Pathophysiology Chapter 2: Inflammation and Healing
Pathophysiology Chapter 2: Inflammation and Healing
I. Review of Normal Defenses in the Body
A. Nonspecific defense mechanisms
1. 1st line of defense - skin, mucous membrane, body secretions
2. 2nd line of defense
a. phagocytosis - neutrophils (leukocytes)and macrophages: engulf bacteria,
cell debris, foreign matter
b. inflammation - sequence of events to limit effects of injury or foreign agent
(interferon)
B. Specific defense mechanisms
1. 3rd line of defense - immune system
2. protection through antibodies/sensitized lymphocytes
II. Review of Normal Capillary Exchange
A. Not all capillaries working all the time
B. Movement out of capillaries
1. arteriolar end - fluids, electrolytes, nutrients, oxygen move out
a. based on net hydrostatic pressure
b. capillary hydrostatic pressure high - osmotic pressure low
c. differences in concentrations of dissolved substances between blood and interstitial fluid promote movement
3. blood cells, plasma proteins (albumin, globulin, fibrinogen) stay inside capillary
C. Movement into capillaries
1. venous end - fluids, carbon dioxide, waste move in
2. capillary hydrostatic pressure low - osmotic pressure high
3. excess fluid/any proteins picked up by lymphatic system - returned to general circulation
III. Inflammation
A. Inflammation not infection
B. Nonspecific response to tissue injury
1. swelling
2. redness
3. warmth
4. pain
5. possible loss of function
6. -itis - ending for inflammation
C. Causes
1. direct damage (cuts, sprains)
2. chemicals (acids)
3. ischemia and cell necrosis or infarction
4. allergic reactions
5. physical agents (burns)
6. foreign bodies (splinters, dirt)
7. infection
IV. Acute Inflammation
A. Sequence of events
1. injured mast cells/platelets release chemical mediators
a. affect blood vessels and nerves in damaged area
b. antihistamines counteract affect
2. local vasodilation and increased capillary permeability (vascular response)
3. formation of exudate (collection of interstitial fluid in inflammed area)
4. leukocytes (cellular response)
a. attracted to inflammed area (chemotaxis)
b. leave capillaries (diapedesis) - move to inflammed area
5. phagocytosis occurs
a. phagocytic cell death causes nearby tissue damage
b. prolongs inflammatory response
6. excess interstitial fluid and proteins slow blood/fluid flow to area
B. Local Effects
1. redness/warmth (erythema)
2. swelling
3. pain
4. exudate - characteristics vary with cause of trauma
a. serous - watery (allergic reaction, burns)
b. fibrinous - thick, sticky (forms possible scar tissue)
c. purulent - thick, yellow-green (pus)
d. abscess ( localized pus in solid tissue)
e. hemorrhagic (bloody)
C. Systemic Effects
1. fever - pyrexia
a. results from release of pyrogens from wbc or macrophages
b. circulate and tell hypothalamus to up thermostat
- shivering - activated to increase metabolism
- involuntary cutaneous vasoconstriction - pale cool skin
- voluntary curling up
2. malaise
3. fatigue
4. headache
5. anorexia
D. Diagnostic Tests
1. blood serum tests
a. leukocytosis
-differential count (proportion of each type of wbc) - bacterial vs viral vs allergic reaction
-wbc - infection?
b. elevated serum C-reactive protein (CRP)
c. elevated erythrocyte sedimentation rate (ESR)
d. increased plasma proteins and cell enzymes (liver problems, severe inflammation, necrosis)
E. Course of the Inflammatory Response
1. short - "no harm no foul"
2. prolonged - extensive tissue damage
F. Potential complications
1. infection
2. deep ulcers and/or perforation
3. skeletal muscle spasms/strong muscle contractions
4. local complications
V. Chronic inflammation - Pathophysiology
A. less swelling and exudate
B. more lymphocytes, macrophages, fibroblasts, collagen, fibrous scar tissue, possible granulomas
C. more tissue damage
VI. Treatment of Inflammation
A. Drugs
1. acetylsalicylic acid - aspirin, ASA - anti-inflammatory, antipyretic, analgesic
2. acetaminophen - Tylenol - antipyretic and analgesic but not anti-inflammatory
3. nonsteriodal anti-inflammatory drugs - NSAIDS - easier on stomach than aspirin; such as ibuprofen (Advil, Motrin), piroxicam (Feldene), diclofenac sodium (Arthrotec), COX-2 inhibitors (Celebrex) - antipyretic, analgesic, and anti-inflammatory
B. Glucocorticoids
1. synthetic corticosteroids or steroidal anti-inflammatory drugs: prednisone - oral, triamcinolone - topical, methylprednisolone - into the joint, dexamethasone - IM/IV injections, and beclomethasone dipropionate - Beclovent inhaler, hydrocortisone.
