoscopy with biopsy (and endoscopic ultrasound)

- CT/MRI for staging

110
Q

TNM staging system

A
  • TNM system = tumour, node, metastasis
  • 1-4 system =
    o 1 = cancer is small
    o Tumour is growing but hasn’t spread to surrounding tissues
    o Cancer may have spread to lymph nodes
    o Metastases
  • T1 = invading lamina propria/submucosa
  • T2 = invading muscularis propria
  • T3 = invading adventitia
  • T4 = invasion of adjacent structures
  • N0 = no nodal spread
  • N1 = regional node metastases
  • M0 = no distant spread
  • M1 = distal metastases
111
Q

Oesophageal cancer treatment

A
  • Poor survival rate
  • Localised T1/T2 disease = radical curative oesophagestomy
  • Pre-op chemo = cisplatin
  • Chemotherapy
  • Palliation aims to restore swallowing with chemoradiotherapy, stenting and laser use
112
Q

M:F ratio for stomach cancer

A

2:1

113
Q

stomach cancer associations

A

Pernicious anaemia, blood group A, H. pylori, atrophic gastritis, lower social class, smoking, nitrosamine exposure

114
Q

Pathology of gastric cancer

A
  • tumours mostly occur in gastric antrum
  • Almost always adenocarcinomas
  • Borrmann classification =
    o Polyploid
    o Excavating
    o Ulcerating and raised
    o Diffusely infiltrative
  • Some are confined to mucosa and submucosa – ‘early’ gastric carcinoma
115
Q

Symptoms of gastric cancer

A

often non-specific, indigestions (dyspepsia), weight loss, vomiting, dysphagia

116
Q

Signs suggesting incurable gastric cancer

A

Epigastric mass, hepatomegaly, jaundice, ascites, large left supraclavicular (Virchow’s) node, Acanthosis nigricans (black hyperpigmentation of skin usually on folds)

117
Q

Gastric cancer spread

A

local, lymphatic, blood-borne, trans-coelemic

118
Q

Diagnostic tests in gastric cancer

A
  • Gastroscopy and multiple ulcer edge biopsies
  • Endoscopic ultrasound
  • CT/MRI for staging
119
Q

Treatment of gastric cancer

A
  • Partial gastrectomy for distal tumours
  • Total gastrectomy if more proximal
  • Combination chemo – Epirubicin, cisplatin, 5-fluorouracil
  • Surgical palliation –> for obstruction, pain or haemorrhage - 5yr survival = <10% overall
120
Q

Small intestine tumours

A

rare - present with abdominal pain, diarrhoea, anorexia and anaemia

121
Q

Treatment of malignant small bowel tumours

A

surgical excision or chemo/radiotherapy

122
Q

What is a colorectal polyp?

A

overgrowth of epithelial cells - project into GI lumen. Normally asymptomatic but some can become malignant

123
Q

Adenomatous polyp

A

most common colon polyp

Forms due to mutation in APC gene (tumour suppressor gene)

124
Q

Histological classification of polyps

A
  • tubular

- villous –> become malignant

125
Q

Pedunculated and sessile classification of polyps

A
  • pedunculated = attached to colon by stalk

- sessile = firmly attached to colon –> become malignant

126
Q

Risk factors for colon polyps

A
  • genetic conditions (familial adenomatous polyposis FAP)
  • injury to bowel wall - smoking, IBD
  • old age
127
Q

Complications of polyps

A
  • polyp ulceration –> rectal bleeding –> anaemia

- bowel obstruction –> abdominal pain and constipation

128
Q

Diagnosis of polyps

A

endoscopy and biopsy

129
Q

Treatment of polyps

A

polypectomy

130
Q

What is CRC?

