GI Flashcards
What is a bowel/intestinal obstruction? What are the three key types? Of these three types, which is the most common? How serious are they?
- A bowel obstruction is an arrest of the onward propulsion of intestinal contents. 3 types:
- Small bowel obstruction
- Large bowl obstruction
- Pseudo-obstruction
- Small bowel obstructions are the most common (60-75%)
- All intestinal obstuctions can be serious and potentially fatal
What are the three big causes (90% of cases) of intestinal obstruction?
- Adhesions (small bowel)
- Hernias (small bowel)
- Malignancy (large bowel)
Describe the aetiology of small bowel obstruction. What are these due to?
- ADHESIONS (~60%) - usually due to previous abdo/pelvic surgery, but can be caused by previous abdo infections, e.g. peritonitis
- Hernias - due to intestinal contents being unable to pass through a strangulated loop
- Malignancy
- Crohn’s disease
Describe the pathophysiology of small bowel obstruction.
- Obstruction of the bowel leads to distension above the blockage due to a build up of fluid & contents
- This causes increased pressure which pushes on the blood vessels within the bowel wall causing them to become compressed
- These compressed vessels cannot therefore supply blood resulting in ischaemia & necrosis, and eventually perforation
What is the clinical presentation of small bowel obstruction?
- Pain - INITIALLY COLICKY BUT THEN DIFFUSE. Pain is higher in the abdomen than LBO
- Profuse vomiting following pain. Vomiting OCCURS EARLIER IN SBO THAN LBO
- Abdominal distension - but less than LBO
- INCREASED BOWEL SOUNDS (TINKLING from AIR/FLUID)
- Tenderness - suggests strangulation/risk of perforation
- Constipation with no passage of gas occurs late in SBO
What are the investigations for small bowel obstruction? What is diagnostic?
- ALL bowel obstructions are are diagnosed first by abdo X-ray and then by a confirmatory CT scan
- Abdominal X-ray (1st line):
- Key finding = DISTENDED LOOPS OF BOWEL proximal to obstruction
- Shows central gas shadows that completely cross the lumen
- Non-contrast CT = Gold standard. Accurately localises the obstruction
- Examination of hernia orifices and rectum
- FBC
Describe the management for small bowel obstruction.
- DECOMPRESSION OF THE BOWEL:
- ‘Drip and suck’ - Nil by mouth and IV fluids with Nasogastric (NG) tube. If this fails, then surgery
- Aggressive fluid resuscitation
- Analgesia & anti-emetics for symptoms
- Antibiotics
- Surgery to remove obstruction - usually laparotomy (open)
Why are large bowel obstructions less common than small bowel obstructions?
Because the lumen is much larger and can distend more, therefore is harder to block
What is the aetiology of large bowel obstruction?
- MALIGNANCY (90%). More common in the EU/West than Africa
- VOLVULUS = rotation/twisting of the bowel on its mesenteric axis. Sigmoid colon is the most common place for this to occur as it has a mesentery
- Diverticulitis
- Crohn’s disease
- Intussusception = when the bowel rolls inside of itself. Almost exclusively in neonates/infants as they have ‘softer’ bowels
Describe how Crohn’s disease can cause intestinal obstruction.
Crohn’s disease -> fibrosis -> contraction -> obstruction
Describe how Diverticular disease can cause intestinal obstruction.
Out-pouching of mucosa -> faeces trapped -> inflammation in bowel wall -> contraction -> obstruction
What is the clinical presentation of large bowel obstruction?
- Abdominal pain = MORE CONSTANT AND DIFFUSE THAN SBO. Usually occurs lower in abdomen, especially LIF
- Abdominal distension - MUCH MORE THAN SBO
- Normal bowel sounds initially, then increased and eventually silent as no movement
- Palpable mass, e.g hernia. Most common in LIF
- VOMITING OCCURS MUCH LATER THAN SBO, AND MAY BE ABSENT
- CONSTIPATION EARLIER THAN IN SBO
What are the investigations for large bowel obstruction? What is diagnostic?
- Abdominal X-ray (1st line):
- Peripheral gas shadows proximal to blockage, but doesn’t show rectum hence why DRE is essential. Caecum and ascending colon will be distended
- CT = gold standard
- Digital rectal exam (DRE):
- Empty rectum
- Hard, compacted stools
- Might be blood
- FBC
What is the management for large bowel obstruction?
