Crohn's Disease Flashcards
(21 cards)
What are the defining features of crohn’s
GALS
Granulomatous inflammation (granulomas)
All parts of the GI tract (mouth to anus)
Layers - Transmural
Skip lesions (discontinuous inflammation) and cobblestone mucosa (fissures and deep ulcers)
Where does Crohn’s most commonly affect?
Distal ileum or proximal colon
What is the microscopic appearance of Crohn’s?
Non-caeseating granulomatous inflammation
What is the risk of transmural disease?
Fistula formation between adjacent structures: Perianal Entero-enteric Rectovaginal Enterocutaneous Entero-vesicular
What are risk factors of Crohn’s?
Family history
Smoking
White European descent
Appendicectomy
What are symptoms of Crohn’s?
Diarrhoea (chronic and may contain blood)
Abdominal pain (Colicky)
Weight loss
Acute attacks
Systemic symptoms: malaise, anorexia, low-grade fever, fatigue
What are signs of Crohn’s disease?
Bowel ulceration, abdominal tenderness, abdominal swelling perianal abscess/fistulae/skin tags, anal strictures
Oral aphthous ulcers (painful, recurring)
Signs of malabsorption or dehydration
What are extra intestinal features of Crohn’s
Clubbing, metabolic bone disease due to malabsorption
Skin: erythema nodosum: tender red/purple subcutaneous nodules, found on patients shins
Pyoderma gangrenous - ulcers on shins
Eye: anterior uveitis
Hepatobiliary - primary sclerosis cholangitis, cholangiocarcinoma, gallstones
Renal: renal stones (reduced absorption of bile salts)
What investigations for Crohn’s?
Bloods: FBC anaemia, albumin, WCC CRP, ESR LFT U&E INR B12 Folate
Stool: MC&S (C.diff, campylobacter, E. coli) Faecal calprotectin (raised in IBD, marker of GI inflammation)
What imaging for Crohn’s?
Colonoscopy with biopsy - coblestone mucosa - fissures and ulcers, non-caeseating granulomatous inflammation
Barium swallow
Pelvic MRI for perianal disease
How is mild Crohn’s managed?
Prednisolonge (oral corticosteroids) for 1 wk then taper for 7 wks
How are acute attack’s of Crohn’s managed?
Admit for IV fluid resuscitation, electrolyte replacement, nutritional support,
IV corticosteroids hydrocortisone, VTE prophylaxis, immunosuppressive agent - mesalazine/azothioprine, exclude infection, consider sepsis!
How do you maintain Crohn’s remission?
Azathioprine/mercaptopurine mono therapy to maintain remission.
Methotrexate in those who cannot tolerate others.
Biological agents - infliximab, adaluminab, tiruximab used as rescue therapy during acute flares in those who have not responded to first line remission agents.
What advice would you give to someone with Crohn’s
Smoking cessation due to increased risk fo colorectal malignancy
How would you assess severity of Crohn’s flare? What would you do?
Raised temperature
Raised HR
Raised ESR, CRP, WCC
Low albumin
Admit for IV steroids
hat would you give to patient refractory to steroids but relapsing on steroid taper?
Azathioprine
Alternaticves: mercaptopurine, methotrexate
What are the side effects of azathioprine?
Abdo pain, nausea, pancreatitis, leucopenia, abnormal LFTs
Monitor FBC, U&E, LFT weekly for 4wks then monthly for 3 months
What type of drugs are infliximab and adalimumab? How do they work? CI? SE?
Anti-TNF alpha
Counter neutrophil accumulation and granuloma formation
Cause cytotoxicity to CD4+ T cells clearing cells driving immune response
CI - infection, sepsis, underlying malignancy, latent TB
SE: rash
What nutrition for Crohn’s patient?
Enteral nutrition
When/How are Crohn’s patients managed surgically?
Indications: drug failure, GI obstruction from stricture, perforation, fistulae, abscess
Resect affected areas or control perianal disease or deduction distal disease with temporary ileostomy
Most commonly ileocaecal resection and form primary anastomosis between ileum and ascending colon
What are complications of Crohn’s?
Stricture(tightening of bowel) formation - bowel obstruction and perforation
Fistula
Perianal abscess or fistula
Malignancy
Malabsorption -growth delay in children, osteoporosis, gall stones due to reduced reabsorption of bile salts, renal stones - malabsorption of fats in small bowel causing calcium to remain in the lumen, oxalate is then absorbed freely as normally young to calcium and excreted –> hyperoxaluria and formation of oxalate stones