505 acute and chronic inflammation

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List the five cardinal, local signs and symptoms of acute inflammation and explain the physiological basis of each.

1. Redness - caused by initial vasodilation
2. Heat - Caused by initial vasodilation
3. Swelling/Edema - transudate formed because of vasodilation that results in increased hydrostatic pressure. Exudate formed because of increased capillary permeability.
4. Pain - caused by stable prostaglandins and bradykinin. Swelling can also cause pain - puts more pressure on pain receptors, and the injury itself can be painful.
5. Loss of function

Define an inflammatory exudate, its contents, and its purpose

Exudate is formed from the increased permeability of the capillaries.
Contents: protein rich - globulins, defensive proteins and WBC
Purpose: to bring WBC to area so they can fight infection

Compare and contrast a transudate and an exudate

Transudate: pitting, very low protein content. Caused by increased blood flow post injury which increases hydrostatic pressure.
Exudate: non-pitting, protein rich. Caused by Increased capillary permeability

Describe the process by which the body delivers leukocytes to the site of inflammation

-RBC starts to clump together because blood gets thicker from all the fluid being pushed into tissues during first phase of inflammation. The RBC clumping together called rouleaux and this clumping causes the WBC to move towards the outside of the flow, closer to the capillary walls.
-margination is the movement of WBC closer to the capillary walls. During inflammation the capillary walls and the WBC produce proteins to make them stick to each other
-Rolling - adhesion molecules become present to help WBC adhere to capillary wall. Adhesion molecules: selectins - up regulate along capillary wall and on WBC to help stick to each other.
-Firm adhesion: integrins on capillary wall and WBC act like super glue and prevent WBC from rolling farther. Now firmly adhered to capillary wall
-Emigration: pores in capillary wall have become wide enough for WBC to leave. WBC acts like amoeba, forms pseudopod and pulls itself through pore in capillary wall - process called diapedesis
-chemotaxis - chemicals produced to attract WBC to injured area. Chemokines can be produced by many different cells
-phagocytosis - WBC in area can phagocytize but needs direction

Describe the 3 processes involved in phagocytosis

Recognition: bacteria has been covered by antibodies, complement proteins and is now called opsonized.

Engulfment: WBC take bacterium into cytoplasm, into vacuole or sac called phagosome. Fuses phagosome with lysosome (where all killing power is) - now called phagolysosome

Killing/degradation: occurs when phagsome fuses with lysosome

List the cell-derived chemical mediators of acute inflammation and explain their physiological effects

Cell-derived mediators are released from cells.
-Histamine
-Neutrophil and eosinophil chemotactic factors
-Eicosanoids
-ROS
-Lyzosomal proteases
-cytokines

Explain the physiological effects of histamine

Mast cells - primarily found in tissues around BV. Close to BV so when histamine released it can easily get into blood.
Basophils - might release histamine
Platelets

Explain the physiological effects of neutrophil and eosinophil chemotactic factors

Mast cells - chemical mediators that attract neutrophils and eosinophil's to site of inflammation. Primarily released from mast cells

Explain the physiological effects of eicosanoids

Formed from free fatty acid called arachidonic acid which is derived whenever the cell membrane breaks down. AA metabolized in body through two pathways: 5-lipoxygenase pathway and cyclooxygenase pathway

Explain prostaglandins

-outcome of AA via COX pathway
Prostacyclin and Thromboxane A2 - work against each other
Prostacyclin: causes vasodilation, inhibits platelet aggregation
Thromboxane A2 causes vasoconstriction and promotes platelet aggregation

Stable prostaglandins: cause BV to dilate potentiation of increase capillary permeability - facilitate exudate formation. Cause pain.

Explain Leukotrienes

-outcome of 5-lipoxygenase pathway
Cause vasoconstriction, bronchospasm, increase permeability.
Leukotriene B4 is the most powerful chemo attractant in body for attracting WBC to area of inflammation

Explain the physiological effects of ROS

Reactive oxygen species including free radicals
Mostly released from phagocytic cells in order to destroy bacteria. When a lot of these are produced they can injure normal cells

Explain the physiological effects of lyzosomal proteases

Usually confined to lyzosymes but when cell dies they release into tissue which can cause degradation of normal tissue

Explain the physiological effects of cytokines

Chemical mediators that are usually released locally in tissues by WBC, not typically found circulating in the blood
-Interferons
-interleukins
-tumor necrosis factor
-colony stimulating factor
-chemokines

List the plasma-derived chemical mediators of acute inflammation and explain their physiological effects