2. long term use/high dosages
a. atrophy of lymph tissue: decrease in # of wbc, lowers immune response
b. catabolic effects - tissue breakdown/repair (due to decrease in protein synthesis), osteoporosis, muscle atrophy, epithelial thinning/breakdown of skin and/or mucosa
c. delayed healing
d. delayed growth in kids
e. retention of sodium and water resulting in high blood pressure and edema
f. adrenal gland atrophy
f. must wean off drug slowly - if too sudden, possible adrenal crisis due to lack of naturally occurring glucocorticoids
C. Other Therapies
1. RICE
a. rest
b. ice - vasoconstriction - decreases edema, swelling, pain
c. compression
d. elevation - improve fluid flow away from damaged area
2. moderate exercise - improve blood flow
3. physical therapy
VII. Healing
A. Types of healing
1. resolution
2. regeneration
3. replacement - fibrous connective tissue replaces normal tissue - scar
B. The healing process
1. blood clot formation
2. inflammation
3. phagocytosis
4. granulation tissue formation
5. mitosis of epithelial cells
C. Factors Affecting Healing
1. youth
2. good nutrition
3. adequate hemoglobin
4. effective circulation
5. clean, undisturbed wound
6. no complications
D. Complications of Healing by Scar Formation
1. loss of function
2. contractures and obstructions (stenosis)
3. adhesions
4. hypertrophic scar tissue (keloid formation)
5. ulceration
VIII. Example of Inflammation and Healing - Burns
A. Classification of Burns
1. superficial thickness (1st degree)
a. epidermis
b. red, minor pain (sunburn)
2. partial thickness - superficial (2nd degree)
a. destruction of epidermis and superficial (papillary) dermis
b. red, blistering, painful
3. partial thickness - deep (3rd degree)
a. destruction of epidermis and deep (reticular) dermis
b. whiter appearance or fixed red staining (no blanching), painful
4. full thickness (4th degree)
a. destruction of epidermis, dermis, and partial damage to subcutaneous fat
b. charred or leathery tissue (eschar), thrombosed blood vessels (coagulation), insensate (no sensation)
c. may need escharotomy
d. skin grafts
5. subdermal (5th degree)
a. complete destruction of epidermis, dermis, subcutaneous fat, and underlying tissue and possibly fascia, bone, or muscle
b. Hard, leather-like eschar, purple fluid, insensate
B. Percentage of Body Surface Area (BSA) Burned - Rule-of-Nines
1. fluid replacement guideline, etc.
2. method for rapid calculation
3. body parts assigned a value of nine/multiple of nine
a. head and each arm - 9% (27%)
b. each leg - 18% (36%)
c. anterior surface and posterior surface of trunk - each 18%
d. groin - 1%
C
C. Effects of Burn injury
1. shock
a. inflammatory response under skin
b. fluids leave blood/move into injured area
c. loss of fluid from blood lowers bp, bv, and hypovolemic shock
2. respiratory problems
a. inspiration of carbon monoxide
b. hot air, steam, chemicals can damage mucosa of trachea and bronchi
-inflammation can occur - edema - obstructs airway
3. pain
4. infection
-could result in septic shock
5. metabolic needs
a. hypermetabolism - need increase in consumption of protein and carbs
b. loss of skin = loss of heat - need more calories to produce heat
c. anemia - loss of erythrocytes due to injury
d. bone marrow function reduced = reduced hematopoiesis (production of blood cells)
D. Healing of burns
1. skin grafts
2. biosynthetic skin
3. elasticized garments
4. splints
5. physiotherapy
6. possible surgery
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