| Front | What are the harmful effects of inflammation? |
| Back | - digestion of normal tissue (collagenase and proteases) - swelling (of epiglottis in children, cranial cavity, -> death) - inappropriate inflammatory response (athergies) |
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| Front | Describe type II hypersensetivity |
| Back | - antibody dependant, complement mediated, cytotoxic hypersensetivity - sensetisation- - firstly immunological encounter drives IgM production - memory Bcells produced - these produce IgG - mechanism- - IgG activate complement via the classic pathway - complement can cause direct cytolysis (MAC) or opsonisation -> phagocytosis - takes a few hours - examples- - can be autoimmune such as Graves disease of thyroid - penicillin has B-lactam ring (behaves as haptan) which can bind to platelets -> immunological responce to platelets - Rhesus diease- RhD negative mothers carrying RhD positive babies, first pregnancy sensetisation, second pregnancy IgG can cross placental barrier and bind to foetal RBCs -> type II hypersensetivity |
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| Front | Describe DVT pathology risk diagnosis outcomes treatment |
| Back | pathology - venous thrombosis - 2/3 of all venous thrombosis - commonly in leg - formation usually at valves at blood flows back (gradual) risk factors - all of venous thromboembolism risk factors - pregnancy, combined pill, immobility, post op etc diagnosis - compression ultrasound or venograph - D-dimer test- fibrin broken down gives D-dimers (days)- recently formed or not - Wells clinical score outcomes - painful swollen leg - pulmonary embolism - recurrent DVT - venous insufficiancy -> ulceration - thrombophlebitis treatment - anticoagulation of 3-6 months - remove risk factors - pain relife - elastic compression stockings for 2 years after DVT - warfarin and heparin ( both for minimum of 5 days) - LMWH if outpatient |
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