-systems of proteins that normally circulate in blood in inactive form
-if one system stimulated they are all stimulated regardless of if they are needed or not
(a) Coagulation system
(b) Fibrinolysis system
(c) Kinin system - along with complement system most related to acute inflammation
Bradykinin (chemical mediator) that activates kinin system. Causes vasodilation, increased permeability and pain
(d) Complement system - 9-10 proteins that are activated during inflammation that cause complement proteins to fragment into pieces. 20-25 mediators that develop from this system. Causes a lot of events: chemo attractants, opsonins, mast cell degranulation, increase vascular permeability, help activate neutrophils, cause cell lysis (membrane attack complex)
Complement proteins drill a hole and destroy lipid bilayer and cause cell death

Explain why fever, leukocytosis, increased ESR, and increased acute phase proteins occur with acute inflammation

All part of systemic signs of acute inflammation
Fever: not same as local heat, some mediators have ability to upregulate thermostat and cuase fever (ex IL1, IL4, TNFa and bacterial products)
Leukocytosis: increase in WBC count. Doesn't tell you which WBC is in excess. Mediators that stimulate fever also stimulate leukocytosis. "Shift to the left" increase in % of bands. More immature WBC in circulation, indicates acute infllmation
Increased ESR (erythrocyte sedimentation rate): don't need to know why occurs
C-Reactive protein: acute phase protein made in liver during inflammation. One of first tests done to measure MI in women.

Discuss the 3 outcomes of acute inflammation

(1) resolution - occurs 95% of time. Minimal tissue loss or scar tissue formation
(2) suppuration/abscess - dead white cells, living whit ecells, dead bacteria, live bacteria form purulent exudate. Body forms fibrous pocket around exudate called abscess which might absolve itselve or might need draining
(3) fibrosis - scarring
(4) can turn chronic - very rare

Explain when and why chronic inflammation occurs

Occurs when one or more of the situations exist
(1) Acute inflammation has failed to eradicate the injurious agent
(2) Injurious agent is an inert substance (splinter of wood, silicon particle, metal fragment)
(3) Injurious agent is a self-molecule (like an autoimmune disease)
(4) Injurious agent is a microorganism whose anatomical structure is unaffected by the cemical mediators of acute inflammation (TB, Sypillis, leprosy)

Differentiate between the characteristics of acute and chronic inflammation

Acute
- short duration
-acute onset
-neutrophils and macrophages are inflammatory cells
-vascular changes: active vasodilation and increased permeability
-fluid exudate and edema
-cardinal clinilca signs of inflammation occur
-usually no tissue necrosis
- no fibrosis
-systemic manifestations: high fever
-changs in perpipheral blood: neutrophil leukocytosis, lymphocytosis

Chronic
- long duration (weeks to months)
- insidious onset
-inflammatory cells: lymphocytes, macrophages, eosinophils, fibroblasts, plasma cells
-vascular changes: new vessel formation
-no fluid exudate or edema
-no cardinal signs of inflammation
-ongoing tissue necrosis
-systemic manifestations: low grade fever, weight loss, anemia
-Changes in peripheral blood: usually none

State the function of chronic inflammation

...

Define the 2 primary outcomes of chronic inflammation

Necrosis
Fibrosis

Describe the types of tissue damage caused by intracellular

(1) cell necrosis - lytic viruses (HIV, Hep B) that destroy host cell as replicate and leave the cell
(2) cell swelling - intracellular oganisms can interfere with cellular processes, impairing ATP production and causing cellular swelling
(3) latent infection - some viruses can remain latent in cells for long periods with no activity; reactivation of the virus may occur at any time (chicken pox)
(4) giant cell formation

Describe the types of tissue damage caused by extracellular organisms

(1) Release of locally-acting enzymes : bacteria release enzymes of one kind or another as they invade tissue; these enzymes break down tissue and can result in cell injury or necrosis
(2) local vasculitis - many highly virulent organisms (anthrax) can cause thrombosis in local small vessels, causing necrosis near infection; may be due to direct invasion by the organism or production of toxins
(3) release of remotely-acting enzymes - some bacteria produce toxins that are carried in the circulation to cause cell injury/death to tissues far removed from the point of infection
(a) endotoxins - dead bacterial compoenents of gram negative organisms. Act on small blood vessels to cause vasodilation, endothelial cell damage, and activation of the coagulation cascasde leading to widespread clot formation. Shock results
(b) exotoxins - substnaces serveted by living bacteria exert their effects at distant locations from infection. Highly antigenic - stimulate the production of antibodies. Heat-labile and usually can dbe destroyed by cooking or heating to tempersautes above 60
(c)enterotoxins - exotoxins affecting intestinal mucosal cells

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