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19 Cards in this Set
- Front
- Back
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What is the treatment of anaphylaxis?
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IM adrenaline
IV chlorphenamine, hydrocortisone Oxygen |
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What is the treatments for asthma and with each more intense regime what is added (step1-5)?
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1:short-acting B2 agonist - salbutamol
2: inhaled corticosteroid 3:long acting - salmeterol 4: increased doses 5: oral steroid |
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What do NSAID inhibit to relieve symptoms?
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COX - cyclo-oxygenase reducing PG synthesis and therefore inflammation
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What immunosupressive effects do steroid have?
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Inhibit cytokine release, phagocytosis, bacterial killing, antigen presentation, arachidonic acid metabolism and its derivatives (LT and PG)
Lymphocyte and monocyte proliferation and numbers |
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What are the side-effects of steriods?
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Cushigoid effects - moon face- obesity
- Protein breakdown - Striae - muscle wasting - Steroidal diabetes - inhibits insulins effects - Adrenal supression - Osteoporosis - mental disturbances - Mineralocorticoid mimicry - HT |
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Name 2 T-cell immunosupressive drugs and reasons for use
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Rapamycin and cyclosporin
AI and transplants |
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What is passive immunisation and an example for use?
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Inoculation with antibody to promote a rapid response without triggering memory - Rhesus, Varicella-zoster, anti-toxins
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How are MAB made?
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Immunisation of a mouse, Ab forming cell taken and hybridised with a tumour cell - Cell then screen for Ab production and cultured
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Infliximab is an anti-TNF. Which diseases is it licensed for and what much be checked before prescribing?
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RA - TB via heaf test as TNF important in maintaining TB in latent state
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How does herceptin work?
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HER-2 (human EGF receptor) over-expressed in 25% breast cancer - more agressive as it tells itself to continually divide. Herceptin blacks this signalling reducing division and targets the immune system towards the cancer
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What are sope causes of the breakdown of self-tolerance?
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Molecular mimicry - foreign antigen has cross reactivity with self-antigen
Defective immunosupression - Failure of regulatory T-cells Expossure of immunoprivaledged sites. Genetic disposition HLA-types (B-27 ankylosing spondylitis) |
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Describe Type 1 hypersensitivity
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Exposure to a antigen - Th2 CD4+ response and IL-5 causing IgE production by Plasma cells - These attach to mast cell membrane waiting for the antigen exposure (sensitised) - Exposure leads to mast cell degranulation and a massive release of cytokines leading to a inflammation and possible anaphylaxis
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Name some common type I hypersensitivity allergens
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Peanut, coconut, animal dander
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Describe type II hypersensitivity
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Ab bind to cell surface antigen (self antigen - intrinsic) or an extrinsic molecule binds to the cell surface and Ab bind to that. This can have blocking or stimulating effects on receptors (grave's hyperthyroidism, Myasthenia gravis) or lead to cell destruction - haemolytic anaemia
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Name some type II hypersensitivity diseases
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Rhesus, Goodpastures (Type IV collagen - kidney, lung basement membrane)
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Describe Type III hypersensitivity - immune complexing
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Soluble antigen binds with Ab and this can lead to large polymerised Ab-Ag chain and small one which deposits in vessels and joints attracting neutrophils and cause microthrombi formation.
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Name some type III hypersensitivity diseases
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ANCA (anti-neutrophil cytoplasmic antibody) - systemic vasculitis
RA |
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Describe Type IV delayed type hypersensitivity (cell mediated - not Ab)
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An antigen (soluble - contact dermatitis or cellular - cytotoxic - diabetes) is presented by macrophages to CD4+ cells which activate and release Th1 cytokines prompting CD8+ recruitment and cell killing
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Name some Type V diseases
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Diabetes mellitus type 1, coeliac disease, gullian-barre syndrome
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