A

most common cancer of GI tract.

most CRCs = adenocarcinomas

131
Q

Aetiology of CRC

A
  • most are due to sporadic mutations

- some are due to known mutations - polyps

132
Q

Risk factors for CRC

A
  • non-modifiable = old age, IBD

- modifiable = smoking, low fibre diet, eating lots of red meat, obesity, high alcohol intake

133
Q

Distribution of CRC

A
  • 27% = rectum
  • 20% = sigmoid colon
  • 14% = caecum
134
Q

CP of CRC in descending colon

A
  • infiltrating masses - ring shaped –> transmural –> bowel obstruction
  • altered bowel habit or obstruction
  • PR mass, tenesmus
135
Q

CP of CRC in ascending colon

A
  • grow outwards –> vague abdominal pain and weight loss

- can ulcerate and bleed –> iron deficiency

136
Q

Urgent referral criteria in CRC

A
  • Over 40 with PR bleeding and bowel habit change
  • Any age with right lower abdominal pain
  • Palpable rectal mass
  • Men/non-menstruating women with unexplained iron deficiency anaemia
137
Q

Diagnostic tests in CRC

A

Diagnostic tests

  • FBC – microcytic anaemia
  • Faecal occult blood – used for UK screening programme
  • Sigmoidoscopy
  • Barium enema or colonoscopy or CT
  • Liver US/MRI
  • DNA test if family history of FAP
138
Q

Spread of CRC

A
  • local
  • lymphatic
  • blood (liver, lung, bone)
  • trans-coelomic
139
Q

Dukes’ criteria

A

o A = limited to muscularis mucosae (93%)
o B = extension through muscularis mucosae (77%)
o C = involvement of regional lymph nodes (48%)
o D = distant metastases (6.6%)

140
Q

Treatment of CRC

A
  • Depends on stage
    o Early –> surgical resection
    o Lymph node involvement –> chemotherapy
    o Metastatic –> incurable – palliation = radiotherapy
141
Q

What is a diverticulum?

A

A diverticulum is an outpouching of colonic mucosa that has herniated through the circular muscular layer of the large bowel at weak sites = entry of perforating arteries

142
Q

Difference between a diverticula and diverticulosis

A
  • Diverticula = multiple outpouchings

- Diverticulosis = many diverticula are present with no symptoms

143
Q

Types of diverticulum

A
  • True = congenital –> all layers of colonic mucosa are involved in the outpouching
  • False = acquired –> only mucosa and submucosa is involved
144
Q

Risk factors for diverticulum

A

age, male gender, obesity, corticosteroids, exercise, NSAIDs, smoking

145
Q

Aetiology of diverticulum

A

a diet low in fibre and high in meat is the strongest risk factor

146
Q

Pathophysiology of diverticulum

A
  • Most occur at sigmoid colon
  • Firm stools require higher intraluminal pressures to propel them through the colon
  • High intraluminal pressures force pouches of colonic mucosa to herniate through the muscle layers at weak points adjacent to penetrating blood vessels
147
Q

Clinical presentation of diverticulum

A
  • Most are asymptomatic
  • Symptoms result from luminal narrowing –> pain and constipation
  • Bleeding
148
Q

Diagnostic tests for diverticulum

A
  • Common incidental finding at colonoscopy
  • Barium enema
  • CT – best way to confirm acute diverticulitis
149
Q

Complications of diverticulum

A
  • altered bowel habit with left-sided colic relieved by defecation
  • nausea and flatulence
150
Q

Treatment of diverticula

A
  • high fibre diet

- anti-spasmodics - mebeverine

151
Q

What is diverticulitis?

A

inflammation of the diverticula - occurs when faeces obstruc the neck of the diverticulum

152
Q

CP of diverticulitis

A 
LIF pain
fever
nausea
pyrexia
raised WCC
tender colon
localised/generalised peritonitis
153
Q

DT for diverticulitis

A

barium enema, CT,

FBC - raised CRP/ESR

154
Q

Treatment of diverticulitis

A
  • analgesia, nil by mouth, IV fluids, CT-guided percutaneous drainage (if abscess)
  • surgical - colectomy (indicated in perforation and fistula)
155
Q

Complications of diverticulitis

A
  • perforation –> abscess formation or peritonitis
  • fistula formation into bladder or vagina
  • intestinal obstruction

Hamzah's GI pathology (2 decks)

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