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78 Cards in this Set
- Front
- Back
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What is the main purpose of inflammation? |
Destroy, dilute, contain, repair & regenerate |
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Aetiology of Inflammatory Reaction |
- Infections and microbial toxins - Trauma - Physical and Chemical agents, thermal, irradiation, environmental factors - Tissue Necrosis - Foreign bodies - Immune reactions |
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Categories of Inflammatory Responses |
Time, Degree of damage, Characteristic picture, Immunopathological mechanisms |
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What is the pathophysiology of vascular inflammation? |
- transient vasoconstriction followed by vasodilation - increased permeability (enlargement of endothelial gap) - increased viscosity (promotes clotting) - peripheral orientation of leucocytes |
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Exudate is a result of ? |
Inflammation |
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Transudate is a result of _________? Which means it has ___________? |
Osmotic imbalance ; low protein count, low cell count, low fibrinogen content, low specific gravity |
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What are the 5 types of Exudate edema? |
- Serous - watery + low protein content - Haemorrhagic -severe tissue damage - Fibrinous - thick sticky meshwork - Membraneous - in mucous membranes - Purulent - contains pus |
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What are the 3 Patterns of Response? |
- Immediate but transient - Immediate sustained response - Delayed Hemodynamic response |
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What is Immediate Sustained Response? |
- Occurs after serious injury - Longer duration - Involves arterioles, venues, caillaries - direct damage to endothelium |
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How long after injury does delayed hemodynamic response set in? |
2-12 hours + lasts for several days |
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What is the sequence of events in Cellular Phase of Inflammation? |
- Leucocyte migration - Leucocyte adhesion to endothelium - Migration of leucocytes across endothelium - Chemotaxis - Activation of phagocytosis |
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What causes leucocyte migration? |
Stasis of blood flow |
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What causes leucocytes to adhere to endothelial cells? |
Release of chemical mediators |
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What are the types of adhesion molecules |
- selectins (adhesion of leucocyte to endothelial) - integrins (promote cell-to-cell + cell to extracellular) - immunoglobin (I CAM-1, ICAM-2 VCAM) |
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What is Transmigration/Emigraton/Diapedsis? |
After firm adhesion leucocytes squeeze across basement membrane; migrate out of vessel *early response = mostly neutrophils *later response = monocytes, lymphocytes |
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What is chemotaxis? |
Directed movement of leucocytes towards chemical stimulus of offending agent; dynamic + energy dependant |
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What are leucocytes guided by in interstitial fluid? |
Guided by chemical gradient created by chemo-attractants |
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What are the steps of Phagocytosis ? |
- Recognition + Adhesion - Engulfment - Intracellular killing |
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What occurs in Intracellular killing? |
- fusion of phagosome with intracellular lysosomes - digestion of ingested microbe enzymes - formation of residual body - discharge of waste material |
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When are the neutrophils and macrophages not the first to arrive at inflammation? |
Viral + rickettsial infections = lymphocytes Allergy + parasitic = eosinophils |
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What are the Benficial Effects of Inflammation? |
- increased fluid dilutes irritant present - blood cells engulf/digest dead cells that could cause further irritation - Antibodies present in fluid neutralise toxic substance - Clotting with fibrin prevents irritation/inflammation from spreading beyond area - Initiates healing and regeneration |
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What are the Harmful effects of inflammation? |
- digestion destruction of normal tissue - loss of function - inappropriate/exaggerated inflammatory response - acute or chronic - Altered blood supply (anoxia, infarcts) |
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What is defective adhesion? |
-impaired adhesion; occurs with recurrent bacterial infection + impaired wound healing |
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If there is impaired locomotion (movement) and impaired lysosomal degranulation what is wrong? |
Defective chemotaxis or phagocytosis |
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Insufficient hydrogen peroixde production resulting in chronic granulomatous is known as ? |
Defects in microbial function |
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Describe deficiency in # of circulating cells. |
There is marrow destruction or infiltration from cancer cells, reduces number of cells produced. Can also occur with radiation effect. |
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What is the clinical manifestation of Acute Inflammation? |
Calor Rubor Tumor Dolor Function Laesa |
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What causes calor and rubor? |
Increased blood flow to the area from arteriolar dilation |
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What happens if there is an inflammatory response in rigid or semi-rigid structures? |
There will be an increase in pressure in a confined space; can constrict vessels and cause ischaemic necrosis. |
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What causes dolor? |
Inflammatory mediators irritating the nerve endings as well as physical tension within limitations of organ/tissue |
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What are acute phase reactions caused by? |
Inflammatory mediators |
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What endogenous factors cause fevers and rigors? |
TNF, IL 2 or PGE2 |
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What is Leucocytosis ? |
- increase in white blood cells (neutrophils + lymphocytes) - mediated by IL + TNF |
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What are fibrinogen and c-reactive proteins? |
Acute Phase Proteins |
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What are the Acute Phase reactions? |
-Fever + rigors - Leucocytosis - Acute Phase Proteins - Endocrine Changes - Lymphadenopathy - Raised ESR |
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What is Raised ESR? |
- Elevated rate at which RBC settles in test tube; due to alterations in plasma proteins |
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What is lymphatic drainage from local infection? |
Lymphadenopathy |
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What is caused by inflammatory mediators? |
Acute phase reaction of clinical manifestation |
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Properties of Mediators : triggered by microbes or host protein, short lived and ______________? |
Act on target cells |
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Where of inflammatory mediators originate from? |
Plasma or cells |
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True or False - plasma derived mediators do not need to be activated? |
False - plasma derived mediators are present in precursor form and must be activated by proteolytic changes; sourced from complement system + kinin system |
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Where are cell derived mediators? |
Intracellular granules |
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What cell derived mediators can be secreted? Synthesized? |
- histamine from mast cell degranulation - prostaglandins and cytokines synthesized on exposure to stimulus |
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What is the most common method mediators use to regulate? |
Bind to specific receptors on target cells |
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What are the two types of target cell mediators? |
- diverse target = same mediator, many different targets, same reaction - differing effects on different cell types |
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What stops mediators? |
- decay - inactivated by enzymes - scavenged by inflammatory cells - inhibited |
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What are the two cellular mediators |
Histamine and serotonin |
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Where is histamine found? When is it activated?What is the stimulus for histamine release? |
In lungs, skin and GIT; activated in mast cell degranulation - physical injury, immune reaction, fragments of complement, neuropeptides and cytokines |
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What is receptor for histamine? How long does reaction last ?