EXACTLY THE SAME AS SMALL BOWEL OBSTRUCTION:
- DECOMPRESSION OF THE BOWEL:
- ‘Drip and suck’ - Nil by mouth and IV fluids with Nasogastric (NG) tube. If this fails, then surgery
- Aggressive fluid resuscitation
- Analgesia & anti-emetics for symptoms
- Antibiotics
- Surgery to remove obstruction - usually laparotomy (open)
What is pseudo-bowel obstruction?
Bowel obstructions that present identically to SBOs or LBOs, dependent on the location (can present as both at the same time if whole bowel is obstructed), although a blockage cannot be found
What is the best way to manage a pseudo-bowel obstruction?
Treat the underlying cause
What is oesophageal cancer? What are the two main histological types? Describe these two types.
- Oesophageal cancer = rare malignancy of oesophageal epithelium
- Two main types:
- Adenocarcinoma = most common in the developed world. Typically found in the lower 1/3 of the oesophagus. Often caused by Barrett’s oesophagus but smoking is also a risk factor
- Squamous cell carcinoma = most common in the developing world. Typically found in the upper 2/3 of the oesophagus. Most common risk factors are smoking and alcohol ingestion
What are the risk factors for oesophageal adenocarcinoma?
- Barrett’s oesophagus
- GORD
- Smoking
- Achalasia
- Obesity
What are the risk factors for oesophageal squamous cell carcinoma?
- Alcohol
- Smoking
- Achalasia
- Obesity
- Low fruit/veg/fibre/vit A/C
- Hot drinks
- Plummer-Vinson syndrome
What is the clinical presentation of oesophageal cancer?
- PROGRESSIVE DYSPHAGIA - solids then liquids
- Vomiting
- Anorexia and weight loss
- Odynophagia, hoarseness, melaena, cough
What are the investigations for oesophageal cancer?
- Upper GI endoscopy and biopsy (1st line)
- CT scan or endoscopic ultrasound (staging)
Describe the management of oesophageal cancer.
- Medically fit and metastases = surgical resection and then adjuvant chemotherapy
- Medically unfit and metastases = palliative care. Stents can help with dysphagia
What is gastric/stomach cancer? What are the two histological types?
- Gastric cancer = aggressive adenocarcinoma arising from gastric mucosa
- Two types:
- Type 1 (intestinal/differentiated, 70-80%)
- Type 2 (diffuse/undifferentiated, 20%)
What are the risk factors, histology, appearance and location of type 1 (intestinal/differentiated) gastric cancer?
- Risk factors: male, H.PYLORI, chronic and atrophic gastritis, older age, diet (nitrates and nitrosamines), smoking, alcohol
- Histology: glandular epithelium
- Appearance: large, irregular (polyploid/ulcerated with heaped up edges)
- Location: antrum and lesser curvature
What are the risk factors, histology, appearance and location of type 2 (diffuse/undifferentiated) gastric cancer?
- Risk factors: blood type A, genetic, younger age, diet (nitrates, nitrosamines), smoking, alcohol
- Histology: poorly differentiated, signet ring cells
- Appearance: GASTRIC LINITIS. Submucosa invasion. No movement on barium swallow (late sign)
- Location: anywhere, especially cardia (defective adhesion because of CDH-1 mutation = defective E-cadherin = increased ability to invade and spread
A mutation in what gene can cause familial diffuse gastric cancer? What is performed in this instance?
CDH1 - 80% chance of gastric cancer.
Prophylactic gastrectomy is done in these patients
What is the clinical presentation of gastric cancer?
- Often late presentation:
- Anorexia, nausea, weight loss, anaemia, dysphagia, vomiting
- Haematemesis
- Malaena
- Epigastric pain - better with ant-acids
- Paraneoplastic syndromes, e.g. polycythaemia
- Metaplastic signs, e.g. Krukenberg tumour
What are the investigations for gastric cancer? When would the endoscopy be urgent?
- Gastroscopy with biopsy: 8-10 biopsies
- CT/MRI/PET
- Endoscopic USS. 2 week wait for endoscopy if upper abdominal mass consistent with stomach cancer and: dysphagia of any age, >55 + weight loss with upper abdominal pain, reflux or dyspepsia. Consider non-urgent endoscopy if haematemesis, treatment resistant dyspepsia, upper abdominal pain + anaemia
- Laparoscopy final line
What is the management for proximal and distal gastric cancer? What do we have to give to the patient for the rest of their lives after this type of surgery?
