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Pathology > Inflammation--Exam 2 > Flashcards

Inflammation--Exam 2 Flashcards

1
Q

Why is initial vasconstriction with acute inflammation important?

A

allows for coagulation

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2
Q

Name 4(5) mediators of vasodilation in acute inflammation

A

histamine
serotonin
Nitric Oxide
Prostaglandins D2 and E2

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3
Q

Principle mediator of vasodilation in acute inflammation? Its source?

A

Histamine; mast cells

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4
Q

Name the 3 histamine receptor subtypes, their location, and if it’s “go” or “stop”

A

H1–on endothelium; “go”

H2–GI tract; “go”

H3–nerve terminals; “stop”

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5
Q

What is the stimulus for serotonin release

A

platelet stimulation and aggregation

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6
Q

3 sources of nitric oxide?

A

endothelial cells–eNOS
macrophages–iNOS
neurons–nNOS

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7
Q

Primary target and action of NO?

A

Targets vascular smooth muscle; causes relaxation (vasodilation)

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8
Q

Name 3 important products of COX pathway?

A

1) Prostacyclin (PGI2)
2) Thromboxane (TXA2)
3) Prostaglandins (PGD2/E2)

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9
Q

Function of PGI2 (prostacyclin)

A

inhibits platelet aggregation; potentiates permeability

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10
Q

Function of TXA2 (thromboxane)

A

STOP SIGNAL

causes platelet aggregation and vasoconstriction

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11
Q

Which neurotransmitter can stimulate nNOS release?

A

Glutamate

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12
Q

What are 3 mechanisms to increase endothelial cell permeability?

A

1) endothelial gap formation
2) non-leukocyte mediated damage
3) leukocyte mediated damage

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13
Q

Uses neurokinin receptors to cause contraction of endothelial cells

A

Substance P

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14
Q

What substance from leukocytes and endothelial cells helps regulate permeability?

A

Bradykinin

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15
Q

Leukotriene that is a chemotactic agent and activator of neutrophils?

A

LTB4

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16
Q

Cyteinyl-containing leukotrienes…cause bronchospasms and increase permeability

A

LTC4, C4, and E4

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17
Q

Where does endothelial gap formation occur?

A

Post-capillary venules

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18
Q

Mechanisms of endothelial gap formation

A

1) cellular contraction
2) increased transcytosis
3) new blood vessel formation

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19
Q

Differentiate btwn the two length of responses

1) immediate sustained
2) delayed prolonged

A

1) directly damages cells causing immediate death and loss of function
2) accumulation of damage induces cell apoptosis

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20
Q

How is fibrin formed?

A

Fibrinogen is cleaved by thrombin to form fibrin

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21
Q

two mechanisms for exudate formation?

A

1) endothelial cell damage

2) increased permeability

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22
Q

Bacterial infections are associated with what type of exudate?

A

Suppurative/purulent

23
Q

Which type of exudate is associated with mucosal surfaces?

A

Catarrhal

24
Q

L-selectins:
expressed on which cells?
Bind to what?

A

Expressed on activated leukocytes

bind to glycoproteins on endothelial cells

25
Q

P-selectins
expressed on which cells?
stored?

A

expressed on endothelium

stored in weibel-palade bodies

26
Q

What two things bind to form a strong bond btwn leukocyte and endothelial cell?

A

Integrins on leukocyte bind to ICAMs on endothelial cells (Ig superfamily)

27
Q

Beta-2 integrins are found on?

CD11d/CD18 found on?

A

beta–>on ALL leukocytes

CD11d/CD18–> macrophages and cytotoxic T-cells

28
Q

Which molecule is upregulated during emigration and mediated diapedesis?

A

PECAM-1 (CD31)

29
Q

An exogenous mediator (AA) unique to prokaryotes that can bind leukocyte receptors

A

N-formyl methionine

30
Q

Name 3 important ENDOGENOUS mediators for leukocyte chemotaxis

A

C5a
LTB4
IL-8 (from activated lymphocytes and macrophages)

31
Q

What important molecule is made available when leukocytes undergo an oxidative burst

A

NADPH

32
Q

What two products can be made from H2O2?

A

1) HOCL (using myeloperoxidase)

2) OH (fenton reaction)

33
Q

Which non-oxygen dependent mechanisms share the same mechanism?

A

Bactericidal permeability increasing proteins

Defensins

34
Q

What cytokines do lymphocytes and macrophages use to communicate with each other?

A

Macrophage secretes IL-1 and TNF to activate lymphocyte

Lymphcytes secrete INF-y to activate macrophages

35
Q

Classic activation of macrophages:
Driving mediators?
Type of response stimulated?

A

Mediators–>IFN-y & IL-12

Th1 response

36
Q

Alternative activation of macrophages:
Driving mediators?
Type of response stimulated?

A

Mediators–>IL-4, IL-13

Th2 response

37
Q

Which lymphocytes are the first to arrive with chronic inflammation? Purpose?

A

Gamma/delta T-lymphocytes

contribute to granuloma formation

38
Q

Which lymphocytes (general) regulate the type of immune response that ensues

A

Alpha/beta lymphocytes (CD4, CD8)

39
Q

Important products of T regulatory lymphocytes

A

IL-10, TGF-b

40
Q

Dendritic cells express:

1) when naive
2) when mature

A

1) CCR6

2) CCR7

41
Q

CCR7 binds what cytokine in the paracortical region?

A

CCL21

42
Q

Type 1 interferon induces what response?

A

Th1 response

43
Q

Granuloma with central necrosis; Langhan’s giant cells have nuclei around periphery

A

Immune granuloma

44
Q

Granuloma due to foreign material; giants cells have nucei in center of cell

A

Foreign body granuloma

45
Q

What 3 things do PPARs inhibit to stop inflammation?

A

NFkB
STATs
AP-1

46
Q

4 possible outcomes of inflammation

A

resolution
regeneration
repair by fibrosis
abscess formation

47
Q

Interaction in ECM are mediated by what?

A

Integrins

48
Q

What is copper required for?

A

Cross-linking of procollagen via lysyl hydroxylase

49
Q

Role of HIF in angiogenesis?

A

in hypoxic conditions, HIF is NOT hydroxylated and goes on to stimulate genes necessary for angiogenesis

50
Q

Order of events in angiogenesis

A 
Digestion
Migration
Proliferation
Maturation
Perivascular cell migration
51
Q

Response produced when:

1) VEGF–>VEGF-R1
2) VEGF–>VEGF-R2
3) Ang1–>tie 2
4) Ang2–>Tie 2

A

1) tube formation
2) proliferation
3) maturation of vessel
4) inhibitory to VEGF

52
Q

Function of MMPs? What inhibits them?

A

degrade ECM in organized manner; inhibited by TIMPs

53
Q

Which growth factor, from macrophages and platelets, is central in fibroblast activity and collagen deposition

A

TGF-b

54
Q

How do corticosteroids inhibit healing?

A

inhibit TGF-b

Pathology (6 decks)

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