Hemodynamics & Cellular Phases Types of Exudates (Role of Chemical mediators in inflammation)

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Transcript of Hemodynamics & Cellular Phases Types of Exudates (Role of Chemical mediators in inflammation)

Page 1: Hemodynamics & Cellular Phases Types of Exudates (Role of Chemical mediators in inflammation)

Hemodynamics & Cellular PhasesTypes of Exudates

(Role of Chemical mediators in inflammation)

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Hemodynamics

• Hemodynamics consist of maintenance of: I-Vessel wall integrity.

• II-Intravascular pressure & osmalarity.

• III-Blood as liquid.

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Hemodynamic Changes

• These are;

• I-Disturbances in cellular phases.

• II-Disturbances in blood.

• III-Non clot formation.

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Hemodynamic Changes

• Disturbances in Cellular Phases: Disturbances occur in blood & endothelium, like:

• I-Changes in volume, pressure & proteins contents.

• II-Alteration in epithelial function.• Both cause movements of water towards

the vessel wall & out side the vessel in the interstitial tissue/spaces, called edema.

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Edema (Changes in Volume & Pressure)

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Hemodynamic Changes

• II-Disturbances in blood:

• Disturbance in fluidity of blood.

• Blood not maintain as fluid with injury, causes clot formation.

• Fixed clot formation in vessel wall lumen called Thrombosis.

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Thrombosis

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Thrombosis

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Thrombosis

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Thrombosis

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Hemodynamic Changes

• II-Disturbances in blood:

• Migration of clot (thrombus) in the vessel lumen is called, Embolism.

• Obstruction in vessel lumen, by clot (thrombosis), obstruct the blood flow to the tissue, cause cell death (infarction).

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Embolism

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Infarction

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Hemodynamic Changes

• III-Non clot formation:

• Inability to clot after vascular injury results in hemorrhage.

• Local bleeding cause, tissue perfusion.

• Extensive hemorrhage results in hypotension (shock) & death.

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Types of Edema

• These are:

• I-Fluid collection in interstitial tissue cause edema.

• II-Inflammatory edema due to increase vascular permeability.

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Types of Edema

• I-Fluid collection in interstitial tissue cause edema:

• There is sever or generalized edema with subcutaneous tissue swelling called Anasarca.

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Types of Edema

• II-Inflammatory edema due to increase vascular permeability:

• i-Dependent edema.

• ii-Fluid collection (edema fluid) in the body cavities.

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Types of Edema

• II-Inflammatory edema due to increse vascular permeability:

• i-Dependent edema;

• In feet.

• In legs.

• At sacral region.

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Types of Edema

• II-Inflammatory edema due to increse vascular permeability:

• ii-Fluid collection (edema fluid) in the body cavities:

• Hydrothorax, (fluid in thoracic cavity).• Hydropericardium, (fluid in pericardial

cavity).• Hydroperitoneum, (fluid in peritoneal

cavity), also called Ascitis.

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Hydrothorax

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Hydropericardium

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Ascitis.

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Hyperermia & Congestion

• Hyperemia is an active process, occurs due to arteriole dilation, cause engorgement of vessels with oxygeneted blood.

• This occur as red area on body in;

• Inflammation.

• Skeletal muscle during exercise.

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Hyperermia & Congestion

• Congestion is a passive process resulting from impaired blood out flow from a tissue

• Blue red color (cyanosis), can occur due to accumulation of deoxygeneted blood.

• Congestion can occur:

• Locally due to an isolated venous obstruction.

• Systematically in cardiac failure.

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Hyperemia

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Sub mucosal Congestion

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Congestion

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Exudate FormationIn Inflammation Vascular changes Cardinal signs RUBOR (Redness ) – Increased arterial blood flow

CALOR (Rise in temperature) – Increased arterial blood flow

DOLOR ( Pain ) – Physical / Chemical irritation of nerve TUMOR (Swelling ) – Collection of exudate

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Exudate

• Exudates it is an inflammatory extra vascular fluid that has a high protein concentration, cellular debris and an specific gravity above 1.020. There is also disturbance in the normal permeability of small blood vessels in the area of injury.

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Types of exudate

• The types are:• Serous.• Fibrinous.• Suppurative.• Hemorrhegic.• Ulceration.

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Types of exudate• Serous / Catarrhal Resorption (No

complication)• Watery, protein-poor effusion (e.g., blister)• Fibrinous Fibrinolysed / Fibrosis (May or may

not have complication)• Fibrin accumulation.

Either entirely removed or becomes fibrotic

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Serous fluid in Pericardial Cavity

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Types of exudate

SuppurativePresence of pus (pyogenic staphylococcal

species).

Often walled-off if persistent.

Haemorrhagic Adherence (Complication)

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Hemorrhage

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Types of exudate

• Ulceration– Necrotic and eroded epithelial surface– Underlying acute and chronic inflammation– Trauma, toxins, vascular insufficiency

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Chronic Inflammtion(Gastric Ulcer)

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Chemical mediators

• Chemical mediators are the chemical complexes induce inflammation.

