Gastrointestinal Flashcards
1
Q
What is dyspepsia and what causes it?
A
The presence of upper GI symptoms (incl nausea, vomiting, pain/discomfort, heartburn) for 4 weeks or more
DDs - functional, ulcer, duodenitis, oesophagitis/GORD, malignancy, gastritis
2
Q
What are the red flag symptoms for dyspepsia?
A
Anaemia (iron deficiency)
Loss of weight
Anorexia
Recent onset/progressive symptoms
Meleana/haematemesis
Swallow difficulty
~~~
3
Q
How should new dyspepsia (for over 4 weeks) be investigated?
A
Under 55 - stop drugs causing dyspepsia, lifestyle changes. antacids etc. If 4 weeks still symptoms, test for H. pylori and treat
Over 55 or ALARMS signs - refer for 2WW endoscopy as need to rule out cancer
4
Q
How long before an H pylori test or OGD should you stop usual meds?
A
2 weeks - PPI, ranitidine
4 weeks - bismuth, antibiotics
5
Q
Describe H pylori testing
A
Choice between:
- Carbon 13 urea breath test
- Stool antigen test
- Lab-based serology
6
Q
When should H pylori eradication therapy be offered?
A
Patients who have tested positive for H pylori and have PUD
7
Q
What is peptic ulcer disease and what causes it?
A
A break in the superficial epithelial cells penetrating down to the mucosa - this can be gastric or duodenal.
Caused by H pylori, NSAID use, smoking, stress
8
Q
How do you differentiate between duodenal and gastric ulcers?
A
DUODENAL - Gnawing epigastric pain BEFORE meals or at night, which is relieved by eating (these are 4x more common)
GASTRIC - Gnawing epigastric pain AFTER meals
9
Q
Where do gastric ulcers usually occur?
A
On the lesser surface of the stomach (elsewhere are usually malignant)
10
Q
How should those with PUD be managed?
A
H PYLORI POSITIVE:
Associated NSAID use - full dose PPI for 2 months then eradication therapy
No NSAID use - first line eradication therapy
H PYLORI NEGATIVE:
- Full dose PPI therapy for 4-8 weeks
11
Q
Describe H pylori eradication therapy
A
7 day, twice daily course of:
- Lansoprazole
- Amoxicillin
- Clarithromycin/metronidazole
If no response try whichever abx was not used first line
If pen allergic do bottom two abx
12
Q
Describe H pylori eradication therapy (if previous exposure to clarithromycin and metronidazole)
A
7 day, twice daily course of:
- Lansoprazole
- Amoxicillin
- Tetracycline
13
Q
What follow up is offered for H pylori eradication therapy?
A
Urea breath test - if not effective try second line regime
14
Q
What is functional dyspepsia?
A
Non ulcer dyspepsia this may be due to a hypersensitive oesophagus or functional heartburn (non acid stimulus) - treat with PPI, psychotherapy, bismuth
15
Q
What is GORD?
A
Reflux of stomach contents causing symptoms (dyspepsia, hoarseness, cough). Often defined as 2 or more episodes of heartburn a week.
16
Q
What causes GORD?
A
- LOS hypotension
- Hiatus hernia
- Loss of oesophageal peristaltic function
- Abdo obesity
- Gastric acid hyper secretion
- Slow gastric emptying
- Overeating
- Smoking/alcohol
- Pregnancy
- Drugs
- Systemic sclerosis
- H. pylori
17
Q
Which drugs can cause GORD?
A
- Tricyclics
- Anticholinergics
- Nitrates
18
Q
How is GORD investigated?
A
BLOODS - FBC, U&E
IMAGING - endoscopy
OTHER - barium swallow, C13 urea breath test or stool antigen test
19
Q
What are the criteria for endoscopy in GORD?
A
ALARM symptoms or over 55
20
Q
What are the complications of GORD?
A
- Oesophagitis
- Benign oesophageal stricture
- Barretts oesophagus
- Iron deficiency
21
Q
How should H pylori negative GORD be managed?
A
Lifestyle:
Pillows, diet, alcohol, stress management
Drugs:
Antacids, alginates
If oesophagitis present:
1st line - high dose PPI for 4 or 8 weeks (eg. lansoprazole)
2nd line - switch to another PPI or H2RA therapy (eg. ranitidine)
22
Q
How should H pylori positive GORD be managed?
A
Triple eradication therapy
23
Q
How is severe GORD managed?
A
Severe GORD must be confirmed by pH monitoring/manometry, if drugs are not working.
Management is surgical - Nissen fundoplication, HALO, stretta ablation.
24
Q
What classification is used to assess severity of GORD?
A
Los Angeles classification - describes the extent of the mucosal break.
25
What is Nissen fundoplication?
Gastric fundus wrapped around the lower oesophageal sphincter to prevent reflux from happening.
26
When is surgery considered in peptic ulcer disease?
- Haemorrhage
- Perforation
- Pyloric stenosis
27
Which elective surgeries can be offered for PUD?
Vagotomy - denervation of the the vagus supply where it supplies the LOS and stomach to reduce the rate of gastric secretion
Gastrectomy - rare! only potentially in Zollinger Ellison syndrome
28
Which emergency surgeries can be offered for PUD?
Haemorrhage - adrenaline, diathermy, surgery
Perforation - laparoscopic repair, commence H pylori eradication post op
Pyloric stenosis - endoscopic balloon dilatation, drainage procedure and vagotomy
29
What are the symptoms of pyloric stenosis in adults?
Vomiting large amounts of food hours after meals - this is due to scarring in duodenal ulcers
30
What is Zollinger-Ellison syndrome?
A rare condition in which one or more tumors form in your pancreas or the upper part of your small intestine (duodenum). These tumors, called gastrinomas, secrete large amounts of the hormone gastrin, which causes your stomach to produce too much acid.
The gastronome is usually found in the pancreas! 60% are malignant.
31
What are the symptoms of Zollinger-Ellison syndrome?
- Abdo pain
- Dyspepsia
- Chronic diarrhoea and steatorrhea
32
How is Zollinger-Ellison syndrome diagnosed?
Measure 3 fasting serum gastrin levels on different days. Positive test is >1000pg/mL, with gastric pH <2.
Use CT/endoscopic US to stage and OGD to evaluate ulceration.
33
How is Zollinger-Ellison syndrome managed?
High dose PPI
| Chemo/surgery if malignancy.
34
Which familial cancer is Zollinger-Ellison syndrome associated with?
MEN1
35
What is Barretts oesophagus?
Replacement of normal squamous epithelium with metaplastic columnar epithelium, due to GORD.
36
How is Barretts oesophagus diagnosed?
Biopsy of endoscopically visible columnar cells
37
Which criteria is used in Barretts?
Prague criteria (looks at C - circumferential extent and M - maximum extent)
38
How is Barretts oesophagus managed?
No premalignant changes - biopsy and endoscopy every 1-3 years
Low grade dysplasia - endoscopy every year
High grade dysplasia - endoscopic therapy, oesophageal resection, eradicative mucosectomy, mucosal ablation
39
What is gastritis?
Inflammation of the lining of the stomach, presenting with epigastric pain, vomiting, haematemesis
40
How can gastritis be prevented?
Give PPI gastroprotection when prescribing long term NSAIDS
41
How can gastritis be treated?
Ranitidine/PPI. H pylori eradication if indicated (may need quadruple therapy with bismuth). Endscopic quarterly.
42
What are the different types of endoscopy?
