Chapter 2 Flashcards
What is inflammation?
a protective response involving host cells, blood vessels and proteins and other mediators that is intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult and to initiate the process of repair.
What are the characteristics of acute inflammation?
rapid in onset
short duration (minutes to days)
fluid and plasma protein exudation
predominantly neutrophilic leukocyte accumulation
what are the characteristics of chronic inflammation?
longer duration (days to years)
lymphocytes and macrophages
vascular proliferation
fibrosis
what are the external signs of inflammation?
heat--calor redness--rubor swelling--tumor pain--dolor loss of fxn--functio laesa
who added the 5th cardinal sign of inflammation?
Rudolf Virchow, the ‘father of modern pathology’
what are the two major components of acute inflammation?
vascular changes–vasodilation and increased vascular permeability
leukocyte recruitment and activation
what are the two most important families of pattern recognition receptors?
- Toll-like receptors (TLRs)
- inflammasome
what do TLRs sense? where are they found (on/in) a cell
- products of bacteria, viruses and other pathogens.
- found on plasma membrane–sense environment
what do inflammasomes sense? where are they found (on/in) a cell?
- products of dead cells, such as uric acid and extracellular ATP
- activate caspase-1
- found in a cell–sense cytoplasm
what is responsible for the redness and warmth characteristic of acute inflammation?
arteriolar vasodilation
what is stasis, as applied to acute inflammation?
the dilation of microvasculature causing blood to become more concentrated and viscous, decreasing circulation
what is margination?
the accumulation of leukocytes along the vascular endothelial surface as stasis develops.
what is exudate?
protein-rich fluid accumulation in vessels as water leaves the blood and enters the tissues due to osmotic pressure imbalance during increased vascular permeability
what is transudate
interstitial fluid accumulations caused by increased hydrostatic pressure, typically a consequence of reduced venous return.
low [protein] and few or no blood cells
which is normally found with acute inflammation, exudate or transudate?
exudate
what causes increased vascular permeability in acute inflammatory reactions?
1-endothelial cell contraction leading to intercellular gaps in postcapillary venules (MC)
2- endothelial injury
3-increased transcytosis
4-leakage from new blood vessels
what do leukocytes do?
1-ingest offending agents, kill bacteria, and other microbes
2-eliminate necrotic tissue and foreign substances
what cell types have surface receptors?
macrophages, mast cells, dendritic cells
what is diapedesis
when a cell goes out of circulation to get to target tissue during acute inflammation
what are the sequence of events in the recruitmentof leukocytes form the vascular lumen to the extravascular space?
1- margination and rolling along the vessel wall
2- firm adhesion to the endothelium
3-transmigration between endothelial cells
4-migration in interstitial tissues toward a chemotactic stimulus
Leukocyte activation results in the enhancement of what functions?
1- phagocytosis
2-intracellular destruction of phagocytosed microbes and dead cells
3-liberation of substances that destroy extracellular microbes and dead tissues
4- production of mediators
what is opsonization?
the process by which leukocytes recognize host proteins (opsonins) that coat microbes and target them for phagocytosis
-most important opsonins are antibodies of IgG class
what are the most important microbicidal substances for killing and degrading phagocytosed microbes?
ROS and lysosomal enzymes (esp. elastase)
when does scarring occur?
after substantial tissue destruction or after chronic inflammation
lymphangitis
inflammation of a lymphatic channel
lymphandenitis
inflammation of a lymph node, increase in size
lymphandenopathy
general disorder of lymph nodes
what cells are predominately found in acute inflammation in the first 24-48 hours? following that time period?
24-48 hours=neutrophils
after= monocytes/macrophages and lymphocytes
what are collectins?
plasma carbohydrate-binding lectins which bind to microbial cell wall sugar groups
what are the possible outcomes of acute inflammation?
1- resolution
2- chronic inflammation
3- scarring
what are the morphologic patterns of inflammation?
1- serous inflammation
2- fibrinous inflammation
3-suppurative (purulent) inflammation
4-ulcerative inflammation
what are the characteristics of serous inflammation?
serum accumulates below epidermis
serous effusion
skin blister: burn, virus, toxin
what are the characteristics of fibrinous inflammation?
- severe injury
- increased vascular permeability–allows large molecules to enter
- fibrin rich exudate —>fibrin-rich scar
- characteristic of peritoneum, pleura cavity and pericardial sac
what are the characteristics of suppurative (purulent) inflammation?
localized infection of pus-forming organism
staph. aureus
Abscess- localization of pus
pus= collection of neutrophils, necrotic tissue, edema
what are the characteristics of ulcerative inflammation?
- near an organ or tissue surface
- local defect
- produced by necrosis of cells and sloughing of necrotic and inflammatory tissue
- peptic ulcers, aphthous ulcer
what is granulomatous inflammation?
a distinctive pattern of chronic inflammation characterized by aggregates of activated macrophages with scattered lymphocytes.
-sarcoidosis, Crohn disease, against certain microbes
How do mediators get to inflammation?
1- produced locally by the cells at site of inflammation
2- derived from circulating inactive precursors that are activated at the site of inflammation
how do most mediators act?
by binding to specific receptors on different target cells