Gastrointestinal Flashcards
1
Q
Coeliac disease
A
Inflammation of the mucosa of the upper small bowel in response to GLUTEN
AUTOIMMUNE (T cell mediated)
Intolerance to PROLAMIN (in wheat, barley, rye, oats) which is a component of gluten protein
Causes VILLOUS ATROPHY
Leads to MALABSORPTION
2
Q
Coeliac disease epidemiology
A
1% of population in the UK
Peaks in infancy + 40-60 years
3
Q
Familial link and risk in coeliac disease
A
10% risk in 1st degree relatives
HLA associated: HLA DQ2 (90%)
4
Q
Coeliac disease risk factors
A
Other autoimmune diseases: T1DM, autoimmune thyroid, Addisons
Test all new cases of T1DM for coeliac
5
Q
Pathophysiology coeliac disease
A
SMALL BOWEL (particularly the jejunum)
Gliadin = breakdown product of gluten
Tissue transglutaminase (tTG) Ab
Ab-gliadin complex is presented to a transferrin receptor
Endocytosed accross the gastric mucosa into lamina propria
Deamidation
Deamidated gliadin phagocytosed by HALDQ8 cells
Macrophages signal an immune response (pro-inflammatory cytokines > cascade)
Results in:
VILLOUS ATROPHY > malabsorption
CRYPT HYPERPLASIA
Raised intraepithelial lymphocytes
6
Q
Clinical presentation of coeliac disease
A
Often asymptomatic Failure to thrive in young children Malabsorption (due to villous atrophy) - STEAORRHOEA (can’t absorb fat) - ANAEMIA (can’t absorb B12, folate, iron) - Osteomalacia (can’t absorb vitamin D) UNINTENTIONAL WEIGHT LOSS Fatigue DIARRHOEA Aphthous ulcers Angular stomatitis Dermatitis herpetiformis
7
Q
Complications of untreated coeliac disease
A
Vitamin deficiency
Anaemia
Osteoporosis
Increased risk of malignancy:
Enteropathy-associated T-cell lymphoma
8
Q
Investigations for coeliac disease
A
1st line: raised anti-tTG antibodies
- very high sensitivity and specificity
- false negatives may occur in people with IgA deficiency as anti-tTG is IgA
Gold standard: endoscopy + duodenal biopsy
- villous atrophy
- crypt hypertrophy
- raised intracellular WBCs
Can also test for IgA endomysial antibody (anti-EMA) but less sensitive
9
Q
Treatment of coeliac
A
Lifelong gluten-free diet
10
Q
Inflammatory Bowel Disease (IBD)
A
Chronic
Autoimmune
Umbrella term for two main diseases that cause inflammation of the GI tract:
Crohn’s disease
Ulcerative colitis
Relapsing & remitting
11
Q
Key features of Crohns: NESTS
A
Not usually blood or mucus (but can occur)
Entire GI tract (mouth to anus)
Skip lesions on endoscopy (non-continuous inflammation)
Terminal ileum and Transmural
Smoking is a risk factor
Cobblestone appearance (ulcers and fissures in mucosa) Non-caseating granuloma inflammatory lesions
12
Q
Key features of Ulcerative colitis: UC CLOSE UP
A
Continuous and circumferential inflammation; crypt abscesses Limited to colon and rectum ONLY superficial mucosa affected Smoking is protective Excrete blood and mucus
Use aminosalicylates and Uveitis
Primary sclerosis cholangitis and pseudo-polyps
DEPLETED goblet cells (mucosal barrier destruction)
13
Q
Risk factors for ulcerative colitis
A
Family history
NSAIDs (can trigger onset and flares) Chronic stress (can trigger flares)
14
Q
Ulcerative colitis epidemiology
A
Presentation at 20-40 years old
Higher incidence than Crohns
Incidence is 3x higher in non-smokers
15
Q
Symptoms of UC
A
Diarrhoea
Abdominal pain
Passing blood and mucus
Weight loss
16
Q
Signs of UC
A
Acute: fever, tachycardia, tender abdomen
Extraintestinal: clubbing, nutritional deficits
