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33 Cards in this Set
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Characteristics of acute inflammation |
Redness dilation of small vessels in area Heat hyperaimia, vascular dilation Swelling accumulation of exudate fluid Pain oedema stretch and distrorts tissues/ chemicals Loss of function (Virchow) movement because of inflammation, pain, reflex, swelling |
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Inflammation definition |
The physiological response of the body to any stimuli |
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Aims of inflammation |
To eliminate and localise causative agent To limit tissue injury To restore tissue normality |
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Benefits of inflammation/inflammatory oedema |
1. Dilution of toxins drainage to lymphatic 2. Delivery of antigens: a. Opsinins for facilitating phagocytosis b. Immunoglobulin: destruction of invading organisms c. Fibrogens to limit spread of infection 3. Delivery of blood and nutrients neutrophils have high metabolic activity 4. Stimulation of specific immune response 5. Delivery of drugs (AB) |
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Disantantages of inflammation |
1. Oedema/swelling traumatized knee 2. Distraction of normal tissue pancreatitis 3. Inappropriate inflammatory response 4. Loss of fluid from the circulatory system septic shock 5. Inflammatory pain rheumatoid arthritis 6. Blockage of tubes/compression Chlamydia infection |
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Acute Vs chronic inflammation |
Acute: a) an initial response to deal with an injury b)the beginning of a the healing process
Chronic: It occurs over a prolonged period of time with tissue destruction and attempted repair. It may also occur secondary to acute inflammation.
1. Response: immediate, initial/adaptive, longstanding response to stimulus 2. Onset: rapid/slow 3. Duration: hours-days/days, weeks, years 4. Immunity: innate/cell mediated 5. Predominant cells: neutrophils/ plasma cells for antibody production, lymphocytes, macrophages for phagocytosis of damaged tissue, slowly increase from acute to chronic, produce growth factors for repair through fibrosis 6. Vascular component: prominent prevents tissue damage, brings WBC /less important 7. Exudate: involves exudate component vascular leakage of protein rich fluid/ blood vessels proliferation and fibrosis (scarring) no exudate 8. Prognosis: resolution or suppuration or organisation or procede to chronic/ poor 9. Characteristics see characteristics of acute and chronic |
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Causes of acute inflammation |
1. Physical: trauma, heat, UV light, radiation 2. Irritant and corrosive chemicals: acids and alkali 3. Microbial infection: pyogenic bacteria 4. Immune-mediated hypersensitive reaction: autoimmune mediated vasculitis, seasonal allergic rhinitis 5. Tissue necrosis: ischaemia in myocardial infarction |
PIMIT |
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Causes of chronic inflammation |
1. Endogenous materials: necrotic adipose tissue, bone, uric acid crystals 2. Exogenous materials silica, asbestis fibres, implanted prosthesis, suture materials 3. Read of infective agents to phagocytosis and intracellular killing: tuberculosis, leprosis, viral infections, brucellosis 4. Some Autoimmune: organ specific chronic gastritis of pernicious anaemia, hashimotos thyroidism non organ specific: reumatoid arthritis contact hypersensitive reaction self antigens altered by nickel 6. Specific disease with unknown aetiology: chronic inflammatory disease ulcerative colitis 7. Primary granulomatous diseases chrons disease, sarcoidosis 8. Drugs ---->hepatic granulomas |
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Characteristics of chronic inflammation |
Colour: pale/blue Temperature: cold Texture: fibrotic Rom: lof |
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Characteristics of acute inflammation |
Colour: redness dilation of small vessels in area Temperature: heat hyperaimia, vascular dilation Texture: swelling accumulation of extravascular fluid Pain: sharp oedema stretch tissues and chemicals Rom: loss of function restricted movement because of inflammation pain, reflex, swelling |
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Characteristics of chronic inflammation |
Colour: pale, blue Temperature: cold Texture: fibrotic Pain: dull, numb ROM: lof, weaker, hypo or hypertonic |
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Roles of acute inflammation |
The initial response to deal with an injuryThe beginning of the healing process |
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Vasodilation |
In acute inflammation, vasodilation occurs when the arterioles and precapillary sphincters relax. This results in an increased blood flow to the injured area. |
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inflammatory oedema mechanism |
1)Local vasodilation In acute inflammation, vasodilation occurs when the arterioles and precapillary sphincters relax. This results in an increased blood flow to the injured area.
