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POD > Acute and Chronic Inflammation > Flashcards

Acute and Chronic Inflammation Flashcards

1
Q

Why does inflammation occur?

A

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

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2
Q

What are the goals of inflammation?

A

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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3
Q

What is acute inflammation?

A

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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4
Q

What is chronic inflammation?

A

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

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5
Q

What is the process of inflammation?

A

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

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6
Q

Mast cell release what?

A

Histamine

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7
Q

What is neutrophils function?

A

Phagocytosis

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8
Q

What are monocytes function?

A

Phagocytosis when they mature they turn into macrophages

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9
Q

What are the five steps of inflammation?

A 
Recognition
Recruitment
Removal
Regulation (control)
Resolution (repair)
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10
Q

What are the five signs of inflammation?

A

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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11
Q

Define Rubor

A

Redness

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12
Q

Define Calor

A

Heat

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13
Q

Define Tumor

A

Swelling

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14
Q

Define Dolor

A

pain

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15
Q

Define Functio Laesa

A

Loss of function

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16
Q

What are systematic effects of inflammation?

A

Fever

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17
Q

What do endogenous pyrogens do?

A

Increase body temperature

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18
Q

What causes acute inflammation?

A 
Infection
Trauma
Agents
Tissue death
immune reactions
Foreign bodies
19
Q

What happen in acute inflammation?

A

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

20
Q

Define margination

A

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

21
Q

What happens when fluid leaks out?

A

More concentrated (more viscous) –> flow is slower

22
Q

How are leukocytes recruited?

A

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

23
Q

What are PECAM-1

A

Platelet endothelial cell adhesion molecules

  • Slip out and the chemokines interact
  • Under the influence of the chemokines it will migrate where it is needed
24
Q

How are leukocytes activated?

A

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

25
Q

How does phagocytosis work?

A

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)

26
Q

Down side to release of lysosomal enzymes to the outside?

A

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

27
Q

What is Amplification?

A

One macrophage gets there and calls others

ROS and lysosome kill the host cell causing inflammation which must then be terminated

28
Q

What is termination?

A

Neutrophils undergo apoptosis

Pro-inflammatory inducers disappar

29
Q

What if something can’t be repaired?

A

Fibroblast turn it into scarring

30
Q

Where does histamine come from and what does it cause?

A

Mast cells, basophils and platelets

Vasodilation, increased vascular permeability and endothelial activation

31
Q

Where does serotonin come from and what does it cause?

A

Platelets

Vasodilation and increased vascular permeability

32
Q

Where does TNF come from and what does it cause?

A

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

33
Q

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

A

Macrophages, endothelial cells and so epithelial cells

Similar to TNF; greater role in fever

34
Q

What are adalimumab and infliximab?

A

monoclonal antibodies that block TNF

35
Q

What are metabolites of arachidonic acid?

A

PGs
Leukotriens
Lipoxins

36
Q

What changes arachidonic acid to PGs?

A

cyclooxygenase

37
Q

What do TXA2 do?

A

Causes vasoconstriction and promotes platelet aggregation

38
Q

What does PGI2 do?

A

Causes vasodilation and inhibits platelet aggregation

39
Q

What does LXA and LXB do?

A

Inhibits neutrophil adhesion and chemotaxis

40
Q

NSAID do what?

A

Blocks cycloogenase

Blocks COX

41
Q

What does celecoxib block?

A

COX 2

42
Q

What does zileuton block?

A

Lipooxygenase

43
Q

PGs play a role in protecting what?

A

The stomach against acid in the stomach

Inhibiting COX 1 would cause the PGs to not be there to protect the stomach

44
Q

COX 1 stimulates what?

A

PGs

POD (10 decks)

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