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Phase 2A conditions > GI conditions > Flashcards

GI conditions Flashcards

1
Q

What is crohn’s disease?

A

Inflammatory bowel disease (IBD) that can affect any part of the GI system.

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2
Q

What are characteristics of CD?

A
  • Inflammation is transmural and granulomatous (macrophages, epithelioid cells and multinucleated giant cells)
  • 50% have non caseating granulomas (no necrotic)
  • Skip lesions i.e. cobblestone appearance (ulcers and fissures)
  • Involved part is often thickened: Commonly terminal ileum or proximal colon
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3
Q

What are RF of crohn’s disease?

A

genetics, smoking, NSAIDs, family hx

chronic stress and depression can trigger flares

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4
Q

How does Crohn’s present?

A

diarrhoea with urgency, pain and bleeding; tenderness of right iliac fossa
weight loss, lethargy, anal strictures (narrowing), oral ulceration, clubbing

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5
Q

How do you test for Crohn’s and what do you expect?

A

Do a stool sample, faecal calprotectin (non specific IBD), FBC (anaemia, raised CRP+ESR, hypalbuminaemia, negative pANCA), colonoscopy + endoscopy

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6
Q

What are complications of Crohn’s?

A

perforation and bleeding, fistula formation, obstruction, colorectal cancer

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7
Q

How do you treat Crohn’s?

A

smoking cessation and treat anaemia, most require surgery at some point (resection)

  • mild: corticosteroids i.e. budesonide
  • moderate/severe: glucocorticoids i.e. prednisolone
  • severe: IV hydrocortisone + antibiotics for abscesses - no improvement give anti-TNF antibodies i.e. infliximab
  • maintain: azathioprine or methotextrate if intolerant
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8
Q

What is Coeliac’s disease?

A

Gluten sensitivity enteropathy: Inflammation of mucosa that is improved when gluten is withdrawn

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9
Q

What is the pathology of Coeliacs and which features would you see?

A
  1. Prolamin a-gliadin is resistant to complete digestion and remains in lumen and triggers inflammatory response.
  2. Passes through wall and binds to antigen presenting cells
  3. activation of gluten sensitive T-cells causing villous atrophy, crypt hyperplasia and intraepithelial lymphocytes
  4. malabsorption
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10
Q

What is the aetiology of Coeliac’s?

A

gliadin, nordeins (barley) and secalins (rye) in 1% of the population

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11
Q

What are RF for coeliac’s?

A

other autoimmune diseases, IgA deficiency, breast feeding, family hx (HLA3 DQ2 + DQ8), age of gluten introduction

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12
Q

How does Coeliac present?

A

third is asymptomatic, steatorrhea(smelly and fatty), abdominal pain, bloating, nausea and vomiting, angular stomatitis (corners of mouth)

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13
Q

How do you test for Coeliac’s?

A

Maintain gluten for at least 6weeks then test: FBC and serum antibody (endomysial AB and tissue transglutaminase AB - only works if not IgA deficient)
Gold standard: duodenal biopsy

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14
Q

How do you treat Coeliac’s?

A

lifelong GF diet, correct deficiencies

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15
Q

What are complications of Coeliac’s?

A

osteoporosis, dermatitis hepetiformis, malignancy

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16
Q

What are the two types of Oesophageal tumours and where are they found?

A
  1. Squamous cell carcinoma: in middle and upper thirds of the oesophagus
  2. Adenocarcinoma: lower third and primarily in columnar epithelium (higher chance in Barrett’s)
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17
Q

What are causes of Squamous cell in the OE?

A

increased alcohol consumption, achalasia, smoking, obesity and reduced fruit and veg consumption

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18
Q

What are the causes of Adenocarcinomas in OE?

A

smoking, GORD and obesity, previous reflux symptoms increase risk

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19
Q

How does Oesophageal cancer present?

A

often asymptomatic until advanced, initially difficulty swallowing solids then later dysphagia for liquids
weight loss, obstruction , hoarseness and cough if in upper third

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20
Q

what is an indication that the tumour is benign?

A

difficulty swallowing for solids and liquids presents at the same time

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21
Q

What is a type of benign oesophageal tumour?

A

leiomyomas (smooth muscle tumours that are slow growing within the mucus wall)

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22
Q

How do you investigate oesophageal tumours?

A

esophagoscopy and biopsy, barium swallow to see strictures and Ct scan for staging (PET for metastases)

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23
Q

How do you treat oesophageal tumours?

A

resection (best chance if stage 1) and chemo beforehand

  • metastatic: systemic chemotherapy
  • treat dysphagia with stent
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24
Q

What type of cancer is common in the gastric section?

A

Adenocarcinoma

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25
Q

What are the two types of gastric tumours?