2) Vascular permeability increased A. Chemicals (histamine, bradykinin, nitric oxide and leukotriene) cause B. Endothelial contractions, which result in C.1 Increased fenestrations between endothelial cells C.2 increased permeability of vessels to plasma proteins D. Therefore, protein leakage into interstitial spaces, this leads to E. PLASMA ONCOTIC PRESSURE DECREASE & INCREASE IN HYDROSTATIC PRESSURE F. Net fluid movement from plasma to tissue: proteins, immunoglobulin, coagulating factors
Inflammatory oedema Usually an exudate (not transudate) because high in proteins (including fibrin) antibodies and albumin
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Types of inflammation |
1. Serous 2. Catarrhal 3. Fibrinous 4. Suppurative 5. Haemorrhagic 6. Membranous 7. Pseudomembranous 8. Gangrenous 9. Granulomatous |
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Serous inflammation |
Characterised by an abundant protein-rich fluid exudate with low cellular content serous cavities: peritonitis, inflammation of synovial joints, acute synovitis, vascular dilation |
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Cattarhal inflammation |
Mucous hypersecretion & inflammation of mucous membrane Common cold |
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Fibrinous inflammation |
When the inflammatory exudate fibrinogen polymerises into thick fibrin coating Pericarditis. Resulting into an increase amount of fibrin deposition on the tissue surface. acute pleurisy secondary to acute lobar pneumonia Resolution: if fibrin is removed Scar tissue: if fibrin persist endomitriosis. |
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Suppurative inflammation |
Characterised by pus production and collection. Caused by pyogenic bacteria infection. Staphylococcus aureus and streptococcus pyogenus The pus may be walked off by granular or fibrous tissue. Then it is surrounded by pyogenic membrane of neutrophils and fibroblasts. Empyema: in hollow organs Abscess: elsewhere |
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Haemorrhagic inflammation |
If damage is severe, blood vessels within the area may rupture Haemorrhagic pneumonia, meningococcal septicemia |
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Membranous inflammation |
In acute inflammation, epithelium becomes coated by fibrin, desquamated epithelial cells, and inflammatory cells. Grey membrane in pharyngitis or laryngitis Heavy smokers |
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Pseudomembranous inflammation |
Superficial mucosal ulceration with an overlying of disrupted mucosa, fibrin, mucus and inflammatory cells Pseudomembranous colitis due to clostridium difficile colonisation of the bowel following broad spectrum of AB treatment |
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Long term AB use |
1. Acne 2. Osteomyelitis 3. Tuberculosis |
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Necrotising/gangrenous inflammation |
High tissue pressure due to oedema may lead to vascular occlusion or thrombosis which results in widespread septic necrosis of the organ. the combination of necrosis and bacterial putrefaction is gangrene. Gangrenous appendicitis, diabetes |
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Granulomatous inflammation |
Chronic inflammation where modified macrophages aggregate to form small granulomas. Causes: microorganisms resistant to intra cellular killing, foreign bodies, idiopathic (Crohn's) drugs (allopurinol ----->hepatic granulomas) |
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Manifestations of inflammation/ systemic effects |
1. Pyrexia macrophages produces pyrogens (interleukin 1) that stimulates action from the hypothalamus 2. Constitutional symptoms malaise, nausea, anorexia 3. Reactive hyperplasia lymph node enlargement 4. Haematological changes increased erythrocyte sedimentation rate, acute phase protein release (c-reactive protein) 5. Weight loss occurs in sever chronic inflammation tuberculosis, Crohn's |
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Prognosis of acute inflammation |
Resolution cholecystitis Suppuration appendicitis Organisation and repair pelvic ID Calcification tendonitis/atheroma Acute/chronic acute on chronic bronchitis Chronic inflammation tuberculosis Septicaemia urinary tract infection Death meningitis |
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Resolution |
A) oedema fluid drains into lymphatics B) inflammatory fibrin is degraded by plasmin C) apoptosis of neutrophils that are not needed D) regeneration of local tissue As a result: local tissue damage is limited and the exciting stimulus is removed |
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Suppuration |
Commonest reason: bacterial infection If it persists and it's not cleared off: may become isolated. This is abscess, empyema if in pleural space. Sinus formation may occur: abscess tunnelling to the surface of the body Fistula tube connection between two hollow organs |
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Organisation |
Replacement by granulation tissue healing tissue Rich in a.capillaries b.fluid c.neutrophils d. fibroblasts e.macrophages, and f. growth factors. Resulting in fibrosis (scar tissue) ---->LOF because original tissue replaced by inert collagen tissue |
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Progression to chronic inflammation |
Persistent stimulus that is not managed by neutrophils Macrophages, lymphocytes, and plasma cells are the cells of chronic inflammation TB granulomas, repetitive strain injuries |
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Cell death/injury |
Reversible or irreversible
Type of damage depends on: a) nature and duration of injury b) type of cells affected c) regeneration ability of tissue
Classic causes: (11) Hypoxia Toxins Chemicals Heat Cold Radiation Microorganisms Immune mechanism Nutritional imbalance Genetic abnormality/damage
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Cell death |
Necrosis and apoptosis
Necrosis 1. The death of cell/tissue (after sever cellular injury) 2. Still part of the organism 3. Pathological process
Apoptosis Can be physiological that often follows DNA damage and cell cycle arrest
Cell death for the deletion of unwanted individual cells
Inhibition of apoptosis results in cell accumulation (neoplasia)
The rate of apoptosis must match the rate of cellular division to maintain a stable tissue size (otherwise atrophy) It can be physiological eg endometrium during mensuration
It can be pathological eg DNA damage-genetically abnormal cells
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