- Nutritional support
- Proximal gastric cancer with no spread: 3 cycles of chemo and then a full gastrectomy. Lymph node removal too
- Distal gastric cancer with no spread: 3 rounds of chemotherapy and then a partial gastrectomy if the tumour is causing stenosis or bleeding. Lymph node removal too
- Gastrectomy = lack of intrinsic factor = give vitamin B12 to prevent pernicious anaemia
What vitamin supplement will a patient need following gastrectomy?
They will be deficient in intrinsic factor and so will need vitamin B12 supplements to prevent pernicious anaemia
What is the epidemiology of colorectal cancer? What are the risk factors?
- 3rd most common cancer in Western world, 4th leading cause of cancer deaths in the US
- Risk factors:
- Family history of bowel cancer
- FAMILIAL ADENAMATOUS POLYPOSIS (FAP) (autsomal dominant)
- HEREDITARY NONPOLYPOSIS COLORECTAL CANCER (HNPCC) - also known as LYNCH SYNDROME
- IBD (Crohn’s or ulcerative colitis)
- Increased age
- Diet (high in red and processed meat and low in fibre)
- Obesity and sedentary lifestyle
- Smoking
- Alcohol
- Radiotherapy
- Hormonal factors; nulliparity, late first pregnancy, early menopause
Where do colo-rectal cancers most commonly occur?
Rectum (38%) and sigmoid colon (20%)
Give three signs of rectal cancer.
- Change in bowel habit, e.g. more frequent and loose stools
- Rectal bleeding
- Unexplained weight loss
Give 4 signs of left-sided colon cancer.
- Change in bowel habit (more loose/frequent stools)
- Abdominal pain
- Abdominal mass upon inspection
- Rectal bleeding
Give 4 signs of right-sided colon cancer.
- Abdominal pain
- Abdominal mass upon inspection
- Unexplained weight loss
- Change in bowel habit (more frequent and loose stools)
What are the investigations for colo-rectal cancer? What is FIT used for?
- Colonoscopy - gold standard
- Flexible sigmoidoscopy, barium enema, CT colonography
- Faecal immunochemical test - look for amount of human haemoglobin in the stool. Used for patients who do not meet the specific criteria for a two week wait referral:
- >50 with unexplained weight loss and no other symptoms
- <60 with a change in bowel habit
How do we grade colo-rectal tumours?
USED to be Dukes’ classification but has been replaced by TNM staging
Describe Dukes’ classification system.
- Dukes A – confined to mucosa and part of the muscle of the bowel wall
- Dukes B – extending through the muscle of the bowel wall
- Dukes C – lymph node involvement
- Dukes D – metastatic disease
Describe TNM staging.
- T for Tumour:
TX – unable to assess size
T1 – submucosa involvement
T2 – involvement of muscularis propria (muscle layer)
T3 – involvement of the subserosa and serosa (outer layer), but not through the serosa
T4 – spread through the serosa (4a) reaching other tissues or organs (4b)
- N for Nodes:
NX – unable to assess nodes
N0 – no nodal spread
N1 – spread to 1-3 nodes
N2 – spread to more than 3 nodes
- M for Metastasis:
M0 – no metastasis
M1 – metastasis
Describe the treatment for colo-rectal cancer.
- Caecal, ascending or proximal transverse colon = right hemicolectomy
- Distal transverse, descending colon = left hemicolectomy
- Sigmoid colon = high anterior resection
- Upper rectum = anterior resection (TME)
- Low rectum = anterior resection (low TME)
- Anal verge = abdomino-perineal resection of rectum
Familial adenomatous polyposis (FAP) is a risk factor for colo-rectal cancer. What is FAP? Describe the investigations and management.
- (FAP) = autosomal dominant condition involving malfunctioning of the tumour suppressor genes called adenomatous polyposis coli (APC). It results in many polyps (adenomas) developing along the large intestine. These polyps have the potential to become cancerous (usually before the age of 40)
- Colonoscopy every 1-2 years, beginning at 10-12 years of age
- Patients have their entire large intestine removed prophylactically to prevent the development of bowel cancer (panproctocolectomy)
Hereditary nonpolyposis colorectal cancer (HNPCC) is a risk factor for colo-rectal cancer. What is it? Describe its investigations and management.
