GI conditions Flashcards
IBD
Microscopic qualities of Ulcerative Colitis
Macroscopic?
Goblet cell depletion
Mucosa affected - superficial
No granulomas
Affects colon only
Continuous inflammation distal –> proximal
Pseudopolyps
3 characteristic symptoms of IBD. Differentials? test to confirm IBD?
Weight loss, diarrhoea, abdominal pain.
(fever, tenderness, tenesmus, muscle spasms, vomiting, rectal bleeding)
Diff: coeliac, ibs, GI cancer, infective causes… History for clues.
Stool test for calprotectin - sensitive, specific to IBD (but not type of IBD)
IBD
Microscopic qualities of Crohn’s
Macroscopic
Transmural inflammation
Granulomas present
Lymphoid hyperplasia
Patchy ulcers, cobblestone appearance, skip lesions.
Can be anywhere in GI tract, but usually terminal ileum/ileocaecal.
Test to differentiate UC and Crohn’s? definitive diagnosis?
UC may have PANCA antibodies
Crohn’s may have ASCA
Definitive diagnosis through endoscopy and biopsy
Treatment for UC
5-aminosalicylic acid (5-asa): sulfasalazine = anti-inflammatory
Prednisolone to induce remission, steroid-sparing agent aziothioprine to maintain remission. Immunosuppresive.
Biological therapy in severe cases such as tnf-alpha inhibitor inflixamab
Surgery - colectomy - if appropriate
Treatment for Crohn’s
Prednisolone/budesonide to induce remission, methotrexate as steroid sparing agent.
Biological therapy in severe cases such as tnf-alpha inhibitor inflixamab
Surgery may be needed but not curative due to patchy inflammation
IBS: who? exacerbating factors? symptoms? diagnosis? treat?
Most common in females under 40.
Ass. with stress, anxiety/psychological issues.
Exacerbated by gastroenteritis (post infective), menstruation, stress.
Symtoms:
Abdo pain, relieved on defaecation
Bloating/cramps
Change in bowel habit: constipation &/ diarrhoea
Diagnosed based on ruling out differentials and on basis of symptoms/history.
Treat:
Lifestyle - diet modification depending on symptoms, stress reduction, small regular meals
Pharmacological: buscopan for bloating, laxative for constipation, loparamide as anti-motility for diarrhoea
Antidepressants such as amitriptyline to reduce gut sensitivity.
Coeliac disease Describe Symptoms Diagnose Treat
Leaky bowel wall means ingested gliadin (/prolamins) able to enter lamina propria. An autoimmune response occurs: CD4+ produce EMA and tTg antibodies which stimulate CD8+ to produce cytokines and cascade of inflammation which damages the bowel wall, leading to:
- villous atrophy
- crypt hyperplasia
- increased intraepithelial lymphocytes
This damage is visible on duodenal biopsy (definitive diagnosis). EMA and tTg ( IgA antibodies) can also be tested for in the serum.
1/3 asymptomatic, diagnosed by altered MCV (indicating anaemia) on FBC. May have signs of malabsorption: weight loss, steatorrhoea, anaemia (iron def/B12&folate def), osteoporosis, increased infection.
Treat: treat problems resulting from malabsorption (DEXA scan for osteoporosis, supplements). Cut out all gluten immediately from diet. Monitor cancer - increased risk but goes away after gluten free for 3yrs
Common causes of GORD.
Diagnosis
Treatment
- sliding hiatus hernia: sphincter + fundus slide above diaphragm via hiatus, compromising sphincter
- smoking, overeating, cough, alcohol, medications, peptic stricture… anything that increases intragastic pressure or decreases sphincter tone, causing it to relax independently of swallow initiation and reflux of acid occurs.
Diagnosed based on history without investigation if under 45, unless red flags present: weight loss, haematemesis, dysphagia/elderly/not relieved by medication. Gastroscopy, barium swallow, 24hr pH monitoring can be used.
TREAT: Lansoprazole, a PPI, to reduce stomach acid. Antacid eg magnesium trisilicate. H2 receptor antagonist such as cimetidine. Surgery such as Nissen fundoplication (wrapping fundus around sphincter to increase strength) may be used.
What are some causes of peptic ulcers?
NSAIDS inhibit Cyclo-oxygenase 1, needed for prostaglandin synthesis which promotes mucous secretion.
H. Pylori: colonises gastric mucosa, often no harm. Secretes urease which breaks urea –> CO2 and ammonia, forms ammonium which is toxic to gastric mucosa. Also promotes increased acid secretion from parietal cells.
Stress, alchol, spicy food, smoking all precipitate.
Complications of peptic ulcers:
Perforation: ulcer erodes through wall, gastric contents enter peritoneal space
Pancreatitis: erodes and causes inflammation pancreas
Haemorrhage: gastric ulcer in lesser curvature of antrum erodes to L gastric artery, duodenal ulcer on post. wall erodes to gastroduodenal artery (emergency!) causing bleed.
Obstruction: long term, near pyloric sphincter, scarring blocks passage of gastric contents
How do gastric and duodenal ulcers differ in presentation?
Both: localised recurrent burning epigastric pain.
Bloating, belching, vomiting.
Gastric: pain worse when eating (–> weight loss)
Duodenal: pain less when eating, worse when hungry (–> weight gain)
Diagnosis of peptic ulcers
treat?
H. pylori testing: ingest C-urea and measure CO2 in breath
If under 55/no red flags, no investigation necessary.
To eradicate H pylori: Clarithromycin + amoxicillin, plus lansoprazole
H2 receptor antagonist (cimetidine) to red. acid
Reduce irritants such as stress/smoking
Surgery if haemorrhage/complication
What are red flag symptoms for colorectal cancer, for which you would consider 2 week wait referral?
Investigations to diagnose?
Age over 55
Unexplained weight loss
Evidence of GI bleeding: bloody stool, melaena (black stool)
Upper abdominal mass/ rectal mass
Change in bowel habits
Anaemia due to bleeding
Investigation: abdo exam, DRE, colonoscopy and biopsy of polyps(key diagnostic), barium enema
What are colonic polyps? adenomas?
A colonic polyp is an abnormal growth of tissue projecting from the colonic mucosa.
Adenoma is a type of polyp that is a precursor to most colorectal cancer. A benign, dysplastic tumour of columnar cells or glandular tissue.
May be inherited (eg familial adenomatous polyposis)
