GI conditions Flashcards
1
Q
What is crohn’s disease?
A
Inflammatory bowel disease (IBD) that can affect any part of the GI system.
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
3
Q
What are RF of crohn’s disease?
A
genetics, smoking, NSAIDs, family hx
chronic stress and depression can trigger flares
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
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
6
Q
What are complications of Crohn’s?
A
perforation and bleeding, fistula formation, obstruction, colorectal cancer
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
8
Q
What is Coeliac’s disease?
A
Gluten sensitivity enteropathy: Inflammation of mucosa that is improved when gluten is withdrawn
9
Q
What is the pathology of Coeliacs and which features would you see?
A
- Prolamin a-gliadin is resistant to complete digestion and remains in lumen and triggers inflammatory response.
- Passes through wall and binds to antigen presenting cells
- activation of gluten sensitive T-cells causing villous atrophy, crypt hyperplasia and intraepithelial lymphocytes
- malabsorption
10
Q
What is the aetiology of Coeliac’s?
A
gliadin, nordeins (barley) and secalins (rye) in 1% of the population
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
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)
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
14
Q
How do you treat Coeliac’s?
A
lifelong GF diet, correct deficiencies
15
Q
What are complications of Coeliac’s?
A
osteoporosis, dermatitis hepetiformis, malignancy
16
Q
What are the two types of Oesophageal tumours and where are they found?
A
- Squamous cell carcinoma: in middle and upper thirds of the oesophagus
- Adenocarcinoma: lower third and primarily in columnar epithelium (higher chance in Barrett’s)
17
Q
What are causes of Squamous cell in the OE?
A
increased alcohol consumption, achalasia, smoking, obesity and reduced fruit and veg consumption
18
Q
What are the causes of Adenocarcinomas in OE?
A
smoking, GORD and obesity, previous reflux symptoms increase risk
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
20
Q
what is an indication that the tumour is benign?
A
difficulty swallowing for solids and liquids presents at the same time
21
Q
What is a type of benign oesophageal tumour?
A
leiomyomas (smooth muscle tumours that are slow growing within the mucus wall)
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)
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
24
Q
What type of cancer is common in the gastric section?
A
Adenocarcinoma
25
What are the two types of gastric tumours?
```
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
```
26
What is the aetiology for gastric tumours?
smoking, pernicious anaemia, dietary factors, H.pylori (causing gastritis), genetics
27
What are RF for gastric tumours?
family history, smoking, high salt diet
| - non-starch veg, fruit, garlic is protective
28
How do gastric tumours present?
Often advanced at time of presentation: epigastric pain (constant and severe), nausea, anorexia, weight loss, vomiting, palpable lymph node in supraclavicular fossa
29
How do you investigate gastric tumours?
gastroscopy and biopsy, endoscopic ultrasound, CT, PET
30
How do you treat gastric tumours?
Treat with nutritional support, surgery and ECF chemo
31
What is ECF chemo?
epirubicin, cisplatin, 5-fluorouracil
32
What type of cancers are intestinal tumours likely to be?
50% adenocarcinoma but sometimes NH lymphoma
33
What are RF for intestinal tumours?
crohn’s and celiac
34
How do intestinal tumours present?
pain, diarrhoea, anorexia, weight loss and anaemia, can have a palpable mass
35
How do you investigate intestinal tumours?
ultrasound, endoscopic biopsy and CT
36
How do you treat intestinal tumours?
resection and radiotherapy
37
How do colonic tumours arise?
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
38
What is the aetiology of clinic tumours?
polyps can be inherited (familial adenomatous polyposis or lynch syndrome) or acquired
39
What are RF for colonic tumours?
increasing age, low fibre diet, UC, adenomas, alcohol and smoking, obesity, sugar and red meat diet
- low dose aspirin can be protective
40
what are the signs of an emergency in patients with colonic tumours?
signs of obstruction: absolute constipation, colicky abdominal pain, vomiting, abdominal distention
41
How does a right sided colonic tumour present?
usually asymptomatic until anaemia due to bleding, mass, weight loss
42
How does a left sided or sigmoid colonic tumour present?
change in bowel habits, blood and mucus in stool, diarrhoea (alternating with constipation)
43
How does a rectal colonic tumour present?
rectal bleeding and mucus, thinner stool, cramping rectal pain
44
What is Duke's classification?