- HNPCC (a.k.a. Lynch syndrome) is an autosomal dominant condition that results from mutations in DNA mismatch repair (MMR) genes. Patients are at a higher risk of a number of cancers, but particularly colorectal cancer. Unlike FAP, it does not cause adenomas and tumours develop in isolation
- Colonoscopy every 1-2 years, beginning at 20-25 years of age. After surgery, sigmoidoscopy every 1-2 years if subtotal colectomy was performed, or colonoscopy if segmental resection was performed
What is gastro-oesophageal reflux disease (GORD)? Why is the oesophagus more sensitive to acid than the stomach?
- GORD is where acid from the stomach refluxes through the lower oesophageal sphincter (due to dysfunction) and irritates the lining of the oesophagus
- The oesophagus has a squamous epithelial lining, whereas the stomach has a columnar epithelial lining, so the oesophagus is more sensitive
What are the risk factors for GORD?
- Lifestyle factors: obesity, smoking, alcoholism, fat rich diet, caffeine
- Medications, e.g. antihistamines, CCBs, antidepressants - inhibit the strength at which the LOS can contract
- Hiatus hernia = lowers LOS pressure = increase reflux
- Pregnancy
What is the clinical presentation of GORD?
Dyspepsia is a non-specific term used to describe indigestion. It covers the symptoms of GORD:
- Heartburn (retrosternal chest pain) - related to meals, worse when lying, relieved by antacids
- Acid regurgitation
- Retrosternal or epigastric pain
- Bloating
- Unexplained weight loss, anaemia, dysphagia, upper abdo mass, persistent vomiting (red flags)
- Nocturnal cough
- Hoarse voice
What are the investigations for GORD? What are the key red flag features for an urgent referral?
- Clinical diagnosis
- First line = therapeutic challenge = give PPI = will get better
- Gold standard = oesophageal manometry = 24hr of pH and pressure montoring
- X-ray with barium contrasts = shows stenosis and ulcers
- Endoscopy to assess for peptic ulcers, oesophageal or gastric malignancy. Red flags for urgent referral:
- DYSPHAGIA (difficulty swallowing)
- >55
- Weight loss
- Epigastric pain / reflux
- Treatment resistant dyspepsia
- Nausea and vomiting
- Low haemoglobin (anaemia)
- Raised platelets
Describe the management for GORD.
- Conservative:
- Quit smoking
- Reduce alcohol
- Weight loss
- Avoid heavy meals before bed time and stay upright after meals rather than lying flat
- Medical:
- PPIs (first line) and H2 receptor antagonists (second line, e.g. ranitidine) - both decrease acidification of gastric acid secretions
- Surgical:
- GOLD STANDARD = Nissen Fundoplication = upper part of stomach wrapped around LOS = strengthens sphincters, prevents acid reflux
What are the complications of GORD?
- Barrett’s oesophagus (pre-malignant condition). This is because the cells try to adapt - stratified squamous to simple columnar
- Oesophageal adenocarcinoma
- Oesophagitis
- Oesophageal strictures
What is Helicobacter pylori? Where does it live? What does it cause?
- H. pylori is a gram negative aerobic bacteria. It lives in the stomach. It causes damage the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer. It avoids the acidic environment by forcing its way into the gastric mucosa. The breaks it creates in the mucosa exposes the epithelial cells underneath to acid
- It also produces ammonia to neutralise the stomach acid, which directly damages the epithelial cells
What are the complications of Helicobacter pylori infection?
- Peptic ulcers
- Gastric carcinomas
- Gastritis
What are the investigations for Helicobacter pylori infection?
- Urea breath test using radiolabelled carbon 13
- Stool antigen test
- Rapid urease test can be performed during endoscopy. Also known as a CLO test (Campylobacter-like organism test). It is performed during endoscopy and involves taking a small biopsy of the stomach mucosa. Urea is added to this sample. If H. pylori are present, they produce urease enzymes that converts the urea to ammonia. The ammonia makes the solution more alkali giving a positive result on when the pH is tested
What is the treatment for a Helicobacter pylori infection?
- TRIPLE THERAPY:
- Proton pump inhibitor, e.g. omeprazole
- 2 antibiotics, e.g. amoxicillin and clarithromycin for 7 days
What is Barrett’s oesophagus? What is it caused by? What is it classified as? What is it a risk factor for? What is its pathology?
- Barret’s oesophagus = metaplasia of lower oesophagus epithelium from stratified squamous to simple columnar
- It is caused by the constant reflux of acid
- It is classified as a ‘premaligant’ condition. It is a risk factor for adenocarcinoma of the oesophagus
- Pathology = squamous - metaplasia (goblet cells) - dysplastic (precancer) - neoplastic (cancer)
What are the risk factors for Barrett’s oesophagus?