17
Q
Complications of UC
A
Colon:
- Blood loss
- Colorectal cancer
Skin:
- Erythema nodosum
- Pyoderma gangrenosum
Joints:
- Ankylosing spondylitis
- Arthritis
Eyes:
- Uveitis
Liver:
- sclerosing cholangitis
18
Q
Investigations of UC
A
Blood tests:
- raised CRP & ESR in active inflammation
- raised WCC
- raised platelets
- anaemia (normocytic of chronic disease)
- pANCA may be +ve (-ve in Crohn’s)
Gold standard:
- DIAGNOSIS: sigmoidoscopy + biopsy
- further: full colonoscopy + biopsy
Further testing:
Abdominal X-Ray
Ultrasound, CT and MRI
19
Q
Treatment of UC
A
MILD TO MODERATE DISEASE 1st line: aminosalicylate - 5-aminosalicyclic acid (5-ASA) - sulfasALAZINE, mesALAZINE, olsALAZINE - oral or rectal route 2nd line: oral corticosteroids e.g. prednisolone
SEVERE DISEASE
1st line: IV corticosteroids e.g. hydrocortisone
2nd line: IV ciclosporin
SEVERE W/ NO RESPONSE: colectomy
- surgery is possible as it only affects the colon and rectum
MAINTAINING REMISSION: Aminosalicylate, AZATHIOPRINE
20
Q
Crohn’s disease risk factors
A
Stronger genetic association than UC Family history Smoking NSAIDs (exacerbate) Chronic stress (trigger flares)
21
Q
Crohn’s epidemiology
A
Northern Europe and North America
Females > males
Presentation mostly at 20-40 years
22
Q
Crohn’s disease symptoms
A
Small bowel: Abdo pain, weight loss
Colon: Bloody diarrhoea, pain on defecation
Systemic: Fever, fatigue, anorexia
23
Q
Crohn’s disease signs
A
Bowel ulceration
Abdo tenderness
Abdo mass
Extraintestinal:
oral aphthous ulcers (more common in Crohn’s than UC)
skin, joint and eye problems
24
Q
Crohn’s disease complications
A
Malabsorption Small bowel obstruction Colorectal cancer Anaemia Perianal disease e.g. fissures
25
Crohn’s disease investigations
Blood tests:
- raised CRP & ESR
- raised WCC
- raised platelets
- anaemia (normocytic of chronic disease)
- pANCA negative
Gold standard: colonoscopy + biopsy
- granulomatous transmural inflammation
Small bowel imaging: to detect proximal disease
Abdominal X-ray
MRI
Ultrasonography
26
Crohn’s disease treatment
MILD/MODERATE DISEASE
1st line: Oral prednisolone
SEVERE DISEASE
1st line: IV hydrocortisone
If NOT RESPONSIVE to steroids: Anti-TNF antibodies (Infliximab)
MAINTAINING REMISSION: AZATHIOPRINE (Methotrexate if intolerant to Azathioprine)
OTHER
Smoking cessation
Correct iron/B12 deficiencies
Antibiotics for perianal disease
27
IBD: upper RIGHT quadrant pain
Crohn’s disease
28
IBD: LEFT quadrant pain
Ulcerative colitis
29
Screening test for IBD
Faecal calprotectin
- release by the intestines when inflamed
- >90% specific and sensitive to IBD in adults
- doesn’t differentiate UC and Crohn’s
30
Surgery in Crohn’s disease
Resection of worst affected areas of bowel
Never fully cures
Indications:
Failure of medical therapy
Obstruction from strictures
Fistulae, abscesses, perianal disease
31
Irritable bowel syndrome (IBS)
Functional bowel disorder = mixed group of abdominal symptoms with no organic cause
32
IBS epidemiology
More common in females
1 in 5 in western world
Age of onset = under 40 years
33
IBS risk factors
GI infections
Anxiety and depression
Eating disorders
Previous severe long term diarrhoea
34
IBS symptoms
Chronic: 6+ months
Exacerbated by stress, food, menstruation
3 types:
IBS-C: with constipation
IBS-D: with diarrhoea
IBS-M: mixed
Consider IBS if a patient reports ANY:
Abdominal pain
Bloating
Change in bowel habit