Proctoscopy - examines the rectum in pts with history of bright red PR bleed
Sigmoidoscopy - examines 20-25cm of distal colon , give phosphate enema before
Flexi sigmoidoscopy - reaches up to the splenic flexure, requires evacuation of distal colon
OGD - can be diagnostic and therapeutic, looks at oesophagus, stomach and duodenum, no PPI for 2 weeks before and NBM for 4 hours
Colonoscopy - can be diagnostc and therapeutic, looks at colon and terminal ileum, no iron for 1 week post op and no solid food for 12-24hr, give sodium picosulfate before, do PR first
Ballooon enteroscopy - examines small bowel from duodenum to ileum using specialized enterescope
Capsule endoscopy - for evaluation of obscure GI bleeding after negative gastroscopy and colonoscopy
43
What are some relative CIs for OGD?
COPD, recent MI
44
What is the first line investigation for abdo distension?
Ultrasound
45
What is the first line investigation for acute abdomen?
CT (although x-ray often used first)
46
What is the first line investigation for evaluation of rectal cancers and abscesses/fistulae in anal region?
MRI
47
What is the first line investigation for staging most GI cancers?
Ct/MRI/PT
48
What is barium swallow used for?
Investigation of dysphagia, hiatus hernia
49
What is a hiatus hernia?
Sliding (80%) - gastro-oesophageal junction slides up into the chest so that it lies above the diaphragm. Often asymptomatic but may cause reflux
Rolling (20%) - gastro-oesophageal junction remains in abdomen but a bulge of stomach herniates up into the chest. Acid reflux uncommon but may cause severe pain due to strangulation
Risk factors include increased abdominal pressure (ascites, multiparty) and obesity
50
How is hiatus hernia managed?
- Weight loss
- Antacids
- Surgery if rolling HH (due to risk of strangulation), only in sliding HH if no improvement despite medical therapy
51
What is a hernia?
The protrusion of a viscus or part of a viscus through a defcet of the walls of its containing cavity into an abnormal position
52
Which is the most common type of hernia?
Inguinal - presents as a lump in the groin
53
What do the following terms mean in reference to hernias:
a) reducible?
b) incarcerated/irreducible?
c) obstructed?
d) strangulated?
a) Reducible – when the contents of the hernia can be manipulated back into its original position through the defect from which it emerges
b) Incarcerated hernia (irreducible) – the hernia is compressed by the defect causing it to be irreducible (i.e. unable to be pushed back into its original position)
c) Obstructed hernia – refers mainly to hernias containing bowel, where the contents of the hernia are compressed to the extent the the bowel lumen is no longer patent and causes bowel obstruction
d) Strangulated hernia – the compression around the hernia prevents blood flow into the hernial contents causing ischaemia to the tissues and pain
54
Where is the deep inguinal ring located?
Just above the mid-point of the inguinal ligament
55
Where is the superficial inguinal ring located?
Above and medial to the pubic tubercle
56
What is a direct inguinal hernia?
A direct inguinal hernia is caused by a weakness in the posterior wall of the inguinal canal. The abdominal contents (usually just fatty tissues, sometimes with bowel) are forced through this defect and enter the inguinal canal. This means that the contents emerge in the canal medial to the deep ring.
57
What is an indirect inguinal hernia?
The abdominal contents pass through the deep inguinal ring, passing through the inguinal canal and can exit via superficial ring.
58
How can you distinguish between direct and indirect inguinal hernias on examination?
- Reduce the hernia
- Occlude the deep internal ring with two fingers
- Ask the patient to cough or stand
- If hernia is restrained it is indirect, if not it is direct.
59
When and how should an inguinal hernia be repaired?
WHEN
Pain, alterered bowel habits, strangulation
HOW
Open - Reduces contents back into abdominal cavity and places a mesh (eg. lichenstein) to strengthen the posterior wall and prevent reherniation.
Laparoscopic - as name suggests, can be transabdominal pre peritoneal (through the peritoneal cavity) or totally extraperitoneal. Benefits of less post-op pain and quicker recovery.
60
What are the features of:
a) congenital inguinal hernia?
b) congenital umbilical hernia?
Congenital inguinal hernia:
- Indirect hernia resulting from failure in closure of processus vaginalus
- More likely to be right sided
- Should be surgically repaired ASAP
Congenital umbilical hernia:
- More common in premature/afro-caribbean babies
- Vast majority self-resolve before 4-5yrs old
61
What is a femoral hernia?
When bowel enters the femoral canal, presenting as a mass in the upper medial thigh, pointing down to the leg. More likely to be irreducible and strangulate. More common in women.
These are found INFERIOR and LATERAL to the puibic tubercle.
High risk of obstruction and strangulation - must be repaired
62
What is NAVY VAN?
Passing beneath the inguinal ligament are some important structures travelling to the upper leg. Most notably this includes the femoral artery, the femoral vein and the femoral nerve. The order in which these structures lie is easily remembered by the ‘NAVY VAN’ mnemonic. With the ‘Y’ signifying the creases of the groin, it illustrates how from lateral to medial the structures lie nerve, artery and then the vein.
63
How are femoral hernias managed?
Same way as inguinal hernias! Surgical repair recommended due to high change of strangulation.
64
Name 3 other hernias
Incisional - follow breakdown of muscle closure after surgery
Epigastric - pass through linea alba above umbilicus
Paraumbilical - just above or below umbilicus, RF include obesity and ascites
65
What is achalasia?
Aperistalsis of the oesophague and impaired relaxation of the LOS - presents as intermittent dysphagia, regurgitation of food from dilated oesophagus, spontaneous chest pain and aspiration pneumonia.
66
What causes achalasia?
- Autoimmune
- Neurodegenerative
- Viral
Mechanism unknown, potentially inflammation and degeneration of myenteric plexus of oesophagus
67
What does CXR/barium swallow of achalasia show, and how is it managed??
CXR: Fluid level in dilated oesophagus
Swallow: Dilated tapering oesophagus
Treat with endoscopic balloon dilatation or laparoscopic Hellers cardiomyotomy, then PPIs. If not suitable for surgery, give botulinum toxin injection/CCBs/nitrates.
Slight risk of squamous carcinoma of oesophagus.
68
What can cause dysphagia?
MECHANICAL - malignant or benign stricture, lung cancer, lymph nodes, restrosternal goitre, aortic aneurosym, pharyngeal pouch
MOTILITY - achalasia, diffuse oesophageal spasm, systemic sclerosis, neurological bulbar palsy
OTHER - oesophagitis, globus (functional)
69
What causes benign oesophageal stricutres?
GORD, corrosvies, surgery, radiotherapy, prolonged NG intubation
70
How are benign oesophageal strictures managed?
Endoscopic balloon dilatation
71
What is diffuse oesophageal spasm?
Swallowing accompanied by marked contraction of the oesophagus, causing chest pain and dysphagia. This is due to high amplitude peristalitic contractions.
72
What does barium swallow show with diffuse oesophageal spasm?
Corkscrew oesophagus
73
How is oesophageal spasm treated?
PPI for reflux.
| Antispasmodics, nitrates, CCBS, GABA receptor agonists (baclofen) for spasm.
74
What are lower oesophageal rings?
1. Mucosal (Schatzkis ring, B ring) - a ring located at squamocolumnar mucosal junction, associated with characteristic history of intermittent bolus obstruction
1. Muscular (A ring) - located proximal to mucosal ring, causes dysphagia
Rings may require dilatation but usually just conservative management.
75
What is Plummer-Vinson syndrome?
