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41 Cards in this Set

  • Front
  • Back
_______ is the presence of microorganisms in a normally sterile host tissue.
Infection
________ is defined as the presence of viable bacteria in the blood.
Bacteremia
_____ is the systemic response to infection. Clinical signs of systemic inflammation are present together with definitive evidence of infection.
Sepsis
Sepsis is a clinical syndrome that complicates severe infection and is characterized by systemic ________ and widespread tissue injury.
inflammation
In sepsis , tissues remote from the original insult display the cardinal signs of inflammation, including _______ , increased microvascular _______, and ________accumulation.
vasodilatation
permeability
leukocyte
Sepsis is considered ________ when it is associated with organ dysfunction, hypoperfusion, or hypotension
severe
______ is sepsis with hypotension despite adequate fluid resuscitation combined with perfusion abnormalities.
Septic shock
Septic shock is in part caused by cytokines produced mainly by activated macrophages. ___ and ____ are principle mediators of septic shock.
TNF
IL-1
Toll Like Receptors on macrophages constitute a molecular “alarm system” to alert the body of intruders (microorganisms). Overactivation of this system can result in ______
septic shock.
Blood is normally _____.
sterile
________ are common and can occur after dental procedures, obstetrical procedures or even brushing teeth. They are rapidly cleared by the host immune system.
Transient bacteremias
For nontransient bacteremia such as continuous or intermittent, it is usually possible to find a _____ of the infection (where it seeded from).
focus
The principal injurious consequences of host responses to extracellular bacteria are inflammation and ______, which are caused by cytokines produced mainly by activated ________.
septic shock
macrophages
Septic shock is the most severe cytokine-induced pathologic consequence of infection by gram ______ and some gram ________ bacteria.
negative
positive
septic shock is a syndrome characterized by circulatory collapse and ________-
disseminated intravascular coagulation
TNF and IL-1 are the principal mediators of septic shock. _____ serum levels are in fact predictive of outcome of severe gram negative infections
TNF
Gram negative bacteria have ________ , which stimulates the innate immune system.
LPS (lipopolysaccharide)
If an individual is infected with a gram negative bacterium and fails to control its replication, LPS levels can rise to such a level as to cause _______.
septic shock
LPS (lipopolysaccharide) or endotoxin binds to a ______ receptor and stimulates secretion of cytokines. This is part of the ____ immune system.
macrophage innate
Critical amount of ____ stimulates septic shock.
LPS
The polysaccharide moieties on LPS can be highly variable and are recognized by the _____ immune system
adaptive
The lipid moiety is highly conserved and is recognized by the ______ immune system.
innate
Circulating LPS is bound to a plasma _________
LPS binding protein (LBP)
The complex docks with ___ and the LBP is released.
CD14
LPS induces __________
cell signaling
The macrophage is activated via this receptor and ____
TLR4
Macrophages are stimulated to produce ______ and ____, and ______
TNF-a
IL-1
IL-6
Macrophage activation leads to _______
tissue damage
TNF-a in combination with IFN-g and IL-1 can induce nitric oxide synthase which produces nitric oxide, which not only has potent micobicidal activities, but is a vasodilator. NO appears to be responsible for _______.
hypotension
_______ may become evident in several ways. Systemic activation of coagulation generates the deposition of ______in small blood vessels and microvascular thrombosis in critical target organs leading to organ failure.
Disseminated intravascular coagulation (DIC)
fibrin
As components of coagulation are consumed, paradoxically the patient may ______from other sites within the body. So clotting and bleeding may occur simultaneously in the same patient.
bleed
Septic shock arises when cardiac output is unable to compensate for falling blood pressure secondary to vasodilatation. At first it is _____ shock due to increased blood flow to the periphery, then ____ shock.
warm
cold
Finally in septic shock, Multiple organs show inflammation and intravascular thrombosis, which can produce organ ______
failure
Tissue injury in response to LPS can result from the activation of ______ before they exit the vasculature, thus causing damage to endothelial cells and reduced blood flow.
neutrophils
The ____ and _____ are particularly susceptible to injury by neutrophils.
lungs
liver
Lung damage is commonly called ___________ and results when neutrophil-mediated endothelial injury allows fluid to escape from blood into airspace.
acute respiratory distress syndrome (ARDS)
Liver injury and impaired liver function result in failure to maintain normal blood _____ levels because of a lack of gluconeogenesis from stored glycogen.
glucose
Toxic Shock occurs when some bacterial toxins stimulate all the ______ in an individual that express a particular set or family of T cell receptor genes. Such toxins are called _______. They activate many T cells with subsequent production of large amounts of cytokines and clinicopathologic abnormalities that are similar to septic shock.
T cells
super antigens
__________ can produce TSST-1 (toxic shock syndrome toxin).
Staphylococcus arueus
____________ is an enterotoxin that is secreted and can bind nonspecifically to the T-cell receptor to stimulate T-cells. This antigen is capable of stimulating ALL T-cells in a given class.
toxic shock syndrome toxin )TSST-1
some strains of streptococci produce _________ that can act as a super antigen. The antigen interacts with T-cells and macrophages stimulating the release of IL-1, IL-2, IL-6, TNF-a, TNF-b, and INF-g
Streptococcal pyrogenic exotoxins-