Multi-system disorder:
- painful periods
- bladder symptoms e.g. frequency
- joint hyper mobility
- fatigue
35
NICE diagnostic criteria for IBS
ABDOMINAL PAIN which is either related to
- DEFECATION
and/or
- associated with altered stool FREQUENCY (increased or decreased)
and/or
- associated with altered STOOL FORM or appearance (hard, lumpy, loose, or watery)
And there are at least two of the following:
Alternative conditions with similar symptoms have been excluded
Passage of rectal mucus
Symptoms worsened by eating
Abdominal bloating (more common in women than men), distension, or hardness
Altered stool passage (straining, urgency, or incomplete evacuation)
36
Differential diagnoses for IBS
IBD
Coeliac
Lactose intolerance
Colorectal cancer
37
Investigations for IBS
Rule out differentials:
- tTG for coeliac
- faecal calprotectin for IBD
- FBC for anaemia
- colonoscopy for IBD + colorectal cancer
38
IBS treatment
1st line: General healthy DIET + exercise ADVICE
- small frequent non-processed meals
- IBS-C: soluble fibre
1st line medication:
IBS-D: Loperamide (Imodium)
IBS-C: Laxatives e.g. docusate, linaclotide
Pain/bloating: antispasmodics e.g. buscopan
```
2nd line medication:
Tricyclic antidepressants (amitriptyline)
```
3rd line medication
SSRI antidepressants
Can be used in conjunction with psychological therapies e.g. cognitive behaviour therapy (CBT)
39
Acute appendicitis
Sudden inflammation of the appendix
Most commonly caused by an obstruction of the appendix which results in the invasion of gut organisms into the appendix wall leading to INFLAMMATION, necrosis and rupture
Most common surgical emergency
40
Causes of obstruction to the appendix
Faecoliths (stony mass of compacted faeces)
Bezoars (partially digested material collected in the stomach)
Trauma
Intestinal worms
Lymphoid hyperplasia
41
Key clinical presentation of appendicitis
ABDOMINAL PAIN
- starts central (umbilicus) and migrates to the right iliac fossa within the first 24 hours
Inflammation irritates overlying peritoneum (peritonitis) causing tenderness at McBurney’s point (1/3 from anterior superior iliac spine to umbilicus)
42
Other classic features of appendicitis
```
Guarding on abdominal palpating
Pyrexia
Nausea and vomiting
Rosvings sign (palpation of LIF causes pain in RIF)
Coughing causes pain
```
43
Key differential diagnoses of appendicitis
```
Ectopic pregnancy: serum hCG
Meckel’s diverticulum
UTI
Constipation
Food poisoning
Crohn’s (acute terminal ileitis)
```
44
Investigations acute appendicitis
Diagnosis:
- Clinical presentation
- Blood tests: raised WCC (neutrophils), raised CRP & ESR (inflammation)
GOLD STANDARD: CT scan (highly specific and sensitive)
Ultrasound: inflamed appendix and appendix mass
Pregnancy test: exclude ectopic pregnancy
Urinalysis: exclude UTI
45
Management of appendicitis
GOLD STANDARD = laparoscopic appendicectomy
IV antibiotics (metronidazole) and IV fluids
46
Complications of appendicitis
Perforation
| Appendix mass: the omentum sticks to the inflamed appendix forming a mass in the RIF
47
Three types of bowel obstruction
Small bowel obstruction (60-75%)
Large bowel obstruction
Psuedo-obstruction
All can be serious and potentially fatal
48
Causes of small bowel obstruction
INTRA-ABDOMINAL ADHESIONS (60%) - usually due to previous abdo surgery or infections e.g. peritonitis
Hernias
Malignancy
Crohn’s disease
49
Pathophysiology of small bowel obstruction
