Inflammation, Healing

Chapter 2: Inflammation and Healing

First line of defense – skin and mucous membranes mechanical barrier, saliva, tears, contain enzymes, chemicals to destroy contaminants
Second line of defense – phagocytosis, inflammation
Phagocytosis – neutrophils (leukocyte) and macrophages ‘vulture cells’ engulf and destroy cell debris and bacteria
Interferons – protect against viruses
Third line of defense – immune system, production of antibodies, sensitized lymphocytes

Normal defense mechanism to localize and remove, S&S warning of a problem,
Inflammation … ‘itis’ response to tissue injury, redness, swelling, warmth, pain, possibly loss of function, appendicitis, laryngitis…
*Inflammation is not the same as infection! Allergies, burns, no microbes

Causes of inflammation:
Physical damage, sprains, cuts; chemical irritants, allergies, heat, cold, foreign bodies, infection.
Infection is one cause of inflammation
Infection always has bacteria, virus, fungi, or microbe present

Introduction to the immune system

What happens during inflammation?
*Remember the players:
Platelets, mast cells release chemicals to sound the alarm!
Neutrophils – phagocytosis of microorganisms (think nutrition)
Basophils – release histamine > inflammation
Eosinophils – are high in allergic responses (think allergy with a capital E, allErgic)
T lymphocytes – active in cell mediated immune response
B lymphocytes – produce antibodies
Monocytes – phagocytosis in blood
Macrophages – phagocytosis, mature monocytes in tissues

Chemically speaking…inflammation...
May be immediate or delayed, short or long process
When tissue is injured Mast cells and platelets release chemical mediators, histamine, serotonin, prostaglandins, leukotrienes into interstitial fluid and blood > Cytokines send messages to lymphocytes, macrophages, immune system, and hypothalamus >These messages rally the body’s defenses.

Physically… inflammation...
The immediate nerve response is to vasoconstrict, but the chemicals released quickly cause vasodilation, which increases the blood supply to the area causing hyperemia. Capillary permeability also increases. This increases fluid to the area diluting any toxins, globulins serve as antibodies and fibrinogen forms fibrin mesh to wall off area.

Leukocytes are attracted to the area by chemotaxis as damaged cells release their contents. First neutrophils then monocytes, macrophages. Here they destroy microorganisms and cell debris by phagocytosis to help with healing. But when phagocytic cells die, lysosomal enzymes are released, this damages nearby cells and the inflammation is prolonged.

So what does this all mean???
Excessive fluid build up decreases circulation, which decreases cell oxygenation, nutrition and waste exchange….
Cardinal signs of inflammation
Redness, warmth, increased blood flow to area
Swelling, edema, shift fluid to interstitial space
Pain, increased pressure on nerves
Possibly, Loss of function, swelling

*Exudate = collection of fluid in the inflamed area

Types of exudate:
Serous – watery with protein, WBCs, burns, allergic rx
Fibrinous – thick, sticky, high cell, fibrin count, likely to scar
Purulent – thick yellow, green contains leukocytes, cell debris, microbes
Abscess – localized pocket of purulent material
Hemorrhagic exudate – if blood vessels have been injured

The body also responds to inflammation especially if caused by infection with malaise, fatigue, headache, and anorexia. Fever or pyrexia is caused by the release of pyrogens from WBCs. These circulate and cause the body’s temperature system in the hypothalamus to be reset. Fevers can be beneficial if it impairs the growth of the offending organism.

*Changes in the blood with inflammation you should know:
Leukocytosis - ^ numbers of WBCs, ^neutrophils, ‘a shift to the left’
Differential - proportion of each WBC detailed, hints to cause of illness, viral vs. bacterial
Allergic rx = eosinophilia
Plasma proteins – increased fibrinogen and prothrombin, response in the liver
Elevated C-reactive protein – protein not normally in blood, appears within 24-48 hrs w/necrosis, inflammation
Increased erythrocyte sedimentation rate (ESR) – elevated plasma proteins ^ rate that red blood cells settle in sample
Cell enzymes – released from necrotic cells, enter tissue fluids, blood
Cell enzymes, isoenzymes can help locate inflammation or necrosis examples AST (SGOT) liver disease, CK-MB specific for cardiac.

Infection - damaged tissue more susceptible to infection due to decreased perfusion, entry of pathogens, exudate perfect medium for growth of organisms
Ulcers, perforation – can occur due to prolonged inflammation, lack of tissue growth
Skeletal muscle spasm – inflammation causes pain, forces bones or joints out of alignment, more pain
Local complications – depending on site of infection and impaired function of that area … lungs, kidneys
Chronic inflammation – due to chronic conditions (arthritis) or irritants (smoking) typically less swelling, exudate but more lymphocytes, macrophages, fibroblasts, fibrous scar, granuloma

Blood cell component models

Treatment of Inflammation
Aspirin (ASA) Acetysalicylic acid mechanism decreases prostaglandin synthesis at the site of inflammation. anti-inflammatory, analgesic, antipyretic. Not for children, why? Reyes syndrome. Can interfere with blood clotting by decreasing platelets. How might this impact care?

Acetaminophen, Tylenol – Analgesic and antipyretic * does not address inflammation!

NSAIDS – Nonsteroidal anti-inflammatory drugs – Motrin, Advil, ibuprofen, reduce prostaglandin production, analgesic and antipyretic

Glucocorticoid – Anti-inflammatory – synthetic chemicals related to steroids produced in the body by the adrenal gland. Blocks the immune system. Short term therapy due to side effects which can resemble Cushings syndrome.
COX-2 – newer NSAIDs, celebrex, Vioxx, off market

Other therapies – RICE, rest, ice, compression, elevate; mild exercise; rest, nutrition; physiotherapy, occupational therapy.

Types of Healing
The healing process

Complications of healing by scar
Loss of function
Contractures and obstructions
Hypertonic scar tissue

Think about it…?s
Name some ways these defense systems can fail…

Inflammation and Healing


Gould, B. E., & Dyer, R. M. (2011). Pathophysiology for the health professions (4 ed.). St. Louis, Missouri: Saunders Elsevier.

Story, L. (2012). Pathophysiology: A practical approach. Sudbury, MA: Jones & Bartlett Learning .


Blood cell models

Introduction to how the immune system works

Inflammation and Healing