- GORD
- Male (7:1)
- Caucasian
- FHx
- Hiatus hernia
- Obesity
- Smoking
- Alcohol
What is the clinical presentation of Barrett’s oesophagus?
CLASSIC HISTORY - middle aged caucasian male with a long history of GORD and dysphagia
What are the investigations for Barrett’s oesophagus?
- Upper GI endoscopy (oesophago-gastro-duodenoscopy)
- Biopsy
What is the management for Barrett’s oesophagus?
- Lifestyle: weight loss, smoking cessation, reduce alcohol, small meals, avoid hot drinks/alcohol/eating <3 hrs before bed, avoid certain drugs (nitrates, anticholinergics, TCAs, NSAIDs, K+ salts, alendronate)
- Endoscopic Surveillance with Biopsies
- High dose PPI if non-dysplastic
- Low grade dysplasia - radiotherapy with endoscopic mucosal resection
- Severe (high grade dysplasia): radiotherapy with oesophagectomy
What are oesophageal varices? What are their potential complications?
- Dilated veins at sites of portosystemic anastomosis (left gastric + inferior oesophageal veins)
- As these vessels are thin and not meant to transport higher pressure blood, they can easily RUPTURE = haematemesis OR rupture = blood digested = malaena
What are the prehepatic, hepatic and post-hepatic causes of oesophageal varices?
- Pre-hepatic = portal vein thrombosis/obstruction
- Hepatic = cirrhosis, schistosomiasis
- Post-hepatic = Budd-Chiari, RHF, constrictive pericarditis, compression
What is the clinical presentation of oesophageal varices?
- Haematemesis and/or melena
- Epigastric discomfort
- Sudden collapse - Sx haemodynamic instability
What are the investigations for oesophageal varices?
1ST LINE/GOLD STANDARD: upper GI endoscopy
- FBC, U+E, clotting (INR), LFTs
- CXR/ascitic tap/further Ix for PHT
How do we treat oesophageal varices?
- GOLD STANDARD - ENDOSCOPIC THERAPY: BAND LIGATION OR SCLEROTHERAPY
- Small oesophageal varices = watch and wait
- ABCDE
- Medical for medium to large = beta blocker to reduce CO -> reduce portal pressure and band ligation
- Acute bleeding = ROCKALL SCORE (predicition of re-bleeding and mortality)
- Nitrate to reduce portal pressure
- Terlipressin – analogue of ADH -> reduce portal pressure
- Surgical:
- Band ligation
- Transjugular intrahepatic portosystemic shunt (TIPSS)
What is a Mallory-Weiss tear? What is it pathophysiology?
- Haematemesis from tear in oesophageal mucosa
- Pathophysiology: severe vomiting = sudden increase in intra-abdominal pressure = partial laceration at gastro-oesophageal junction = bleeding from mucosa
What are the risk factors for a Mallory-Weiss tear?
- Alcoholism
- Hypermesis gravidarum
- Gastroenteritis
- Bulimia
- Chronic cough
What is the clinical presentation of a Mallory-Weiss tear?
- Haematemesis
- Malaena
- Sx of hypovolaemic shock
What are the investigations for a Mallory-Weiss tear?
- Rockall score (assess blood loss: <3 = low risk)
- Endoscopy
- FBC, U+E, coagulation studies, haematocrit
- ECG + cardiac enzymes
What is the treatment for a Mallory-Weiss tear?
- ABCDE
- Urgent endoscopy
- Anti-emetics if N+V persists
- PPI to suppress acid
What is Boerhaave syndrome? What is it caused by? What are the main symptoms?
- Rupture through the oesophagus
- Caused by an increased intraoesophageal pressure and a negative intrathoracic pressure
- Meckler’s triad: vomiting, chest pain and subcutaneous emphysema
What is achalasia? What is its pathophysiology? How is it different to oesophageal carcinomas?
- Rare disorder that makes it difficult for food to pass through oesophagus (LOS won’t relax)
- Degeneration of ganglion cells = oesophageal smooth muscle fibres fail to relax = oesophageal sphincter remains closed/fails to open
- Will affect solids at the SAME POINT it affects liquids as it is a MOTILITY problem. In carcinomas, it will be PROGRESSIVE DYSPHAGIA (important)
What are the signs and symptoms of achalasia?