Distension above the blockage > increased pressure pushes blood vessels within bowel wall > compressed vessels results in ischaemia, necrosis, perforation
50
Clinical presentation of SBO
PAIN: initially COLICKY but then diffuse, higher in the abdomen than LBO, INTERMITTENT
Profuse VOMITING following pain (occurs earlier in SBO than LBO) - think SB IS CLOSER TO MOUTH
Increased bowel sounds (tinkling)
Abdominal distention
51
Small bowel obstruction Ix
1st line: abdominal X-ray
- distended loops of bowel proximal to obstruction
- no gas distal to obstruction (i.e. large bowel)
GOLD STANDARD: non-contrast CT - localises the obstruction
52
Causes of large bowel obstruction
MALIGNANCY (90%) - more common in West
Volvulus (twisting of the bowel on its mesenteric axis, sigmoid colon most common place)
Diverticulitis
Crohn’s disease
53
Clinical presentation of LBO
Abdominal pain
- more CONSTANT & DIFFUSE than SBO
- usually occurs lower in the abdomen (LIF)
Much more ABDOMINAL DISTENTION than SBO
Palpable mass e.g. hernia
54
Investigations for LBO
Digital rectal exam (DRE)
- empty rectum
- hard compacted stools
1st line: Abdo X-Ray
- peripheral gas shadows proximal to blockage
Gold standard: CT
55
Management of an obstructed bowel (SBO, LBO)
Aggressive fluid resuscitation
Decompression of the bowel “drip and suck”
- IV fluids to hydrate
- NG tube
Analgesia, anti-emetics
Antibiotics
Surgery to remove obstruction
56
Pseudo bowel obstructions
Present identically to SBO/LBO but underlying cause should be treated first
57
Bacterial causes of diarrhoea
Campylobacter jejuni
E. Coli
Salmonella
Shigella
58
Viral causes of diarrhoea
Majority of diarrhoea cases are VIRAL
```
Children = rotavirus
Adults = norovirus
```
59
Management of diarrhoea
Oral rehydration therapy (IV fluids given if very severe)
Treat the underlying causes (bacterial normally treated with metronidazole)
Anti-emetics e.g. metoclopramide
Anti-motility agents e.g. loperamide
60
Ischaemic bowel diseases
Acute mesenteric ischaemia
Chronic mesenteric ischaemia (intestinal angina)
Ischaemia colitis
61
Causes of acute mesenteric ischaemia
Superior mesenteric artery (SMA) THROMBOSIS
SMA EMBOLISM (due to AF)
Mesenteric venous thrombosis
62
Presentation of acute mesenteric ischaemia
Classic triad:
Acute, severe abdo pain (constant and central)
No abdo signs on examination
Rapid hypovolaemia > shock
AF + severe abdo pain = AMI
63
Acute mesenteric ischaemia investigations
Diagnostic: CT angiography
- visualise blockages (difficult to perform)
Bloods:
- increased Hb concentration due to blood loss
- metabolic acidosis + raised lactate
64
Management of AMI
Fluid resuscitation
IV heparin
Antibiotics (metronidazole)
Surgery to remove necrotic bowel
Mortality: >50%
65
Causes of ischaemic colitis
Thrombosis
Emboli
Low flow states (low CO/arrhythmias)
Surgery
66
Presentation of ischaemic colitis
Sudden onset LIF pain
Passage of bright red blood
Signs of hypovolaemic shock (tachycardia, fatigue)
67
Ischaemic colitis investigations
1st line: CT to rule out rupture
Gold standard: colonoscopy + biopsy
68
Mallory Weiss tear
Haematemesis from tear in oesophageal mucosa
69
Causes and risk factors for Mallory Weiss tear
```
ALCOHOLISM
Hyperemesis gravidarum (severe nausea and vomiting during pregnancy)
Gastroenteritis
Bulimia
Chronic cough
```
70
Tar like, black, greasy and offensive stools caused by digested blood