A 
Type 1 (intestinal): well formed and differentiated glandular, sits in mucosa in distal stomach, strong environmental association, commonly with H.pylori or gastritis
Type 2 (diffuse): poorly differentiated, infiltrates in any part of the stomach, worse prognosis
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26
Q

What is the aetiology for gastric tumours?

A

smoking, pernicious anaemia, dietary factors, H.pylori (causing gastritis), genetics

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27
Q

What are RF for gastric tumours?

A

family history, smoking, high salt diet

- non-starch veg, fruit, garlic is protective

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28
Q

How do gastric tumours present?

A

Often advanced at time of presentation: epigastric pain (constant and severe), nausea, anorexia, weight loss, vomiting, palpable lymph node in supraclavicular fossa

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29
Q

How do you investigate gastric tumours?

A

gastroscopy and biopsy, endoscopic ultrasound, CT, PET

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30
Q

How do you treat gastric tumours?

A

Treat with nutritional support, surgery and ECF chemo

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31
Q

What is ECF chemo?

A

epirubicin, cisplatin, 5-fluorouracil

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32
Q

What type of cancers are intestinal tumours likely to be?

A

50% adenocarcinoma but sometimes NH lymphoma

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33
Q

What are RF for intestinal tumours?

A

crohn’s and celiac

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34
Q

How do intestinal tumours present?

A

pain, diarrhoea, anorexia, weight loss and anaemia, can have a palpable mass

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35
Q

How do you investigate intestinal tumours?

A

ultrasound, endoscopic biopsy and CT

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36
Q

How do you treat intestinal tumours?

A

resection and radiotherapy

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37
Q

How do colonic tumours arise?

A

Develops from polyps (abnormal growth of tissue from mucosa):

  1. Adenoma polyps are a precursor lesion to cancer (adenocarcinoma). Spreads through direct infiltration of the bowel wall and then to the lymphatics
  2. Benign: asymptomatic and found by chance
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38
Q

What is the aetiology of clinic tumours?

A

polyps can be inherited (familial adenomatous polyposis or lynch syndrome) or acquired

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39
Q

What are RF for colonic tumours?

A

increasing age, low fibre diet, UC, adenomas, alcohol and smoking, obesity, sugar and red meat diet
- low dose aspirin can be protective

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40
Q

what are the signs of an emergency in patients with colonic tumours?

A

signs of obstruction: absolute constipation, colicky abdominal pain, vomiting, abdominal distention

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41
Q

How does a right sided colonic tumour present?

A

usually asymptomatic until anaemia due to bleding, mass, weight loss

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42
Q

How does a left sided or sigmoid colonic tumour present?

A

change in bowel habits, blood and mucus in stool, diarrhoea (alternating with constipation)

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43
Q

How does a rectal colonic tumour present?

A

rectal bleeding and mucus, thinner stool, cramping rectal pain

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44
Q

What is Duke’s classification?

A

A: limited to muscular mucosae
B: extension through MM
C: regional lymph nodes
D: distant metastases

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45
Q

How to you investigate colonic tumours?

A

faecal occult blood (for screening) and tumour markers (not specific)

Gold standard: colonoscopy, 2nd is double contrast barium enema

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46
Q

What are differentials for colonic tumours?

A

IBD, diverticulum, haemorrhoids

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47
Q

How do you treat colonic tumours?

A

only chance of cure is surgery: hemicolectomy or laparoscopy

obstruction: endoscopting stenting
radiotherapy
chemo for Duke’s C and rectal (hard to excise so try and shrink it first)

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48
Q

What is the pathology of GORD?

A

Gastro-oesophageal reflux disease: transient relaxation of the lower oesophageal sphincter due to reduced tone.

Allows gastric acid to backflow into oesophagus
Clinical features appear when anti-reflux mechanism fail and acid makes prolonged contact with oesophageal mucosa

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49
Q

What is the aetiology of GORD?

A

LOS hypotension, hiatus hernia, loss of oesophageal peristalsis function and gastric acid hypersecretion
- delayed gastric emptying and an increase in mucosal sensitivity contribute

50
Q

What are RF for GORD?

A

abdominal obesity, slow gastric emptying, overeating, smoking, alcohol, pregnancy, drugs (CCB), systemic sclerosis

51
Q

How does GORD present?

A

2+ heartburn episodes a week (worse when bending or lying down), belching, food or acid brash, increased saliva and odynophagia (painful swallowing)
- nocturnal asthma, chronic cough, laryngitis, sinusitis

52
Q

What are differentials of GORD?

A

coronary artery disease, biliary colic, PUD, malignancy

53
Q

How do you diagnose GORD?

A

You can make a diagnosis without investigations as long as there are no red flags (over 45, dysphagia, haematemesis)

54
Q

What investigations could you order for GORD?

A 
Endoscopy: maybe hernia, assess oesophagitis (this or Barrett’s can confirm diagnosis)
Los angles classification to class extend of damage
55
Q

What are complications of GORD?

