Inflammation and Wound Healing Flashcards
Three lines of defense
- Mechanical barriers and body secretions.
- Phagocytosis, inflammation, and interferons.
- Immune response, very specific.
Phagocytosis
Process by which neutrophils and macrophages randomly engulf and destroy bacteria, cell debris, or foreign matter
Interferons
nonspecific agents that protect uninfected cells against viruses
Immune response
stimulates the production of unique antibodies or sensitized lymphocytes following exposure to specific substance
inflammation
Body’s nonspecific response to tissue injury, resulting in redness, swelling, warmth, pain, and sometimes the loss of function
suffix for inflammation
-itis
Acute inflammation
Occurs rapidly in reaction to cell injury, rids the body of the offending agent, enhances healing, and terminates after a short period. Hours or days.
Prevents the spread of infection with antibodies or other chemicals.
Attempts to wall off, destroy, and digest bacteria and dead or foreign tissue.
After insult is contained, repair can begin.
Chronic inflammation
May develop following an acute episode of inflammation when the cause is not completely eradicated.
Examples of chronic inflammation
Smoking, certain bacteria, or long-term abnormal immune response.
Granulocytes
Neutrophils
Basophils
Eosinophils
Agranulocytes
Lymphocytes
Monocytes
Arrive first at the site of cell injury, are the most numerous leukocyte, are part of the innate immune system.
Neutrophils
Active in allergic responses ,releasing their stores of inflammatory chemicals including histamine, serotonin, and leukotrienes. Contain heparin. Fight parasitic infections
Basophils
Active in larger parasitic infections, allergy responses, and some cancers
Eosinophils
B (humoral), T (cell mediated), and Natural Killer (NK) Cells
Identify and destroy foreign invaders
Found in lymph and blood
NK cells defend against tumors and viruses
Lymphocytes
Largest WBC; differentiates into macrophages that clean up cellular debris in the inflammatory process
Monocytes
Cytokines
short-lived proteins that are released by one cell as intracellular messengers
inflammatory mediators
send out signals, enabling the blood vessels to dilate and become more permeable, allowing fluids, WBC to enter
three stages of acute inflammation
- vascular permeability
- cellular chemotaxis
- systemic responses
WBC line up along endothelium when arriving at site of injury
margination
Three outcomes of acute inflammation
Complete resolution
Healing by connective tissue
Chronic, persistent inflammation that does not recede
Complete resolution of acute inflammation
normalization of vascular permeability
deactivation of chemical mediators
elimination of cellular debris and edema
apoptosis of WBC
Healing by connective tissue acute inflammation
In tissues that cannot regenerate cells or exudates and cellular debris cannot be adequately cleared.
Cellular debris and exudates are instead reabsorbed and fibrous scar tissue replaced damaged cells.
Characteristics of chronic inflammation
less swelling, more lymphocytes, macrophages, fibroblasts, more collagen
small mass of cells with necrotic center, covered by connective tissue
granuloma
local complications of chronic inflammation
depend on the site of the inflammation
infection complications of chronic inflammation
microorganisms can more easily penetrate when the skin or mucosa is damaged and the blood supply is impaired.
skeletal muscle spasms
result by inflammation from musculoskeletal injuries. can cause additional pressure on the nerves, increasing pain.
chemicals released during acute inflammation
histamine, kinins, prostaglandins
cardinal signs of inflammation
- Redness and heat- increased blood flow into the damaged area (erythema)
- Swelling- shift of protein and fluid into the interstitial space.
- Pain- increased pressure of fluid on the nerves and by local irritation of nerves by chemical mediators.
- Loss of function- cells lack nutrients or swelling interferes mechanically with function.
- Exudate- collection of interstitial fluid formed in the inflamed area. The characteristics of the exudate vary with the cause of the trauma.
Clinical cellulitis
Erysipelas
Exudation of inflammation (5)
- Serous
- Fibrinous
- Purulent
- Abscess
- Hemorrhagic
Examples of serous exudates
allergic reactions or burns. primarily of fluid with small amounts of protein and WBC.
Fibrinous exudate
thick and sticky, have high cell and fibrin content. Increases the risk of scar tissue in the area.
Purulent exudates
thick, yellow-green in color, contain more leukocytes and cell debris and microorganisms. Indicates bacterial infection.
Abscess
Localized pocket of purulent exudate or pus in a solid tissue. Around a tooth or in the brain
Hemorrhagic exudate
present if blood vessels have been damaged.
Systemic responses of inflammation
Pyrexia.
Malaise.
Fatigue.
Headache.
Anorexia.
Weight loss.
Lethargy/sleepiness.
Lymphadenopathy.
Common systemic effect if inflammation is extensive, microbial organisms bacterial products and cytokines act as pyrogens
Pyrexia
Agents that cause fever
Pyrogens
Where is the body temperature control system
Hypothalamus
Cells that mature inside the lymph nodes
Lymphocytes
Increased number of white cells in the blood
leukocytosis
measures the rate at which red blood cells precipitate out of the plasma, indicating damage to these cells during the inflammation process
erythrocyte sedimentation rate (ESR)/ sed rate
C-reactive protein (CRP)
produced by the liver, also indicating presence of inflammation
High WBC, 90% neutrophils
bacterial infection
High WBC, 90% lymphocytes
viral infection
immature neutrophils
bands - present in patients with leukocytosis
increased number of bands
acute inflammatory process
increased number of white blood cells, especially neutrophils
leukocytosis
proportion of each type of white blood cell altered, depending on the cause
differential count
Increased fibrinogen and prothrombin
plasma proteins
a protein not normally in the blood, but appears with acute inflammation and necrosis within 24-48 hours.
C-reactive protein
Elevated plasma proteins increase the rate at which red blood cells settle in a sample
Increased erythrocyte sedimentation rate
released from necrotic cells and enter tissue fluids and blood: may indicate the site of inflammation
cell enzymes
COX-1 inhibitors protect against
myocardial infarction and stroke
other first-generation NSAIDs inhibit
COX-1 and COX-2
Non-aspirin NSAIDs cause __ inhibition
reversible
Ibuprofen is the prototype of
Propionic acid derivatives
severe hypersensitivity reaction that causes blistering of the skin and mucous membranes, can result in scarring, blindness, and death
Stevens-Johnson syndrome
rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, mild pain, primary dysmenorrhea, and migraine
diclofenac
This NSAID can cause fluid retention, which can exacerbate hypertension and heart failure.
Diclofenac
NSAID for arthritis, bursitis, tendinitis, and acute gouty arthritis
Indomethacin
Given IV to preterm infants to promote closure of the ductus arteriosus
Indomethacin
Can cause frontal headache, CNS effects, seizures and psychiatric changes, GI effects, hematologic reaction
Indomethacin
Powerful analgesic with minimum anti-inflammatory actions
Keterolac