Chp 3 Flashcards
Blood vessel inflammatory response?
Dilation –> slows blood flow, increase permeability –> allows proteins to site of damage, recruitment of leukocytes –> ingest and destroy microbes/dead cells
Harmful consequences of inflammation
pain, tissue damage
inflammatory reaction steps
1) offending agent recognized by host cells
2) leukocytes and proteins recruited to site
3) leukocytes and proteins destroy offending agent
4) reaction controlled and terminated
5) tissue is repaired
Local vs systemic inflammation
local - reaction confined to the site of tissue damage
systemic - widespread inflammation causing pathologic abnormalities, called sepsis
Acute vs chronic inflammation
Acute - minutes to hours, causes exudation of fluid and plasma proteins (edema) and emigration of leukocytes (neutrophils), innate immunity
Chronic - lymphocytes, macrophages, proliferation of blood vessels, deposition of connective tissue. adaptive immunity
acute disorders and inflammatory molecules associated with each
acute respiratory distress syndrome - neutrophils
asthma - eosinophils, IgE antibodies
glomerulonephritis - antibodies and complement, neutrophils, monocytes
septic shock - cytokines
chronic disorders and inflammatory molecules associated with each
arthritis - lymphocytes, macrophages
asthma - eosinophils, IgE antibodies
atherosclerosis - macrophages, lymphocytes
pulmonary fibrosis - macrophages, fibroblasts
4 causes of inflammation
infection, tissue necrosis, foreign bodies, immune reactions, trauma
cellular receptors for microbes
Toll like receptors - triggers production of adhesion molecules, cytokines, mediators
sensors of cell damage - recognize uric acid, ATP, DNA, reduced intracellular [K+], activate inflammasome, induces IL-1
mediators of inflammation (8), source, action
1) histamine - mast cells, basophils, platelets - vasodilation, vascular permeability, endothelial activation
2) prostaglandins - mast cells, leukocytes - vasodilation, fever
3) leukotrienes - mast cells, leukocytes - vascular permeability, chemotaxis, leukocyte adhesion, activation
4) cytokines - macrophages, endothelial cells, mast cells - endothelial activation, fever, metabolic abnormalities, hypotension (shock)
5) chemokines - leukocytes, macrophages - chemotaxis, leukocyte activation
6) platelet activating factor - vasodilation, vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst
7) complement - plasma - leukocyte activation and chemotaxis, direct target killing, vasodilation
8) kinins - plasma - vascular permeability, smooth muscle contraction, vasodilation, pain
vascular reactions in acute inflammation (3)
1) vasodilation causes erythema, stasis of blood flood
2) increased vascular permeability produces gaps in endothelial cells allowing leukocytes and plasma proteins to enter sites of infection
3) lymphatic vessels and lymph nodes cause redness and swelling
Steps of leukocyte adhesion to endothelium
1) Margination - leukocyte redistribution to peripheral position along endothelial surface
2) Rolling - leukocytes adhere transiently to endothelial surface, detach and rebind. chemokines bind to proteoglycans, activate leukocytes
3) adhesion - via complementary adhesion molecules (selectins and integrins). firm adhesion via integrin VCAM-1/ICAM-1 binding
4) migration - adhesion molecules PECAM-1 binds leukocytes and allows migration through post capillary venules
5) chemotaxis - chemoattractants take leukocytes to site of injury (cytokines, complement, leukotrines).
podoconiosis
dust foot in desert dwellers from plugged lyphatics
Milroys
malformed lymphatics producing lifelong edema
orangepeel skin
ominous sign of breast cancer
chylous effusion
damaged lymphatics, usually thoracic duct, turbid, lipid rich fluid
transudate
low protein effusion
exudate
high protein effusion
edema first in feet
cardiac
