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Pathology Midterm > Inflammation (part 2) > Flashcards

Inflammation (part 2) Flashcards

1
Q

cells move out of vessels into the area of inflammation recruited by ________ agents

A

chemotactic

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2
Q

name the 4 stages of the cellular events of inflammation

A
  1. margination and rolling of WBC
  2. Migration of leukocytes
  3. chemotaxis
  4. phaocytosis
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3
Q

what are eicosanoids

A

lipid mediators in the innate immune repsonse

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4
Q

name the 3 cell signaling molecules in the inflammatory process

A

1st, lipid mediators (eicosanoids) are released from activated cells - early recruitment of inflammatory cells from the bone marrow into vascular system

proinflammatory cytokines activate resident tissue cells

these resident tissue cells release chemokines to amplify inflammatory cell recruitment

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5
Q

leukocyte tethering/rolling is mediated by….

A

selectins

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6
Q

transmigration is also known as….

A

diapedesis

leukocyte crossing tight junction between endothelial cells

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7
Q

what inflammatory mediators are involved in firm adhesion and diapedesis

A

chemokines – induce the expression of icams to allow for tight adhesion

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8
Q

what is marginationn/tethering

A

leukocytes moving from axial flow to the margin of the vessels

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9
Q

marginated leukocytes begin to roll on the endothelial surface by transient adhesion molecules.
WHAT ARE THESE MOLECULES

A

selectins

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10
Q

adhesion of PMNs to endothelium occurs via…..

A

selectins and integrins

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11
Q

what structure ON THE LEUKOCYTE mediates firm adhesion to endothelial cells

A

beta 2 integrins – binds to icam 1

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12
Q

leukocyte diapedesis occurs mostly where?

A

in postcapillary venules

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13
Q

name 3 different selectins.
what is their general function

A

P-selectin
L-selectin
E-selectin

aid in tethering/rolling

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14
Q

ICAM-1 binds to….

A

beta 2 integrins on the leukocyte

aids in adhesion, arrest, and transmigration

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15
Q

what is another term for CD31

A

PECAM-1

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16
Q

what does CD31/PECAM-1 do

A

involved in arrest and transmigration

on the endothelial cell AND leukocyte

MAJOR MEDIATOR OF DIAPEDESIS

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17
Q

of the selectins, which is the only one to NOT roll lymphocytes?

A

L-selectin

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18
Q

what accomplishes firm adhesion

A

integrins

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19
Q

define chemotaxis

A

process in which WBCs are attracted to the inflammation area according to the high concentration of certain products (ie: CXCL8/C5a/leukotriene b4)

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20
Q

explain the mechanism of phagocytosis

A

bacterium containing opsonins such as C3b gets recognized by neutrophil C3b receptor and gets internalized through changes in the cytoskeleton. pseudopods form around teh microbe to enclose it within a phagosome. the phagosome releases ROS (O2 becomes O2- by NADPH oxidase and rapidly converted to H2O2.

primary granules containing “_ases” are released. phagosome fuses with lysosome to form a PHAGOLYSOSOME. death of pathogen and neutrophil itself

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21
Q

name 6 phagocytic cells

A

microglia in the brain
macrophages
neutrophils
monocytes
dendritic cells
osteoclasts

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22
Q

true or false

leukocytes can also kill microorganisms by nonoxidative mechanisms

A

true

-lysosomal hydrolases
-defensins
-lactoferrin
-lysozyme
etc

23
Q

disease: LAD (leukocyte adhesion deficiency)

what is the defect?

A

LAD-1 - defective B2 integrin expression or function

pathogenesis - leukocytes can’t reach the site of infection and no damage is done to the pathogen

24
Q

disease: hyper IGE recurrent infection syndrome

what is the defect?

