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5 cardinal signs of inflammation
redness, swelling, warmth, pain, loss of function
acute inflammation
-vasodilation
-hyperemia
-increase in capillary permeability
-chemotaxis to attract cells of the immune system
chronic inflammation
(Follows acute episode of inflammation)
-less swelling
-presence of more lymphocytes
-macrophages, and fibroblasts
-continued tissue destruction
-more fibrous scar tissue
-granuloma may develop around foreign object.
histamine
a chemical mediator from mast cell granules that causes immediate vasodilation and increased capillary permeability to form exudate
chemotactic factors
a chemical mediator from mast cell granules that attracts neutrophils to the site
platelet-activating factors
a chemical mediator from cell membranes of platelets that activates neutrophil's platelet aggregation
cytokines
a chemical mediator from T lymphocytes and macrophages that increases plasma proteins, erythrocyte sedimentation rate, induces fever, chemotaxis, and leukocytosis- ie. interleukins and lymphokines)
leukotrines
a chemical mediator from synthesis from arachidonic acid in mast cells that causes vasodilation, increased capillary permeability, and chemotaxis
prostaglandins
a chemical mediator from synthesis from arachidonic acid in mast cells that causes vasodilation, increased capillary permeability, pain, fever, and potentiate histamine effect
kinins
a chemical mediator from activation of plasma protein (kinogen) that causes vasodilatation and increased capillary permeability, pain, and chemotaxis
complement system
a chemical mediator from activation of plasma protein cascade that causes vasodilation and increased capillary permeability, chemotaxis, and increased histamine release.
exudate
collection of interstitial fluid formed in the inflamed area
serous
watery exudates from infected wound that consists primarily of fluid with small amounts of protein and WBC- ie. from allergic reactions or burns
fibrinous
thick and sticky exucates from infected would that have high cell and fibrin content- increases risk of scar tissue- ie. from deep traumatic wounds, burns, bites
purulent
thick and yellow-green exudates from infected wound and contains more leukocytes, cell debris, and microorganisms (pus)- ie. usually seen in bacterial infections- diagnosed througn CNS (culture and sensitivity)
abscess
localized pocket of purulent exudate/ pus in a solid tissue- ie. boil, can be around tooth, or in brain
effects of burn injuries
shock, respiratory problems, pain, infection, hypermetabolism
superficial burns
first degree- damages the epidermis and may involve the upper dermis, usually red and painful but heal without scar- ie. sunburn/ mild scald
partial thickness burn
second degree- destruction of epidermis and part of dermis, usually red, blistered, and hypersensitive and can appear waxy with red margin, may need to be grafted, can lead to infection
full thickness burns
third/ fourth degree- destruction of all skin layers, and underlying tissue (in fourth), appears coagulated/ charred and is hard and dry to surface, healing tissue shrinks
9 steps of inflammation
-release of bradykinin from injured cells
-activation of pain receptors by bradykinin
-mast cells and basophils release histamine
-capillary dilation
-increased blood flow and capillary permeability
-bacteria may enter the tissue
-neutrophil and monocytes come to injured site
-neutrophils phagocytize bacteria
-macrophages leave bloodstream for phagocytosis of microbes
erysipelas
common bacteria skin infection effecting upper layer of skin and nearby lymph vessels
systemic effects of inflammation
-mild fever (pyrexia)
-malaise
-fatigue
-headache
-anorexia
leukocytosis
common change in blood with inflammation- increased number of WBC cells especially neutrophils
differential count
common change in blood with inflammation- proportion of each type of WBC is altered, depending on cause
plasma proteins
common change in blood with inflammation- increased fibrinogen and prothrombin
C- reactive protein
common change in blood with inflammation- a protein not normally in blood, but appears with acute inflammation and necrosis within 24-48 hours
increased ESR
common change in blood with inflammation- elevated plasma proteins increase the rate at which red blood cells settle in a sample
cell enzyme
common change in blood with inflammation- released from necrotic cells and enter tissue fluids and blood, may indicate the site of inflammation
erythrocyte sedimentation rate
common diagnostic test for inflammation- should be elevated if present
treatment of inflammation
-acetylsalicylic acid (asa) (aspirin)
-acetaminophen (Tylenol)
-nonsteroidal anti-inflammatory drugs (NSAIDs)
-glucocorticoids (corticosteroids)
anti-inflammatory effects of glucocorticoids
-decreased capillary permeability
-enhanced effectiveness of epinephrine and norepinephrine
-reduced number of leukocytes and mast cells
-reduces immune response
adverse effects of glucocorticoids
-atrophy of lymphoid tissue
-catabolic effects (tissue breakdown/ decreased protein synthesis)
-delayed healing
-delayed growth in children
-retention of sodium and water
-increased gluconeogenesis
resolution
type of healing that results in minimal tissue damage
regeneration
type of healing where damaged tissue is replaced with cells that are functional
replacement
type of healing where functional tissue is replaced by scar tissue, results in loss of function
types of burns
thermal, chemical, radiation, electricity, light, friction
children and burns
growth of children can be affected during burn recovery because metabolic needs are compromised, increase in inflammatory mediators may cause renal problems, and additional surgery/ grafts may be required to accommodate growth and ease effects of scaring
Infection
Entry and multiplication of microorganisms in the body that can cause tissue damage and disease.
Inflammation
The body's nonspecific response to tissue injury; infection can cause inflammation, but inflammation can also occur without infection.
Relationship between infection and inflammation
Microorganisms enter and reproduce, causing tissue injury, which activates the inflammatory response.
Pathogenicity
The ability of a microorganism to cause disease.
