GI Flashcards
Crohn’s disease definition
A disorder of unknown aetiology characterised by granulomatous transmural inflammation of the GI tract. Usually seen in the terminal ilial, proximal colon and perianal location, but can affect ANY PART of the GI tract. Unlike ulcerative colitis, CD may have non-continuous skip lesions (normal bowel mucosa found between diseased areas). The transmural inflammation can also result in sinus tracts that burrow through and penetrate the serosa, giving rise to perforations and fistulae.
Macroscopic appearance: skp lesions, cobblestone appearance, thickened and narrowed.
Microscopic appearance: transmural, granulomas (non-ceseating), goblet cells present
Crohn’s disease aetiology
Unknown
Genetic - potential: inappropriate immune response against (possibly abnormal) colonic flora in genetically susceptible individuals
Environment: smoking, oral contraceptive pill, NSAIDs, stress
Crohn’s disease risk factors
Peak age of onset 14-40yrs Smoking Family history Mutation on NOD2 gene Equally present in men and women More common in white northern Europeans and N. America
Crohn’s disease pathophysiology
Acute transmural inflammation results in bowel obstruction due to mucosal oedema associate with spasm. Scarring, luminal narrowing and stricture formation occur due to the chronic inflammation.
Chronic inflammation damages the mucosa leading to deficient absorptive ability
Involvement at the terminal ileum interferes with bile acid absorption, leading to steatorrhea, fat-soluble vitamin deficiency and gallstone formation
Crohn’s disease key presentations
Can have mild symptoms in periods of remission followed by ‘flare ups’/exacerbatiions. Oral ulcers are common
Dependent on area affected:
Small bowel
- abdo pain
- weight loss
- right iliac fossa pain (less common)
Colon
- bloody diarrhoea
- pain on defecation
Systemic symptoms in attacks
- fever
- anorexia
- malaise
- fatigue
Signs
- bowel ulceration
- abdo tenderness
- abdo mass
- perianal disease
- extraintestinal signs: clubbing; oral apthous ulcers; more common than UC; skin, joint and eye problems
Crohn’s disease 1st line investigations
Ask for travel history, family history and medications to see any contributing causes.
Blood tests - raised WCC, raised platelets, raised CRP and ESR, normocytic anaemia of chronic disease, iron, folate, B12 deficiency, hypoalbuminaemia in severe, pANCA negative
Stool sample - exclude infection
Faecal calprotectin - raised in IBD
Gold standard
Colonoscopy with biopsy - can help determine severity, further radiological examinations can determine severity and transmural complications (eg fissure)
Crohn’s disease differential diagnosis
Ulcerative colitis, infective colitis, intestinal ichaemia, acute appendicitis, diverticulitis, IBS, malignancy such as tumour
Crohn’s disease management
No cure so treatment is intended to manage and improve symptoms.
1st treatment: corticosteroids such as prednisolone tablets or hydrocortisone injections (severe) - reduce inflammation. Side effects: weight gain, swelling of the face and osteopenia or osteoporosis. If the case is severe, immunosuppressants are considered. Surgery can also be considered if symptoms arent relieved.
Smoking cessation, treat iron/folate/B12 deficiency
Anti-TNF antibodies if no response to steroids: inflicimac, adalimumab
Azathioprine to maintain remission
Surgery last resort to remove most damaged area - short bowel syndrome = diarrhoea and malabsorption
Crohn’s disease monitoring
A surveillance colonoscopy is generally recommended eight to ten years after diagnosis of ulcerative colitis or Crohn’s disease involving the colon and every one to two years thereafter
Crohn’s disease complications
SAMPANOO
Systemic - amyloidosis. Thisis where the myloid protein builds up in organs + interferes with their function
Anemia
Malabsorption - due to the reduced absorptive function
Perforation
Anal issues - fistula, abscesses, fissure and skin tags
Neoplasia - colorectal cancer
Osteoporosis
Obstruction - due to acute swelling and chronic fibrosis
Crohn’s disease prognosis
Great prognosis - mortality rates low with management
Ulcerative colitis definition
A type of inflammatory bowel disease that usually involves the rectum and extends proximally to affect a variable length of the colon. It is recognised as a multifactorial poygenic disease.