Melaena
71
Presentation of Mallory Weiss tear
Haematemesis
Melaena
Sx of hypovolaemic shock
72
Investigations Mallory Weiss tear
1. Rockall score (risk of bleeding: <3 = low risk)
2. Haemoglobin (FBC), Urea (U&Es), coagulation (INR, FBC for platelets), Liver disease (LFTs), Crossmatch blood
3. ECG and cardiac enzymes
73
Management Mallory Weiss tear
```
ABCDE
Terlipressin (oesophageal varices)
Urgent endoscopy (oesophagogastroduodenoscopy/OGD)
```
74
Oesophageal varices
Dilated veins at sites of portosystemic anastomosis (left gastric & inferior oesophageal veins)
75
Causes of oesophageal varices
Pre-hepatic: portal vein thrombosis
Hepatic: CIRRHOSIS > PORTAL HYPERTENSION
Post hepatic: Budd Chiari syndrome, RHF
76
Oesophageal varices clinical presentation
Haematemesis
MELAENA
Sudden collapse (Sx of haemodynamic instability)
77
Investigations oesophageal varices
1. Urgent endoscopy
2. FBC, U&Es, clotting (INR), LFTs
4. CXR, Ix PHT
78
Treatment for oesophageal varices
ABCDE
Rockall score
TERLIPRESSIN + prophylactic broad spectrum AB (ciprofloxacin)
79
Barrett’s Oesophagus
Metaplasia of the lower oesophageal mucosa (STRATIFIED SQUAMOUS to COLUMNAR epithelium with goblet cells)
Pre-malignant: RF for adenocarcinoma of the oesophagus
80
Causes and RF for Barrett’s oesophagus
```
GORD
Male (7:1)
Caucasian
FHx
Hiatus hernia
Obesity
Smoking
Alcohol
NSAIDs
```
81
Classic patient Px of Barrett’s oesophagus
Middle aged Caucasian male with long history GORD and dysphasia
82
Investigations Barrett’s oesophagus
Endoscopy + Biopsy
83
Management of Barrett’s oesophagus
Lifestyle advise: weight loss, reduce caffeine, avoid smoking
Acid neutralising medication: Gaviscon
Proton pump inhibitors: OmePRAZOLE, LansoPRAZOLE
Endoscopic surveillance with biopsies
84
Risk factors for progression to adenocarcinoma in Barrett’s oesophagus
```
Male
Older age
>8cm segment
Intestinal metaplasia
GORD duration
Alcohol, smoking, obesity
Achalasia
```
85
Adenocarcinoma oesophageal cancer
Most common type in the DEVELOPED world e.g. UK
RF: GORD, Barrett’s, Smoking, Obesity
Location: Lower 1/3 (near GO junction)
86
Squamous oesophageal cancer
Most common type in the DEVELOPING world
RF: SMOKING, Alcohol, Low fruit/veg/fibre, Hot drinks
Location: Upper 2/3
87
Presentation of oesophageal cancer
THROAT LUMP
LONG HISTORY OF DYSPEPSIA
```
ALARMS:
Anaemia
Loss of weight
Anorexia
Recent onset progressive symptoms
Regurgitation
Swallowing difficulties: PROGRESSIVE DYSPHAGIA
```
88
Oesophageal cancer investigations
1st line: Upper GI endoscopy + biopsy
(REFER WITHIN 2 WEEKS)
Staging: CT scan or endoscopic ultrasound
89
Oesophageal cancer management
OPERABLE: surgical resection + adjuvant chemotherapy
Palliation (relief of symptoms without cure)
90
Gastrooesophageal reflux disease
Lower oesophageal sphincter (LOS) dysfunction
Leads to reflux of gastric contents leading to symptoms of OESOPHAGITIS
91
RF GORD
```
Hiatus hernia
Smoking
Alcoholism
Obesity
Pregnancy
```
92
Oesophageal presentation of GORD
Heartburn/retrosternal pain: related to meals, worse when lying down, relieved by antacids
Acid regurgitation
Odynophagia: painful sensation in the oesophageal regions that occurs in relation to swallowing
93
Dyspepsia
Non specific term to describe indigestion symptoms e.g. heartburn
94
Extra oesophageal symptoms of GORD
Nocturnal asthma
Chronic cough
Laryngitis, Sinusitis
95
GORD Red Flags
