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Cell Pathology 2 (Pathology) > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is the main role of the selectin family of proteins?

A

Mediates the rolling interactions of leukocytes on the vessel wall.

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2
Q

What do selectin molecules bind to on leukocytes?

A

The ligands for selectins are the Sialyl-Lewis X oligosaccharides that are on leukocytes. This is how they mediate the rolling effect of leukocytes along the vessel wall.

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3
Q

What induces release of P-selectin, and from what cell? What induces the release of E-selectin, and from what cell?

A

P-selectin release is induced by histamine from Weibel-Palade bodies on endothelial cell granules.
E-selectin release is induced by TNF and IL-1 and is from endothelial cells

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4
Q

What family of proteins mediates the adhesion of leukocytes (specifically neutrophils) to the endothelium?

A

The integrins

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5
Q

What two molecules upregulate the expression of integrins on the vessel wall?

A

TNF and IL-1 upregulate integrins

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6
Q

What are the two main integrin proteins that are upregulated on the vessel wall?

A

VCAM-1 and ICAM-1

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7
Q

What upregulates the expression of integrins on leukocytes?

A

C5a and LTB4

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8
Q

What is the most likely cause of leukocyte adhesion deficiency?

A

Most commonly due to autosomal recessive defect of integrins (CD18 subunit)

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9
Q

What is the physiologic process that produces exudate? Transudate?

A

Exudate is produced by an increase in permeability of small blood vessels due to ongoing inflammatory response. Transudate is produced as a result of osmotic or hydrostatic imbalances.

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10
Q

What cell type contains the most histamine that is released in acute inflammation?

A

Mast cells

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11
Q

What are the activator of mast cells?

A
  1. trauma
  2. complement proteins C3a or C5a
  3. Antigen binding to IgE and cross linking (allergies happen via this mechanism)
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12
Q

Where are mast cells located?

A

In the connective tissue surrounding endothelial cells

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13
Q

What two lipid mediators of the acute inflammation are produced from arachidonic acid?

A

Prostaglandins and leukotrienes

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14
Q

What acts on the phospholipid cell membrane to release arachidonic acid?

A

phospholipase A2

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15
Q

What two enzymes act on arachidonic acid to create (1) prostaglandins and (2) leukotrienes?

A

(1) cyclooxygenase and (2) 5-lipoxygenase

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16
Q

Which prostaglandin are major players in vasodilation (at the level of the arteriole) and vascular permeability (at the post-capillary venule)?

A

PGI2, PGD2, and PGE2.

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17
Q

What prostaglandin mediates pain and fever?

A

PGE2 (feeever)

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18
Q

Which leukotriene is a key attractant for neutrophils during an acute inflammatory response?

A

LTB4

19
Q

Which leukotrienes are involved in vasoconstriction, bronchospasm, and increased vascular permeability of the venules?

A

LTC4, LTD4, and LTE4

20
Q

By what mechanism do NSAIDS reduce pain?

A

Pain is mediated by the prostaglandin PGE2. NSAIDS block the COX enzymes which create prostaglandins including PGE2.

21
Q

Which eicosanoids are involved in vasodilation?

A

PGI2, PGE1, PGE2, and PGD2

22
Q

Which eicosanoids are involved in vasoconstriction?

A

TXA2, LTC4, LTD4, LTE4

23
Q

Which eicosanoids are involved in increased vascular permeability?

A

LTC4, LTD4, and LTE4 (the leukotrienes)

24
Q

Which eicosanoids are involved in chemotaxis and leukocyte adhesion?

A

LTB4

25
Q

What receptor is present on cells of the innate immune system and are activated by pathogen-associated molecular patterns?

A

Toll-like receptors

26
Q

What is the mechanism by which toll-like receptors are activated and how they produce multiple immune mediators?

A

TLRs are activated when pathogen-associated molecular patterns are recognized by CD14 (a coreceptor for TLR4) on the outside of gram negative bacteria.
They function by upregulation NF-kB which activates immune response genes leading to production of many mediators.

27
Q

What are the key roles of TNF and IL-1?

A

Key role in induction of the systemic acute-phase response.

  • in endothelial activation (allowing for neutrophil arrival and function; via E selection induction and cell adhesion molecules)
  • for induction of fever
  • for production of leukocytes
28
Q

How is fever induced in an inflammatory response?

A

Pyrogens (eg from bacteria) cause macrophages to release IL-1 and TNF which increase COX activity in the perivascular cells of the hypothalamus.
fever is also induced

29
Q

What 3 factors attract neutrophils to the site of injury?

A

IL-8, C5a, LTB4, and bacterial products

30
Q

What is the pathway by which HOCl is generated?

A

O2 -> O2- via NADPH oxidase
O2- -> H2O2 via superoxide dismutase
H2O2 -> HOCL by myeloperoxidase (MPO)

31
Q

What are NETs?

A

Neutrophil extracellular traps which provide a high concentration of antimicrobial substance sat site of infection and prevent the spread of microbes by trapping them.

32
Q

What type of proteins enhances phagocytosis of neutrophils?

A

Opsonins (IgG and C3b)

33
Q

What are the 3 ways that the complement protein C3 can become cleaved?

A

Classical: C1 binding to IgM or IgG bound to antigen
Alternative: microbial products activate complement
Lectin: mannose-binding lectin in plasma binds to carbohydrates on microbes and directly activates C1

34
Q

Which complement protein acts as a C5 convertase to make C5a and C5b?

A

C3b (cleaved from C3 to make C3a and C3b)

35
Q

How is the MAC formed?

A

C5b binds C6-C9 to make the MAC and lyse cells

36
Q

Which complement proteins stimulate histamine release?

A

C3a, C5a and C4a

37
Q

Which complement proteins are chemotaxic for neutrophils, eosinophils, and basophils?

A

C5a

38
Q

Which complement proteins are opsins?

A

C3b

39
Q

What is a factor of the coagulation cascade that is also an inactive proinflammatory protein? How does it become active?

A

factor XII. Activated when XII leaks out of vessels and comes in contact with extracellular components. Activates kinin and coagulation cascades

40
Q

What does factor XIIa do that connects it to the inflammatory response?

A

Cleaves C3 in the complement protein system

41
Q

What are the 3 morphological patterns of acute inflammation?

A

Serous inflammation
Fibrinous inflammation
Purulent (suppurative) inflammation

42
Q

What characterizes serous inflammation?

A

Marked by the exudation of cell-poor fluid into spaces created by cell injury or into body cavities.

43
Q

What characterizes fibrinous inflammation?

A

Fibrinous exudate develops when the vascular leaks are large (happens with a more pronounced increase in vascular permeability.

44
Q

What characterizes purulent inflammation?

A

Characterized by production of pus, especially as in an abscess

Cell Pathology 2 (Pathology) (9 decks)

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