A: limited to muscular mucosae
B: extension through MM
C: regional lymph nodes
D: distant metastases
45
How to you investigate colonic tumours?
faecal occult blood (for screening) and tumour markers (not specific)
Gold standard: colonoscopy, 2nd is double contrast barium enema
46
What are differentials for colonic tumours?
IBD, diverticulum, haemorrhoids
47
How do you treat colonic tumours?
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)
48
What is the pathology of GORD?
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
49
What is the aetiology of GORD?
LOS hypotension, hiatus hernia, loss of oesophageal peristalsis function and gastric acid hypersecretion
- delayed gastric emptying and an increase in mucosal sensitivity contribute
50
What are RF for GORD?
abdominal obesity, slow gastric emptying, overeating, smoking, alcohol, pregnancy, drugs (CCB), systemic sclerosis
51
How does GORD present?
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
What are differentials of GORD?
coronary artery disease, biliary colic, PUD, malignancy
53
How do you diagnose GORD?
You can make a diagnosis without investigations as long as there are no red flags (over 45, dysphagia, haematemesis)
54
What investigations could you order for GORD?
```
Endoscopy: maybe hernia, assess oesophagitis (this or Barrett’s can confirm diagnosis)
Los angles classification to class extend of damage
```
55
What are complications of GORD?
peptic stricture, Barrett’s oesophagus (and therefore cancer)
56
How do you treat GORD?
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
What is Barrett's oesophagus?
change in oesophageal lining to resemble intestinal lining (squamous to columnar)
58
What is the cause of BO?
LT exposure to acid
59
How do you treat Barrett's?
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
What is IBS?
Mixed group of abdominal symptoms without organic cause: problems with intestinal motility and hypersensitivity
61
What are the types of IBS?
IBS-C (constipation)
IBS-D (diarrhoea)
IBS-M (both)
62
What causes IBS?
psychological stress, GI infections and eating disorders
| common problem in Females under 40
63
What are RF for IBS?
female, previous severe and long diarrhoea, high hypochondrial anxiety
64
How does Its present?
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
What do the ROME III diagnostic criteria say?
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
What are differentials for IBS?
coeliac, lactose intolerance, IBD, cancer
67
How do you treat IBS?
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
What is Ulcerative colitis?
Chronic autoimmune inflammatory disorder of the colonic mucosa
69
Where can UC occur?
1. just the rectum (proctitis)
2. rectum and the left colon (left sided)
3. the entire colon (pancolitis)
!!never proximal to ileocecal valve!!
70
What are characteristics of UC?
relapsing and remitting, circumferential and continuous lesions, limited to mucosa, depleted goblet cells and increased crypt abscesses - ulcers and pseudo-polyps
71
What is the aetiology of UC?
```
enetic aetiology (HLA-27) and potentially linked to diet
affects 15-30 year old non smokers, incidence higher than crohns
```
72
RF of UC?
family history, NSAIDs
| chronic stress and depression triggers flares
73
How does UC present?
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
How do you investigate UC and what do you expect?
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
What are complications of UC?
blood loss, perforation, toxic dilation, cancer, arthritis, uveitis
76
How do you treat UC?
mild: oral 5-ASA (amino salicylate) for left sided and give rectally for proctitis
severe: glucocorticoid
last resort is colectomy and ileoanal anastomosis
77
What is peptic ulcer disease?
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
What is the aetiology of PUD and why?
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
What are RF for PUD?
H.pylori infection, NSAID use, smoking, increased age, history
80
How does PUD present?
Presents with burning epigastric pain (worse when hungry and relieved by antacids), nausea, weight loss and anorexia
81
What are complications of PUD?
massive haemorrhage after gastroduodenal rupture, pancreatitis
82
Who should have invasive tests for PUD and what test is it?
Endoscopy in all red flags patients and patients over 55
83
Who does not need invasive testing to diagnose PUD?
| What are the alternatives?
In patients under 55 non invasive testing is enough to start treatment
serology (IgG), c-urea breath test, stool antigen
84
How do you treat PUD?