```
Dysphagia
>55 years
Weight loss
EPIGASTRIC PAIN
Treatment resistant DYSPEPSIA
Anaemia
Raised platelets
```
= ENDOSCOPY (Refer for Upper GI endoscopy within 2 weeks)
96
Management of GORD
Non-pharmacological: smoking cessation, stop drinking alcohol, lose weight, sleeping position
Pharmacological: PPIs e.g. lansoprazole, H2 receptor antagonists (antihistamines) e.g. ranitidine, Alginates (form a gel raft at top of stomach)
Surgical: laparoscopic/Nissen fundoplication (tying fungus around the LO to narrow the LOS)
97
Peptic ulcers
Break in the lining of the GASTRIC or DUODENAL MUCOSA
98
RF peptic ulcers
H. pylori
NSAIDs e.g. ibuprofen
ZE syndrome
Increased acid: stress, alcohol, caffeine
99
Investigations Peptic Ulcer
Diagnosis: Endoscopy
| - Rapid Urease Test (H. pylori test)
100
Peptic ulcer management
Lifestyle modifications
Treat underlying cause:
- stop NSAIDs
- eradicate H. pylori (PPI, clarithromycin, amoxicillin)
101
Helicobacter pylori
Gram negative aerobic bacteria
Damages the epithelial lining of the stomach resulting in gastritis, ulcers and increased risk of stomach cancer
Damages epithelial cells:
Avoids the acidic environment by forcing its way into the gastric mucosa
Produces ammonia to neutralise the stomach acid
102
Gastric ulcer
Location: lesser curvature of gastric antrum
RF: H. pylori, Smoking, Drugs, Stress, NSAIDs, mucosal ischaemia
Presentation: Epigastric pain WORSE ON EATING and RELIEVED BY ANTACIDS, Haematemesis, Melaena (DARK blood in stools due to degradation by intestinal enzymes)
103
Duodenal ulcer
MORE COMMON
Location: 1st part of duodenum
RF: H. Pylori, Smoking, Drugs, Alcohol
Presentation: Epigastric pain BEFORE MEALS and AT NIGHT and RELIEVED BY EATING
Haematemesis, Melaena (DARK blood in stools due to degradation by intestinal enzymes)
104
Complications of peptic ulcers
Haemorrhage
Perforation
Gastric outflow obstruction
Malignancy
105
Drugs that cause peptic ulcer
NSAIDs
SSRI
Corticosteroids
Bisphosphonates
106
Gastritis
Inflammation of the stomachs mucosal lining
107
RF Gastritis
```
Autoimmunity
H. Pylori
Bile reflux
NSAIDs
Stress
Alcohol
```
108
Gastritis clinical presentation
Epigastric pain
Nausea and vomiting
Dyspepsia
109
Gastritis investigations
H. pylori (Urease test)
| Endoscopy + biopsy
110
Management of gastritis
Addressing cause
H. pylori eradication (PPI, Clarithro, Amox)
Correction of vitamin deficiency
111
Diverticulum
Outpouching of the gut mucosa with penetrating arteries
112
Diverticulosis
Presence of multiple diverticula
“Wear and tear of the bowel”
Very common >50 years
113
Diverticulitis
Inflammation in the diverticula
RF: low fibre diets, obesity, NSAIDs
114
Diverticula disease
Diverticula are symptomatic
115
Meckel’s diverticulum
Common congenital abnormality of the GI tract
2-3% of population
Usually asymptomatic
116
True diverticula
Contain all the layers of the GI wall (mucosa, muscularis propria, adventitia) e.g. Meckel’s
117
False diverticula
Only involve the submucosa and mucosa
118
Where in the colon are diverticula most likely to form
SIGMOID COLON
- Smallest luminal diameter
- Highest pressure
- presents in LIF
DESCENDING COLON
119
Presentation of diverticulitis
```
Left iliac fossa pain with tenderness
Palpable LIF mass
Constipation
Tachycardia
Fever
```
120
Diverticulitis investigations
Bloods: raised WCC, ESR & CRP
Imaging: Erect CXR, AXR and CT
121
Treatment of diverticulitis
