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USMLE Step 1 Notes

USMLE Step 1 Notes

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Published by villarex
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Published by: villarex on Nov 12, 2009
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IL-2- T cell growth factor secreted by Ag-stim T helper cells; enhancescytotoxicity of NK cellsIl-3- lymphokine secreted by activated T cells, major immunologicmediator of myeloid diff; causes prolif of granulocytes and macs; diff of megakaryocytic, erythrocytic, mast cell precursorsIL-5- B-cell diff factor produced by T helper cells and mast cells; causesprolif of activated B cells, increased eosinophil; enhances IgMsecretion, class switching of IgAIL-7- hematopoietic growth factor secreted by bone marrow stromalcells; growth factor for T cell and B cell precursors; enhances cytotoxicactivity on lymphocytes and monocytesIL-8- inflamm cytokine secreted by monocytes and macrophages;chemotactic for both neutrophils and T cells; causes activation of neutrophils to release lysosomal enzymes, leads to SOD productionIL-10- produced by activated T cells and mast cells; inhibits cytkinesynth and T cell prolif in presence of monocytes; inhibits IL-2 and IFN-gproduction by T helper cells; enhances B cell diff 
Ab responseincreasedIL-13- produced by T helper cells; regulator of inflamm response b/cinhibits activity and release of inflamm cytokines by macsVascoactive amines are histamine and serotonin (present in plateletsand enterochrommafin cells)Complement system consists of 20 component proteins (and theircleavage products), which are found in
greatest concentration inplasma
; system functions in both innate and adaptive immunity fordefense against microbial agents; in process of complement activation,a number of complement components are elaborated that causeincreased vascular permeability, chemotaxis, and opsonization. The
classical pathway is triggered by fixation of C1 to antibody(IgM or IgG)
that has combined with antigen, and proteolysis of C2and C4, and subsequent formation of a
C4b2b complex thatfunctions as a C3 convertase
. The alternative pathway can be triggered by
microbial surfacemolecules (e.g., endotoxin, or LPS), complex polysaccharides,and cobra venom
; involves a distinct set of plasma components(properdin, and factors B and D); spontaneous cleavage of C3 thatoccurs normally is enhanced and stabilized by a complex of C3b and abreakdown product of Factor B called Bb;
the C3bBb complex is aC3 convertase.
In the lectin pathway,
mannose-binding lectin,
binds to
carbohydrate-containing proteins on bacteria and viruses anddirectly activates C1
C3b generated by any of the pathways binds to the C3 convertase andproduces C5 convertase, which cleaves C5.
C5b remains attachedto the complex and forms a substrate for the subsequentbinding of the C6-C9 components. Polymerized C9 forms achannel in lipid membranes, called the membrane attack complex, which allows fluid and ions to enter and causes celllysis.C1INH interferes with the enzymatic activity of two of theproteins in the C1 complex. Excessive complement activation isalso prevented by a number of proteins that act to inhibit MACformation (e.g., CD59, also called membrane inhibitor of reactive lysis).
Deficiency of C3 results in increased susceptibility to infections that isfatal unless treated. Deficiencies of the alternative pathway proteinsare also associated with defective resistance to infections.Paradoxically,
deficiencies of C2 and C4 are associated withautoimmune diseases, notably systemic lupus erythematosus,
probably because of a failure to clear immune complexes that areformed.In late component and MAC deficiency the only infections thesepatients appear to suffer from are by Neisseria organisms.Bradykinin increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain when injected intothe skin.Activated Hageman factor (factor XIIa) initiates four systems involvedin the inflammatory response: (1) the kinin system, (2) the clottingsystem, (3) the fibrinolytic system, which produces plasmin anddegrades the fibrin; and (4) the complement system, which producesanaphylatoxins.Arachidonic acid (AA) is a 20-carbon polyunsaturated fatty acid;derived from dietary sources or by conversion from the
essentialfatty acid linoleic acid.
Inflammatory Actions of Eicosanoids:
Vasoconstriction - TXA2, LTs C4, D4, E4; Vasodilation PGI2,PGE1, PGE2, PGD2; Increased vascular permeability- LTs C4,D4, E4; Chemotaxis-, leukocyte adhesion LT B4, HETE, lipoxins
5-lipoxygenase (5-LO) is the predominant enzyme in neutrophils. Themain product, 5-HETE, which is chemotactic for neutrophils, isconverted into a family of compounds collectively called leukotrienes.LTB4 is a potent chemotactic agent and activator of neutrophilfunctional responses, such as aggregation and adhesion of leukocytesto venular endothelium, generation of oxygen free radicals, andrelease of lysosomal enzymes.
The principal actions of lipoxins are to inhibit leukocyterecruitment and the cellular components of inflammation.Resolvins inhibit leukocyte recruitment and activation, in partby inhibiting the production of cytokines. Thus, the anti-inflammatory activity of aspirin is likely attributable to itsability to inhibit cyclooxygenases (see below) and, perhaps, tostimulate the production of resolvins.In addition to platelet stimulation, PAF causes vasoconstrictionand bronchoconstriction, and at extremely low concentrationsit induces vasodilation and increased venular permeability witha potency 100 to 10,000 times greater than that of histamine.TNF and IL-1 are two of the major cytokines that mediateinflammation; systemic responses include fever, loss of appetite, slow-wave sleep, the release of neutrophils into thecirculation, the release of corticotropin and corticosteroidsand, particularly with regard to TNF, the hemodynamic effectsof septic shock—hypotension, decreased vascular resistance,increased heart rate, and decreased blood pH
NO is synthesized from L-arginine by the enzyme nitric oxide synthase(NOS)- eNOS and nNOS are constitutively expressed at low levels andcan be activated rapidly by an increase in cytoplasmic calcium ions.Influx of calcium into cells leads to a rapid production of NO.
iNOS, incontrast, is induced when macrophages and other cells areactivated by cytokines (e.g., TNF, IFN-γ) or other agents.
Different granule enzymes serve different functions. Acid proteasesdegrade bacteria and debris within the phagolysosomes, in which anacid pH is readily reached. Neutral proteases are capable of degradingvarious extracellular components. These enzymes can attack collagen,basement membrane, fibrin, elastin, and cartilage, resulting in thetissue destruction that accompanies inflammatory processes. Neutralproteases can also cleave C3 and C5 directly, releasinganaphylatoxins, and release a kinin-like peptide from kininogen.Neutrophil elastase has been shown to degrade virulence factors of 

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