• They originate from:

• Plasma, (plasma derived mediaters).

• Cells, (cells derived mediaters).

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Chemical mediators

• Plasma-derived:– Complement, kinins, proteins & coagulation

factors present in plasma.– Many in “pro-form” requiring activation

(enzymatic cleavage like proteolytic enzymes)

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Chemical mediators

• Cell-derived:– Preformed, sequestered and released (mast

cell histamine, in intercellular granules of mast cells).

– Synthesized as needed (prostaglandin & cytokines).

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The cells which release mediators

• These are;

• Platelets.

• Neutrophils.

• Monocytes.

• Macrophages.

• Mast cells.

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Activation of Mediators

• Mediators are triggered by;

• Microbial products.

• Damaged tissue.

• By host proteins from;

• -Complement system.

• -Kinin system.

• -Clotting system.

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Types of Chemical Mediaters

• Vasoactive amines:

• -Histamine.

• -Serotonin.

• Plasma proeases:

• -Complement system.

• -Kinin system.

• -Clotting system.

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Types of Chemical Mediaters

• Arachidonic acid metabolies:• -Prostaglandis.• -Leukotriens.• -Lipoxins.• Platelet activating factors (PAF).• Cytokines & Chemokines:• -Tumor necrosis factors.• -Inteleukin-1

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Types of Chemical Mediaters

• Lysosomal constituents of leukocytes.

• Oxygen derived free radicals.

• Neuropeptides.

• Other mediates:

• -Hypoxia induce factor-1.

• -Necrotic tissue.

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Chemical mediators

• Vasoactive amines:

• Histamines & Serotonin-1st mediaters released in inflammation.

• Mast cells, Basophils, Platelets & connective tissue (around the blood vessels), released histamine.

• Pre-formed histamine is present in mast cells granules.

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Chemical mediators

• Vasoactive amines:

• Histamine is mainly released by mast cells granules in response of different stimuli:

• Physical injury- trauma, cold or heat.

• Immune reaction- binding of antibodies to mast cells.

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Chemical mediators

• Vasoactive amines, (histamin release):

• Anaphylotoxins- C3a & C5a.

• Histamine releasing proteins- from leukocytes.

• Neuropeptides- substance P.

• Cytokines- IL-1 & IL-2.

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Chemical mediators

• Functions of Histamine:

• - Dilation of arterioles.

• - Increase permeability of venules.

• - Constriction of large arteries.

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Chemical mediators

• Serotonin:• Pre-formed vasoactive mediater.• Functions are same as Histamine.• Activated by platelets aggregates.• Serotonin & platelet aggregates are

stimulated by platelet activating factor (PAF).

• Serotonin cause increase permeability during immunologic reaction.

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Chemical mediators

• Plasma proteins:

• -Complement system.

• -Kinin system.

• -Clotting system.

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Chemical mediators

• -Complement system:

• Consists of 20 component proteins with cleavage products.

• The system is consist of;

• Innate immunity.

• Adaptive immunity.

• Both types immunity act against microbial agents.

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Chemical mediators

• -Complement activation causes:

• - Increased vascular permeablity.

• - Chemtaxis.

• - Opsonization.

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Chemical mediators

• -Kinin system:

• Kinin system form the vasoactive peptides- Kininogens from the plasma proteins.

• Kinin system also release nonpeptide bradykinin- produce histamin like effect.

• Hog man factor also release bradykinin.

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Chemical mediators

• -Kinin system:

• Function nonpeptide bradykinin:

• Increase vascular permeability.

• Dilation of blood vessels.

• Contraction of smooth muscles.

• Pain when injected in the skin.

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Chemical mediators

• -Clotting system:

• It is divided into two;

• Intrinsic pathway.

• Extrinsic pathway.

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Chemical mediators

• -Clotting system:• Intrinsic pathway- is a series of plasma

proteins, activated by Hogman factor (factor xii).• Hogman factor (inactive protein) synthesized in

liver. • Hogman factor with negatively charged surfaces

(collagen, platelets, basement membrane & in endothelial injury) form, factor XIIa & activate a verity of mediaters.

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Chemical mediators

• Arachidonic acid metabolites:

• - Prostaglandins.

• - Leukotriens.

• - Lipoxins.

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Chemical mediators

• Arachidonic acid metabolites:

• Arachidonic acid is a 20-carbon polyunsaturated fatty acid (from diet or from essential fatty acids).

• Present in cell membrane, as phospholipids.

• It release from cell membrane by phospholipase (phospholipase A2).

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Chemical mediators

• Arachidonic acid metabolites:• It release from cell membrane by

phospholipase (phospholipase A2).• The cellular phospholipase is activated by;• Mechanical stimuli.• Chemical stimuli.• Physical stimuli.• Mediaters like C5a.

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