Transcript Document

Hemodynamics & Cellular Phases
Types of Exudates
(Role of Chemical mediators in
inflammation)
Hemodynamics
• Hemodynamics consist of maintenance of:
I-Vessel wall integrity.
• II-Intravascular pressure & osmalarity.
• III-Blood as liquid.
Hemodynamic Changes
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These are;
I-Disturbances in cellular phases.
II-Disturbances in blood.
III-Non clot formation.
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.
Edema
(Changes in Volume & Pressure)
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.
Thrombosis
Thrombosis
Thrombosis
Thrombosis
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).
Embolism
Infarction
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.
Types of Edema
• These are:
• I-Fluid collection in interstitial tissue cause
edema.
• II-Inflammatory edema due to increase
vascular permeability.
Types of Edema
• I-Fluid collection in interstitial tissue
cause edema:
• There is sever or generalized edema with
subcutaneous tissue swelling called
Anasarca.
Types of Edema
• II-Inflammatory edema due to increase
vascular permeability:
• i-Dependent edema.
• ii-Fluid collection (edema fluid) in the body
cavities.
Types of Edema
• II-Inflammatory edema due to increse
vascular permeability:
• i-Dependent edema;
• In feet.
• In legs.
• At sacral region.
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.
Hydrothorax
Hydropericardium
Ascitis.
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.
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.
Hyperemia
Sub mucosal Congestion
Congestion
Exudate Formation
In 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
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.
Types of exudate
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The types are:
Serous.
Fibrinous.
Suppurative.
Hemorrhegic.
Ulceration.
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
Serous fluid in Pericardial Cavity
Types of exudate
Suppurative
Presence of pus (pyogenic staphylococcal
species).
Often walled-off if persistent.
Haemorrhagic Adherence (Complication)
Hemorrhage
Types of exudate
• Ulceration
– Necrotic and eroded epithelial surface
– Underlying acute and chronic inflammation
– Trauma, toxins, vascular insufficiency
Chronic Inflammtion
(Gastric Ulcer)
Chronic Inflammtion
(Gastric Ulcer)
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)
Chemical mediators
• Cell-derived:
– Preformed, sequestered and released (mast
cell histamine, in intercellular granules of mast
cells).
– Synthesized as needed (prostaglandin &
cytokines).
The cells which release mediators
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These are;
Platelets.
Neutrophils.
Monocytes.
Macrophages.
Mast cells.
Activation of Mediators
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Mediators are triggered by;
Microbial products.
Damaged tissue.
By host proteins from;
-Complement system.
-Kinin system.
-Clotting system.
Types of Chemical Mediaters
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Vasoactive amines:
-Histamine.
-Serotonin.
Plasma proeases:
-Complement system.
-Kinin system.
-Clotting system.
Types of Chemical Mediaters
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Arachidonic acid metabolies:
-Prostaglandis.
-Leukotriens.
-Lipoxins.
Platelet activating factors (PAF).
Cytokines & Chemokines:
-Tumor necrosis factors.
-Inteleukin-1
Types of Chemical Mediaters
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Lysosomal constituents of leukocytes.
Oxygen derived free radicals.
Neuropeptides.
Other mediates:
-Hypoxia induce factor-1.
-Necrotic tissue.
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.
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.
Chemical mediators
• Vasoactive amines, (histamin release):
• Anaphylotoxins- C3a & C5a.
• Histamine releasing proteins- from
leukocytes.
• Neuropeptides- substance P.
• Cytokines- IL-1 & IL-2.
Chemical mediators
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Functions of Histamine:
- Dilation of arterioles.
- Increase permeability of venules.
- Constriction of large arteries.
Chemical mediators
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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.
Chemical mediators
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Plasma proteins:
-Complement system.
-Kinin system.
-Clotting system.
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.
Chemical mediators
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-Complement activation causes:
- Increased vascular permeablity.
- Chemtaxis.
- Opsonization.
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.
Chemical mediators
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-Kinin system:
Function nonpeptide bradykinin:
Increase vascular permeability.
Dilation of blood vessels.
Contraction of smooth muscles.
Pain when injected in the skin.
Chemical mediators
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-Clotting system:
It is divided into two;
Intrinsic pathway.
Extrinsic pathway.
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.
Chemical mediators
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Arachidonic acid metabolites:
- Prostaglandins.
- Leukotriens.
- Lipoxins.
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).
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.
Thank You