- A rare disease characterised by difficulty swallowing, IDA, glossitis, cheilosis and oesophageal webs
- Treat with iron supplementation and mechanical widening of the oesophagus
76
What is eosinophilic oesophagitis?
An allergic inflammatory condition of the oesophagus, causing dysphagia, food impaction, heartburn, pain. Male, white, middle aged.
Mucosal furrowing, loss of vascular pattern seen on endoscopy, due to a thickened mucosa.
77
How is eosinophilic oesophagitis managed?
Swallowed inhaled steroids preparations eg. fluticasone, budesonide, systemic steroids, monoclonal antibodies.
78
What causes oesophageal perforation/rupture and how is it managed?
Endoscopic dilatation, NG tube insertion. More likely if malignant strictures.
Rupture occurs from violent vomiting, alcohol ingestion.
Place stent over the hole and perform water soluble contrast x-ray after 2-3 days to check.
79
What are the RF for oesophageal cancer?
Alcohol, diet, smoking, achalasia, Plummer-Vinson syndrome, obesity, Vit A/C deficiency, nitrosamine exposure, reflux/barrets oesophagus
80
What is the histopathology of oesophageal cancer?
Squamous carcinoma in upper and middle third (55%) - related to alcohol, achalasia
Adenocarcinoma in lower third (45%) - related to GORD, barretts (THIS IS NOW MORE COMMON IN UK/US)
81
How does oesophageal cancer present?
Dysphagia, weight loss, retrosternal chest pain, hoarseness, cough. Usually around age 60-70.
82
How is oesophageal cancer diagnosed?
Oesophagoscopy with biopsy
83
How is oesophageal cancer staged?
TNM staging system
T - tumour invasion (Tis, T1-4)
N - lymph node invasion (Nx unable to be assesed, N0, N1)
M - metastases (M0, M1)
Do F-18 FDG PET CT, EUS to determines this.
84
What is the prognosis for oesophageal cancer?
Since over 70% preesnt after stage 3, 5 year survival rates are LOW (10%)
85
How is oesophageal cancer managed?
Surgery - only if tumour has not infiltrated outside of oesophageal wall (T1/T2)
Chemoradiation - stage 2b/3
Palliative - endoscopic dilatation, laser and brachytherapy, insertion of metal stent to aid feeding.
86
Describe the mucosal structure of the stomach
Smooth muscle has 3 layers - outer longitudinal, inner circular and inner oblique.
Mucosa of upper 2/3 of stomach contains parietal cells that secrete hydrochloric acid and chief cells that secrete pepsinogen. Antrum mucosa contains mucus secreting cells and G cells that secrete gastrin, and D cells that secrete somatostatin.
Mucosal barrier protects gastric epithelium; prostaglandins stimulate mucus secretion (these are inhibited by NSAIDS - cause ulcers!)
87
How does stomach acid secretion work?
1. Histamine stimulates Gs via H2 receptors to ACTIVATE secretion
2. Prostaglandin E2 activates the Gi protein to INHIBIT secretion
3. Somatostatin inhibits histamine and gastrin release and therefore acid secretion
88
Which factors affect gastric emptying?
Osmoreceptors in duodenal mucosa control gastric emptying by local reflexes and release of gut hormones
89
What is the difference between gastritis and gastropathy?
Gastritis - inflammation associated with mucosal injury
| Gastropathy - epithelial cell damage without inflammation
90
What causes gastritis?
H. pylori (80%)
Autoimmune (5%)
Viruses (5%)
91
What causes gastropathy?
```
Irritants - NSAIDS, alcohol
Bile reflux
Severe stress
Trauma/shock
Renal failure
```
92
What is the incidence and RF for gastric cancer?
Geography (Japan, eastern europe), male, H. pylori, EBV, diet high in nitrosamines, smoking, genetic, pernicious anaemia (due to atrophic gastritis)
93
Describe the histopathology of gastric cancer
Adenocarcinoma, two types:
1. Intestinal - differentiated, ulcerating/polypoid - strong environmental association and with atrophic gastritis
2. diffuse - undifferentiated, worse prognosis, loss of E-cadherin
94
What are the symptoms of gastric cancer?
Non-specific - EARLY SATIETY, dyspepsia, weight loss, vomiting, dysphagia, anaemia, mass, Virchows node
Due to this most patients present with advanced disease with mets
95
What is a krukenberg tumour?
A Krukenberg tumor refers to a malignancy in the OVARY that metastasized from a primary site, classically the GI TRACT, although it can arise in other tissues such as the breast. Gastric adenocarcinoma, especially at the pylorus, is the most common source.
96
How is gastric cancer diagnosed?
Gastroscopy and multiple ulcer edge biopsies
97
How is gastric cancer staged?
EUS for depth of invasion, CT/MRI for staging, laparoscopic staging if advanced
```
TNM classification (as oesophageal)
Stage 1 - T1N0M0, T1N1M0, T2N0,M0
Stage 2 - T1N2M0, T2N1M0, T3N0M0
Stage 3 - T2N2M0, T3N1M0, T4N0M0, T3N2M0
Stage 4 - everything else
```
ie - as soon as there are mets, it is stage 4
98
What is the prognosis for gastric cancer?
Poor, <10% overall for 5 year survival.
99
How is gastric cancer treated?
Surgery - most effective if suitable
Chemoradiation (cisplatin)
Palliative
Targeted therapy if HER2 positive (trastuzumab)
100
What is dumping syndrome?
Fainting and sweating after eating due to food of high osmotic potential being dumped in the jejunum - this is a side effet of gastrectomy.
101
What other lumps may be found on gastrocopy?
GIST - GI stromal tumours, sometimes malignant and may ulcerate and bleed
Polyps - usually asymptomatic, may be cystic, adenomatous, fibroid
102
How can you distinguish between UGI bleed and LGI bleed?
UGI - haematemesis 'coffee ground', meleana,
| LGI - passage of dark blood and clots without shock
103
What causes GI bleed?
- Peptic ulceration (most comm0on)
- Varices
- NSAIDS
- Mallory Weiss tear
- Viral infections (developing countries)
- Malignancy
- Bleeding after PCI
104
How should patients with upper GI bleed be managed initially?
1. ABCDE, high flow 02
2. Insert two large bore cannulae and take FBC, U&E, LFT, group and save, cross match
3. Give IV fluids whilst waiting for crossmatch
4. Insert catheter, monitor urine output
5. Organise ABG, CXR, ECG, stop NSAIDS/aspirin/clopidogrel/warfarin
6. Consider central line for inotropes (but not for fluid resus)
7. Transfuse until haemodynamically stable (consider platelets and FFP)
8. Monitor obs until stable
9. Give PPI (omeprazole) if bleeding ulcer
10. Arrange urgent endoscopy - may need banding/angiography/embolization
IF ON WARFARIN GIVE PCC TO REVERSE
105
When should platelets and FFP be given in an UGI bleed?
Platelets - actively bleeding and have a platelet count of less than 50 x 109/litre.
Prothrombin complex - actively bleeding and on warfarin
FFP - actively bleeding and have a prothrombin time (or international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal. Also needed if over 4 units transfused in one go?
Cryoprecipitate - If a patient's fibrinogen level remains less than 1.5 g/litre despite fresh frozen plasma use
106
Why should calcium be given to patients receiving multiple blood transfusions?
Transfusions associated with hypocalcemia - risk of fatal neurological and cardiovascular dysfunction
107
Which risk assessment scores can be used in UGI bleed?
