Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Chapter 14 Inflammation, Tissue Repair, and Fever

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Inflammation Inflammation is an automatic response to cell injury that: –Neutralizes harmful agents –Removes dead tissue

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Damaged cells release inflammatory mediators These compounds stimulate inflammation Corticosteroids NSAIDs Inflammation

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins damaged cells release inflammatory mediators local responses vascular stage cellular stage systemic (whole- body) responses white blood cell response acute-phase response

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Vascular stage –Prostaglandins and leukotrienes affect blood vessels –Arterioles and venules dilate ºIncreasing blood flow to injured area ºRedness and warmth result –Capillaries become more permeable ºAllowing exudate to escape into the tissues ºSwelling and pain result Acute Inflammation

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Vascular Stage

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question What mechanism causes the redness (erythema) associated with the inflammatory process? a.Prostaglandins b.Leukotrienes c.Arachidonic acid d.All of the above e.a and b

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer e.a and b Rationale: Prostaglandins and leukotrienes cause vasodilation, which brings more blood to the injured/affected area. The symptoms caused by this vasodilation are redness/erythema and warmth.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Kinds of Exudate Serous Hemorrhagic Fibrinous Membranous Purulent

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Scenario A woman has peritonitis. She has a distended abdomen, low blood pressure, and fluid in her abdominal cavity After surgery, she is told to report any GI distress as it may indicate fibrous adhesions Question: What kinds of exudate are involved? What useful purposes do they serve? What complications may they cause?

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Cellular Stage White blood cells enter the injured tissue: –Destroying infective organisms –Removing damaged cells –Releasing more inflammatory mediators to control further inflammation and healing

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins White Blood Cells Involved in Inflammation Granulocytes –Neutrophils –Eosinophils –Basophils –Mast cells Monocytes –Monocytes  macrophages

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Leukocytes Leukocytes enter the injured area Leukocytes express adhesive proteins Attach to the blood vessel lining Squeeze between the cells Follow the inflammatory mediators to the injured area Pavementing Emigration Chemotaxis

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Leukocytes (cont.) Leukocytes release many inflammatory mediators at the injured area: Histamine and serotonin Platelet-activating factor Cytokines –Colony-stimulating factors –Interleukins –Interferons –Tumor necrosis factor Nitric oxide

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Which leukocytes participate in the acute inflammatory response? a.Eosinophils b.Monocytes c.Neutrophils d.All of the above e.a and c

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer d.All of the above Rationale: Granulocytes and monocytes play a role in the acute phase of the immune response. Eosinophils and neutrophils are granulocytes, so all of the leukocytes listed participate.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Other Inflammatory Mediators Other inflammatory mediators travel in the plasma Kinins Coagulation and fibrinolysis proteins Complement system C-reactive protein

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins damaged cells release inflammatory mediators local responses vascular stage cellular stage systemic (whole- body) responses white blood cell response acute-phase response

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Acute-phase Response Leukocytes release interleukins and tumor necrosis factor –Affect thermoregulatory center  fever –Affect central nervous system  lethargy –Skeletal muscle breakdown Liver makes fibrinogen and C-reactive protein –Facilitate clotting –Bind to pathogens –Moderate inflammatory responses

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Fever

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins

Question Tell whether the following statement is true or false. Body temperature is controlled through negative feedback loops.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer True Rationale: When the body senses a change out of the norm (as illustrated in the previous slides), it activates mechanisms that oppose that change (vasodilation and sweating with increased temperatures; vasocontriction and shivering with decreased temperatures). This is known as negative feedback. Positive feedback, on the other hand, senses a change, but activates a mechanism that exaggerates the change.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Scenario Mr. X says he has “chills and fever.” His daughter wants you to explain how he could have both at the same time and from the same disease Question: Should she be keeping him warmer or helping him cool off?

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins White Blood Cell Response Inflammatory mediators cause WBC production WBC count rises Immature neutrophils (bands) released into blood

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Chronic Inflammation Macrophages accumulate in the damaged area and keep releasing inflammatory mediators Nonspecific chronic inflammation –Fibroblasts proliferate –Scar tissue forms Granulomatous inflammation –Macrophages mass together around foreign bodies –Connective tissue surrounds and isolates the mass

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Scenario A man had tuberculosis long ago and when he first had the disease, he had a fever, productive cough, and bloody sputum Later, he had trouble breathing and the doctor said his lungs were “consolidated” with fibrous proteins He recovered and his fever went down; he thought he was cured Three years later, an x-ray showed nodules in his lungs and he was told they contained the TB bacteria Question: Identify inflammatory events in his case

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Tissue Repair Growth factors stimulate local cells to divide Tissue organization is controlled by the extracellular matrix New cells are laid down on the extracellular matrix –Tissue regeneration: injured tissue is replaced by the same kind of cells –Fibrous tissue repair: injured tissue is replaced by connective tissue ºGranulation tissue  scar tissue

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Question Tell whether the following statement is true or false. If you get a paper cut, epithelial tissue will be replaced with connective tissue.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Answer False Rationale: The surface epithelial cells of the skin are most likely to be damaged in this instance. Surface epithelial tissue has the ability to regenerate, replacing the damaged tissue with the same type (epithelial).

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins Wound Healing Inflammatory phase Proliferative phase Remodeling phase