3. Acute Inflammation Flashcards
What is (acute) inflammation?
What are some exogenous causes of inflammation?
What are some endogenous causes of inflammation?
Response of living tissue to injury. The reaction of microcirculation and its contents to injury. Defence mechanism produced to contain/isolate/destroy/neutralise injury and achieve healing and repair. Ideally resolves. May become chronic. “itis”. Vascular changes, inflammatory mediators, neutrophil recruitment and phagocytes sum it up!
Trauma, infection, chemicals, temperature, radiation
Anoxia, antigen/antibody complexes, body chemicals, metabolic products
What are 5 macroscopic changes (5 cardinal signs) of inflammation?
What are some microscopic changes of inflammation?
Distinguish between exudate and transudate.
Redness, swelling, heat, pain, function loss
Initial constriction then dilation of BVs, increased blood flow and permeability, exudate formation, leucocoyte migration through wall, oedema.
Exudate: high protein content, cell debris, high SG (>1.020), vessel alteration.
Transudate: low protein content, no debris, low SG (<1.012). ultrafiltrate
Essentially, transudate is fluid pushed through the capillary due to high pressure = plasma ultrafiltrate. Exudate is fluid that leaks around the cells of the capillaries caused by inflammation = everything!
How does the permeability of post-capillary venules (mainly) assist inflammation?
What might gaps in BVs be due to?
How does cellular action assist inflammation?
Enhances cell migration, toxin dilution, stimulates lymphatics/immune repsonse, deposition of proteins e.g. fibrin to form mechanical barrier.
Endothelial contraction (venules, vasoactive mediators), direct injury (e.g. toxins, burns), leukocyte-dependant injury (mostly venules), increased transcytosis (venules)
Chemotaxis, phagocytosis, movement of WBC from blood flow to injury focus (margination, pavementing, transmigration/diapedesis). Most migratory cells = polymorphonuclear lymphocytes.
Describe extravasation.
Describe the first cells to arrive at the site of injury.
Describe the second main cell of acute inflammation?
What other cells arrive early?
What cells arrive especially after allergy and helminth infections?
Neutrophil polymorphs, predominant cell for 6-24h, mobile, phagocytic, responds to chemotaxis, segmented nucleus, granular cytoplasm full of granules containing enzymes etc.
Monocytes/macrophages, circulating/in tissue, predominate after 24h, mobile, phagocytic, responds to chemotaxis, attacks and clears up, bean shaped nucleus, copious cytoplasm. Tissue damage/infection = monocytes leave blood and enter affected tissue/organ -> changes to become macrophages.
Basophils/mast cells, blue/purple cytoplasm, degranulates with release of vasoactive amines. Mast cells = histamine release.
Eosinophils, bilobed, red granules
What is chemotaxis? List things which demonstrate this.
What are the 3 stages of phagocytosis?
Movement of an organism in response to a chemical stimulus (i.e. along a chemical gradient), stimulated by exogenous agents (bacteria, fungi, toxins), or endogenous agents (immune complexes, complement components, lipoxygenase products, white cell breakdown products)
1) Recognition and attachment (mechanical contact, opsonisation)
2) Engulfment (pseudopods, phagosome)
3) Killing and degradation (lysosomal contents)
Bystander injury.
What is opsonisation?
What controls the inflammatory response?
Identifies particles such as bacteria and targets them for destruction via binding of an opsonin e.g. antibody, complement proteins, or circulating proteins, to an epitope on an antigen, attracting phagocytes.
Mediators - connection between stimulus and response. Circulate in plasma or intracellular (preformed/synthesised). Released from damaged tissue.
List some preformed cellular mediators.
List some synthesised cellular mediators.
How do steroids and COX1 and COX2 inhibitors and asprin work?
Histamine, serotonin, lysosomal enzymes. Source = mast cells, basophils, platelets, neutrophils, macrophages.
Prostaglandins, leukotrienes, NO (vasodilation), cytokines (leukocyte activation), platelet-activating factors. Source = leuokocytes
Also plasma -> complement activation and factor XII activation
Steroids inhibit phospholipases = can’t make arachidonic acid. COX1/2 inhibitors and asprin inhibit cylooxygenase so can’t make prostaglandins.
List some gerenal and organ specific clinical features of inflammation.
Describe 5 possible outcomes of acute inflammation.
General: pyrexia, drowsiness, lethargy, leukocytosis, decreased appetite, acute phase proteins. Organ specific: e.g. headache.
1) Resolution: clearance of injury, inflammatory cells and mediators, replacement of injured cells, normal function resumed. Spontaneous or with treatment e.g. pneumonia
2) Repair: some tissue lost may not be able to regenerate therefore replaced with granulation tissue and fibrosis. Less than ideal function.
3) Chronic inflammation: if injury can’t be dealth with, repeated episodes
4) Suppurative inflammation: pus more exaggerated form of acute inflammation, neutrophils, dead cells, bacteria and debris. If walled off and surrounded by fibrous rim = abcess.
5) Septicaemia: organism gains access to lymphatics then blood, or blood direct. Response heightened. High mortality.
