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
Pain relief is equivalent to morphine and other opioids
ketorolac
Usual indication for ketorolac
Postoperative pain
Approved only for rheumatoid arthritis and osteoarthritis
piroxicam
Half-life of 50 hours
Piroxicam
inhibits COX-1, selectivity for COX-2 at low doses
meloxicam
Derivative of salicylic acid
Diflunisal
Should not be given to children with chickenpox or influenza, for Reye’s syndrome precipitation
Nonacelytated salicylates
should be avoided in patients on a sodium-restricted diet
sodium salicylate
may accumulate to toxic levels in patients with chronic renal insufficiency
magnesium salicylates
prodrug that breaks down to release two molecules of salicylate in the alkaline environment
salsalate
Developed on the theory that selective inhibition of COX-2 should be able to suppress pain and inflammation with no gastric ulceration
COX-2 inhibitors/coxibs
First selective COX-2 inhibitor to reach market
Celecoxib
Off-label use for familial adenomatous polyposis - predisposes colorectal cancer
Celecoxib
devoid of clinically useful anti-inflammatory and anti rheumatic actions
acetaminophen
does not suppress platelet aggregation, cause gastric ulceration, decrease renal blood flow, cause renal impairment
acetaminophen
used more than any other analgesic
acetaminophen
inhibition of CNS is limited to CNS
acetaminophen
decreases prostaglandin synthesis in the CNS
acetaminophen
regular alcohol consumption increases the risk of liver injury when taken at excessive doses
acetaminophen
evidence that there is increased risk of bleeding in patients taking
warfarin
routine use of these drugs to prevent vaccination-associated pain/fever is discouraged
acetaminophen
preferred NSAID for children suspected of having chickenpox or influenza
acetaminophen
preferred NSAID for patients with peptic ulcer
acetaminophen
not preferred for arthritis or rheumatic fever
acetaminophen
principal feature of overdose is hepatic necrosis
acetaminophen
drug used to minimize liver damage
acetylcysteine - acetaminophen antidote
NSAIDs are contraindicated for patients with a history of
severe NSAID hypersensitivity
NSAIDs (especially aspirin) are contraindicated for children with
chickenpox or influenza
Celecoxib is contraindicated for patients with
sulfa allergy
synthetic chemicals related to the naturally occurring glucocorticoids
corticosteroids
hormones produced by the adrenal cortex gland in the body
glucocorticoids
beneficial anti-inflammatory effects of glucocorticoids
- decreasing capillary permeability - epinephrine and norepinephrine - vascular systems stabilized.
- reducing the number of leukocytes and mast cells at the site - decreases release of histamine and prostaglandins.
- Blocks immune response - common cause of inflammation.
increased intake reduces normal hormone secretion and adrenal gland atrophy
glucocorticoids
glucocorticoids influence the metabolism of
carbohydrates, proteins, and fats
principal effect of carbohydrate metabolism
elevation of blood glucose - promoting synthesis of glucose from amino acids, reducing peripheral glucose utilization, reducing glucose update by muscle and adipose tissue.
protein metabolism with glucocorticoids
suppress synthesis of proteins from amino acids and divert amino acids for production of glucose. Reduce muscle mass, decrease protein matrix of bone, thinning of skin, nitrogen balance is negative.
low endogenous glucocorticoid levels
capillaries are more permeable, vasoconstriction is suppressed, bp falls
increase the number of circulating red blood cells and polymorphonuclear leukocytes
glucocorticoids
Decrease counts of lymphocytes, eosinophils, basophils, and monocytes
glucocorticoids
physiologic stress releases which two hormones
glucocorticoid and epinephrine
synthesis and release regulated by negative feedback loop
glucocorticoids
components of negative feedback loop of synthesis and release of glucocorticouds
hypothalamus, anterior pituitary, adrenal cortex
ways in which glucocorticoids differ from most drugs
- receptors are located inside the cell, not on surface.
