A clinical overview of autoimmune disease Flashcards
What is autoimmunity?
T cells with high affinity for self antigens should be removed by negative selection in the thymus
Some T cells will escape - these are CD4+ cells (checkpoint 1)
APC present on MHC I
Some CD4+ cells recognise this antigen and mount immune response (autoimmunity)
Checkpoint 2: Treg cells stimulate CD4+ to apoptosis and dampen immune response
If no Treg cells, DC presents self-antigen to CD4+ cell
For CD4+ to be activated, needs interaction between CD80 on DC and CD28 on CD4+
CD80 upregulated on inflammation
Autoimmune diseases in childhood
T1DM, Rheumatic fever, Kawaski’s disease
Risk factors for autoimmune disease
Family history
Genetics - HLA DR2 (narcolepsy and Goodpasture’s and MS), HLA DR3 (myasthenia graves, Hashimoto’s), HLA DR4 (RA and SLE)
Drugs increase SLE risk and smoking increases RA risk
What is elevated in gut inflammation?
Calprotectin
How to differentiate between UC and Crohn’s?
UC has bloody diarrhoea and only affects the mucosal wall of the colon in a continuous fashion
Crohn’s affects the whole GIT, affects all layers, causes vaginal involvement, granulomas, abscesses etc
Treatment for UC and Crohn’s
Steroids Elemental diet Anti-TNF (infliximab) 5-ASA drugs (mesalazine) DMARDs (methotrexate)
Sx Grave’s
Hypothyroidism, non-tender goitre, proptosis
Risk factors Grave’s
Age 30-50, pregnancy, smoking
Tests Grave’s
Anti-TSH ABs
Treatment Grave’s
Anti-thyroid drugs (carbimazole), radiodiodine and thyroidectomy
Sx Coeliac’s
Cramps and diarrhoea
ABs coeliac’s
Anto-TTG, IgA subtype
Treatment Coeliac’s
Avoid gluten, steroids, imunosuppressants
Where is IgA found?
Secretions (saliva, tears, breast milk)
IgA diseases
IgA nephropathy, HSP, coeliacs
When is IgE made?
parasitic infections
Allergy, atrophy, anaphylaxis
When will IgM be made?
Acute infection - diagnoses acute vs chronic infection
Sx RA
Symmetrical small joint swelling and redness Worse in morning Swan neck deformity Ulnar deviation Boutonniere deformity
Tests for RA
Rheumatoid factor (sensitive, not specific) and anti-CCP (specific, not sensitive)
Treatments RA
Steroids, DMARDs (methotrexate, leflunomide), infliximab
Sx Addison’s
Low sodium, high potassium ,low BP, pigmentation
Why do you get pigmentation with Addison’s
No cortisol means no neg feedback - more ACTH made (formed by cleaving of POMC to ACTH and MSH) and more melanin made
Short synACTH test
SynACTH given
Monitor at baseline, 30 min and 60 min
Cortisol should double
If not, indicated adrenal insufficiency
Tx Addison’s
Hydrocortisone and fluid/glucose management
