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Pathology > Mediators of Inflammation > Flashcards

Mediators of Inflammation Flashcards

1
Q

What are mediators of inflammation?

A

Substances that initiate and regulate inflammatory reactions

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2
Q

Which cells secrete inflammatory mediators?

A

Macrophages, dendritic cells, mast cells

- other cells could also be induced: platelets, neutrophils, endothelial cells, epithelial cells

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3
Q

Where are mediators located inside cells?

A

Sequestered in intracellular granules for rapid secretion (histamine) or may be synthesized de novo (prostaglandins, leukotrienes, cytokines)

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4
Q

Mediators of inflammation are produced only _________

A

In response to various stimuli

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5
Q

How do inflammatory mediators function?

A

Bind to receptors on target cell to secrete additional inflammatory mediators

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6
Q

General characteristics of inflammatory mediators

A
  • have short half lives and quickly decay
  • are enzymatically destroyed
  • are scavenged by antioxidants
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7
Q

T/F: one mediator can stimulate the release of other mediators

A

True

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8
Q

Prostaglandins, leukotrienes, and PAF are from the ______

A

Plasma membrane

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9
Q

Nitric oxide is from ______

A

Macrophages

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10
Q

Defensins are produced ______

A

At the epithelial surface, will up regulate production when cell is induced

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11
Q

Inflammatory mediators from plasma proteins are constantly being secreted by the ________

A

Liver as precursors

- activated via proteolytic cleavage in circulatory system

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12
Q

Look at list of mediators and their source!!!

A

1st ppt

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13
Q

What are the 2 preformed inflammatory proteins?

A

Histamine: mast cells, basophils, platelets
Serotonin: mast cells, platelets

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14
Q

What are the functions of histamine?

A
  • vasodilation

- increased vascular permeability

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15
Q

What are 3 synthesized mediators?

A
  • cytokines
  • chemokines
  • arachidonic acid metabolites
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16
Q

Cytokines

A

Primarily produced by activated macrophages, lymphocytes, dendritic cells

  • regulate immune and inflammatory rxns
  • acute inflammation: TNF, IL-1, IL-6!!!
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17
Q

Functions of cytokines

A
  • endothelial activation
  • leukocyte recruitment
  • leukocyte activation
  • systemic acute phase response
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18
Q

TNF

A

Macrophages, mast cells, T cells

  • stimulates expression of endothelial adhesion molecules
  • secretion of other cytokines = systemic effects
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19
Q

IL-1

A

Macrophages, endothelial cells, some epithelial cells

- similar to TNF, greater role in liver

20
Q

IL-6

A

Macrophages

- systemic effects (acute phase response)

21
Q

Chemokines

A

Cytokines that promote leukocyte chemotaxis and migration

- IL-8: secreted by activated macrophages, endothelial cells = chemotaxis of neutrophils

22
Q

Arachidonic acid metabolites

A

Lipid mediators (prostaglandins, leukotrienes) produced from arachidonic acid present in membrane phospholipids

23
Q

What do prostaglandins and leukotrienes release?

A

Mechanical, chemical, physical stimuli releases AA from the membrane

  • prostaglandins: cyclooxygenase
  • leukotrienes and lipoxins: lipoxygnease
24
Q

AA metabolites function

A

Mediate virtually every step of acute inflammation!

  • vasodilation: prostaglandins
  • vasoconstriction: leukotrienes, thromboxane
  • increased vascular permeability: leukotrienes
  • chemotaxis, leukocyte adhesion: leukotrienes
25
Q

Which is more potent: leukotrienes or histamine?

A

Leukotrienes!

- more important for increasing vascular permeability

26
Q

Steroids inhibit ____

A

Phospholipases

27
Q

COX1 and COX2 inhibitors, aspirin, indomethacin inhibit _______

A

Cyclooxygenase

28
Q

Prostacyclin (PGI2)

A

Causes vasodilation, inhibits platelet aggregation

29
Q

Thromboxane A2

A

Causes vasoconstriciton, promotes platelet aggregation

30
Q

PGD2, PGE2

A

Causes vasodilation, increased vascular permeability

= pain, fever

31
Q

Leukotriene receptor antagonists inhibit

A

Leukotrienes C4, D4 and E4

- funciton in bronchospasm, increased vascular permeability

32
Q

5-HETE

A

Chemotaxis

33
Q

Complement

A

Collection of soluble proteins and membrane receptors that function in host defense
- present in inactive forms in the plasma, activated via antibody detection or direct microbe binding

34
Q

What are 3 functions of complement?

A
  • inflammation: C3a and C5a to stimulate histamine release (anaphylatoxins) –> C5a is a chemotactic for leukocytes
  • opsonization and phagocytosis: C3b when fixed to microbial cell wall acts as opsonin and promotes phagocytosis
  • cell lysis: deposition of membrane attack complex, kills by making cells permeable to water
35
Q

Activated factor XII (Hageman factor)

A

Activates intrinsic coagulation and catalyzes formation of kallikrein

36
Q

Brakykinin

A
  • short lived
  • increased vascular permeability
  • vasodilation
  • pain
37
Q

Kallikrein acts on ______ to form ______

A

Plasminogen; plasmin

- breaks down fibrin polymers and cleaves C3

38
Q

Coagulation factors require _______

A

Balance between formaiton and degradation of fibrin

  • fibrin polymers provide a surface to facilitate phagocytosis and prevent spread of infectious agents
  • excessive fibrin obstructs the microvasculature resulting in ischemic injury
  • excessive activation of fibrinolytic system leads to depletion of fibrinogen and possibly hemorrhage
39
Q

Oxygen derived free radicals

A

Released from neutrophils and macrophages following exposure to chemokines and after phagocytosis

  • lipid peroxidation
  • DNA damage
  • can alter signaling molecules (increase/decrease cytokines)
  • antioxidant mechanisms in place to minimize damage
40
Q

Nitric oxide

A

Synthesized by endothelial cells and macrophages

  • vasodilation
  • inhibits platelet aggregation and adhesion
  • oxidizes lipids
41
Q

Platelet activating factor

A
  • phospholipid derived mediator
  • leukocytes, platelets, endothelial cells can elaborate the factor
  • vasoconstriction and bronchoconstriction
  • 100 to 1,000x more potent than histamine!!
42
Q

Vasodilation

A
  • histamine

- prostaglandins (PGI2)

43
Q

Increased vascular permeability

A
  • histamine
  • serotonin
  • C3a and C5a by liberating vasoactive amines from mast cells
  • leukotrienes
44
Q

Chemotaxis, leukocyte recruitment and activation

A
  • TNF, IL-1, IL-8 (neutrophil chemotaxis)
  • chemokines
  • C3a, C5a
  • leukotriene B4
45
Q

Fever

A
  • IL-1, TNF

- prostaglandins

46
Q

Pain

A
  • prostaglandins

- bradykinin

47
Q

Tissue damage

A
  • lysosomal enzymes of leukocytes

- reactive oxygen species

Pathology (19 decks)

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