Glasgow Blatchford score - used at first assessment, if=0 may not need admission
Rockall score - can be used pre and post endoscopy to predict chance of bleed in non-variceal upper GI haemorrhage. Looks at age, shock, comorbodity (pre) and diagnosis/signs of recent haemorrhage (post)
108
When should endoscopy be performed in UGI bleed?
Haemodynamicaly unstable - immediately after resus
| Haemodynamically stable - within 24h
109
Which endoscopic signs are associated with rebleeding?
- Active arterial bleeding
- Visible vessel
- Adherent clot/black dot
110
What are the best ways of monitoring blood transfusion for adverse effets?
Pulse rate and venous pressure - a CVP line may be needed if organ failure/risk of heart failure
111
How should bleeding ulcers be treated at endoscopy?
2 or 3 haemostatic methods:
- Adrenaline injection
- Thermal coagulation with heat probe
- Endoscopic clipping
Also start PPI and eradication therapy if indicated AFTER endoscopy
112
What are the indications for surgery in UGI bleed?
- Severe bleeding despite transfusion 6U if >60yo
- Active or uncontrollable bleeding at endoscopy
- Initial rockall >3 or final >6
113
What are oesophageal varices?
Enlarged veins in the oesophagus. Form from portal hypertension and formation of collateral veins between the portal and systemic systems, secondary to liver fibrosis.
They develop when portal pressure is >10mmHg.
114
What are the RF for variceal bleeds?
- Increased portal pressure
- Variceal size
- Endoscopic features of variceal wall eg. haematocystic spots
- Child pugh score >8
115
How are varices managed prophylactically?
Propranolol
Endoscopic variceal band ligation - 2 weekly until all varices eradicated
| Secondary - as above + transjugular intrahepatic porto-systemic shunt (TIPS)
116
How is acute variceal bleeding managed?
1. Resuscuitate until haemodynamically stable but avoid saline
2. Correct clotting abnormalities + prophylactic IV antibiotics
3. IV TERLIPRESSIN!!!!!!!
4. Endoscopic banding
5. Balloon tamponade with Minnesota tube/Sengstaken-Blakemore tube if uncontrollable bleeding
6. TIPSS (shunt) if all measures fail
117
What causes lower GI bleed?
Massive bleeds
- Ischaemic colitis
- Diverticular disease
Small bleeds
- Haemorrhoids
- Anal fissures
- Solitary rectal ulcer
-
118
How is LGI bleed managed acutely?
Usually stop by themselves - if not or haemodynamically unstable follow the protocl for UGI bleed.
119
What causes chronic GI bleed?
Cancer (particularly ascending colon)
| Coeliac disease
120
How should chronic GI bleed be investigated?
Usual bloods, endoscopy, colonoscopy, CT
If no cause found, capsule endoscopy
121
Describe the structure of the small intestine
Duodenum - jejunum - ileum
Mucosal folds called villi and microvili found on enterocytes - these greatly increase the surface area.
Each villus has a core containing blood vessels, lymphatics, plasma cells and lymphocytes. The lamina propria is a thin layer of connective tissue that lies underneath the epithelial layer, containing plasma cells, lymphocytes, macrophages, eosinophils and mast cells.
Enterocytes are found at the bottom of the crypts of Lieberkuhn.
122
What artery supplies that small intestine?
Branches of the superior mesenteric artery
123
What is the enteric nervous system?
The nervous system that controls bowel functioning, involving two plexuses - the myenteric plexus and submucosal plexus.
This controls gut motility!
124
What is the physiology of the small bowel?
- Digestion and absorption of nutrients and ions
- Regulation of fluid absorption and secretion
It has physical and innate defence systems to prevent colonization and invasion by pathogens.
125
What is the role of the duodenum?
1. Takes in secretions from the pancreas and gallbladder, by producing CCK and secretin
2. Slows gastric emptying
3. Increases pancreatic activity
126
What is the role of the jejunum?
Lots of villi to increase surface area, involved in nutritional absorption and regular peristalsis
127
What is the role of the ileum?
Absorption of vitamin B12 and bile salts and whatever products of digestion were not absorbed by the jejunum
128
What are taenia coli?
Three separate longitudinal ribbons of smooth muscle on the outside of the ascending, transverse, descending and sigmoid colons. They contract lengthways to produce haustra
129
What is the role of the large intestine?
1. Absorption of water and minerals
2. Mass movement (peristalsis twice an hour)
3. Defaecation
130
What are the symptoms of intestinal obstruction?
- Vomiting
- Colicky pain (may be faeculent = severe)
- Constipation (may not be absolute) or diarrhoea
- Distension (due to increased production of gas - can compress surrounding veins and cause ischaemia)
- Tinkling bowel sounds
- Fever and tachycardia (sepsis may occur as anaerobic bacteria produce toxins which get into the bloodstream)
- Hypotensive or septic shock
131
What are the main causes of small bowel obstruction?
- Post op adhesions (75%)
- Hernias
(intussusception rare but if so will be at the ileocaecal valve)
132
What are the main causes of large bowel obstruction?
- Colon cancer
- Constipation
- Diverticular stricture
- Volvulus (sigmoid or caecal)
133
What is an ileus?
A functional obstruction of the bowel from reduced motility - painless, bowel sounds will be absent.
This is due to absence of normal peristaltic contractions - may be due to surgery, peritonitis, electrolyte imbalances, spinal injury.
134
How can you differentiate between small and large bowel obstruction on AXR?
Small bowel - AXR shows central gas shadows with VALVULAE CONNIVENTES the completely cross the lumen and no gas in the large bowel. Considered dilated if small bowel >3cm in diameter
Large bowel - AXR shows peripheral gas shadows proximal to the blockage but not in the rectum. You can also see HAUSTRA which do not cross the lumens width.
135
What is Riglers sign?
A sign of pneumoperitoneum from bowel perforation - when gas is outlining both sides of the bowel wall - 'double wall sign'
If perforation suspected should do an erect CXR to look for air under the diaphragm
136
What do simple/closed/strangulated mean in reference to bowel obstruction?
Simple - one obstructing point with no vascular compromise
Closed - obstruction at two points forming a loop of grossly distended bowel at risk of perforation (usually at caecum where bowel is thinnest
Strangulated - compromised blood supply, PERITONITIS
137
What is a sigmoid volvulus?
Occurs when the bowel twists on its mesentery to produce rapid, severe strangulated obstruction
AXR: coffee bean!!
138
How is sigmoid volvulus managed?
- Sigmoidoscopy
| - Insertion of flatus tube
139
What investigations should be done for bowel obstruction?
BLOODS: FBC, U&E, amylase, LFTs
IMAGING: AXR, erect CXR (CT if unclear)
OTHER: gastrografin contrast XR, consider colonoscopy but risk of perforation
140
How is bowel obstruction managed?
Drip and suck - NGT and IV fluids to rehydrate and correct electrolyte imbalance
If strangulated or closed loop, emergency surgery needed (usually only large bowel!)
141
How is abdominal wound dehiscence managed?
- Cover wound with saline soaked gauze
- Broad spectrum IV abx
- Analgesia and IV fluids
- Return to theatre
142
What is acute mesenteric ischaemia and what causes it?
```
Acute reduced blood supply to the intestine. Small bowel requires a lot of blood and nutrients!
Due to :
- Arterial thromobosis/embolus
- Non-occlusive disease (related to cardiac output, hypovolaemia)
- Venal thrombosis
- Trauma
- Vasculitis
- Radiotherapy
- Strangulation
```
143
How does acute mesenteric ischaemia present?
