Topic 12 Immune Response & Inflammation part 2 Flashcards
Non-specific response to tissue damage:
Response to cut is the same as a burn/radiation/infection, etc.
(Pathogens, Abrasions, Chemical irritations, Distortion / cell disturbance, Extreme temps)
Inflammation 4 signs
Redness
Pain
Heat
Swelling
3 stages of Inflammation
- Vasodilation - Increase permeability of blood vessels
- Emigration - Movement of phagocytes from blood to interstitial fluid
- Tissue repair
Factors that cause vasodilation and increased
permeability:
Histamine, Kinins, prostaglandins, leukotrienes, Complement
Histamine
Mast cells in the tissues release
Basophils and platelets stimulate the release of
histamine in the blood
Causes increased dilation and permeability
Kinins induce/act as what?
Polypeptides
Induce vasodilation and increase permeability
Act as chemotaxic agent phagocytes
Ex: bradykinin
Prostaglandins
Lipid
Released by damaged cells
Stimulate emigration of phagocytes
Leukotrienes
Basophils and mast cells produce
Increase permeability
Complement
Stimulate histamine release
Attract neutrophils
Promote Phagocytosis
Within 1hour of start of inflammatory process
what appears?
Phagocytes appear
Fibrinogen converted to fibrin forms what?
Forms fibrin mesh
Inflammation Neutrophils stick to blood vessel wall with increased blood flow – and do what?
Squeeze through blood vessel wall to tissues-“emigration”
Depends on chemotaxis
Neutrophils attempt to destroy via what?
phagocytosis
Monocytes follow neutrophils and do what?
Transform into macrophages
More potent phagocytes than neutrophils.
Eventually macrophages die
Redness of inflammation is caused by?
Large amount of blood in damaged area
Local temperatures increase
Metabolic reactions speed up
More heat released
Swelling of inflammation is caused by?
Increased permeability
More fluid in the area
Pain caused by inflammation is caused by?
Symptom of inflammation–neuron injury or increased pressure (edema)
Fever in inflammation is caused by and do what?
Bacteria toxins increase body temperature
Trigger release of interleukin-1 (cause fever)
Helps to inhibit the growth of some microbes
Helps to speed up body reactions
Aids in repair
Inflammation two major components
vascular reaction
cellular reaction
Acute inflammation
rapid onset / short duration / emigration of
neutrophils
chronic inflammation
long duration / lymphocyte involvement /
proliferation of blood vessels / tissue necrosis
Components of acute inflammation (3)
*dilation of capillaries and surrounding blood
vessels–increase blood flow
*structural changes in capillaries-allow plasma proteins and leukocytes to enter interstitial space
*emigration of leukocytes from capillaries where they accumulate in focus of injury-activation to eliminate offending agent
Stimulation for acute inflammation
Infections and microbial toxins Trauma Physical and chemical agents Tissue necrosis Foreign bodies Immune reactions
Vascular changes do what?
Maximize movement of plasma proteins and
appropriate circulating cells into the site of injury or infection
Vasodilation
Increased capillary permeability
Vasodilation what is involved first?
Arterioles involved first, followed by opening of new capillary beds
Increased Capillary Permeability results in what?
Osmotic & hemodynamic changes force fluid into interstitial space (results stasis) /
neutrophils begin adhering to endothelium and moving into interstitial space /
physical openings in endothelium allow more fluid /
protein /
cells to migrate
Margination
movement of leukocytes toward the wall of the capillary
Rolling:
leukocytes tumble slowly along endothelium, adhere transiently, then are finally attached–endothelium completely lined with white cells
Transmigration (diapedesis):
insert pseudopods into junctions between endothelial cells–move through the junction
Chemotaxis:
migrate thru interstitial fluid to source of problem
Extravasation:
movement of leukocytes from vessel lumen to interstitial space
Chemotaxis how does it work?
Locomotion along chemical gradient
Most common exogenous agents are bacterial products
Common endogenous agents
Common endogenous agents of chemotaxis (3)
- components of complement (C5a)
- products of lipoxygenase pathway (leukotriene B4)
- cytokines
Results of Leukocyte activation (5)
production of arachidonic acid metabolites
degrannulation and secretion of lysosomal enzymes
secretion of cytokines
modulation of surface receptors
phagocytosis
Leukocyte activation induced by what?
microbes / products necrotic cells / antigen-antibody complexes / cytokines
Chemical mediators plasma derived must what?
plasma-derived must be activated
Cell-derived chemical mediators usually stored where?
usually stored in intracellular granules
Once activated and the chemical mediators released have what life span?
most are short lived
Production of active mediators triggered by microbial products or host proteins (complement, etc.)
chemical mediators
SIRS
systemic inflammatory response - common systemic response to a wide variety of insults
2 or more of these must be present to diagnosis SIRS (4)
Body temp above 38*C or below 36*C
HR >90 BPM
Respiratory Rate >20/min
Or PaCO2 12,000 cell/mm2
Or <10% immature neutrophilsWidely accepted that SIRS is induced in what % of patients undergoing bypass?
ALL
Incidence and severity or type of response-variable
Most have a few clinical symptoms
Minority develop severe hemodynamic changes or organ failure after bypass.
Risk factor–Length of CPB
Most common culprit of SIRAB is ?
= contact with foreign surface Other factor: Altered arterial blood flow patterns Sheer stress (blood pumps) Cardiotomy suction Tissue ischemia Reperfusion Hypothermia Relative anemia anticoagulants
What contact proteins are activated during SIRAB?
Coagulation factors XII and XI
Prekallikrein
High molecular weight kininogen
End result of SIRAB: formation of what? converts what?
Formation of bradykinin
Conversion of plasminogen into plasmin
Initiates fibrinolysis
Triggers classical complement cascade
Chemokine mediated generalized whole boy inflammation response
Activates vascular endothelium
Further neutrophil-mediated injury
