Pathophysiology Chapter 2: 1.

venous end - fluids, carbon

Inflammation and Healing dioxide, waste move in
2. capillary hydrostatic
I. Review of Normal Defenses in the pressure low - osmotic pressure high
Body 3. excess fluid/any proteins
A. Nonspecific defense picked up by lymphatic system -
mechanisms returned to general circulation

1. 1st line of defense - skin, mucous III. Inflammation

membrane, body secretions A. Inflammation not infection
B. Nonspecific response to tissue
2. 2nd line of defense injury
a. phagocytosis - 1. swelling
neutrophils (leukocytes)and 2. redness
macrophages: engulf bacteria, 3. warmth
cell debris, foreign matter 4. pain
b. inflammation - sequence 5. possible loss of function
of events to limit effects of injury or 6. -itis - ending for
foreign agent inflammation
c. interferon – protect C. Causes
uninfected cells from virus 1. direct damage (cuts, sprains)
2. chemicals (acids)
B. Specific defense mechanisms 3. ischemia and cell necrosis
1. 3rd line of defense - immune or infarction
system protection through 4. allergic reactions
antibodies/sensitized lymphocytes 5. physical agents (burns)
6. foreign bodies (splinters, dirt)
II. Review of Normal Capillary 7. infection
Exchange
IV. Acute Inflammation
A. Not all capillaries working all the
time A. Sequence of events

B. Movement out of capillaries 1. injured mast cells/platelets

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
2. blood cells, plasma proteins
(albumin, globulin, fibrinogen) stay
inside capillary
C. Movement into capillaries
1
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
blood serum tests
a. leukocytosis
differential count (proportion of each
type of wbc) - bacterial vs viral vs
2
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 -
Acute episode ( not completely
eradicated)
Pathophysiology
A. less swelling and exudate
B. more lymphocytes,
macrophages, fibroblasts, collagen,
fibrous scar tissue, possible
granulomas (small mast cell necrotic
center covered by connective tissue)
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- B. Other Therapies
inflammatory drugs - NSAIDS - easier a. RICE
on stomach than aspirin; such as : 1. rest
ibuprofen (Advil, Motrin), 2. ice - vasoconstriction -
piroxicam (Feldene), decreases edema, swelling, pain
diclofenac 3. compression
sodium (Arthrotec), 4. elevation - improve fluid
COX-2 inhibitors (Celebrex) - flow away from damaged area
antipyretic, analgesic, and b. moderate exercise - improve
anti-inflammatory blood flow
c. physical therapy
4. Glucocorticoids
a. synthetic corticosteroids or VII. Healing
•steroidal anti-inflammatory drugs: A. Types of healing
prednisone - oral, 1. resolution
•triamcinolone - topical, 2. regeneration
•methylprednisolone - into the 3. replacement - fibrous
joint connective tissue replaces normal
•dexamethasone - IM/IV injections tissue - scar
•beclomethasone dipropionate - B. The healing process
Beclovent inhaler, hydrocortisone. 1. blood clot formation
2. inflammation
b. long term use/high dosages 3. phagocytosis
1. atrophy of lymph 4. granulation tissue formation
tissue: decrease in # of wbc, lowers 5. mitosis of epithelial cells
immune response 6. fibroblasts
2. catabolic effects - C. Factors Affecting Healing
tissue breakdown/repair (due to 1. youth
decrease in protein 2. good nutrition
synthesis), osteoporosis, muscle 3. adequate hemoglobin
atrophy, epithelial 4. effective circulation
thinning/breakdown of 5. clean, undisturbed wound
skin and/or mucosa 6. no complications
3. delayed healing D. Complications of Healing by
4. delayed growth in kids Scar Formation
5. retention of sodium 1. loss of function
and water resulting in high blood 2. contractures and
pressure and edema obstructions (stenosis)
6. adrenal gland atrophy 3. adhesions
7. must wean off drug 4. hypertrophic scar tissue
slowly - if too sudden, possible (keloid formation)
adrenal crisis due to 5. ulceration
lack of naturally occurring
glucocorticoids

3
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%
4
d. groin - 1%
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 increase in hematocrit
2. respiratory problems
a. inspiration of carbon
monoxide ; toxic / irritating fumes
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