Virulence
The degree of disease-producing ability or aggressiveness of a microorganism.
Host resistance
The ability of the body to defend itself against infection.
Factors that decrease host resistance
Extremes of age, poor nutrition, chronic disease, damaged skin or mucous membranes, immunodeficiency, and immunosuppressive therapy.
Bacteria
Unicellular microorganisms that can survive and reproduce independently of human cells.
Cocci
Round-shaped bacteria.
Bacilli
Rod-shaped bacteria.
Vibrio
Curved or comma-shaped bacteria.
Spirilla
Spiral-shaped bacteria.
Diplococci
Cocci arranged in pairs.
Staphylococci
Cocci arranged in clusters.
Streptococci
Cocci arranged in chains.
Binary fission
The process by which bacteria reproduce by duplicating their DNA and dividing into two cells.
Why can bacterial infections increase rapidly?
Bacteria can reproduce quickly by binary fission, causing the bacterial population and tissue injury to increase.
Gram-positive bacteria
Bacteria with a thick peptidoglycan cell wall that retain the Gram stain and appear purple.
Gram-negative bacteria
Bacteria with a thinner peptidoglycan layer plus an outer membrane containing lipopolysaccharide.
Lipopolysaccharide (LPS)
A component of the outer membrane of gram-negative bacteria that can act as an endotoxin.
Endotoxin
A toxin associated with the structure of gram-negative bacteria that can trigger a strong systemic inflammatory response.
Pathophysiology of severe endotoxin effects
Endotoxin can trigger widespread inflammatory mediator release, vascular changes, capillary leakage, hypotension, impaired tissue perfusion, and potentially shock.
Exotoxin
A toxin produced and secreted by certain bacteria that can damage host cells and tissues.
Difference between exotoxin and endotoxin
Exotoxins are secreted by bacteria, while endotoxin is associated with the gram-negative bacterial cell structure.
Bacterial spores
Highly resistant, inactive forms produced by some bacteria during unfavorable environmental conditions.
Purpose of bacterial spores
Allow bacteria to survive harsh conditions until the environment becomes favorable again.
Virus
An infectious agent containing DNA or RNA that must use a living host cell to reproduce.
Why can't viruses reproduce independently?
They lack the complete cellular machinery needed for reproduction and must use the host cell.
General viral replication sequence
Virus attaches to host cell, enters the cell, releases genetic material, uses host machinery, produces viral components, assembles new viruses, and releases them.
How do viruses damage tissues?
Viral replication disrupts normal host cell function and can cause cell injury or death, leading to inflammation.
Why don't antibiotics treat viral infections?
Antibiotics target bacterial structures or processes that viruses do not have.
Fungi
Eukaryotic organisms that include yeasts and molds and may cause infection under certain conditions.
Candida albicans
A fungus that may normally live in the body but can cause opportunistic infection if normal microbial balance is disrupted.
Opportunistic infection
An infection caused by an organism that takes advantage of weakened host defenses or disruption of normal flora.
Why can broad-spectrum antibiotics cause Candida infection?
They may destroy normal bacterial flora, decreasing competition and allowing Candida to overgrow.
Protozoa
Single-celled eukaryotic organisms that may cause infections through contaminated food, water, sexual contact, or vectors.
Examples of protozoa
Entamoeba histolytica, Giardia, Plasmodium, and Trichomonas.
Plasmodium
The protozoan responsible for malaria and transmitted by mosquitoes.
Vector transmission
Transmission of a microorganism through an animal or insect such as a mosquito or tick.
Helminths
Multicellular parasitic worms such as tapeworms, roundworms, and pinworms.
How can helminths cause disease?
They may consume nutrients, damage tissues, obstruct structures, and trigger inflammation.
Resident flora
Microorganisms that normally live on or in the body without causing disease under normal conditions.
Common locations of resident flora
Skin, mouth, nose, pharynx, intestine, vagina, and portions of the genitourinary tract.
Why are resident flora protective?
They compete with pathogens for nutrients and space and may inhibit growth of harmful organisms.
What can happen when resident flora are destroyed?
Opportunistic or resistant microorganisms may multiply and cause a secondary or superinfection.
Superinfection
A new infection that develops when antimicrobial therapy disrupts normal flora and allows resistant or opportunistic organisms to overgrow.
Chain of infection
Infectious agent → reservoir → portal of exit → mode of transmission → portal of entry → susceptible host.
Why is the chain of infection important?
Breaking any link can prevent transmission of infection.
Reservoir
A place where an infectious organism normally lives, grows, or multiplies.
Portal of exit
The route by which an organism leaves its reservoir or host.
Portal of entry
The route by which an organism enters a new host.
Susceptible host
A person whose defenses are insufficient to prevent infection.
Direct transmission
Transfer of microorganisms directly from one person to another.
Indirect transmission
Transfer of microorganisms through contaminated objects, food, water, or equipment.
Fomite
A contaminated inanimate object that can transmit microorganisms.
Droplet transmission
Spread of microorganisms through larger respiratory droplets produced by coughing, sneezing, or talking.
Airborne transmission
Spread by very small particles that remain suspended in the air.
Why does damaged skin increase infection risk?
It removes an important first-line physical barrier and creates a portal of entry for microorganisms.
Local infection
An infection limited to a specific area of the body.
Common local signs of infection
Redness, warmth, swelling, pain, and possibly purulent drainage.
Why does infection cause redness and warmth?
Inflammation causes vasodilation and increased blood flow to the infected area.
Why does infection cause swelling?
Inflammation increases capillary permeability, allowing fluid and proteins to enter the interstitial space.