inflammtion - KAHOOT & HINTS Flashcards
what is one cardinal sign of inflammation?
heat & redness
what can cause inflammation?
infection
thorn
heat/ burn
T/F - endorphins are released into bloodstreams by platelets & mast cells in response to injury?
FALSE
=histamines released
what cell is most prominent in allergic & parasitic reactions?
eosinophils
T/F - RBCs are directly involved with inflammation
FALSE
cells involved: neutrophils, PMNs, eosinophils, basophils, macrophages, platelets
phagocytosis is…
a process where macrophages engulf & digest foreign objects
what type of inflammation produces exudate rich in fibrin?
fibrinous
T/F - a popped blister is an example of purulent inflammation
FALSE
5 stages of deep wound healing in order
inflammatory, migratory, proliferative, maturation, scar formation
a keloid scar…
is elevated & exceeds boundary of original wound
T/F - intrinsic & extrinsic pathways both merge to form fibrin which then turns into fibrin clot
FALSE
= prothrombinase then prothrombin → thrombin → fibrin thread → fibrin clot
purpose of inflammation
Start the healing process
FUNCTION: protective role
-inactivate injurious agent
-breakdown & remove dead cells
-initiate healing of tissues
Cardinal signs/ symptoms of inflammation
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
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
HISTAMINES
released from platelets & mast cells, stimulates endothelial cells to contract making gaps between them wider & leakier
BRADYKININ
released from plasma, slower reaction, accounts for pain with inflammation
COMPLEMENT SYSTEM
proteins activated (by 3 different things) in cascade that forms membrane attack complex (MAC) that kills cell but also causes more histamine release
ARACHIDONIC ACID
leukotrienes (promote chemotaxis & increased permeability) & prostaglandins (vasodilation, increased permeability, mediates pain & fever)
CYTOKINES
produced by leukocytes (WBCs)
-Interleukin-1: promotes inflammatory reaction
-Tumor Necrosis factor (TNF)
NEUTROPHILS / POLYMORPHONUCLEAR cells (PMNs)
60-70% of all WBCs – most numerous, first to arrive, highly mobile, phagocytes (engulfing cells), contain bactericidal lysosomes, produce cytokines
EOSINOPHILS
2-3% of all WBCs, arrive 2-3 days after, phagocytes, bactericidal, in chronic, in allergies & parasitic reactions
BASOPHILS
less than 1%, IgE reactions, release histamine, morph into mast cells
MACROPHAGES
arrive 3-4 days after onset, in chronic, derived from monocytes, in tissues NOT blood stream, phagocytes, secrete cytokines that produce inflammatory mediators
PLATELETS / THROMBOCYTES
early to arrive with PMNs, contain many substances: histamine, clotting proteins, growth factor – released if damage to endothelial lining/ ECM, cause coagulation
complement system - activated in 3 ways
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 that release chemicals that cause liver to produce lectins
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
wound healing stages
-1st intention: clean wound edges close together
-2nd intention: wound left open due to too much tissue damage, more scar & granulation tissue allowed to build up before closing wound
-Delayed: wound left open
CELLS in wound healing
Leukocytes, macrophages, connective tissue cells, epithelial cells, PMN’s.
*macrophages are most important - stay long time & contribute by producing cytokines, growth factors, mediators, myofibroblasts, angioblasts, fibroblasts
EXTRINSIC pathway
tissue damage, activated by presence of tissue factor (TF), releases thromboplastin & activates clotting factor VIII
INTRINSIC pathway
blood vessel wall damage, activated by exposed collagen fibers in wall, activates clotting factor XIII
clot formation - intrinsic & extrinsic pathway
require Ca2+ to produce prothrombinase then prothrombin → thrombin → fibrin thread → fibrin clot (scab)