Clinical triad!!!
1. Acute severe abdo pain
2. No abdo signs (soft)
3. Rapid hypovolaemia and shock
Infarction usually happens about 12 hours later causing vomiting and bloody diarrhoea
144
What do investigations show in acute mesenteric ischaemia?
Bloods - raised Hb, raised WCC, raised amylase, metabolic acidosis, lactate
Imaging - AXR shows gasless abdomen, CT/MRI angiography may show occlusion
Other - MR oximetry is reduced
145
What are the complications of acute mesenteric ischaemia?
1. Ileus
2. Septic peritonitis (ischaemia causes ROS production and cell death. Reperfusion injury then causes damage/inflammation to epithelial lining of the small intestine)
3. SIRS and multi organ dysfunction
146
How is acute mesenteric ischaemia managed?
1. Resuscitation with fluids
2. Gentamicin and metronidazole
3. Heparin
4. Infusion of thrombolytics through angiography catheter
5. Surgical removal of ischaemic bowel
147
AF with abdo pain?
INVESTIGATE FOR MESENTERIC ISCHAEMIA
148
What is chronic mesenteric ischaemia and what causes it?
aka 'intestinal angina'
Chronic hypoperfusion of the intestine due to vascular disease.
149
What are the symptoms of chronic mesenteric ischaemia?
Clinical triad!!
1. Severe, colicky post-prandial abdo pain (gut claudication)
2. Weight loss as eating hurts!
3. Upper abdo bruit
May have PR bleed, malabsorption, nausea and vomiting
150
How is chronic mesenteric ischaemia diagnosed?
CT angiography and contrast enhanced MR angiography
151
How is chronic mesenteric ischaemia managed?
SURGERY - percutaneous transluminal angioplasty and stent insertion
152
What is chronic colonic ischaemia?
aka 'ischaemic colitis'
Hypoperfusion of the colon due to low flow in the IMA territory. Commonly affects the splenic flexure due to anatomy of vascular supply.
153
How does chronic colonic ischaemia present?
Lower left abdo pain, bloody diarrhoea
154
How is chronic colonic ischaemia diagnosed?
Flexi sigmoidoscopy and biopsy (shows epithelial cell apoptosis and lamina propria fibrosis) - barium swallow shows thumb printing at splenic flexure
155
How is chronic colonic ischaemia managed?
Fluids and antibiotics!!!
If gangrenous (peritonitic/shock) need rests and surgical resection of affected bowel with stoma formation.
156
What causes bloody diarrhoea?
Campylobacter (should stay off work!!), UC/Crohns, colorectal cancer
157
What causes mucus in stools?
IBS, colorectal cancer, polyps
158
What causes pus in stools?
IBD, diverticulitis, fistula
159
What causes explosive diarrhoea?
Cholera, giardia, rotavirus
160
What bloods should be done for diarrhoea?
FBC (look for iron deficiency anaemia, corresponding with IBD)
ESR/CRP (if raised, implies inflammatory or infective process, or cancer)
U&E (low potassium may be caused by severe D&V)
TSH (hyperthyroid can cause bowel symptoms)
Coeliac serology
161
What other tests may be necessary in diarrhoea?
- PR
- Stool sample
- C13 breath test
- Sigmoidoscopy
- Colonscopy
162
How should diarrhoea be managed?
Lifestyle factors - drink fluids, stay off work
Primary care - codeine/loperamide to stop, treat cause (avoid antibiotics!!)
Secondary care - referral to specialist clinic (eg IBD)
163
What bloods should be done for constipation?
Often none necessary, especially in the young.
If over 40, change in bowel habit, associate symptoms you should investigate.
FBC, ESR, U&E, Calcium, TFT
164
What other tests may be necessary in diarrhoea?
- Sigmoidoscopy
- Colonoscopy
- Barium enema
165
How should constipation be managed?
Lifestyle factors - eat more fibre, drink fluids, exercise
Primary care - Bulking agents (eg bran/ispaghula husk), stimulant laxatives (eg. docusate, senna), stool softeners (eg. liquid paraffin), osmotic laxatives (eg. macrogol, lactulose)
Secondary care - if laxatives dont work, refer to secondary care for further invesitgations.
166
What are the indications and contraindications for bulk forming laxatives?
eg. isphagula husk
I: colostomy, IBS, chronic constipation (affect takes days)
CI: faecal impaction, colonic atony
167
What are the indications and contraindications for stool softeners?
eg. docusate
I: angina, stroke, hernia, post surgery, faecal impaction (any time you want to avoid straining)
CI: peanut allergy
168
What are the indications and contraindications for stimulants?
eg. senna, bisacodyl
I: diet, bed rest, bowel prep
CI: crampy abdo pain, obstruction
169
What are the indications and contraindications for osmotic laxatives?
eg. lactulose, phosphate, macrogol
I: hepatic encephalopathy
CI: bloating
170
Which laxatives should be used for opiate induced constipation?
Stool softeners or osmotic
171
Which laxatives should be used for faecal impaction?
Docusate or macrogol (?)
172
Describe the structure of the colon and rectum
- Made up of caecum, ascending, transverse, descending, sigmoid, rectum.
- Muscle wall has inner circular layer and outer longitudinal layer.
- The outer layer comes together to form the taenia coli which produces the haustral pattern seen.
173
Describe the mucosa of the colon and rectum
Colon - columnar epithelial
| Rectum - squamour epithelial
174
Describe the blood supply to the colon
Caecum to splenic flexure - SMA
| Splenic flexure to rectum - IMA
175
How does defecation occur?
1. Stool propelled into the rectum by colonic contractions
2. After 100ml of stool filled, the rectum contracts and the internal anal sphincter relaxes
3. This pushes the stool down into the proximal anal canal
4. This increases the defecatory urge which can only be suppressed by contraction of the external sphincter and puborectalis muschles
5. Once these relax, stool is expelled
176
What are the common causes of incontinence?
- Anal sphincter dysfunction (surgery, obstetric injury, trauma, crohns, radiation)
- Rectal prolapse
- Faecal impaction with overflow diarrhoea
- Severe diarrhoea (infective, IBS, UC)
- Neurological (spinal trauma, stroke, MS, diabetes, dementia)
177
How can anal sphincter damaged by assessed?
Endoanal USS or pelvic MRI
178
What is the difference between a diverticulum, diverticulosis, diverticulitis and diverticular disease
DIVERTICULUM - outpouching of gut wall, usually at site of entry of perforating arteries (occur in over 50% of patients over 50)
DIVERTICULOSIS - presence of diverticulum
DIVERTICULAR DISEASE - symptomatic presence of diverticulum (often inflamed)
DIVERTICULITIS - inflammation of a diverticulum (often when faeces obstruct the neck of the diverticulum, allowing bacteria to multiply and produce inflammation?
179
What are the symptoms of diverticular disease and diverticulitis?
95% asymptomatic with disease. Often incidental finding on colonoscopy. May have intermittent LIF pain and rectal bleed.
Diverticulitis presents as severe LIF pain pyrexia, PR bleed, constipation, peritonoism. O/E tenderness, guarding, rigidity (similar to appendicits but opposite side!)
180
What are the complications of diverticular disease?
- Bowel perforation
- Abscess formation
- Fistulae
- Peritonitis
181
Where does diverticular disease usually occur?
Sigmoid colon
182
How should diverticular disease be investigated and treated?
