quiz #2 - inflammation Flashcards
INFLAMMATION
Non-specific response to injury
Purpose: start healing process
Interconnected events form coordinated reaction by cells
Involves blood vessels & cells, nerves & chemicals
May last minutes → years
Causes redness, swelling, warmth & pain
May be acute/ chronic
FUNCTION of inflammation
has protective role – serious side effects may go too far
-Inactivate injurious agent
-Breakdown & remove dead cells
-Initiate healing process
5 cardinal signs of inflammation & what they are caused by
HEAT: vasodilation & increased blood flow
ERYTHEMA (redness): vasodilation & increased blood flow
EDEMA (swelling): too much fluid & cells leak into interstitial spaces – imbalance
PAIN/ TENDERNESS: direct trauma, bradykinins, histamines, swelling of nerves
LOSS OF USE/ dysfunction: joint, ligament, mm, tendon damage
4 KEY COMPONENTS in response to injury
- Circulatory changes
- Vessel wall changes
- Immune response
- Cellular response
Circulatory changes (components in response to injury)
first response, increased blood flow: causes redness, swelling & warmth
Vessel wall changes (components in response to injury)
damage to endothelial lining in blood vessel walls causes them to become more permeable/ leakier via 4 processes
Vessel wall changes (components in response to injury): 4 processes
-increase in BP
-decrease in speed of circulation in area
-WBCs & platelets stick to endothelial lining (adhesion)
-release of mediators locally
Immune response (components in response to injury)
release of mediators/ chemicals → cytokines, histamines, bradykinins, arachidonic acid, activation of complement system
HISTAMINES (immune response)
released from platelets & mast cells, stimulates endothelial cells to contract making gaps between them wider & leakier
BRADYKININ (immune response)
released from plasma, accounts for pain with inflammation
COMPLEMENT SYSTEM (immune response)
proteins activated (by 3 different things) in cascade that forms membrane attack complex (MAC) that kills cell but also causes more histamine release
COMPLEMENT SYSTEM: 3 pathways
Classical pathway: activated by antibodies binding to antigens
Alternative pathway: activated by bacteria endotoxins (fungi, snake venom etc.) that are carbohydrates on surface of bacteria
Lectin pathway: activated by macrophages that digest bacteria, release chemicals that cause liver to produce lectins
*all 3 pathways lead to formation of the membrane attack complex (MAC) -> kills cells by boring hole in membrane
ARACHIDONIC ACID (immune response)
leukotrienes (promote chemotaxis & increased permeability) & prostaglandins (vasodilation, increased permeability, mediates pain & fever)
CYTOKINES (immune response)
produced by leukocytes (WBCs)
-Interleukin - 1
-Tumor Necrosis factor (TNF)
Cellular response (components in response to injury)
fluid imbalance, emigration of leukocytes, phagocytosis
CELLS of inflammation
Neutrophils
polymorphonuclear cells (PMN’s)
Eosinophils
Basophils
Macrophages
Platelets
Other cells
CAUSES of inflammation
Infections: bacteria, virus, fungus, protozoa, worms
Chemical: industrial, medicinal, exogenous & endogenous
Physical: heat, irradiation, trauma
Foreign bodies: thorn, bee sting
Immune: hypersensitivity reactions
TYPES of inflammation (by duration)
ACUTE: rapid onset, short duration, all 5 cardinal signs
-EXUDATE: full of PMNs, monocytes, eosinophils
CHRONIC: delayed onset, longer duration, may or may not have cardinal signs
-EXUDATE: full of lymphocytes, macrophages, plasma cells
TYPES of inflammation
Serous
Fibrinous
Purulent
Ulcerative
Pseudomembranous
Granulomatous
SEROUS (types of inflammation)
mildest form, early stages
EXUDATE: clear fluid, no cells, lots of proteins
Common: viral infections (herpes)
FIBRINOUS (types of inflammation)
caused by severe inflammation, does not resolve easy
EXUDATE: lots of proteins (fibrin), dead neutrophils
Common: bacterial infections (strep throat)
PURULENT (types of inflammation)
caused by pus forming bacteria, may accumulate & form an abscess
EXUDATE: viscous, yellow fluid, dead PMNs, dead tissue, lytic enzymes
Common: bacteria (streptococci, staphylococci)
ULCERATIVE (types of inflammation)
on body surfaces or mucosa of hollow organs (stomach, small intestine), epithelial lining lost or ulcerated creating a hole
PSEUDOMEMBRANOUS (types of inflammation)
combination of ulcerative, purulent & fibrinous
EXUDATE: made of fibrin, pus & cellular debris form membrane on surface of ulcer
Common: diphtheria (throat)
GRANULOMATOUS (types of inflammation)
formation of granulomas made of T lymphocytes, macrophages & multinucleated giant cells that clump together into small nodules that destroy tissues over long period of time
Common: tuberculosis, hypersensitivity reactions
SYSTEMIC CLINICAL FINDINGS with inflammation
Fever: caused by pyrogenic cytokines
Leukocytes: increase in circulating WBCs
General symptoms: fatigue, weakness, depression, malaise, lack of appetite, achiness
Wound healing
sequence of events that occur after skin injury
CELLS in wound healing
leukocytes, macrophages, CT cells, epithelial cells, PMN’s
Leukocytes (WBCs) / POLYMORPHONUCLEAR (PMNs)
act as scavengers at site
Macrophages (most important)
stay the longest, produce cytokines, growth factors, mediators, myofibroblasts, angioblasts, fibroblasts
Connective tissue
produce scar tissue:
Myofibroblasts – smooth mm & fibroblasts combined, holds wound margins together
Angioblasts – precursor to blood vessels, form new blood vessels & blood supply
Fibroblasts – produce extracellular matrix & two most important proteins:
-Fibronectin → forms scab
-Collagen type III → scar tissue
Epithelial cells
undergo mitosis & duplicate to extend to cross gap over wound to fill gap
1st intention healing
clean wound edges close together
2nd intention healing
wound left open due to too much tissue damage, more scar & granulation tissue allowed to build up before closing wound
delayed wound healing
wound left open
angioblasts
precursors to blood vessels, proliferate like sprouts from close-by blood vessels at margins of wound
-appear 2-3 days after injury, provide new blood supply
DETERMINANTS of wound healing
Site of wound: skin heals well, brain does not
Mechanical factors: if margins are close, no tension around wound, not over joint
Size of wound: small wounds heal faster
Presence/ absence of infection: sterile wounds heal faster
Circulatory status: if wound is in ischemic tissue, will heal slower (diabetes mellitus)
Nutritional & metabolic factors: if healthy, wounds heal faster
Age: wounds heal fastest in children
EPIDERMAL wound healing
effects dermis, minimal damage
DEEP wound healing
effects epidermis, dermis & subcutaneous layers
clot formation - INTRINSIC pathway
blood vessel wall damage, activated by exposed collagen fibers in wall, activates clotting factor XIII
clot formation - EXTRINSIC pathway
tissue damage, activated by presence of tissue factor (TF), releases thromboplastin & activates clotting factor VIII
clot formation - what do both pathways require?
require Ca2+ to produce prothrombinase then prothrombin → thrombin → fibrin thread → fibrin clot (scab)
COMPLICATIONS of wound healing
Deficient scar formation
Excessive scar formation
Loss of function
Infection
Hypertrophic scar
elevated scar within original boundaries of wound
Keloid scar
elevated scar that exceeds original boundaries of wound
Contracture
over joint, fixation/ deformity
Adhesions
bands of scar tissue that join two normally separated surfaces