A

peptic stricture, Barrett’s oesophagus (and therefore cancer)

56
Q

How do you treat GORD?

A

Lifestyle changes
antacids (magnesium trisilicate mixture), alginates (Gaviscon), PPI (lansoprazole), H2 receptor antagonists (cimetidine)
In severe cases can do surgery to increase resting LOS pressure: Nissen fundoplication (can cause dysphagia)

57
Q

What is Barrett’s oesophagus?

A

change in oesophageal lining to resemble intestinal lining (squamous to columnar)

58
Q

What is the cause of BO?

A

LT exposure to acid

59
Q

How do you treat Barrett’s?

A

without dysplasia (no pre-cancerous cells): PPI and observe
low grade dysplasia: ablation and potentially some mucosal resection
high grade dysplasia: ablation, resection and PPI

60
Q

What is IBS?

A

Mixed group of abdominal symptoms without organic cause: problems with intestinal motility and hypersensitivity

61
Q

What are the types of IBS?

A

IBS-C (constipation)
IBS-D (diarrhoea)
IBS-M (both)

62
Q

What causes IBS?

A

psychological stress, GI infections and eating disorders

common problem in Females under 40

63
Q

What are RF for IBS?

A

female, previous severe and long diarrhoea, high hypochondrial anxiety

64
Q

How does Its present?

A

multisystem with non-intestinal symptoms i.e. painful periods, fatigue, backpain or urinary complaints

  • exacerbated by stress
  • Look out for red flags for cancer
65
Q

What do the ROME III diagnostic criteria say?

A

recurrent abdominal pain at least 3 days a month in last 3 months and 2 of:

  1. change in frequency of stool
  2. change in appearance 3. improvement with defecation
66
Q

What are differentials for IBS?

A

coeliac, lactose intolerance, IBD, cancer

67
Q

How do you treat IBS?

A

education, reassurance and dietary change
if more severe try antispasmodics for bloating and laxatives or anti-motility agents
antidepressants (amytripteline) and therapy may help

68
Q

What is Ulcerative colitis?

A

Chronic autoimmune inflammatory disorder of the colonic mucosa

69
Q

Where can UC occur?

A
  1. just the rectum (proctitis)
  2. rectum and the left colon (left sided)
  3. the entire colon (pancolitis)

!!never proximal to ileocecal valve!!

70
Q

What are characteristics of UC?

A

relapsing and remitting, circumferential and continuous lesions, limited to mucosa, depleted goblet cells and increased crypt abscesses - ulcers and pseudo-polyps

71
Q

What is the aetiology of UC?

A 
enetic aetiology (HLA-27) and potentially linked to diet 
affects 15-30 year old non smokers, incidence higher than crohns
72
Q

RF of UC?

A

family history, NSAIDs

chronic stress and depression triggers flares

73
Q

How does UC present?

A

left lower quadrant pain, diarrhoea with blood and mucus and cramps, clubbing, oral ulcers, amyloidosis, erythema nodusum

acute: can experience fever, tachycardia, tender and distended abdomen, bloody diarrhoea (10-20 day)

74
Q

How do you investigate UC and what do you expect?

A

stool sample faecal calprotectin, FBC (iron deficiency anaemia, pANCA may be positive)

Gold standard: colonoscopy (inflammatory infiltrate, mucosal ulcers and crypt abscesses)
if too severe to x-ray

75
Q

What are complications of UC?

A

blood loss, perforation, toxic dilation, cancer, arthritis, uveitis

76
Q

How do you treat UC?

A

mild: oral 5-ASA (amino salicylate) for left sided and give rectally for proctitis
severe: glucocorticoid
last resort is colectomy and ileoanal anastomosis

77
Q

What is peptic ulcer disease?

A

Damage to epithelium due to increased acid and destruction of mucin layer

Ulcer: break in superficial cells down to mucosa in stomach or duodenum

78
Q

What is the aetiology of PUD and why?

A
  1. NSAIDs (prostaglandins stimulate mucusal secretion)
  2. H.pylori (increases acidity, destruction and produces ammonium)
  3. Ischaemia (less mucin)
    other: alcohol, smoking, delayed gastric emptying
79
Q

What are RF for PUD?

A

H.pylori infection, NSAID use, smoking, increased age, history

80
Q

How does PUD present?

A

Presents with burning epigastric pain (worse when hungry and relieved by antacids), nausea, weight loss and anorexia

81
Q

What are complications of PUD?

A

massive haemorrhage after gastroduodenal rupture, pancreatitis

82
Q

Who should have invasive tests for PUD and what test is it?

A

Endoscopy in all red flags patients and patients over 55

83
Q

Who does not need invasive testing to diagnose PUD?

What are the alternatives?