INVESTIGATION: Colonoscopy, barium enema, flexi sig.
TREATMENT: conservative eg. high fibre diet, smooth muscle relaxants eg. mebevarine
183
How should diverticulitis be investigated?
BLOODS: FBC, ESR, U&E
IMAGING: CT colonography, erect CXR, US (these are also to look for complications)
184
How do you treat uncomplicated acute diverticulits?
- Analgesia
- Oral co-amoxiclav if systemically unwell
- Safety netting
185
How do you treat complicated acute diverticulitis and the complications?
a) No complications- NBM, IV fluids, IV co-amoxiclav
b) Abscess - CT guided percutaneous abscess drainage
c) Perforation - surgical - primary anastamoses or Hartmann procedure at laparotomy (temporary colostomy and partial colectomy)
d) Haemorrhage - ABCDE (see LGI bleed)
e) Fistulae - surgical
186
What is Hartmanns procedure?
Resection of the bowel with stoma formation
187
What is a primary anastamosis?
Join in the bowel, with ot without stoma formation
188
What is a sporadic adenoma?
A benign colorectal polyp which has the potential to become malignant. There are 3 types:
1. Tubular
2. Tubulovillous
3. Villous
189
How are sporadic adenomas managed, incl surveillance?
Endoscopic removal is usually advised due to the malignant potential.
Colonic surveillance is advised for people who have had adenomas removed and are at high risk of developing colorectal cancer (multiple large polyps)
Low risk - 5 year colonoscopy
Medium risk - 3 year colonoscopy
High risk - 1 year colonoscopy
190
What are the 2WW criteria for colorectal cancer?
- Age >40 with unexplained weight loss
- Age >50 with unexplained rectal bleeding
- Age>60 with iron deficiency anaemia or change in bowel habit
- Positve FIT test (faecal immunochemical test - looks at occult blood)
191
What is the most common type of colorectal cancer?
Adenocarcinoma, usually located in the sigmoid colon
192
How do patients with bowel cancer present?
Acute - bowel obstruction, perforation, peritonitis
| Chronic - iron deficiency anaemia, change in bowel habit, tenesmus, palpable mass
193
What are the typical features of a cancer in the ascending colon?
Iron deficiency anaemia, weight loss, abdo pain
194
What are the typical features of a cancer in the descending colon?
Change in bowel habit, PR bleed (as lumen is narrower and stool is hard), obstruction more likely, tenesmus
195
What are the RF for colorectal cancer?
- Neoplastic polyps
- Genetic predisposition (FAP, HNPCC)
- IBD
- Diet/alcohol/smoking
196
What is the pathology of FAP?
Mutation in the APC gene, involved in the tumour suppressor pathway.
Can be classical or attenuated (presents later)
197
How are Lynch syndrome and FAP transmitted?
Dominant inheritance
198
What are the colonic and extracolonic features of FAP?
Colonic - abdo pain and >6wk change in bowel habit at age 16
Extracolonic - retinal pigmentation, childhood hepatoblastoma, thyroid cancer
199
How is FAP managed?
Affected individuals should be offered a total colectomy as malignancy is inevitable
200
A patient with known FAP presents with an osteoma and a soft tissue tumour. What are you worried about?
Gardners syndrome
201
A patient with known FAP presents with confusion and CT scan shows brain tumour. What are you worried about?
Turcot syndrome
202
What is the pathology of Lynch Syndrome/Hereditary non polyposis colorectal cancer?
Mutation in MLH1 mismatch repair gene, leading to a cascade of mutations that cannot be repaired.
This will occur at areas of repeated DNA sequences known as microsatellites.
This leads to a frameshift mutation and a new truncated peptide.
This has two actions:
1. Generation of adenomas
2. The body mounts an inflammatory response against this foreign peptide
203
What is microsatellite instability?
Failure to repair repetitive sequences of DNA, due to faulty mismatch repair genes. This is characteristic of lynch syndrome and is rarely seen in sporadic colorectal cancer
204
What are the symptoms and complications of Lynch syndrome?
Usually asymptomatic
Can progress to COLORECTAL and ENDOMETRIAL cancer (aged 40)
205
How is Lynch Syndrome diagnosed?
Amsterdam Criteria
206
How is Lynch Syndrome managed?
1. Surveillance
2. Chemoprophylaxis with low dose aspirin
3. Surgical prophylaxis
207
How can biopsy differentiate between Lynch syndrome and sporadic colon cancer?
Do a biopsy of tumour tissue and do MSI and BRAF test.
MSI high - lynch syndrome
BRAF high - sporadic cancer
208
A person with known lynch syndrome presents with sebaceous skin tumours. What are you worried about?
Miur Torre Syndrome
209
What tests should be done to diagnose colorectal cancer?
Colonoscopy with biopsy
| CT colonography with air inflation
210
What tests should be done to stage colorectal cancer?
CT thorax and abdomen
Do MRI if rectal cancer
211
What tests should be done to monitor disease and effectiveness of treatment in colorectal cancer?
CEA
212
Describe the staging of colorectal cancer
TNM staging - if any nodal spread should have chemo
| Dukes Criteria
213
How is colorectal cancer managed surgically?
Right hemicolectomy - caecal, ascending or proximal transverse tumour
Left hemicolectomy - distal transverse, descending tumour
High anterior resection- sigmoid tumour
Anterior resection (TME) - upper or low rectal tumour
Abdomino-perineal excision of rectum - anal verge tumour
Hartmanns (resection of sigmoid colon and end colostomy) - emergency surgery due to perforation (don't form anastamosis due to risk of leak)
CONSIDER LAPAROSCOPIC AND ENDOSCOPIC SURGERY
214
Which types of bowel surgery will result in a permanent colostomy?
Abdomino-perineal resection for rectal cancer
215
What is the use of radio/chemo in colorectal cancer?
Radiotherapy usually just palliative (this is due to risk of toxicity) but used preop in rectal cancer
Chemotherapy used as an adjuvant in advanced disease or if squamous cancer (commonly FOLFOX and FOLFIRI)
Targeted theraies (bevacizumab and cetuximab) for metastatic disease
216
What is the prognosis of colorectal cancer?
5 year survival is 50%
217
Describe the screening programme for colorectal cancer
People age 60-75 have 2 yearly FIT tests (50-74 in Scotland)
People aged 55 have one-off flexi sig (not available nationally)
218
What are haemorrhoids?
Dilated anal cushions, causing bleeding, itch and potential discharge.
219
How should haemorrhoids be investigated?
- Abdo exam
- PR exam
- Proctoscopy - internal haemorrhoids
- Rigid segmoidoscopy
220
How are haemorrhoids classified?
1st degree - remain in rectum
2nd degree - prolapse through anus on defecation but spontaenously reduce
3rd degree - prolapse but require digital reduction
4th degree - persistently prolapsed
221
How are haemorrhoids managed?
Conservative - increase fluids and fibre
Medical - topical analgesics, stool softener
Non-operative - rubber band ligation, sclerosants (phenol injected into pile), cryotherapy, infra-red coagulation
Surgical - excisional haemorrhoidectomy or stapled haemorrhoidopexy
222
What are the symptoms of an anal fissure?
Severe pain, minimal blood
Visible tear (usually posterior midline due to pressure - if unusual location/size, think CROHNS/syphilis/herpes/trauma)
Acute <6 weeks
Chronic > 6 weeks
223
How is an anal fissure managed?
