Bacteremia & Sepsis

Front 1

_______ is the presence of microorganisms in a normally sterile host tissue.

Back 1

Infection

Front 2

________ is defined as the presence of viable bacteria in the blood.

Back 2

Bacteremia

Front 3

_____ is the systemic response to infection. Clinical signs of systemic inflammation are present together with definitive evidence of infection.

Back 3

Sepsis

Front 4

Sepsis is a clinical syndrome that complicates severe infection and is characterized by systemic ________ and widespread tissue injury.

Back 4

inflammation

Front 5

In sepsis , tissues remote from the original insult display the cardinal signs of inflammation, including _______ , increased microvascular _______, and ________accumulation.

Back 5

vasodilatation
permeability
leukocyte

Front 6

Sepsis is considered ________ when it is associated with organ dysfunction, hypoperfusion, or hypotension

Back 6

severe

Front 7

______ is sepsis with hypotension despite adequate fluid resuscitation combined with perfusion abnormalities.

Back 7

Septic shock

Front 8

Septic shock is in part caused by cytokines produced mainly by activated macrophages. ___ and ____ are principle mediators of septic shock.

Back 8

TNF
IL-1

Front 9

Toll Like Receptors on macrophages constitute a molecular “alarm system” to alert the body of intruders (microorganisms). Overactivation of this system can result in ______

Back 9

septic shock.

Front 10

Blood is normally _____.

Back 10

sterile

Front 11

________ are common and can occur after dental procedures, obstetrical procedures or even brushing teeth. They are rapidly cleared by the host immune system.

Back 11

Transient bacteremias

Front 12

For nontransient bacteremia such as continuous or intermittent, it is usually possible to find a _____ of the infection (where it seeded from).

Back 12

focus

Front 13

The principal injurious consequences of host responses to extracellular bacteria are inflammation and ______, which are caused by cytokines produced mainly by activated ________.

Back 13

septic shock
macrophages

Front 14

Septic shock is the most severe cytokine-induced pathologic consequence of infection by gram ______ and some gram ________ bacteria.

Back 14

negative
positive

Front 15

septic shock is a syndrome characterized by circulatory collapse and ________-

Back 15

disseminated intravascular coagulation

Front 16

TNF and IL-1 are the principal mediators of septic shock. _____ serum levels are in fact predictive of outcome of severe gram negative infections

Back 16

TNF

Front 17

Gram negative bacteria have ________ , which stimulates the innate immune system.

Back 17

LPS (lipopolysaccharide)

Front 18

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 _______.

Back 18

septic shock

Front 19

LPS (lipopolysaccharide) or endotoxin binds to a ______ receptor and stimulates secretion of cytokines. This is part of the ____ immune system.

Back 19

macrophage innate

Front 20

Critical amount of ____ stimulates septic shock.

Back 20

LPS

Front 21

The polysaccharide moieties on LPS can be highly variable and are recognized by the _____ immune system

Back 21

adaptive

Front 22

The lipid moiety is highly conserved and is recognized by the ______ immune system.

Back 22

innate

Front 23

Circulating LPS is bound to a plasma _________

Back 23

LPS binding protein (LBP)

Front 24

The complex docks with ___ and the LBP is released.

Back 24

CD14

Front 25

LPS induces __________

Back 25

cell signaling

Front 26

The macrophage is activated via this receptor and ____

Back 26

TLR4

Front 27

Macrophages are stimulated to produce ______ and ____, and ______

Back 27

TNF-a
IL-1
IL-6

Front 28

Macrophage activation leads to _______

Back 28

tissue damage

Front 29

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 _______.

Back 29

hypotension

Front 30

_______ 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.

Back 30

Disseminated intravascular coagulation (DIC)
fibrin

Front 31

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.

Back 31

bleed

Front 32

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.

Back 32

warm
cold

Front 33

Finally in septic shock, Multiple organs show inflammation and intravascular thrombosis, which can produce organ ______

Back 33

failure

Front 34

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.

Back 34

neutrophils

Front 35

The ____ and _____ are particularly susceptible to injury by neutrophils.

Back 35

lungs
liver

Front 36

Lung damage is commonly called ___________ and results when neutrophil-mediated endothelial injury allows fluid to escape from blood into airspace.

Back 36

acute respiratory distress syndrome (ARDS)

Front 37

Liver injury and impaired liver function result in failure to maintain normal blood _____ levels because of a lack of gluconeogenesis from stored glycogen.

Back 37

glucose

Front 38

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.

Back 38

T cells
super antigens

Front 39

__________ can produce TSST-1 (toxic shock syndrome toxin).

Back 39

Staphylococcus arueus

Front 40

____________ 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.

Back 40

toxic shock syndrome toxin )TSST-1

Front 41

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

Back 41

Streptococcal pyrogenic exotoxins-