- Dysphagia affecting solids and liquids AT THE SAME POINT
- Heartburn
- Weight loss
- Coughing while lying horizontally
What are the investigations for achalasia?
- Barium swallow X-ray and continuous fluoroscopy - normal peristalsis not seen
- Oesophageal endoscopy with or without endoscopic ultrasound
What is the treatment for achalasia?
- Medications: CCBs for mild to moderate, nitrates effective before dilation occurs, PPIs effective after surgery
- Gold standard = Laparoscopic Heller myotomy = oesophageal dilation via surgical cleaving of muscle
- Endoscopic myotomy
What are the three main types of ischaemic bowel disease? What do they affect?
- Ischaemic bowel diseases can be classified into 3 main types:
- Acute mesenteric ischaemia
- Chronic mesenteric ischaemia
- Ischaemic colitis
- Acute & chronic mesenteric ischaemia almost always affect the small bowel, whereas ischaemic colitis affects the large bowel
Where does the bowel get the majority of its blood supply from? Which areas are most susceptible to ischaemia?
- The bowel mostly gets its blood supply from the superior & inferior mesenteric arteries
- “Watershed areas” like the splenic flexure + caecum are the most susceptible to ischaemia
What is mesenteric ischaemia? What is its aetiology?
- Mesenteric ischemia occurs when narrowed or blocked arteries restrict blood flow to your small intestine
- Aetiology:
- Superior mesenteric artery (SMA) THROMBOSIS
- SMA EMBOLISM (DUE TO AF)
- Mesenteric vein thrombosis - typically young patients who are in hypercoaguable states
- Non-occlusive disease, e.g. poor blood flow, poor cardiac output
What is the clinical presentation of mesenteric ischaemia?
- Classical triad:
- Acute, severe abdo pain - usually constant & central
- No abdo signs on exam
- Rapid hypovolaemia > shock
- The symptoms are often way out of proportion with clinical signs
- IF YOU SEE AF WITH SEVERE ABDOMINAL PAIN, THINK AMI
What is the difference between chronic mesenteric ischaemia and AMI in terms of presentation? What is chronic mesenteric ischaemia described as?
Chronic mesenteric ischaemia is very similar to AMI, except the symptoms are on a lower level & persist for much longer. It is described as “abdominal angina”
What are the investigations for mesenteric ischaemia?
- Bloods = ^^Hb due to blood loss and persistent metabolic acidosis due to ischaemia
- ABDOMINAL X-RAY = used to rule out bowel obstruction
- Laparoscopy = used to visualise the necrosis
- CT/MRI ANGIOGRAPHY = non-invasive way to look at arteries to see blockages, but is a difficult scan to perform
Describe the management of mesenteric ischaemia.
- FLUID RESUSCITATION
- Antibiotics - Metronidazole, Gentamicin
- IV HEPARIN TO REDUCE CLOTTING
- Surgery to remove necrotic bowel
What are the complications of mesenteric ischaemia?
- Sepsis
- Peritonitis
What is ischaemic colitis? What is its aetiology?
- Ischaemic colitis = inflammation of the large intestine resulting from a lack of blood flow
- Aetiology:
- Thrombosis
- Emboli
- Low flow states
- Low cardiac output/arrhythmias
- Surgery
- Vasculitis
- Coagulation disorders
- Oral contraceptive pill
- Idiopathic
What is the clinical presentation of ischaemic colitis?
- SUDDEN ONSET LIF PAIN
- Passage of bright red blood
- SIGNS OF HYPOVOLAEMIC SHOCK
What are the investigations for ischaemic colitis?
- Urgent CT to rule out perforation
- Flexible sigmoidoscopy w/ biopsy - will show epithelial cell apoptosis
- Colonoscopy w/ biopsy = Gold standard = only done AFTER patient has fully recovered to exclude the formation of a strictures at the site and to confirm mucosal healing
- Barium enema
Describe the management for ischaemic colitis.
- Most patients will be fine with only symptomatic treatment
- Fluid replacement
- Antibiotics = reduce infection risks due to translocation of bacteria across the drying bowel wall
- Strictures at the disease site are common
- Gangrenous ischaemic colitis = peritonitis & hypovolaemic shock, will require surgical intervention
What is Coeliac’s disease? What is it an intolerance to? What does it cause?