Oral co-amoxiclav
Oral/IV ciprofloxacin
Analgesia + clear liquid diet
Severe: surgical resection
122
Presentation of diverticular disease
Altered bowel habit
Abdominal pain
Bleeding PR
123
Investigations for diverticular disease
CT (acute)
| Colonoscopy
124
Management for diverticular disease
High fibre diet and fluids +/- laxatives
| Surgery
125
Gastric cancer types
Type 1: intestinal/differentiated (70-80%)
| Type 2: diffuse/undifferentiated (20%)
126
Gastric cancer risk factors
Male
H. Pylori
Chronic gastritis
Older age
127
Signet ring cell carcinoma
Type of adenocarcinoma (mucus producing)
| Most often found in gastric cancer
128
Criteria for 2 week wait endoscopy in gastric cancer
```
Upper abdominal mass +
- Dysphagia (any age)
Or
- Aged >55 + weight loss and:
- Upper abdominal pain
- Reflux
- Dyspepsia
```
129
Clinical presentation of gastric cancer
Often late presentation
Anorexia, nausea, weight loss, anaemia, dysphagia, vomiting
Epigastric pain (better with antacids)
Paraneoplastic syndromes
130
Gastric cancer investigations
Gastroscopy: 8-10 biopsies
Endoscopic USS: depth of invasion
CT/MRI/PET
131
Management of gastric cancer
Nutritional support (fruit, veg, fibre = protective)
Surgical resection
Chemo
Prognosis: 60% 5 year survival
132
Risk factors for colon cancer
```
Family Hx - younger presentation
IBD
Diet (red meat, low fibre)
Obesity
Colorectal polyps
Smoking
```
133
Diagnosis of colon cancer
1. Faecal occult blood test
a) >50 + bowel habit change or IRON DEFICIENT ANAEMIA
b) >60 + anaemia
2. Colonoscopy + biopsy
3. Flexible sigmoidoscopy / Barium enema / CT colonoscopy
134
Management of colon cancer
Surgical resection depending on area
| E.g. descending colon = left hemicolectomy
135
Example of hereditary causes of colon cancer
Familial adenomatous polyposis (FAP) - AUTOSOMAL DOMINANT
136
Staging of colon cancer
Dukes staging system
A) confined to submucosa
B) invasion through muscularis without lymph node involvement
C) invasion through muscularis with lymph node involvement
D) presence of distant metastases
137
Types of diarrhoea
```
Inflammatory
Dysentery
Secretory
Osmotic
Exudative
```
138
Clinical tool to classify faeces
Bristol stool chart
139
Red flags for abdominal cancer
```
PR bleeding
Abdominal mass
Weight loss
FHx
Anaemia
Age >60
Bowel habit
```
140
Complications of bowel obstruction that would lead to emergency surgery
Bowel ischaemia
| Strangulation
141
Non-invasive tests for H. pylori
C-Urea breath test
| Faecal antigen test
142
Gastritis differentials
GORD
Gastric carcinoma
Peptic ulcer
143
Clinical features of haemorrhoids
Bright red bleeding
Discomfort/pain
Pruritis ani
Pain on passing stools
144
Pathophysiology of haemorrhoids
Swelling and inflammation of veins in the rectum and anus
145
Two types of haemorrhoids
Internal: painless covered in mucus, prolapse
External: painful, covered with skin
146
Treatment of haemorrhoids
```
Stool softeners
High fibre diet
Adequate fluid intake
Band ligation
Haemorrhoidectomy
```
147
Causes of acute diarrhoea
Bacterial: salmonella from food poisoning
Viral: norovirus (associated with cruise ships)
IBS/IBD
Anxiety
Drugs e.g. NSAIDs, PPIs
148
Potential complications of diverticulitis
```
Large bowel perforation
Fistula formation
Large bowel obstruction
Bleeding
Mucosal inflammation
```
149
If Terlipressin is contraindicated in oesophageal varices, what drug should be used?