Macroscopic appearance: continuous inflammation (no skip lesions), ulcrs, pseudo-polyps
Microscopic appearance: mucosal inflammation (no transmural inflammation_, no granulomata, depleted goblet cells, increased crypt abscesses
Ulcerative colitis epidemiology
More prevalent in Northern European population
Most patients are aged 20-40 at diagnosis with another peak at 60yrs
Uncommon in children
High incidence than Crohn’s
Smoking is protective
Ulcerative colitis aetiology
Unknown, possibly autoimmune: inappropriate immune response against (possibly abnormal) colonic flora in genetically susceptible individuals
Exacerbated by NSAIDs and stress
Ulcerative colitis pathophysiology
Relapses strongly associated with infectious enteritis
Ulcerative colitis key presentations
Remission and exacerbation
Ulcerative colitis signs and symptoms
Symptoms:
- pain in lower left quadrat
- diarrhoea with blood and mucus
- lower back pain from spondylitis (inflammation of spinal bones)
- systemic fever, anorexia, malaise, weight loss
Signs:
- fever (in acute UC)
- clubbing
- erythema nododsum (inflammation of subcutaneous fat)
- pyoderma gangrenosum - painful ulcers on skin
- malnutrition
- real ulcers
Ulcerative colitis 1st line investigations
Still studies: elevated feacal calprotein (useful for DDx but seen in both UC and Crohn’s), C.difficile toxins often present and associate with increase mortality (need at least 4 sample)
FBC: ESR and CRP may be elevated in flare-up, raised WCC and platelets, normocytic anaemia of chronic disease
pANCA: antibody found in 70% of UC patient (helps with DDx of CD)
Imagining:
- plain abdominal radiography
- ab x-ray
Ulcerative colitis gold standard investigations
Colonscopy with biopsy
- sigmoidoscopy for diagnosis
- full colonoscopy to define extent once controlled
Ulcerative colitis management
Aminosalicylate (1st lines): mesalazine or sulfasalzine
Add oral prednisolone if no response, IV hydrocortisone if severe
Azathioprine to maintain remission
Colectomy indicated in patients with severe UC and not responding to treatment
Ulcerative colitis complications
Toxic megacolon can occur with associated risk of perforation
Bpwel adenocarcinoma is a complication in 3-5% of patients
Joint problems such as arthritis
Hepatobiliary such as chronic pericholangitis and sclerosing cholangitis
Irritable bowel syndrome defintiion
A chronic condition characterised by abdominal pain associated with bowel dysfunction. There are no structural abnormalities to explain the pain
IBS-C: with constipation
IBS-D: with diarrhoea
IBS-M: mixed, with alternating constipation and diarrhoea
Irritable bowel syndrome epidemiology
Occurs in abotu 15% of the adult population - 1 in 5 western world
More common in female
Under 40s
Irritable bowel syndrome aetiology
Likelt multifactorial
Irritable bowel syndrome risk factors
Stress, female, GI infection
Irritable bowel syndrome pathophysiology
Altered gut reactivity (motility and secretion) due to environmental effects such as stress and certain foods
Irritable bowel syndrome key presentations
Abdominal pain associated with 2+ of:
- relived by defacating
- altered stool form
- altered bowel frequency
Irritable bowel syndrome signs and symptoms
ABC:
Abdominal dyscomfot
Abdominalbloating or distention
Change in bowel habits
Normal examination of abdomen
Can affect variety of other systems eg painful periods, back pain, bladder dysfunction
Irritable bowel syndrome 1st line investigations
FBC: normal; anaemia suggests non-IBS disease; ESR/CRP-inflammation
Faecal Calprotein - raised in IBD
Faecal occult blood: may be positive in IBS or colorectal cancer
Irritable bowel disease differential diagnosis
Crohn’s: faecal occult blood will be positive
Coeliac disease: usually have weight loss
Irritable bowel disease management
Dietary midifcations - food diary, avoid FODMAPs
Pain/bloating: antipasmodics; buscopan
Contstipation: laxative eg Senna, linaclotide
Diarrhoea: antimotility eg Loperamide
If no better: tricylic antidepressants (amitryptiline SE: drowsiness)
3rd line: SSRIs
CBT
Coeliac disease definition
Systemic autoimmune disease tirggered by Prolamin (dietary gluten peptide) found in wheat, rye, barley etc. Inflammation of upper small bowel mucosa
Leads to villous atrophy, hyperplasia of the intestinal crypts and increased numbers of lymphocytes in the epithelium and lamina propria. Leads to GI symptoms and malabsorption. Systemic manifestations are diverse, potentially affecting almost every organ system.
