Acute and Chronic Inflammation Flashcards by Beth Cocker

Why does inflammation occur?

Protective/Defensive
Inappropriately triggered/controlled
Against self tissue/food allergies
tissue injury

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What are the goals of inflammation?

Destroy pathogens that caused initial injury
Get rid of necrotic cells and tissues which arise due to injury
Initiation of the repair process

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What is acute inflammation?

Rapid onset
Short duration
Edema (swelling)
Migration of neutrophils (come right away but die via apoptosis)
If not resolved leads to chronic inflammation

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What is chronic inflammation?

Longer duration
Macrophages and lymphocytes
Proliferation of blood vessels
Fibrosis and tissue destruction (scar tissue)

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What is the process of inflammation?

Chemicals are released by damaged cells
Blood clot forms
Abscess starts to form

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Mast cell release what?

Histamine

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What is neutrophils function?

Phagocytosis

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What are monocytes function?

Phagocytosis when they mature they turn into macrophages

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What are the five steps of inflammation?

Recognition
Recruitment
Removal
Regulation (control)
Resolution (repair)

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What are the five signs of inflammation?

Redness: induce vasodilation (more blood flowing
Heat: Blood picks up heat from the body and brings it to the area
Swelling: Blood vessel fluid leaks out
Pain: Swelling puts press on the nerve endings
Loss of function: Cannot do what it is supposed to do

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Define Rubor

Redness

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Define Calor

Heat

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Define Tumor

Swelling

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Define Dolor

pain

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Define Functio Laesa

Loss of function

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What are systematic effects of inflammation?

Fever

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What do endogenous pyrogens do?

Increase body temperature

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What causes acute inflammation?

Infection
Trauma
Agents
Tissue death
immune reactions
Foreign bodies

What happen in acute inflammation?

Vasodilation
Increase in vascular permeability (blood vessels are more leaky), endothelial cell contraction. cytoskeleton changes (histamine causes more space between endothelial cells) and leukocyte damage (release damaging particles

Define margination

Big stuff get pushed to the edges of the vesicles and once they are close they can interact and penetrate –> leaving the blood vessels

What happens when fluid leaks out?

More concentrated (more viscous) –> flow is slower

How are leukocytes recruited?

Macrophage with microbes is lead to the membrane via cytokines
Leukocyte has glycoproteins that bind to P and E selectins on the membrane causing a rolling effect.
The integrin are then activated by chemokines and convert from low affinity to high affinity state leading to a stable adhesion to the membrane. After this it migrates through the endothelium

What are PECAM-1

Platelet endothelial cell adhesion molecules

Slip out and the chemokines interact
Under the influence of the chemokines it will migrate where it is needed

How are leukocytes activated?

Toll-like Receptors –> PRRs
GPCRs
Receptors for cytokines and opsonins

How does phagocytosis work?

Pathogen is covered (opsonization) Phagosome merges with lysosome to make a phagolysosome - Pathogen is destroyed by enzymes or respiratory burst (creats ROS to kill the bacteria)

Down side to release of lysosomal enzymes to the outside?

Kill the invader but then kill good cells to (chronic inflammation)

What is Amplification?

One macrophage gets there and calls others | ROS and lysosome kill the host cell causing inflammation which must then be terminated

What is termination?

Neutrophils undergo apoptosis | Pro-inflammatory inducers disappar

What if something can't be repaired?

Fibroblast turn it into scarring

Where does histamine come from and what does it cause?

Mast cells, basophils and platelets | Vasodilation, increased vascular permeability and endothelial activation

Where does serotonin come from and what does it cause?

Platelets | Vasodilation and increased vascular permeability

Where does TNF come from and what does it cause?

Macrophages, mast cells, T lymphocytes Stimulates expression of endothelial adhesion molecules and secretion of other cytokines Systemic effects

Where does IL-1 come from and what does it cause?

Macrophages, endothelial cells and so epithelial cells | Similar to TNF; greater role in fever

What are adalimumab and infliximab?

monoclonal antibodies that block TNF

What are metabolites of arachidonic acid?

PGs Leukotriens Lipoxins

What changes arachidonic acid to PGs?

cyclooxygenase

What do TXA2 do?

Causes vasoconstriction and promotes platelet aggregation

What does PGI2 do?

Causes vasodilation and inhibits platelet aggregation

What does LXA and LXB do?

Inhibits neutrophil adhesion and chemotaxis

NSAID do what?

Blocks cycloogenase | Blocks COX

What does celecoxib block?

COX 2

What does zileuton block?

Lipooxygenase

PGs play a role in protecting what?

The stomach against acid in the stomach | Inhibiting COX 1 would cause the PGs to not be there to protect the stomach

COX 1 stimulates what?

PGs