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level: Acute Inflammation

Questions and Answers List

level questions: Acute Inflammation

Question	Answer
Edema, presence of neutrophils in tissue	Hallmarks of acute inflammation
Infection, Tissue necrosis	Causes of acute inflammation
Activators of Toll-like receptors (TLRs)	Pathogen-associated molecular pattern (PAMP)
A TLR on macrophages which recognizes lipopolysaccharide on the outer membrane of Gram negative bacteria	CD14
Nuclear transciption factor upregulated by TLR activation which leads to production of inflammatory mediators	NF-kB
Releases arachidonic acid from plasma membrane	Phospholipase A2
Produces prostaglandins from AA	Cyclooxygenase
Mediates arterial vasodilation and increased vascular permeability at the postcapillary venule	PGI2, PGD2, PGE2
Location of increased vascular permeability	Postcapillary venule
Also mediates fever and pain ("E2" = "fee-ver")	PGE2
Produces leukotrienes from AA	5-lipoxygenase
Activates neutrophils	LTB4
Slow reacting substances of anaphylaxis; mediates vasoconstriction, vasospasm and increased vascular permeability	LTC4, LTD4, LTE4
Contractile cells which increase space between endothelial cells -> increased permeability	Pericytes
Tissue trauma, C3a and C5a, crosslinking of surface IgE by an antigen	Activators of mast cells
LTB4, C5A, IL-8, Bacterial products	Activators of neutrophils
Degranulation-> histamine release -> arteriolar vasodilation, increased vascular permeability of postcapillary venule	Immediate response of mast cells
Leukotriene release and activation	Delayed response of mast cells
C1 binds to IgG or IgM bound to an antigen ("GM makes CLASSIC cars")	Classical complement pathway
Microbial products directly activate complement	Alternative complement pathway
MBL binds to mannose on microorganisms and activates complement	Mannose-binding lectin (MBL) pathway
Cleaves C3 -> C3a and C3b	C3 convertase
cleaves c5 -> c5a and c5b	C5 convertase
C5bC6C7C8C9; lyses microbes by creating a hole on cell membrane	Membrane attack complex
Anaphylatoxins which trigger mast cell degranulation	C3a and C5a
Chemotactic for neutrophils	C5a
Opsonin for phagocytosis	C3b
Proinflammatory protein produced in liver; activated by exposure to subendothelial and tissue damage; Activates coagulation,fibrinolytic systems, complement system and kinin system	Hageman factor (Factor XII)
Cleaves high molecular weight kininogen (HMWK) to bradykinin -> similar effects as histamine + mediation of pain	Kinin system
Rubor, calor, tumor, dolor	Cardinal signs of inflammation
Histamine	Key mediator of rubor and calor
Increase COX activity in perivascular cells of hypothalamus -> Increased PGE2 -> elevated temperature set point -> fever	IL 1 and TNF