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50 Cards in this Set

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  • Back
There is always an initial innate immune response when a pathogen enters the body. Describe how it is triggered.
1. using toll receptors, the body recognizes microbial macromolecules (usually mannose or lipopolysaccharides) in bacterial cell wall
2. this activates macrophages, neutrophils, and fibroblasts which release chemokines and cytokines that cause the inflam response
How do neutrophils multiply?
1. The main proliferative cells that are neutrophil precursors, myeloblasts and promyeloblasts, are activated to multiply by G-CSF, GM-CSF, and IL-3.
What happens to neutrophils after they are made from myeloblasts and promyeloblasts?
They are placed in a maturation pool.
What chemical factors cause neutrophils to mature and get released?
IL-1, IL-6, IL-8
What two types of cells can cause neutrophils to both proliferate and mature?
Pathogens and activated macrophages
In patient's with severe infections what is wrong with their bodies neutrophils?
Many neutrophils will be immature because there is alot of IL-1, IL-6, IL-8 that causes immature neutrophils to leave the maturation pool early.
Which blood has more neutrophils in it: marginated or core flow?
Marginated blood
What five things amplifies inflammation? How? Where are they from?
IL-8 and PAF - from macrophages, platelets, endothelium and fibroblasts - regulates production, traffic, and local blood flow

TNF-alpha - from macrophages - accelerates proinflammatory cytokine production and release.


Coagulation system
How do neutrophils kill and phagocytose?
By using the NADPH oxidase system which uses MPO to convert H2O2 into HOCl and induces cell toxicity.
How do macrophages kill and phagocytose?
By using nitric oxide synthase (iNOS) regulated by cytokines and chemokines (TNF-alpha, IL6, IL8). In this process NO (a lipid soluble gas) reacts with oxygen to form a toxic radical and kill the cell.
What is the role of TGF-beta?
It regulated the inflammatory response my downregulating action on inflammatory cell recruitment and upregulating fibrosis and wound healing
What are the major sources of TGF-beta?
Macrophages and fibroblasts
What works with TGF-beta to regulate the inflammatory response?
IL-10 from macrophages and t-cells
IL-10 is an inflammatory response regulator, what regulates this regulator?
T regulator lymphocytes
What cytokine moves the body's response away from inflammation and toward repair?
What general marker can be used to tell the severity of an MI?
Leukocytes, the higher the leukocyte count the greater the damage on the heart.
What do events need to occur before the body can transition to fibrosis and healing?
1. inflammatory stimulus must be silenced
2. necrotic debris and infection are scavenged and destroyed
Three acute phase reactions caused from acute systemic effects of inflammation?
1. fever
2. constitutional symptoms like aches and pains
3. anorexia
What four pro-inflammatory cytokines drive the acute systemic effects of inflammation?
Cytokines IL-1, -6, -8, TNF alpha
What is C-reactive protein?
A critical early indicator of inflammation
What produces C-reactive protein?
IL_-6 (from pathogen or activated macrophage) causes liver to produce many acute phase reactants, including C-reactive protein.
If C-reactive protein is high how is the albumin level?
Albumin is reciprically low
As inflammation is being treated, what happens to albumin levels?
Albumin increases
If a patient has a normal CRP (C-reactive protein) what is their diagnosis?
They are not infected (no inflammation)
Along with CRP (C-reactive protein) what also increases at onset of infection?
serum amyloid A
What three other things increase with infection (thought their increases are delayed compared to CRP)?
Along with albumin what else decreases reciprically as inflammation occurs?
What is ARDS (acute respiratory distress syndrome)?
A syndrome that induces a massive recruitment of neutrophils into the lung
What neutrophil related problem can occur in an MI?
Neutrophil mediated myofiber loss
What can prevent neutrophil damage after an MI?
Neutrophils can be blocked with a CR-1 antagonist
What are two diseases associated with excessive TGF-beta?
Keloids - big band of fibrose scarring

Retroperitoneal fibrosis - TGF-beta is not working and have relentless TGF-beta driven fibrosis
What is pseudoleukopenia?
Redistibution of neutrophils from the core to the marginated pool as they respond to cytokine signals during the early phase of inflammation
If neutrophils are defective in any way but the rest of the immune response is normal will there be any problems in the inflammatory response?
No - there will be profound defects in the inflammatory response and overwhelming infection
What does a bacteria have to be able to do to become a successful intracellular parasite?
It has to be able to prevent formation of a functional phagolysosome
What type of bacteria are highly pathogenic?
encapsulated bacteria like meningococci, streptococci, and pneumococci

What is chronic granulomatous disease?
A disease caused by a defect in neutrophil killing secondary to a genetic defect in NAPH oxidase

What is the standard bearer of host inability to response an inflammatory stimulus?
Why does chronic inflammation occur?
Because of persistant inflammation that is unable to be eliminated
During chronic inflammation what does persistant macrophage activation lead to?
High proinflammatory cytokine levels that impair iron utilization and albumin synthesis
In chronic inflammation what does elevated IL-6 cause?
thrombocytosis (high platelet counts)
In chronic inflammation what does the combination of elevated IL-6, IL-1, and TNF-alpha cause?
Cachexia (loss of weight, muscle atrophy, fatigue, weakness and anorexia)
In chronic inflammation what does high levels of TGF-beta cause?
What five things are elevated during chronic inflammation?
1. C-reactive protein
2. serum amyloid A
3. IL-6 (makes platelets)
4. platelets
5. IgG (B-cells are trying to find a good antibody)
What three things go down during chronic inflammation?
1. albumin
2. transferrin
3. hemoglobin
What does a high sedementation rate tell us?
The patient is more likely effected with inflammation (but does not guarantee they are since the increase can be due to elevated immunoglobulins)
What does a high CRP tell us?
The patient is more likely to have inflammation (but does not guarantee they do because adipocytes of an enlarged panniculus can stimulate increased baseline production of CRP)

Panniculus: term describing a dense layer of fatty tissue growth, usually in the abdominal cavity. It generally coincides with morbid obesity and can be mistaken for a tumor or hernia
What can changes hemoglobin (and other serum proteins) tell us about an inflammatory stimulus?
Can be used as a crude index of the severity and length of time an inflammatory stimulus has been present.
If hemoglobin and other serum protein levels do not change while monitoring a patient what can this tell us?
Inflammation may actually not be present since changes should occur during the inflammatory process
What is present in persistant inflammation? Why are these around?
Granulomas - host is unable to remove them

Five things avaible to give a patient who is experiencing inflammation?
1. growth factors for production of inflammatory mediators
2. cytokines for amplification
3. IL-8 for neutrophil recruitment and mobilization
4. TGF-beta to manipulate inflammation into healing
5. TNG-alpha inhibitors