Coeliac disase risk factors
Family history, other autoimmune diseases
Coeliac disease epidemiology
Affects up to 1% of gneeral population
Peaks at infancy + 40-60yrs
Coeliac disease aetiology
Almost all patient carry one of two major histocompatibility complex class-II molecules (human leukocyte antigen [HLA]-DQ2 or -DQ8)
Coeliac disease pathophysiology
- Gliadin (a prolamin found in wheat) binds to secretory IgA in the mucosal membrane
- The gliadin-IgA is transcytosed to the laminate propria
- Gliadin binds to tTH and is deamidated
- Deamidated gliadin is taken up by macrophages via HLA and expressed on MHC2
- T helper cells release inflammatory cytokines and stimulate B cells
- This causes gut damage
Note that gliadin is deamidated not deaminated
Inflammation of the mucosa of the upper small bowel in response to gluten
Autoimmune - T cell mediated
Intolerance to prolamin (in what, barely, rye, oats) - component of gluten protein
Causes villous atrophy and crypt hyperplasia
Leads to malabsorption
Coeliac disease signs and symptoms
Symptoms: diarrhea, bloating, abdo pain, nausea and vomiting
Signs: anaemia, weight loss, steatorrhoea and stinking stools (malabsorption), angular stomatitis, apthous stomatitis (non-contagious mouth ulcers), osteomalacia (decreased vitamin D absorption), failure to thrive (children), dermatitis herpetiformis
Coeliac disease 1st line investigations
IgA-tTG blood test: positive, very high sensitivity and specificity
FBC and blood smear: low Hb, folate, ferritin, B12
Genetic testing
Coeliac disease gold standard investigations
Duodenal biopsy:
- required for definitive diagnosis
- villous atrophy, crypt hyperplasia
- increase epithelial WBCs
Coeliac disase managemet
Gluten free diet
Vitamin and mineral supplementation
Coeliac disease prognosis
Up to 90% of people will have complete and lasting resolution of symptoms on a gluten-free diet alone
GORD definition
Complications due to the reflux of gastric contents into or beyond the oesophagus
GORD epidemiology
GORD is common - exists when the reflux of the stomach contents become troublesome - more than 2 heartburn episodes a week
GORD aetiology
Usually as a result of the ring at the bottom of the oesophagus becoming weakened. Causes can include lower oesophageal sphincter hypertension, hiatus hernia
GORD risk factors
Overweight or obese, eating large amounts of fatty foods, smoking, alcohol, coffee, chocolate intake, pregnancy, hiatus, certain medicines such as NSAIDs
GORD pathophysiology
Transient lower oesophageal sphincter relaxations and other lower oesophageal sphincter pressure abnormalities. As a result, reflux of acid, bile, pepsin and pancreatic enzymes occur, leading to oesophageal mucosal injury.
GORD clinical manifestations
- heartburn. This is aggravated by bending, stooping and lying down. May be relieved by antacids.
- belching
- food/acid regurgitation
- increased salvation (water brash)
- odynophagia (painful swallowing)
- nocturnal asthma
- chronic cough
GORD investigations
Diagnosis can usually be made without investigation.
NO ALARM BELLS - weight loss, haematemesis and dysphagia require further investigation:
- endoscopy - symptoms longer than 4 weeks, persistent vomiting, GI bleed or palpable mass. Also required if symptoms persist after treatment
- barium swallow - to exclude hiatus hernia
These investigations assess the oesophagus - Barrett’s oesophagus confirms reflux
GORD differential diagnosis
Chronic Artery Disease, biliary colic, peptic ulcer disease, malignancy
GORD management
LIfestyle changes: weight loss, smoking cessation, small and regular meals, avoiding hot drinks, alcohol, citrus fruits. Don’t eat within 3 hours of going to bed
Pharmacology: antacids such as magnesium trisilicate mixture. This relieves symptoms by forming a gel with gastric contents to reduce reflux. Side effects could be diarrhoea.
Alginates such as gaviscon can also relieve symptoms.
PPI - proton pump inhibitors such as lansoprazole reduces gastric acid production H2 receptor antagonists - cimetidine - blocks histamine receptors on partial cells and reduces acid release.
Surgery: nissen fundoplication - laparoscopically increase the resting lower oesophageal sphincter. This is used when they aren’t responding to treatment.
GORD monitoring
not much monitoring required if responding well to treatments. Make patient aware of increased risks and alarm bell symptoms so they know went to come back.
GORD complications
Peptic stricture - inflammation of the oesophagus (aka oesophagitis) due to gastric acid exposure. Results in narrowing and stricture change. Usually occurs in patients over 60. Presents as gradually worsening dysphagia.
Barrett’s oesophagus - distal oesophageal epithelium undergoes metaplasia from squamous to columnar. Increased risk of oesophageal cancer.
GI cancers definition
Oesophageal cancers: most are mucosal lesions originating from the epithelial cells of the oesophagus. Associated with metaplastic condition. Barrett’s oesophagus (‘precancerous’ condition) (stratified squamous to columnar epithelium with goblet cells)
Stomach cancers: most common is type 1 (interstitial/differentiated) usually in the antrum and lesser curve, type 2 (diffuse/undifferentiated) occurs anywhere but often the cardia
Colon cancer: majority are adenocarcinomas