Treat with lifestyle adjustment and potential H.pylori eradication:
PPI (lansoprazole) and 2 of clarythromycin, amoxicillin, tetracycline or bismuth
- H2 antagonists
85
What is appendicitis?
obstruction in lumen resulting in invasion of gout organisms into appendix wall
86
What is the aetiology of appendicitis?
faecolith, lymphoid hyperplasia, filarial worms
87
What are RF for appendicitis?
smoking and low dietary fibre
88
How does appendicitis present?
Presents as a surgical emergency: consider in all right sided pain, pain migrates to McBurney’s point, anorexia, nausea, vomiting, pyrexic, tender mass
89
What is the gold standard for appendicitis?
CT
90
what are differentials of appendicitis?
ectopic pregnancy, UTI, diverticulitis
91
What are complications of PUD?
perforations, abscess or appendix mass
92
How do you treat appendicitis?
removing appendix (laparoscopic appendectomy) and IV antibiotics
93
What is gastroparesis?
Delayed gastric emptying
94
What is a intestinal obstruction?
Blockage of onward propulsion of intestinal contents
95
What are the main causes of small bowel obstruction?
Adhesions and hernias
96
How does small bowel obstruction present?
pain, vomiting then constipation later, increased bowel sounds
97
What is the gold standard investigation for small bowel obstruction?
CT
98
How do you treat small bowel obstruction?
fluid resuscitation, analgesia and antiemetic, antibiotics, decompression
99
What are common causes of large bowel obstruction?
(less common) malignancies
100
How does large bowel obstruction present?
onstant abdominal pain, mass, late or no vomiting, increased then quiet bowel sounds
101
How do you investigate large bowel obstruction?
Digital rectal exam, FBC, xray, CT
102
How do you treat large bowel obstruction?
aggressive fluid resuscitation, bowel decompression, antibiotics, surgery
103
What are the two mechanisms of bowel obstruction?
Mechanical: adhesion, tumour, hernia, volvulus, intersusseption, IBD, gallstones
Functional (not physical): paralytic ileum, abscess, idiopathic
104
What can cause intestinal obstruction?
tumours, IBD, diverticulitis, Hischprung’s disease (incomplete innervation from colon to rectum), adhesions, volvulus (twist)
105
What is a pseudo obstruction?
clinical picture minces obstruction but no mechanical cause
106
How do you treat a pseudo obstruction?
IV neostigmine and treat underlying
107
what is diverticulitis?
```
Inflamed diverticula (bulging pouches in lining of GI system)
increased intraluminal pressure leading to erosion and inflammation, potentially causing perforation
```
108
What is diverticulosis?
development of diverticula (due to abnormal motility leading to high pressure)
109
How does diverticulitis present?
LLQ pain (sigmoid), palpable mass, diarrhoea and constipation, nausea, fever
110
How do you investigate diverticulitis?
CT with contrast and X ray
111
What are complications of diverticulitis?
stricture, abscess, fistula formation
112
How do you treat diverticulitis?
antibiotics and nil by mouth
| severe cases may need resection
113
What is gastritis?
Inflammation of the stomach lining
114
What are the two types of gastritis and what are their causes?
Acute: NSAIDS, H pylori, alcohol and stress
Atrophic (chronic): mainly infections (80%, H pylori, ulcers) or autoimune (autoimmunity against parietal cells, adenocarcinoma)
115
How does gastritis present?
Can be asymptomatic: epigastric pain, nausea, vomiting, ulcers
autoimmune can also present with iron deficiency and pernicious anaemia
116
How do you investigate gastritis?
Endoscopy with biopsy
H pylori detection (c-urea breath test, IgG and stool antigen)
Anti IF antibodies
117
How do you treat Gastritis?
removing cause i.e. stop NSAIDs or eradicate H pylori
118
What is Mallory Weiss syndrome?
bleeding from a laceration in the mucosa at the junction of stomach and oesophagus
119
What is a Mallory Weiss tear?
Laceration in mallory Weiss syndrome
120
What causes a Mallory Weiss tear?
severe vomiting: mainly alcoholism or bulimia but can be any cause of vomiting
121
How do you treat a Mallory Weiss Tear?
Can significantly heal within 48 hours
| - Treat with acid suppression (PPI) and antiemetics