A

In patients under 55 non invasive testing is enough to start treatment
serology (IgG), c-urea breath test, stool antigen

84
Q

How do you treat PUD?

A

Treat with lifestyle adjustment and potential H.pylori eradication:
PPI (lansoprazole) and 2 of clarythromycin, amoxicillin, tetracycline or bismuth
- H2 antagonists

85
Q

What is appendicitis?

A

obstruction in lumen resulting in invasion of gout organisms into appendix wall

86
Q

What is the aetiology of appendicitis?

A

faecolith, lymphoid hyperplasia, filarial worms

87
Q

What are RF for appendicitis?

A

smoking and low dietary fibre

88
Q

How does appendicitis present?

A

Presents as a surgical emergency: consider in all right sided pain, pain migrates to McBurney’s point, anorexia, nausea, vomiting, pyrexic, tender mass

89
Q

What is the gold standard for appendicitis?

A

CT

90
Q

what are differentials of appendicitis?

A

ectopic pregnancy, UTI, diverticulitis

91
Q

What are complications of PUD?

A

perforations, abscess or appendix mass

92
Q

How do you treat appendicitis?

A

removing appendix (laparoscopic appendectomy) and IV antibiotics

93
Q

What is gastroparesis?

A

Delayed gastric emptying

94
Q

What is a intestinal obstruction?

A

Blockage of onward propulsion of intestinal contents

95
Q

What are the main causes of small bowel obstruction?

A

Adhesions and hernias

96
Q

How does small bowel obstruction present?

A

pain, vomiting then constipation later, increased bowel sounds

97
Q

What is the gold standard investigation for small bowel obstruction?

A

CT

98
Q

How do you treat small bowel obstruction?

A

fluid resuscitation, analgesia and antiemetic, antibiotics, decompression

99
Q

What are common causes of large bowel obstruction?

A

(less common) malignancies

100
Q

How does large bowel obstruction present?

A

onstant abdominal pain, mass, late or no vomiting, increased then quiet bowel sounds

101
Q

How do you investigate large bowel obstruction?

A

Digital rectal exam, FBC, xray, CT

102
Q

How do you treat large bowel obstruction?

A

aggressive fluid resuscitation, bowel decompression, antibiotics, surgery

103
Q

What are the two mechanisms of bowel obstruction?

A

Mechanical: adhesion, tumour, hernia, volvulus, intersusseption, IBD, gallstones

Functional (not physical): paralytic ileum, abscess, idiopathic

104
Q

What can cause intestinal obstruction?

A

tumours, IBD, diverticulitis, Hischprung’s disease (incomplete innervation from colon to rectum), adhesions, volvulus (twist)

105
Q

What is a pseudo obstruction?

A

clinical picture minces obstruction but no mechanical cause

106
Q

How do you treat a pseudo obstruction?

A

IV neostigmine and treat underlying

107
Q

what is diverticulitis?

A 
Inflamed diverticula (bulging pouches in lining of GI system)
increased intraluminal pressure leading to erosion and inflammation, potentially causing perforation
108
Q

What is diverticulosis?

A

development of diverticula (due to abnormal motility leading to high pressure)

109
Q

How does diverticulitis present?

A

LLQ pain (sigmoid), palpable mass, diarrhoea and constipation, nausea, fever

110
Q

How do you investigate diverticulitis?

A

CT with contrast and X ray

111
Q

What are complications of diverticulitis?

A

stricture, abscess, fistula formation

112
Q

How do you treat diverticulitis?

A

antibiotics and nil by mouth

severe cases may need resection

113
Q

What is gastritis?

A

Inflammation of the stomach lining

114
Q

What are the two types of gastritis and what are their causes?

A

Acute: NSAIDS, H pylori, alcohol and stress

Atrophic (chronic): mainly infections (80%, H pylori, ulcers) or autoimune (autoimmunity against parietal cells, adenocarcinoma)

115
Q

How does gastritis present?

A

Can be asymptomatic: epigastric pain, nausea, vomiting, ulcers
autoimmune can also present with iron deficiency and pernicious anaemia

116
Q

How do you investigate gastritis?

A

Endoscopy with biopsy
H pylori detection (c-urea breath test, IgG and stool antigen)
Anti IF antibodies

117
Q

How do you treat Gastritis?

A

removing cause i.e. stop NSAIDs or eradicate H pylori

118
Q

What is Mallory Weiss syndrome?

A

bleeding from a laceration in the mucosa at the junction of stomach and oesophagus

119
Q

What is a Mallory Weiss tear?

A

Laceration in mallory Weiss syndrome

120
Q

What causes a Mallory Weiss tear?

A

severe vomiting: mainly alcoholism or bulimia but can be any cause of vomiting

121
Q

How do you treat a Mallory Weiss Tear?

A

Can significantly heal within 48 hours

- Treat with acid suppression (PPI) and antiemetics

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