769152
Description
Flashcards by Chloe Zaydner, updated more than 1 year ago
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Created by Chloe Zaydner
over 10 years ago
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| Question | Answer |
| What is stearic hinderence? | Where immune proteins are bound, preventing them from reacting with their receptor. (or binding to the receptor to prevent the immune protein from binding) |
| Which cytokine produced by the innate immune response is released in rheumatoid arthritis/peridontal disease. | IL-1beta |
| What is the name of IL-1betas normal receptor? | IL-1R1 |
| Describe how decoy receptors can regulate IL-1B | Receptor IL-1R2 is upregulated and so IL-1beta binds to this instead of its normal IL-1R1. This new receptor does not produce a downstream effect --> natural control of IL-1Beta |
| What additional way can IL-1R2 help control IL-1Beta concentrations? | A cell may release soluble IL-1R2 which can mop up IL-1Beta in the microenvironment. |
| What does IL-1Ra do? | It is a competitive inhibitor of IL-1Beta and has affinity but not efficacy so no downstream effects are produced. |
| Is control of IL-1beta specific or broad ranging? | It is specific |
| Why might anti TNF-a antibodies cause problems? | They bind to TNF-a so it can't bind elsewhere leading to immune complex formation which may lead to deposits in areas such as the kidneys. |
| Why would you want to control TNF-a in the first place? | If an animal had a granuloma, TNF-a can lead to breakdown and release of the mycobacterium inducing the disease (Tb) |
| Describe the action of corticosteriod mimics? | Bind to receptor. GC + receptor get internalised. Enter nucleus and bind to promoter region. Induce upregulation of anti-inflammatory cytokines such as IL-10 |
| What affect do glucocorticoids have on NFkB? | They act as an inhibitory protein, binding the NFkB so that they cannot enter the nucleus to transcribe inflammatory cytokines |
| If a drug has an increased mineralocorticoid effect what would be the outcome? | Increased water output (may cause incontinence). This increased clearance may decrease half life. |
| Is immunosupression by corticosteroids specific or broad ranging? | Broad ranging |
| Which drug is more potent? Dexamethasone or prednisolone? | Dex is 5 x more potent than pred. |
| How do NSAIDs work? | Inhibit COX1 and COX2 and therefore prostaglandin production |
| Which Cox is responsible for production of Pgs? | Cox-2 |
| Why must you give NSAIDs with food? | Because COX-1 is responsible for protective mucus production in the intestinal tissues so inhibition of this may lead to gastric ulcers/bleeding. |
| What is an action of PGE2? | Downregulates Fas/FasL on activated T-cells, preventing apoptosis. |
| How are CD4+ lymphocyte populations controlled? | Fas on CD4+ binds to FasL on CD8+ and vise versa. The CD8+ then releases perforin to punch holes in the CD4+ and then releases granzyme which enters the pores and causes luteolysis. |
| What affect does thromboxane have? | Induces platelet aggregation and constricts blood vessels. |
| What is the name of the group which has prostaglandins and thromboxanes in it? | Eicosanoids - NSAIDs inhibit production of these. |
| GIve some examples of some neutroceuticals? | Devils claw and green lipped mussel have anti-inflammatory effects. |
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