A

poor chemotaxis

25
Q

disease: chediak-higashi syndrome

what is the defect

A

defective lysosomal granules, poor chemotaxis

26
Q

disease: neutrophil-specific granule deficieny
what is the defect

A

absent neutrophil granules (AND THUS DEFECTIVE PHAGOCYTOSIS)

27
Q

disease: chronic granulomatous disease

what is the defect

A

deficient NADPH oxidase with absent H2O2 production.

inability to destroy pathogen with ROS

28
Q

vasoactive mediators cause what?
name some vasoactive mediators

A

cause vasodilation and increased vascular permeability, leading to EDEMA

histamine
serotonin
bradykinin
anaphylatoxins

29
Q

what do chemotactic factors do? name some chemotactic factors

A

recruit and stimulate inflammatory cells

C5a
chemokines

30
Q

name 3 things involved in acute inflammation and 3 things involved in chronic inflammation

A

acute:
neutrophils
platelets
mast cells

chronic:
macrophages
lymphocytes
plasma cells

31
Q

mediators may be produced either ___ or ____

A

locally by cells at the site of inflammation OR circulate in the plasma (typically synthesized by the liver)

32
Q

name 3 plasma derived mediators as well as how they circulate and how they’re activated

A

circulate as inactive precursors and are activated by proteolytic cleavage

complement, kinin, and coagulation cascasdes

33
Q

name 5 cell derived mediators and how they’re stored, and activated

A

histamine
serotonin
bradykinin
prostaglandins
leukotrienes

stored in intracellular granulation and are secreted upon activation

34
Q

most mediators act by..

A

binding to specific receptors on target cells

35
Q

true or false

mediators only have 1 target

A

FALSE

may only have one, a few, or many targets

36
Q

mediators can stimulate their target cells to do what

A

release secondary effector molecules

37
Q

true or false

mediator function is generally tightly regulated

A

TRUE

mediators can be potentially harmful, so they quickly decay once activated and released from the cell. they are inactivated by enzymes and are either eliminated or inhibited

38
Q

all 3 plasma derived cascades – coagulation, kinin and complement — are mechanistically linked by initial activation of what?

A

HAGEMAN FACTOR – factor XII of the coagulation cascade

39
Q

what is factor 12 (hageman factor) synthesized by? how is it activated?

A

synthesized by the liver and circulates in inactive form. is activated by collagen, basement membrane, or activated platelets

40
Q

what is responsible for pain during inflammation

A

bradykinin

41
Q

kinins act quickly and are rapidly inactivated by….

A

kinases

42
Q

name 4 effects of activation of Hageman factor (factor 12)

A

-conversion of plasminogen to plasmin (cleaves complement components to generate anaphylotoxins C3a and C5a)
-conversion of prekallikrein to kallikrein (cleaves HMWK to kinins)
-activation of alternative complement pathway
-activation of the coagulation system

43
Q

_____ separate pathways can activate complement to form the membrane attack complex

A

THREE – alternative, classical, mannose binding

44
Q

name 3 anaphylotoxins

what do they do

A

C3a, C4a, C5a

mediate smooth muscle contraction (bronchial and vascular constriction) and increase vascular permeability (EDEMA)
-partly through stimulating mast cells which releases histamine causing vasoconstriction

PROINFLAMMATORY

45
Q

name 2 opsonins

what do they do

A

C3b iC3b

bind to bacterium and enhance phagocytosis by allowing receptors on phagocytic cell membranes to recognize and bind

46
Q

name 2 proinflammatory molecules

what do they do

A

C5a and MAC (membrane attack complex)

induce mast cell and basophil degranulation

47
Q

what does factor p (properdin) do

A

stabilizes C3 convertase - C3bBb on pathogen surface

48
Q

what does factor H do?

A

works with factor I to turn C3b to iC3b (inactivated)

factor I is the one that actually cleaves

49
Q

what does DAF and MCP do

A

disrupts C3 convertase - C3bBb on human cell surface and inactivates it to iC3b

MCP uses factor I to cleave

second class of complement control proteins

50
Q

another name for MCP

A

protectin

51
Q

explain anaphylactic shock

A

sudden blood pressure drop, airways narrow which blocks breathing

rapid, weak pulse, skin rash, nausea, vomiting

52
Q

what can cause anaphylaxis

A

too many anaphylotoxins due to sepsis and other conditions

53
Q
A

Pathology Midterm (10 decks)

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