Infection, Inflammation and the Gut Flashcards
Infective causes in the Gut
Giardiasis
Whipples disease
Psuedomembrane colitis
Giardisis
Protozoa
Waterbourne infection
Rare in Glasgow
Usually a chronic infection
Symptoms- diarrhoea, malabsorption, weight loss but often asymptomatic
RFs- immunodeficiency
Tbx - metronidazole
Whipples disease
Tropheryma whipplei
Patients have lack of immmunity to ogansim . Absorption of digested food in the intestine is reduced.
Rfs- Middle aged men
Symptoms- Abdominal pain, skin pigmentation, arthrlagia (joint pain), diarrhoea
Diagnosis - Biopsy of dudoenum - PAS positive macrophages
Tbx- antibiotics
Psuedomembrane colitis
Clostridium difficile
Overgrowth with toxin producing clostridium difficile after abx therapy with clindimycin
Symptoms- Feverm abdominal pain, diarrhoea, necrosis
Diagnosis - toxin in stool
Treatment - Vancomycin
Non infective causes of gut inflammation
Acute appendicitis
Coeliac disease
Coeliac disease Definition
A condition where there is inflammation of the jejunum mucosa that improves when the patient is treated with a glten free diet and relapses when gluten is introduced
Clinical featues of coeliac
- fatty diarrhoea: bulky, pale, greasy and offensive
- Weight loss
- Reduced bone density with increased risk of fracture (osteomalacia)
- iron deficiency aneamia (can digest but not absorb)
- oral apthous ulcers
- Dermatitis herpetiforms
Investigations for coeliac disease
a. Duodenal/jejunual biopsy
b. Endomysial (EMA) Ab
c. Haematology
d. Biochemistry
Risk factors of coeliac disease
RFs - genetic predispostiion (HLA-Dq)
Epidemiology of coeliac
Epideimiology - commonest cause of villous atrophy in UK (1in 200)
Pathophysiology of coeliac disease
Cause - triggered by ingestion of gluten
- Prolamins (gliadin from wheat, Hordeins from barley, seclans from rye) are damaging factors
- Gluten is fractioned to give alpha, beta and gamma-gliadin peptides (alpha-gliagin is main damaging factor)
- gliadin peptides pass through the epithelium
- deaminated by tissue transglutamase
- Gliadin peptides then bind to APC and presented to CD4 T cells in lamina propria via HLA Dq2/8
- T cells produce pro-inflammatory cytokines
- T cells also interact with B cells to produce autoantibodies (transglutaminase + antiendomysial autoantibodies) against self tissue
- Leads to:
a. Villous atrophy - normally cells created at the pit of tge crypt and regenerate
b. Crypt hyperplasisa - proliferative component increased
Classification used in coeliac
Marsh classification
0- Normal mucosa
1- Increase number of intra-epithelial lymphocytes >20 per 100 enterocytes)
2- Proliferation of the crypts of liberkuhn
3 - Variable villous atrophy
3a- Partial villous atrophy
3b- Subtotal villous atrophy
3c - total villous atrophy
4. hypoplasia of the small bowel architecture
Treatment of coeliac disease
Treatments with gluten free diet - recovery of villous atrophy in three months
Complications of coeliac disease
-TTG antibodies are a good measure of compliance. If the diet is good they will stay low.
They are at risk of enteropathy associated T cell lymphoma
They are prone to osteoporosis – therefore bone should be screened regularly. Would not use bisphosphonates at such a young age – save them for later in life.
Can have side effect of causing spontaneous mid shaft femur fractures.
Use regular biopsies to monitor bowel
Acute appendicitis
Bacterial infection of blocked appendix
Right iliac fossa pain!!!
Chi;dren
Histo- acute inflammation followed by ulceration and trasnmural inflammation
Complications - transmural gangrene leading to perforation, generalised peritonitis