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70 Cards in this Set
- Front
- Back
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inflammation
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-dynamic response of vascularised tissue to injury.
-reaction of microcirculation -protective response |
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microcirculation
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movement of fluid and leukocytes from blood into extravacular tissues
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Causes of inflammation
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-infection
- trauma -thermal sources -ionizing radiation - chemical sources - immunologic causes - tissue death |
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acute inflammation
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-neutrophils first come
- vascular damage - little or no fibrosis -exudate |
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chronic inflammation
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-little signs
-fibrosis - neo-vascularisotis -lymphocytes - no exudate |
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PRINCIPAL CELL EFFECTORS
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-1st 24 hours: NEUTROPHILS
-Bacterial infections, infarction -Come from the bone marrow reserve pool -Band neutrophils: less mature cells -2nd-3rd day: neutrophils are replaced by monocytes-macrophages -Tuberculosis, salmonellosis |
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-Band neutrophils:
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less mature cells
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Eosinophils
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FIGHTS
Allergic reactions Parasitic infections Hodgkin lymphoma |
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Mast cells and basophils
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-store and produce histamine and heparine
-chronic myelogenous leukemia: unregulated growth of myeloid cells in bone marrow -myeloproliferative dieases |
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myeloproliferative dieases
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excess cells produced in bone marrow
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cellular response of leukocytes
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emigration
margination pavementing rolling firm adhesion transmigration chemotaxis phagocytosis intracellular microbial killing |
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margination
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-adhesion of leukocytes to the luminal surface of blood vessel walls
-THE ENDOTHELIAL CELLS ARE ACTIVATED, ATTRACT THE SURFACE GLYCOPROTEINS ON NEUTROPHILS |
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transmigration
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like DIAPEDESIS- change of place form one part of the body to the other (crosses membrane into extracellular tissues)
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diapedesis process
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-INSINUATION OF THE NEUTROPHILS THRU THE ENDOTHELIAL CELLS
-BASEMENT MEMBRANE -EXTRAVASCULAR TISSUES |
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CHEMOTAXIS
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- cells/organisms direct their movement according to certain chemicals
-NEUTROPHIL DIRECT ITS MIGRATION TOWARDS THE CHEMOATTRACTANT |
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MARGINATION, CHEMOTAXIS AND DIAPEDESIS
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CAN DELIVER HUGE NUMBERS OF NEUTROPHILS IN A FEW HOURS
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PUS:
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CELLULAR ACUTE INFLAMMATORY EXUDATE WITH PMN CELLS AND CELLULAR DEBRIS
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PHAGOCYTOSIS
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FORMATION OF PHAGOSOME
+ LYSOSOME = PHAGOLYSOSOME |
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phagosome
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vacuole formed around a particle
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phagocytosis of a particle
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opsonization -> attachment -> engulfment -> intracellular killing
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Intracellular microbial killing:
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phagocytosis activates HMP -> oxidative burst -> supplies e's to NADPH oxidase -> superoxide anion -> H2O2
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HMP shunt
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generate NADPH and pentose syn
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H2O2
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Oxides microbial proteins and disrupts cell walls
Myeloperoxidase-halide system of bacterial killing |
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DEGRANULATION
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- releases antimicrobial cytotxic molecules from granules (secretory vesicles)
-THE TOXIC SUBSTANCES MAY CAUSE LOSS OF FUNCTION (FUNCTIO LAESA) |
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rubor
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redness
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calor
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heat
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tumor
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swell
-contraction of capillary endothelial cells - mildest: extravasation of wter, low molecular weight proteins - moderate: + HMW prteins -severe: + bl. cells |
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rubor and calor
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increase bl. flow due to relaxation of the terminal arteries
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functioles
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loss of function
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dolar
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pain
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Histamine
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-increase capillary permeability
-contracts postcapillary venules -Source: basophils, mast cells,platelets -Stimuli: binding of IgE, binding of C3a and C5a:”anaphylotoxins” heat, cold Interleukin-1 |
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Serotonin
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5-hydroxytryptamine
Action: similar to histamine Source: platelets |
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Cyclooxygenase pathway
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-Enzymes:COX-1,COX-2
-Products: Platelet TxA2 2. Endothelial prostacyclin |
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Platelet TxA2
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-vasoconstrictor,platelet aggregator
