4365496
Beschreibung
Karteikarten von Sebastian Bassi , aktualisiert more than 1 year ago
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Erstellt von Sebastian Bassi
vor fast 9 Jahre
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| Frage | Antworten |
| Define: acute inflammation | A local response by living tissue to tissue injury resulting in the formation of a fluid rich -protein -cells (polymorphs , later macrophates) |
| Exudate accumulates at the site by: | 1. An increase in blood flow to area under attack 2. An increase in permeability of the basement membrane of the blood vessels Achieved through chemical mediators released when injured |
| Vascular phase | - Increased blood flow to the area - Slowing of blood flow in the distended blood vessels due to : >increased permeability of blood vessels > Loss of axial flow > Higher MWt proteins leak out of blood vessels( antibiotics too) |
| Cellular phase: Neutrophils | - Attachment of neutrophils to walls of blood vessels - Movement of cells through vessel wall - Phagocytosis of debris/organisms by neutrophils - Intracellular killing/digestion by neutrophils |
| Local response by staph. aureus | - Coagulase produced by the organism precipitates fibrin out around the lesion, containing it. - Boil of the skin (well circumscribed) |
| Local response by Strep. pyogenes | - Hyaluronidase produced by organism which breaks down hyaluronic acid (component of CT in dermis. - Organism "digest pathway for self - Causing spreading superficial infection -poorly demarcated - Cellulitis/impetigo |
| Cardinal signs of acute inflammation | 1. Rubor (redness) 2. Calor (heat) 3. Tumor (swelling) 4. Dolor (pain) 5. Loss of function |
| Tissues and acute inflammation | 1) expansion of tissue (NB brain and bone) 2) Surface area covered by exudate (Shock) 3) Tissue release further dmg substances (chemical dmg) 4) Physiologically respond different (alveoli bv contract) |
| Beneficial effects of acute inflammation (fluid) | 1. Dilutes toxins 2. Contain antibodies 3. Fibrin (localize) 4. Polymorphs (destroy pyogenic) 5. Macrophages (ingest proteins) |
| Possible outcomes of acute inflammation | 1. Resolution 2. Suppuration 3. Healing by fibrosis 4. Progression to chronic inflammation 5. Spread 6. Death |
| Destroys harmful enzymes in neutrophils | Alpha-1-antitrypsin (deficiency = emphysema) |
| Vascular phase steps | - Transient, brief, vasoconstriction - Dilatation of blood vessels - Increased blood flow (active hyperaemia, prostaglandins) - Exudate into tissues - Slowing of blood flow - Increased lymphatic flow |
| Local responses | A) various organisms B) Therapeutic intervention (local peritonitis) C) Toxins (gangrene) |
| Kinin and histamine | lead to an immediate but transient increased vascular permeability through walls of VENULES ONLY |
| Endothelial cell injury | Leads to a delayed but persistent vascular peermeability through both capillaries and venules |
| 2 main cell types | 1) Neutrophil : - definitive cell of acute inflammation - produced in bone marrow - initial phagocytosis 2) Macrophage : - Phagocytosis - Antigen presentation - Secrete factors which stimulate fibrosis - Production of complement components |
| Cellular phase | 1) sloiwing of blood flow 2) Margination of leukocytes 3) Triggering 4) Strong adhesion (integrins) 5) Motility 6) Phagocytosis 7) Intracellular killing (superoxide, halides) |
| Consequences of acute inflammation | - Resolution - Suppuration - Fibrosis - Progression (to chronic) - Death |
| Systemic effects | 1) Fever 2) Leucocytosis 3) Alterations in serum proteins |
| Specific patterns | - Suppuration - Cellulitis (phlegmon) - Pseudomembranous (fibrinopurulent) inflammation - Serous inflammation - Catarrhal inflammation - Ulceration |
| Local response implications | - Low grade sensing system - Coagulation systems - Inflammatory mediators - Complement cascade - Cells of chronic inflammation |
| Treatment of Non-infective causes | i) Antibodies to chemical mediators of inflammation ii) Suppression of immune response : steroids iii) Plasmapheresis iv) Antipyretics v) non-steroidal anti inflammatories |
| Prevention of sepsis | i) Preparation of skin ii) Haemostasis iii) debridement iv) Prophylactic antibiotics |
| Suturing of laceration | i) cleaning ii) haemostasis iii) needle iv) Thread v) threaded or not |
| Aftercare | - Wound dressing + ointments - Antibiotics - analgesic - antipyretics - anti-inflamms. (NSAIDS) |
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