- modulate the production of regulatory proteins, not signaling pathway.c
ironic disease similar to RA, not limited to just joints
systemic lupus erythematosus (SLE)
can be used to treat severe cases of ulcerative colitis and Crohn’s disease
glucocorticoids
most effective antiasthma agent
glucocorticoids
Adverse effects of glucocorticoids
adrenal insufficiency, osteoporosis, infection, glucose intolerance, myopathy, fluid and electrolyte disturbance, growth delay, psychologic disturbances, cataracts, glaucoma, peptic ulcer disease, Cushing’s syndrome
induce hypokalemia, when used with digoxin can cause dysthymia
glucocorticoids
when a microbe or parasite is able to reproduce in or on the body’s tissues
infection
proteins produced by human host cells in response to viral invasion of the cell
interferons
factors that decrease host resistance
-age
-genetic susceptibility
-immunodeficiency of any type
- malnutrition
-chronic disease
-severe physical or emotional stress
-inflammation or trauma affecting the integrity of skin or mucosa
-impaired inflammatory response
capacity of microbes to cause disease
pathogenicity
percentage of deaths occurring in the number of persons who develop the disease
case fatality rate
time the body is expose to the organism and the appearance of clinical signs of disease
incubation period
early symptoms stage when the infected person may feel fatigued, lose appetite, or have headache
prodromal period
stage where infectious disease develops fully and the clinical manifestations reach a peak
acute period
organism enters the Boyd and remains confined to a specific location
local infections
pathogen spreads from a local infection to other tissues
focal infection
infection spreads to several sites and tissue fluids, typically through the circulatory system
systemic infection
caused by multiplication of pathogenic organisms in the blood and the cause of sepsis
septicemia
presence of bacteria in the blood
bacteremia
presence of toxins in the blood
toxemia
presence of viruses in the blood
viremia
several infectious agents concurrently establish themselves path these are site
mixed infections
appear rapidly with severe symptoms but are short lived
acure infections
less severe symptoms than acute but persist for a long period
chronic infections
initial or fist time exposure/infection
primary infection
follows a primary infection caused by a microbe other than the causing the primary infection - usually opportunistic pathogens
secondary infections
do not cause apparent signs or symptoms, although they may persist over long periods of time
subclinical infection
Local signs of infection
pain/tenderness, swelling, redness, and warmth
swollen and tender lymph nodes
lymphadenopathy
hospital-acquired infection
nosocomial
agent applies to living tissue
antiseptic
preparations applied to
objects
complete destruction of all microorganisms
sterilization
drug that suppresses the growth and replication of microorganisms but does not kill them
germistatic drug
inactive against bacterial spores and has erratic behavior with lungi
ethanol
somewhat more germicidal than ethanol, vasodilation properties
70%-100% isopropanol
lethal to all microorganisms, must be immersed for 10 hours
glutaraldehyde
reasons formaldehyde is less desirable than glutaraldehyde
acts slowly, more volatile than glutaraldehyde
most widely germicidal agents
iodine
preferred for intact skin - iodine
tincture
treatment of wounds and abrasions - iodine
solution
rod-shaped organisms, include vibrio, and pleomorphic
bacilli
spirochetes and spirilla, wavy-like
spirals
spherical forms
cocci
pairs of bacteria, prefix
diplo-
chains of bacteria, prefix
strep(to)
irregular, grapelike clusters of bacteria
staph(ylo)
cells groups in a packet or square of four cells bacteria
tetrads
cells lying together with the long sides parallel bacteria
palisade
present in the cell wall of gram-negative organisms and released after the bacterium dies
endotoxins
produced by gram-positive organisms and diffuse through body fluids
exotoxins
small obligate intracellular parasite that requires a living host for replication
virus
protein-like agents that are transmitted by consumption of contaminated tissues such as muscle or use of donor tissues
prions
creutzfeld-jakob disease
prion disease - degenerative disease of the nervous system
drugs or substances that can kill or inhibit the growth of microorganisms. Originally derived from organisms, such as penicillin from mold, many drugs are now synthetic or semisynthetic.
antibiotics
classified by the type of microbe against which the drug is active, such as antibacterials, antivirals, and antifungals. These drugs are unique to the type of organism and are not interchangeable.
antimicrobials
drugs that kill organisms, whereas bacteriostatic applies to drugs that inhibit reproduction and rely on the host’s defenses to destroy the organisms.
bactericidal
antibacterials that are effective against both gram-negative and gram-positive organisms
broad-spectrum antibiotics
