a set of serum proteins which can be activated early in pathogen invasion by bacterial products or by the immune system via antigen-antibody complexes.

with activation, a large complement molecule is cleaved into its active components

1. chemotaxis

2. opsonization

3. increased vascular permeability

4. cell lysis

clotting system

1. inflammation results in activation of the coagulation system

2. PLATELETS serve as inflammatory mediators

1. produce clotting to control bleeding, trap bacteria and debris
2. adhere to fibrin to form meshwork, release HEPARIN and SEROTONIN
3. endothelial cells produce prostacyclins which prevent platelet aggregation--endogenous anticoagulants, injury leads to clotting
4. platelets also produce thromboxanes, which promotes further platelet aggregation
5. ratio of prostacyclins to thromboxanes regulate platelet aggregation 

active peptides are KALLIDIN and BRADYKININ which stimulate VASODILATION

increased VASCULAR PERMEABILITY and PAIN 

1. synthesized by the liver: promote or regulate the inflammatory response
2. c reactive protein--enhances platelet and complement activation
3. lead to INCREASED ESR

fall, winter, fecal/oral, unwashed hands, contaminated water, shellfish.

incubation period 2 wks- 2 mo's 

flu-like symptoms

fever, myalgias, malaise, fatigue, n/v, diarrhea, weightloss, tender enlarged liver

hep A management

fluids, rest, antiemetics

isolate: most infections during 2 wks prior to onset of symptoms, usually not infectious 1 wk after icteric phase entering

treat exposures with immunoglobulin

vaccine or immuno globulin prior to travel to endemic areas

not seasonal, blood and body fluids, sexual contact, IVDA, dialysis, needle stick

incubation - 2-6 months

its the IMMUNE response that is hepatocytophatic. 

5-10% become chronically infected with either chronic active, or chronic persistant or carrier state

if HBV not eradicated

chronic active

significant persistent inflammation with elevation of ALT 

+ HBsAG (hep b surface antigen)

LOW anti HBC IgG

mild persistent inflammation with slight elevation of ALT

no inflammation with normal ALT

+HBsAG 

antiHBc IgG very low

no HBsAG 

HIGH antiHBcIgG

may have subclinical illness--more likely to become chronically infected.

if illness occurs, n/v, jaundice, rashes and arthralgias

HBsAg or HBV DNA PRESENT, in acute and carrier

anti-HBc IgM = ACUTE INFECTION

anti-HBs IgG = immunity - past infection or vaccination

ALT indicates ongoing liver damage

HBV vaccine for all infants, healthcare workers

fluids, rest, antiemetics, isolation, infectious upto 6 months, lifetime for carriers

treat known exposures with HBIG and HBV vaccine

if chronic active hepatitis 

interferon+lamivudine or adefovir, entecavir

transplant