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H1 receptor on smooth muscle; 1 hour |
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What is serotonin ? |
Preformed vasoactive mediator; comes from platelets + enterochromaffin cells |
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What is the stimuli for serotonin? |
Platelet aggregation - in contact with collagen, thrombin ADP + antigen-antibody complexes; - platelet activating factor from mast cell |
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What are the plasma mediators? |
- complement system - kinin system - eicosanoids - cytokines + chemokines - clotting and fibrinolytic systems |
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What is the complement system? |
- consist of large # of proteins + cleavage products - functions in both innate + adaptive immunity |
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What is the mode of action of the complement system? |
- increase vascular permeability with C3a + C5a - chemotaxis + adhesion (C5a) - opsonization (C3b) - Direct lysis of organism (C5b-C9) |
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What does the Kinin system do? |
- forms vasoactive peptides from plasma proteins activated by hangman factor |
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What does bradykinin do? |
- causes increased vascular permeability, vasodilation, pain production and non-vascular smooth muscle contraction ` |
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What do Eicosanoids do? |
- increases vascular permeability - chemoattractant |
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Glucocorticoids vs NSAID |
NSAID inhibits prostaglandin, cyclooxyrgenase + pain Glucococorticoids inhibit release of arachidonic, histamine, IL-1, TNF-a + inflammation |
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What is the mode of action of Platelet Activating Factor? |
- platelet aggregation + release - vasodilation + increased vascular permeability - leucocyte adhesion (integrin), chemotaxis + degranulation of mast cells - boost synthesis of other mediators - bronchoconstriction |
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What is the mode of action of Cytokines and Chemokines? |
- increase endothelial adhesion - regulate immune and hemopoietic cell proliferation and activity |
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What does the clotting + fibrinolytic system act as during inflammation? |
Chemical mediator |
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What are the outcomes of Acute Inflammation? |
- complete resolution - abscess, suppuration or cellulitis - scarring fibrosis |
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What is scaring fibrosis? |
- in tissue unable to regulate - due to organization of excess fribrin deposition - chronic inflammation |
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What is chronic inflammation? |
- Prolonged duration of active inflammation, tissue destruction and attempts at repair |
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What is the aetiology of chronic inflammation? |
- sequence of unresolved acute inflammation - persisted low grade infection with/without symptoms - Prolonged exposure to potentially toxic agents - Autoimmunity - Factors that delay healing - Repeated episodes of acute inflammation - Underlying disease - Genetic factors |
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What is the hallmark of chronic inflammation? |
- infiltration with mononuclear cells including lymphocytes, macrophages + plasma cells - tissue destruction - granulation tissue - scar formation |
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What are the different types of macrophages and where can you find them? |
- Microglia = CNS - Kupffer cells = liver - Alveolar = lungs - Osteoclasts = bone |
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What are plasma cells differentiated from? |
B cells |
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Where can you find mast cells? |
In connective tissue |
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What reactions are Eosinophils present in?? |
Parasitic infections + malignancies (connective tissue disorder) |
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What is non-specific chronic inflammation? |
- Occurs as a sequence of acute inflammation and continued destruction |
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Granuloma is an example of which type of chronic inflammation? |
Specific - there are histologically characteristic tissue reactions |
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Does a foreign body granuloma cause an inflammatory response? |
NO - inert body |
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What is an immune granuloma? |
- insoluble or poorly soluble particle that induce a cell mediated immune response - can be caveating or non caseating |
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What is a supparting granuloma? |
Necrotic tissue and pus produced |
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What are the outcomes of chronic inflammation? |
- ulcers - fibrosis/strictures - fistulas - any combination of above |
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What is a pyogenic granuloma? |
- NOT A TRUE GRANULOMA - small red/brown lesions which bleed easily and may ulcerate - endothelial cell proliferation, new blood vessel formation, edema + inflammation |
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What are the 5 models that make up Vertebral Subluxation Complex ? |
- Kinesiopathology - restrict/increase movement in vertebral joint - Neuropathology - pinched nerve - Myopathology - strained muscle - Histopathology - changes in disk, nerve root/spine - Pathophysiology - change in normal function |