- Inflammation of the mucosa of the upper small bowel in response to GLUTEN (general name for proteins found in wheat)
- AUTOIMMUNE - T cell mediated
- Intolerance to PROLAMIN (in wheat, barley, rye, oats) - component of gluten protein
- Causes VILLOUS ATROPHY, which leads to MALABSORPTION
What is the epidemiology of Coeliac’s disease?
- 1% of the UK population (yet only 25% diagnosed)
- Males and females equally
- Any age, peaks in infancy and 40-60 years
What are the risk factors for Coeliac’s disease?
- FAMILY history - 10% risk in 1st degree relatives
- HLA associated - HLA-DQ2 and HLA-DQ8
- Other AUTOIMMUNE diseases, e.g T1DM
- IgA deficiency
What is the pathophysiology of Coeliac’s disease?
- ALPHA-GLIADIN is resistant to digestion from protease enzymes (pepsin & chymotrypsin) in small intestine lumen
- Passes through damaged epithelial wall, into cells
- Deaminated by tissue TRANSGLUTAMINASE
- Interacts with antigen-presenting cells via HLA-DQ2 or HLA-DQ8
- These activate gluten-sensitive CD4+ T-CELLS
- T-cells produce pro-inflammatory cytokines -> inflammatory cascade
- Causes VILLOUS ATROPY and CRYPT HYPERPLASIA
What does villous atrophy lead to?
Villous atrophy leads to MALABSORPTION
What is the clinical presentation of Coeliac’s disease?
- Steatorrhoea + stinking stools - inability to properly absorb fat from diet
- Anaemia - due to inability to absorb B12, folate, iron
- Weight loss, fatigue & weakness, diarrhoea, abdominal pain, bloating, N+V
- Aphthous ulcers
- Angular stomatitis
- Osteomalacia - decreased absorption of Vitamin D
- Failure to thrive (children)
- Dermatitis herpetiformis:
- Raised red patched of skin
- Blisters, burst with scratching
- Elbows, knees, buttocks, torso, scalp
- Deposition of IgA in skin
What are the complications of Coeliac’s disease?
- Most patients who follow a strict diet recover, but a few are non-responsive
- ANAEMIA
- Osteoporosis
- Hyposplenism
- Neuropathies
- Increased risk of MALIGNANCY:
- T-cell lymphoma = increased T-cells in GI wall
- Gastric, oesophageal, small bowel, colorectal cancer = increased cell turnover
What are the investigations for Coeliac’s disease?
- Serum antibody testing = FIRST LINE:
- IgA TISSUE TRANSGLUTAMINASE (tTG) (can also test for IgA anti-endomysial antibody (EMA) = less sensitive)
- Very high sensitivity & specificity, false negatives in IgA deficiency, offered to people with other autoimmune diseases
- Positive/negative with high index of suspicion = biopsy
- Duodenal BIOPSY = GOLD STANDARD:
- Endoscopically, required for definite diagnosis
- Postive findings: villous atrophy, crypt hyperplasia, increased epithelial WBCs
- FBC: low Hb, low folate, low ferritin, low B12, ~50% have mild anaemia
- Genetic testing: HLA-DQ2 and HLA-DQ8 genotyping
- DEXA scan - because of the increased risk of osteoporosis
What is the management for Coeliac’s disease? What is the main reason for recurrence?
- Lifelong GLUTEN-FREE DIET:
- Avoid foods containing wheat, barley, rye, oats
- GLUTEN-FREE FOOD are now more available
- Poor compliance is the main reason for recurrence
- Symptoms and serology used to monitor response and compliance
What is inflammatory bowel disease? What are the two major forms? What is the general pathophysiology? Which group are the most affected?
- Inflammatory bowel disease = a term used to mainly describe two CHRONIC and AUTOIMMUNE conditions:
- ULCERATIVE COLITIS
- CROHN’S DISEASE
- Mucosal immune system responds inappropriately to luminal antigens, e.g. bacteria when they enter mucosa via leaky epithelium
- Jewish people are the most affected group
What is ulcerative colitis? Describe it on a macroscopic and a microscopic level.
- Ulcerative colitis = inflammation of colon, ulcers are present
- MACROSCOPIC:
- ONLY COLON affected
- STARTS AT RECTUM, can progress as far as ileocaecal valve
- CIRCUMFERENTIAL AND CONTINUOUS inflammation – no skip lesions
- ULCERS + PSEUDO-POLYPS in severe disease
- MICROSCOPIC:
- MUCOSA ONLY inflamed - no deeper (not transmural)
- CRYPT ABCESSES
- Depleted goblet cells
What is the cause of ulcerative colitis? What are the risk factors?