Somatostatin
150
MOA of terlipressin in oesophageal varices
Increase in ARTERIAL vascular resistance = decrease in arterial blood supply = reduction of pressure in portal circulation
151
Abdominal pain
Mucousy stools
Painful diarrhoea
Suspect IBD
152
Mouth ulcers
| Which IBD?
Crohn’s - from mouth to anus
153
Young child: underweight, tired all the time, intermittent stomach pain, nausea, diarrhoea
FH: autoimmune conditions
Coeliac disease
FIRST LINE: serology for TTG (IgA)
GOLD STANDARD investigation: endoscopic intestinal biopsy
- duodenal/jejunal biopsy: villous atrophy + crypt hyperplasia
OTHER: FBC (anaemia), CRP & ESR (inflammation)
154
Treatment in acute variceal haemorrhages
Endoscopic variceal band ligation
155
Achalasia
Lower oesophageal spinchter fails to relax causing failure of oesophageal peristalsis
156
HNPCC
hereditary nonpolyposis colorectal cancer gene
increases the risk of cancers including COLORECTAL and ENDOMETRIAL CANCER
157
Why does a Mallory Weiss tear occur following SEVERE VOMITING
Sudden rise in intragastric pressure causes the oesophageal mucosa to tear
158
Virchows node
```
Left supraclavicular lymph node
Gastric cancer (Trosiers sign)
```
159
Gastroenteritis
Bacterial or viral causes
Diarrhoea and vomiting (dehydration)
(Unlikely to be associated with bleeding)
160
Absorption location: bile salts
Terminal ileum
161
Absorption location: iron
Duodenum
162
Absorption location: Vitamin B12
terminal ileum
163
Absorption location: folate
Duodenum and jejunum
164
Why do NSAIDs cause stomach irritation
Mucus secretion is stimulated by prostaglandins
COX-1 is needs for prostaglandin synthesis
NSAIDs inhibit COX-1 = no mucus for protection
165
Causes of diarrhoea
```
Viral: rotavirus (children), norovirus
Bacterial: E. coli, Salmonella, C.diff
Parasitic
Antibiotics: rule of Cs (cephalosporins)
Other: anxiety, food allergy
Chronic: IBS, IBD, coeliac, bowel cancer
```
166
Risk factors for infective diarrhoea
Foreign travel
Crowded area
Poor hygiene
167
Commonest dermatological manifestation of IBD
Erythema nodosum
168
Most likely part of bowel affected in UC
Rectum (starts here)
169
Large bowel blood supply
170
Explain this diagram
171
AF + severe abdo pain
Acute mesenteric ischaemia
172
Parietal cells secretions
```
Gastric acid (HCl) - H+/K+ ATPase (action of PPIs)
Intrinsic factor
```
173
Location of action of ranitidine
Enterochromaffin cells secrete histamine which works on parietal cells via H2 receptors
Ranitidine is a H2 antagonist = reduce gastric acid secretion from parietal cells
174
Skin turgor and dry mucus membranes
Dehydration