Conservative - increase fibre, fluids, hygeine advice
Medical - bulk-forming laxatives/stool softeners, lubricants, topical GTN/lidocaine
Other - botox injection/sphinceterotomy (if not effective after 8 weeks for GTN)
Acute 1st line - bulk-forming laxatives
Chronic 1st line - topical GTN,
224
What are the symptoms of a perianal abscess?
Pain, discharge, itch. May be systemically unwell. Usually caused by gut organisms but associated with DM, Crohns, malignancy, fistulae
225
How is a perianal abscess managed?
Surgery - incise and drain under GA
226
What are the symptoms of a fistulae?
This is an abnormal communication between the skin and the anal canal - due to blockage of deep IM gland ducts causing an abscess and bursting to form a fistulae.
Causes pain, discharge, itch
227
How is an anal fistula managed?
Fistulotomy and excision (depends on depth of fistula)
High - seton suture
Low - laid open to heal by secondary intention
228
What can cause abdominal distension?
Flatus, fat, fluid, faeces, fetus
229
What can cause ascites (with/without portal hypertension)?
WITH - Cirrhosis, portal nodes, Budd-Chiari syndrome
WITHOUT - Malignancy, infections eg. TB, CCF, pancreatitis, nephrosis, myxoedema
230
What is the first line investigation for abdominal lumps?
Ultrasound
231
What is peritonitis?
Inflammation of the peritoneum, typically caused by perforation of a peptic/duodenal ulcer, diverticulum, appendix, bowel or gallbladder. Generalised peritonitis is a surgical emergency, often involves E coli infection.
Signs: prostration, shock, lying still, positive cough test, tenderness, rebound, guarding, rigidity
232
How is peritonitis managed?
Tests - FBC, CRP, U&E, amylase, LFT, ABG, urinalysis, erect CXR (gas), AXR, USS/CT
Treatment - Laparotomy (after resuscitation) but quickly to prevent abscess formation
233
What is colic?
Regularly waxing and waining pain, caused by muscular spasm in a hollow viscus. Pt will be walking around the room.
234
What does sudden onset acute abdo pain suggest?
- Perforation
- Rupture (eg. ectopic pregnancy, aorta, spleen)
- Torsion
- Acute pancreatitis
- Mesenteric infarction
235
How does acute appendicitis occur?
Obstruction of the lumen of the appendix with a faecolith (stone made of faeces), causing colonisation by E coli and Bacteroids, oedema, ischaemia, necrosis and perforation
236
What are the symptoms of acute appendicitis?
Periumbilical pain that moves to the RIF
Anorexia
Vomiting (often from the pain)
Constipation/diarrhoea
237
What are the specific signs in appendicitis?
Rosving's sign - pain > in RIF when you press on LIF
Psoas sign - pain on extending hip if retrocaecal appendix
Cope sign - pain on flexion and internal rotation of right hip
238
What is the gold standard imaging in acute appendicitis?
CT however may be too slow! (always do FBC, CRP and urinary pregnancy test to rule out ectopic)
239
How is acute appendicitis managed?
Appendicectomy (can be open or laparoscopic) then IV fluids and ?IV antibiotics
240
What are some DDs for acute appendicitis?
- Non specific mesenteric lymphadenitis
- Acute terminal ileitis due to Crohns
- Gynae eg. ruptured ectopic
- Inflamed Meckels diverticulum
- Functional bowel disease
- Pyelonephritis
- Ovarian torsion
241
What is Rovings sign?
Palpation of the left lower quadrant produces pain in the right lower quadrant - this is indicative of appendicitis
242
What is Murphys sign?
Pain on taking a deep breath, when the examiner is pressing down on the right upper quadrant - this is indicative of cholecystitis
243
What is McBurneys point?
A point that lies one-third of distance laterally on a line drawn from the umbilicus to the right anterior superior iliac spine - this is where the appendix lies
244
How is IBD investigated, diagnosed and monitored?
Investigations:
- FBC - anaemia, malabsorption
- Low albumin
- Raised CRP/ESR
- Faecal calprotectin
Diagnosis:
- Colonoscopy with biopsy (UC) or radiology (Crohns)
*avoid colonoscopy if severe colitis due to risk of rupture > flexsig
Monitoring:
TPMT - used often for monitoring treatment
245
Where does UC affect?
Anywhere distal to the ileocaecal valve (often anal sparing)
Most common site is rectum
Spreads proximally from rectal sigmoid area to splenic flexure - left sided colitis
If reaches transverse colon - extensive colitis
246
Describe the inflammation in UC
Uniform and continuous
Confined to the sunmucosa (superficial)
Crypt abscesses
Pseudopolyps
Drainpipe colon
247
What are the symptoms of UC?
Crampy abdo pain, bloody diarrhoea, tenesmus, fatigue, systemically unwell during attacks
Extra-intestinal:
- Arthritis
- Erythema nodosum
- Osteoporosis
- Uveitis
- PSC
- Clubbing
Mild <4 stools daily
Moderate 4-6 stools, some blood
Severe >6 bloody stool, systemic upset
248
What are the complications of UC?
- Perforation
- Toxic megacolon
- Venous thrombosis
- Colon cancer (should have colonoscopy everey 1-5 years with multiple biopsies at regular intervals
These may necessitate a stoma (about 20% of patients)
249
How is UC treated?
Mild to moderate:
- Topical aminosalicylate eg. mesalazine/sulfasalazine suppositories/enema
If no remission in 4 weeks or extensive colitis:
- Add oral aminosalicylate or oral/topical steroids
Moderate to severe:
- Topical aminosalicylate and high dose oral salicylate (+/- steroids after 4 weeks)
- Tofacitinib, Vedolizumab, Infliximab (should have tried other options first unless contraindicated)
Acute severe:
- IV hydrocortisone
- IV cyclosporin
- Infliximab
Maintaining remission:
- Topical aminosalicylate or oral salicylate if extensive
- Oral azathioprine/mercaptopurine if multiple relapses or severe disease
250
Where does Crohns disease affect?
Mainly terminal ileum and proximal colon, but can affect anywhere in the gut (often rectal sparing)
251
Describe the inflammation in Crohns disease
Transmural, skip lesions (unaffected bowel between areas of active disease)
Granulomas, cobblestone appearance, pseudopolyps
252
What are the symptoms for Crohns disease?
Abdo pain, diarrhoea, fatigue, mouth ulcers (primary), systemically unwell
More common in females
Extra-intestinal:
- Arthritis
- Erythema nodosum
- Episcleritis
- Pyoderma gangrenosum
- Clubbing
253
What are the complications of Crohns?
- Small bowel obstruction (due to narrowing and thickening)
- Abscess formation
- Fistulae
- Perforation and rectal haemorrhage
- Anal strictures
- Granulomas
- Colon cancer
COMPLICATIONS MORE SERIOUS DUE TO TRANSMURAL PATHOLOGY
254
How is Crohns treated?
First presentation/single episode:
- Prednisolone PO
- Hydrocortisone IV
- Budenoside (if steroids CI)
INDUCING REMISSION (if >2 exacerbations in a year and TPMT positive):
- Azathioprine PO
- Mercaptopurine PO
- Methotrexate (if cant tolerate above two)
- Add in infliximab (if refractory or fistulating)
255
How can you tell if a stoma bag is an ileostomy or colostomy?
Ileostomy - protect skin due to enzymes, right sided
| Colostomy - ok to touch skin, left sided
256
What drug should be used in fistulating Crohns?
Metronidazole/ciprofloxacin (if isolated peri-anal disease)
Infliximab
257
What are the extracolonic features of IBD?