- Cause: “Inappropriate immune response against (possibly abnormal) colonic flora in genetically susceptible individuals
- Risk factors:
- Family history
- NSAIDS
- Chronic stress + depression
What is the epidemiology of ulcerative colitis?
- Highest prevalence in northern Europe & North America
- Affects males + females equally
- Presentation mostly at 20-40 YEARS
- Higher incidence than Crohn’s
- SMOKING IS A PROTECTIVE FACTOR against UC
- Incidence is 3x higher in non-smokers
- Symptoms may relapse on stopping smoking
What are the symptoms of ulcerative colitis?
- Remissions + exacerbations
- Abdo pain – lower left quadrant
- Abdo cramps/discomfort
- Episodic or chronic diarrhoea: blood and mucus, urgency, frequency relates to severity, night & day in severe attacks
- Systemic symptoms in attacks: fever, anorexia, malaise, weight loss
What are the signs of ulcerative colitis?
- Might be no signs
- Acute, severe UC = fever, tachycardia, tender, distended abdomen
- Extraintestinal signs = clubbing, oral aphthous ulcers, nutritional deficits
- Extraintestinal complications
What are the complications of ulcerative colitis in the colon, skin, joints, eyes, and liver?
- Colon: blood loss, perforation, toxic dilatation, colorectal cancer
- Skin: erythema nodosum (tender red bumps, symmetrically on shins), pyoderma gangrenosum (painful ulcers on skin)
- Joints: ankylosing spondylitis, arthritis (HLA-B27 associated)
- Eyes: iritis, uveitis, episcleritis
- Liver: fatty change, chronic pericholangitis, sclerosing cholangitis
- Venous thromboembolism
What are the investigations for ulcerative colitis?
- Blood tests: raised WCC, raised platelets, raised CRP + ESR
- Anaemia: normocytic of chronic disease most likely
- pANCA may be POSITIVE (it’s negative in Crohn’s)
- Liver biochemistry may be abnormal
- Hypoalbuminaemia - in severe disease
- COLONOSCOPY - BIOPSY = GOLD STANDARD. Sigmoidoscopy - diagnosis, full colonoscopy - to define extent, once controlled
- Stool samples = to exclude C.diff, Campylobacter + others
- Faecal calprotectin - indicates IBD if raised, doesn’t differentiate UC and Crohn’s
- Abdominal X-ray = to exclude colonic dilatation. Also useful when UC is too severe for colonoscopy
Describe the management for ulcerative colitis.
- Aiming to induce REMISSION
- Aminosalicylates: Active component is 5-AMINOSALYCYLIC ACID (5-ASA). Commonly prescribed 5-ASAs: SULFASALAZINE, mesalazine, olsalazine (all used in mild to moderate cases). Oral – FIRST LINE for left sided/extensive. Rectal (suppository) – for proctitis (inflammation of rectal lining)
- Mild/moderate: ORAL PREDNISOLONE (glucocorticoid steroid). SECOND LINE – if they don’t respond to a 5-ASA. Also used in severe cases
- Severe with systemic features: IV Hydrocortisone, ciclosporin, infliximab
- Maintaining remission: 5-ASA or azathioprine if still relapsing on 5-ASA
- SEVERE cases with NO RESPONSE to treatment = surgery:
- Colectomy:
- Whole colon removed
- Ileoanal anastomosis OR ileostomy -> stoma
What is Crohn’s disease? Describe its macroscopic and microscopic features.
- Crohn’s disease = inflammation in the GI tract
- MACROSCOPIC:
- Affects ANY PART of GI tract – MOUTH TO ANUS - especially terminal ileum & proximal colon
- NON-CONTINUOUS inflammation – SKIP LESIONS
- Cobblestone appearance – ulcers + fissures in mucosa
- MICROSCOPIC:
- TRANSMURAL inflammation – through all layers of bowel wall
- GRANULOMAS - non-caseating
- Increased chronic inflammatory cells + lymphoid hyperplasia
What is the cause of Crohn’s disease? What are its risk factors?
- Cause: inappropriate immune response against (possibly abnormal) colonic flora in genetically susceptible individuals
- Risk factors:
- Family history
- Stronger genetic association than UC
- Smoking - 2-4x risk
- NSAIDs - exacerbate it
- Chronic stress + depression - triggers flares