Autoimmune Diseases Flashcards
Autoimmunity
Breakdown of self tolerance. Genetically determined
Autoimmune diseases
Distinct autoimmune processes with distinct clinical entities-environmental factors acting on favourable genetic background
Which cells have HLA type 1
All cells
Which cells have HLA type 2
Professional APCs
Central tolerance
B cell tested against self antigens and deleted if they don’t react. This results in auto-reactive B cells in the bone marrow.
Peripheral tolerance
If some cells in the blood react against self antigens, regulatory processes e.g. in the lymph nodes, protect against this.
Who is most likely to develop autoimmune diseases?
Females. Elderly. environmental triggers include infection, trauma, and smoking
2 examples of Autoimmune thyroid disease
Hashimotos Thyroiditis
Grave’s disease
Hashimotos Thyroiditis
Destruction of thyroid follicles by autoimmune process leads to hypothyroidism
Grave’s Disease
Inappropriate stimulation of thyroid gland by TSH receptor-stimulates autoantibodies and leads to hyperthyroidism
Myasthenia Gravis
Usually caused by a tumour in the thymus. Antibodies bind to ACh receptor at neuromuscular junction-block neurotransmitters from sending signal-no stimulation. Results in weakness and fatigue-actions gadually suppress as ACh levels decrease
Microcytic anaemia
Low iron, small cells
Macrocytic anaemia
Low folic acid/B12. Autoantibodies block intrinsic factor- can’t bind B12
3 examples of non organ specific autoimmune diseases
SLE
ANCA vasculitis
Raynauds
SLE
Photosensitive malar rash-UV induced. Arthralgia, alopecia, pleural effusion/pleuricy, cerebral lupus-seizures, strokes. Anti nuclear antibodies bind to skin cells that have been damaged by UV light i.e. undergone ‘unhealthy cell death’ Antibodies and their antigens form immune complexes that bind to complement and cause inflammation in any tissue
Lupus nephritis
Kidney involvement of SLE patients. Immune complex deposition in glomeruli-inflammation-leaky glomeruli-loss of renal function-scarring-irreversible renal failure
ANCA vasculitis
Anti neutrophil cytoplasmic antibodies- inflammation of small blood vessels caused by WBCs that have been stimulated by ANCA. ANCA activates neutrophils and causes them to leave the vessels.
3 forms of ANCA vasculitis
Microscopic polyangitis
Granulomatosis with polyangitis (Wegener’s granulomatus)
Eosinophilic granulomatosus with polyangitis
Granulomatosis
Mass of inflammed tissue
Polyangitis
Inflammation of many small vessels
Primary Raynauds
Common in young women. Runs in families. Harmless. ANCA -ve
Secondary Raynauds
ANCA +ve. May be associated with scleroderma
Scleroderma
Digital ulcers due to tightening and ischaemia. Lung fibrosis. Skin fibrosis and tightening.
Autoinflammation
Immmulological disruption in the innate immunity e.g. Crohn’s disease
