Hello and welcome to the zero to finals podcast. My name is Tom and in this episode I'm going to be

talking to you about celiac disease. And you can find written notes on this topic at zero to finals.com

slash celiac or in the gastroenterology section of the second edition of the Zero to Finals Medicine

book. So let's get straight into it. Celiac disease is an autoimmune condition triggered by

eating gluten. It can develop at any age and is thought to be caused by genetic and environmental factors.

There's a link with other autoimmune conditions, particularly type 1 diabetes and thyroid disease.

A tom tip for you, remember for your exams that all new cases of type 1 diabetes or autoimmune thyroid disease get tested for

celiac disease, even if they don't have any symptoms. Let's talk about the pathophysiology.

In patients with celiac disease, auto-antibodies are created in response to exposure to gluten.

These auto-antibodies target the epithelial cells of the small intestine, leading to inflammation.

These antibodies relate to disease activity and will rise with more active disease and may disappear with effective management.

There are three antibodies related to celiacs, particularly worth remembering the first two.

And these are anti-tissue transglutamines antibodies, or anti-T-G, anti-endomizial antibodies, or anti-EMA,

and anti-deaminated gliadin peptide antibodies, or anti-DGP.

Inflammation affects the small bowel, particularly the geigenum.

The surface of the small intestine is covered in projections called villi,

and these increase the surface area and help with nutrient absorption.

Celiac disease causes atrophy of the intestinal villi, resulting in malabsorption.

Celiac disease is associated with certain human leukocyte antigen or HLA genotypes or genetic variations,

and these are HLA DQ2 and HLADQ8.

Let's talk about the presentation.

Celiac disease is often asymptomatic and is underdiagnosed, so have a low threshold for testing

...