- Conjunctivitis
- Iritis
- Mouth ulcers
- Fatty liver
- Liver abscess
- Venous thrombosis
- Large joint arthritis
- Erythema nodosum
- Pyoderma gangrenosum
These are due to release of cytokines eg. TNFa
258
When do you diagnose IBS?
Abdo pain and discomfort, bloating or a change in bowel habit for at least 6 months.
This pain should be relieved by defection or associated with altered bowel frequency or stool form.
This should be accompanied by at least 2 of:
- Altered stool passage
- Abdominal bloating
- Symptoms exacerbating by eating
- Passage of mucus
259
What test is performed to diagnose IBS?
Diagnosis of exclusion.
Do FBC, ESR, CRP and faecal calprotectin, coeliac test to distinguish from IBD
260
How is IBS managed?
CONSERVATIVE:
High fibre diet (FODMAP), fluids, encourage physical activity
MEDICAL:
1st line: antispasmodics eg mebevarine, hyoscyamine or laxatives, loperamide if needed
2nd line: linaclotide, TCA, SSRI
OTHER:
CBT, psychological therapy (often associated with ME, fibromyalgia, affective disorders)
261
What is the cause of Coeliac disease?
Autoimmune - associated with HLADQ2 and DQ8 genetics
262
How does coeliac disease present?
- Foul smelling stools and steatorrhoea
- Abdo pain/bloating
- Nausea and vomiting
- Mouth ulcers
- Angular stomatitis
- Weight loss, failure to thrive
- Fatigue
- Osteomalacia
- Unexplained iron deficiency and folate anaemia
Peak presentation in infancy and aged 50-60
263
How does coeliac present biochemically?
Macrocytic anaemia (low B12/ferritin)
Positive IgA and tTG - if weakly positive, do EMA or DGP
HLA typing - HLA-DG2/8 in most individuals (this is not used in initial diagnosis, only in specialist setting or refractory coeliac)
264
What does small bowel biopsy show in coeliac?
- SUBTOTAL VILLOUS ATROPHY
- Biopsy should be of duodenal or jejunum
| - Increased intra epithelial WBCS and crypt hyperplasia
265
How is coeliac managed?
Lifelong gluten free diet - this can be monitored by serial tests for EMA and TTG
Patient should have pneumococcal vaccinations every 5 years (due to splenic atrophy)
266
What are the complications of coeliac?
- Anaemia
- Secondary lactose intolerance
- GI T-cell lymphoma
- Risk of malignancy
- Myopathies
- Neuropathies
- Hyposplenism
- Ulcerative jejunitis
267
What is dermatitis herpetiformies?
Blistering, sub epidermal eruption of skin associated with gluten-sensitive enteropathy - improves from gluten free diet
268
What conditions can cause malabsorption in the small bowel?
- Coeliac disease
- Whipples disease
- Parasite
- Thyrotoxicosis
- Zollinger-Ellison syndrome
- Lymphoma
- Diabetes mellitus
269
Which tumours can arise in the small intestine?
Relatively resistant to neoplasia!
- Adenocarcinoma of small intestine (duodenum)
- Lymphoma (ileum)
- IPSID
- Carcinoid tumours
270
What are 3 different types of colostomy?
1. Loop - entire loop of bowel is exteriorised and partially divided, forming 2 stomas that are joined together. These are usually temporary
2. End - bowel divided and proximal end brought out as a stoma. Distal end may be resected (AP resection), closed and left (Hartmanns procedure) or exteriorised forming a mucus fitstulae
3. Paul-Mikulicaz - double barrelled colostomy in which colon is divided completely and each end is exteriorised as two separate stomas.
271
What is a low anterior resection?
When all or part of the rectum is excised and the proximal colon anastomosed to the top of the anal canal
272
How is parenteral nutrition administered?
Nutrition given through central venous line or PICC (peripherally inserted central catheter). Insertion is sterile and requires x-ray to check.
Check weight, fluid balance, urine glucose daily through PEG nutrition.
273
What is refeeding syndrome?
After a period of starvation, insulin and phosphate levels drop. When refeeding begins, insulin rises and this increases cellular uptake of phosphate
Causes hypophosphatemia within 4 days, leading to rhabdomyolysis, red and white cell dysfunction, respiratory insufficiency, arrhythmias, cariogenic shock, seizures and sudden death.
Treat with parenteral phosphate and oral supplementation.
274
What is Boerhaaves syndrome?
Transmural tear of distal oesophagus, induced by a sudden increase in pressure
Classical triad:
1. Vomiting (often with alcohol excess)
2. Abdo/chest pain
3. Subcutaneous emphysema
275
What is a paralytic ileus?
Complication of bowel surgrey - no peristalsis causing pseudo-obstruction
May be caused by deranged electrolytes, replace IV
276
What does it mean if a stoma is spouted?
That it is an ileostomy - protects skin from acidic bowel contents
277
What is an end ileostomy?
An end ileostomy is usually done following complete excision of the colon or where the ileocolic anastomosis is not planned. It may be used to defunction the colon, but a reversal is difficult.
278
What is a loop ileostomy?
A loop ileostomy involves taking a loop of the ileum, performing a horizontal incision and bringing it up to the skin. It is indicated to defunction the colon, for example, after rectal cancer surgery. Eventually, it can be reversed.
279
What is a loop jejunostomy?
A loop jejunostomy is rarely used as a very high output stoma. It may be used following emergency laparotomy with planned early closure.
280
What is a percutaneous jejunostomy?
A percutaneous jejunostomy involves the insertion of a feeding tube directly into the jejunum. You would notice a tube on the abdomen of the patient rather than a stoma bag.
281
What is the grading system for internal haemorrhoids?
Grade I Do not prolapse out of the anal canal
Grade II Prolapse on defecation but reduce spontaneously
Grade III Can be manually reduced
Grade IV Cannot be reduced
282
What is the location of a femoral hernia?
Inferolateral to pubic tubercle
283
What is the location of an inguinal hernia?
Supermedial to the pubic tubercle
284
What is a pharyngeal pouch?
Posteromedial diverticulum through Killians dehisecnce (area in pharynx)
Presents with dysphagia, regurgitation, aspiration, neck swelling which gurgles on palpitation, halitosis
Investigate with barium swallow
Surgical management
285
What is Peutz-Jeghers syndrome? How is it managed?
- AD condition for gene encoding LKB1 or STK11
- Numerous hamartomatous polyps in GI tract
- Pigmented freckles on lips, face, palms and soles
- Pts will die from GI tract cancer
Management:
- Conservative unless complications develop
286
How is c.difficile infection classified?
Mild
- Normal WCC
Moderate
- High WCC
- 3-5 loose stools daily
Severe:
- high WCC/creatinine/temp 38.5/severe colitis
Life threatening:
- Hypotension
- Partial or complete ileus
- Toxic megacolon or severe disease on CT
287
How is c.difficle managed?
First episode:
- 1st line oral vancomycin 10d
- 2nd line oral fidaxomicin
- 3rd line oral vancomycin +/- IV metronidazole
Recurrent episodes:
- Oral fidaxomicin if within 12 weeks
- Oral vanc/fidax if after 12 weeks
- Consider faecal transplant
Life threatening:
- ADMIT
- Oral vanc + IV metro
- May require surgery
288
What is melanosis coli?
- Disorder of pigmentation of the bowel wall
- Histology shows pigment-laden macrophages
- Associated with laxative abuse esp senna f
289