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2. Endothelial prostacyclin
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-vasodilator,inhibits platelet aggregation
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COX-1
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responsible for baseline levels of prostoglandins
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COX-2
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produces prostoglandins through stimulation
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Lipooxygenase pathway
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Products: hydroperoxyeicosatetraenoic acid (HPETE)
5-HPETE -leukotrienes -cause intense vasoconstiriction, bronchospasm, and increased vascular permeability. |
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LTB4:
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chemotactic for neutrophils
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LTC4,LTD4,LTE4
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“slow reacting substance of anaphylaxis”
vasodilatation bronchoconstriction increase capillary permeability |
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Cytokines
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-Soluble proteins
-Secreted by numerous cells(monocytes-macrphages) -Act as “effector molecules” -“acute phase response” -Fever, increase WBC: systemic -Synthesis of C-reactive proteins, complement components, fibrinogen, prothrombin -Synthesis of adhesion molecules -Neutrophil degranulation |
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IL-1
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interluekin 1 could induce feverm control lymphocytes
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TNF
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tumor necrosis factor
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kinin system
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-Formed during active secretion in sweat glands, salivary glands, pancreas, kidneys
-End product: bradykinin -Actions: vascular permeability arteriolar dilation pain |
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Complement system
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-biochemical cascade that helps to move pathogens from the injured area of an organism
-20 Plasma proteins -source: HEPATOCYTES, MACROPHAGES, GIT CELLS |
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COMPLEMENT CASCADE
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classical pathway-initated by C1
alternative pathway |
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How Complement system kill bacteria
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-OPSONIZE BACTERIA
-ACTIVATE PMN, MACROPHAGES -REGULATES AB RESPONSE -CLEARS AWAY IMMUNE COMPLEXES -INFLAMMATION, after- TISSUE DAMAGE -ANAPHYLAXIS- acute systemic and severe -Type 1 hypersensitivity |
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Classical pathway
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Starts with C1 + antigen-antibody
Ends with the membrane attack complex |
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alternative pathway
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Bacterial surface activates the pathway
Works in the absence of antibodies Less efficient |
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C3b:
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opsonin
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C3a and C5a:
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anaphylotoxins
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C5b-C9:
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“MAC”
membrane attack complex |
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abscess-
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cavity filled with pus
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ulcer-
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discontinuity of the skin
-Loss of surface epithelium |
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fistula
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-abnormal connection bw two surfaces or organs
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scar-
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areas of fibrous tissue that replace the normal skin when there is injury or wound
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Chronic nonspecific inflammation
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-Proliferation of fibroblasts and new vessels
-Increased macrophages, lymphocytes, plasma cells -Macrophage+antigen ---> B lymphocyte activation ----> antibody-producing plasma cells -Scarring and distortion of tissue architecture |
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Granulomatous inflammation
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-Granuloma: nodular collection of macrophages called “epitheloid cells”
-Surrounded by rim of lymphocytes -Macrophage+antigen----> presented to CD4+lymphocytes---> release of cytokines ----> monocytes/macrophages transform-----> epitheloid cells and giant cells |
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healing
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REPAIR + REGENERATION
NEW EPITHELIUM GROWTH |
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steps in wound healing
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COAGULATION- clotting
HEMORRHAGE- CLOT FORMATION FIBRIN, PLATELETS HEMOSTASIS-stop bleeding |
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NEUTROPHILS-
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can be seen within 24-48 HRS
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MACROPHAGES
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48 HRS-72 HOURS
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FIBROBLASTS
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5 -7DAYS
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ANGIOGENESIS
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-formation of new blood vessel
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EPITHELIALIZATION
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IN 24-48 HOURS
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1ST SIGN
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THICKENING OF THE BASAL CELL LAYER-
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COLLAGEN SYNTHESIS
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3-5 DAYS POST INJURY
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6 WEEKS,
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80-90% WOUND STRENGTH
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CAUSES OF HYPERTROPHIC SCAR
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FOREIGN BODY IN THE WOUND
SCRATCHING HEMATOMA SECONDARY INTENTION EXCESSIVE TENSION INADEQUATE WOUND CLOSURE |
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KELOIDS
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-hypertrophic scar
- overgrowth growth of tissue at the site of healed skin injury |
