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41 Cards in this Set
- Front
- Back
_______ is the presence of microorganisms in a normally sterile host tissue.
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Infection
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________ is defined as the presence of viable bacteria in the blood.
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Bacteremia
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_____ is the systemic response to infection. Clinical signs of systemic inflammation are present together with definitive evidence of infection.
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Sepsis
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Sepsis is a clinical syndrome that complicates severe infection and is characterized by systemic ________ and widespread tissue injury.
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inflammation
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In sepsis , tissues remote from the original insult display the cardinal signs of inflammation, including _______ , increased microvascular _______, and ________accumulation.
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vasodilatation
permeability leukocyte |
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Sepsis is considered ________ when it is associated with organ dysfunction, hypoperfusion, or hypotension
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severe
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______ is sepsis with hypotension despite adequate fluid resuscitation combined with perfusion abnormalities.
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Septic shock
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Septic shock is in part caused by cytokines produced mainly by activated macrophages. ___ and ____ are principle mediators of septic shock.
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TNF
IL-1 |
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Toll Like Receptors on macrophages constitute a molecular “alarm system” to alert the body of intruders (microorganisms). Overactivation of this system can result in ______
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septic shock.
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Blood is normally _____.
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sterile
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________ are common and can occur after dental procedures, obstetrical procedures or even brushing teeth. They are rapidly cleared by the host immune system.
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Transient bacteremias
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For nontransient bacteremia such as continuous or intermittent, it is usually possible to find a _____ of the infection (where it seeded from).
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focus
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The principal injurious consequences of host responses to extracellular bacteria are inflammation and ______, which are caused by cytokines produced mainly by activated ________.
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septic shock
macrophages |
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Septic shock is the most severe cytokine-induced pathologic consequence of infection by gram ______ and some gram ________ bacteria.
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negative
positive |
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septic shock is a syndrome characterized by circulatory collapse and ________-
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disseminated intravascular coagulation
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TNF and IL-1 are the principal mediators of septic shock. _____ serum levels are in fact predictive of outcome of severe gram negative infections
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TNF
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Gram negative bacteria have ________ , which stimulates the innate immune system.
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LPS (lipopolysaccharide)
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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 _______.
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septic shock
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LPS (lipopolysaccharide) or endotoxin binds to a ______ receptor and stimulates secretion of cytokines. This is part of the ____ immune system.
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macrophage innate
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Critical amount of ____ stimulates septic shock.
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LPS
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The polysaccharide moieties on LPS can be highly variable and are recognized by the _____ immune system
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adaptive
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The lipid moiety is highly conserved and is recognized by the ______ immune system.
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innate
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Circulating LPS is bound to a plasma _________
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LPS binding protein (LBP)
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The complex docks with ___ and the LBP is released.
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CD14
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LPS induces __________
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cell signaling
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The macrophage is activated via this receptor and ____
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TLR4
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Macrophages are stimulated to produce ______ and ____, and ______
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TNF-a
IL-1 IL-6 |
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Macrophage activation leads to _______
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tissue damage
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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 _______.
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hypotension
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_______ 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.
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Disseminated intravascular coagulation (DIC)
fibrin |
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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.
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bleed
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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.
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warm
cold |
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Finally in septic shock, Multiple organs show inflammation and intravascular thrombosis, which can produce organ ______
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failure
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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.
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neutrophils
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The ____ and _____ are particularly susceptible to injury by neutrophils.
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lungs
liver |
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Lung damage is commonly called ___________ and results when neutrophil-mediated endothelial injury allows fluid to escape from blood into airspace.
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acute respiratory distress syndrome (ARDS)
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Liver injury and impaired liver function result in failure to maintain normal blood _____ levels because of a lack of gluconeogenesis from stored glycogen.
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glucose
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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.
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T cells
super antigens |
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__________ can produce TSST-1 (toxic shock syndrome toxin).
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Staphylococcus arueus
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____________ 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.
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toxic shock syndrome toxin )TSST-1
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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
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Streptococcal pyrogenic exotoxins-
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