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Pathology > 2.5 Inflammation and adhesion > Flashcards

2.5 Inflammation and adhesion Flashcards

1
Q

Stimuli for Inflammation

A 
infection, 
truama, 
physical chemical agents, 
necrosis, 
foreign bodies, 
immune reactions (foreign and auto)
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2
Q

features of inflammation

A 
complex, 
nonspecific, 
mostly vascular and connective tissue reaction to injury,
 migration of leukocytes, 
systemic reactions, 
closely linked to immune system, 
coagulation system and repair process
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3
Q

Goal of inflammation

A

to eliminate, dilute or wall off injurious agent, but can be very harmful

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4
Q

inflammation overlaps with

A

immunity,
coagulation,
repair

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5
Q

host resistance is divided into

A

innate and adaptive immunity

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6
Q

coagulation system is divided into

A

dual function of clotting factors and factors as mediators

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7
Q

usually inflammation leads to

A

induction of repair and repair inhibits inflammation. But not always resulting in disease

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8
Q

inflammation time course can be

A

acute or chronic (granulomatous)

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9
Q

5 cardinal signs of acute inflammation

A

rubor, tumor, calor, dolor, functio laesa

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10
Q

rubor

A

redness

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11
Q

tumor

A

swelling

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12
Q

calor

A

heat

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13
Q

dolor

A

pain

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14
Q

functio laesa

A

loss of fn

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15
Q

cells of inflammation

A

neutorphil, basophil, platelet, eosinophil, monocyte/macrophage, lymphocyte, plasma cell

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16
Q

neutrophil

A

poly or PMN (many lobed nucleus) seen in acute inflammation

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17
Q

basophil

A

accute/allergic - dark granules

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18
Q

platelet

A

acute

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19
Q

eosinophil

A

chronic/allergic

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20
Q

monocyte/macrophage

A

chronic - kidney shaped nucleus

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21
Q

lymphocyte

A

chronic - little bigger than a red cell

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22
Q

plasmacell

A

chronic - eccentric nucleus filled with mrna for Ig

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23
Q

difference btw eosinophil and mast cell

A

eosinophil will be red granules and mast cell will be purpleish

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24
Q

band form

A

immature neutrophil looks like a wll defined horse shoe - not normal to have lots - tells you there is overproduction

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25
Q

other cells also important for inflammatory process

A

fibroblasts

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26
Q

simple demonstration of inflammatory response

A

wheal and flare reaction

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27
Q

first thing when you scrape arm

A

goes white due to vasoconstriction of arteries and arterioles

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28
Q

why does the white scratch turn red

A

you induced an inflammatory response so there is hyperemia as more blood rushes there

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29
Q

what governs efflux and influx of fluid in vessels

A

mediators - inflammation gets things out of the vessels where you need them,
they don_t have to be damaged and leaky bc the mediators will direct them

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30
Q

transudate

A

fluid accumulation in body cavity with low protein/specific gravity - ultrafiltrate - i.e. water squeezed out of vessels

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31
Q

exudate

A

fluid accumulation in body cavity with high protei/ specific gravity

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32
Q

edema

A

interstitial fluid accumulation (may be transudate or exudate)

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33
Q

purulent

A

pus

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34
Q

exudate in lungs

A

pneumonia

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35
Q

transudate in lungs

A

heart failure

36
Q

duet to normal laminar flow and arterial and venou pressure

A

hydrostatic pressure forces fluid out and osmotic pressure draws fluid back in but only 80%. The other 20% goes to lymphatics

37
Q

with increased flow during vasodialation you get

A

increased hydrostatic pressure and transudate

38
Q

when endothelial cells get “leaky” you get

A

exudate - endothelial cells have increased permeability for proteins increasing the osmotic pressure

39
Q

hemoconcentration and stasis

A

loss of lamnar flow, rolling, attachment, transmigration

40
Q

factors affecting vascular permeability (leakage)

A 
endothelial gap formation, 
endothelial retraction, 
increasaed trancytosis, 
direct injury, 
delayed prolonged leakage (like sunburn), 
leukocyte-mediated damage, 
leakage from new blood vessels
41
Q

Endothelial gap formation

A

most common mechnaism of non damage active vascular leakage

42
Q

endothelia gap formation is the major effecto of mediators such as

A

histamine, bradykinin, leukotrienes, substance P

43
Q

where does endothelial gap formation occur

A

exclusively in post capillary venules of 20 to 60 um in diameter (receptor density)

44
Q

how long does endothelia gap formation last

A

rapid and short lived - immediate transient response

45
Q

cytoskeletal reorganization/endothelial retraction

A

cytoskeleton changes and endothelial cells retract from one another

46
Q

how is endothelial retraction induced

A

by cytokines such as Il1 and TNF alpha or hypoxia and sublethal injury

47
Q

how long does cytoskeletal reorganization take

A

endothelial retraction is delayed 4-6 hrs and lasts longer up to 24 hrs

48
Q

is endothelial retraction localized

A

not perfectly localized bc injury can induce it

49
Q

increased trancytosis

A

movement of fluid and material across endothelial cytoplasm, occurs through clusters of uncoated vesicles and vacuoles called the vesiculovacular organelle

50
Q

how is trancytosis induced

A

vascular endothelial growht factor (VEGF) - also may be induced by histamine

51
Q

Direct endothelial injury resulting in necrosis results in

A

leakage from damaged vessels, immediate and long lasting (immediate sustained response), happens in small and large vessels, and is associated with platelet aggregation and thrombosis

52
Q

Delayed prolonged leakaged

A

2-12 hours lasting for hours to dayes, occurs at venules and capilaries

53
Q

how is delayed prolonged leakage induced

A

by mild thermal burns, ionizing and UV radiation (sunburn–get pain not just on skin but all over, chills..)

54
Q

delayed prolonged leakage mechanism

A

maybe apoptosis from DNA damage

55
Q

leukocyte mediated damage

A

leukocytes adhere to activated or damaged endothelium, secrete reactive and toxic products that damage self as well as microbes, location dependent on why and where leukocytes bind

56
Q

leakage from new blood vessels

A

during repair angiongenesis occurs and new vess are nleaky before new endothelial cells fully differentiate and form gap junctions, VEGF induces increased vascular permeability, new endothelium has an increased density of receptors for vasoactive signals

57
Q

what allows for pure collection of white exudate (pus)

A

mediators allowing collection of neutrophoils - so don’t need vessel trauma for inflammation

58
Q

Margination

A

a hemodynamic effect where lamina flow of leukocytes changes to peripheral and contacto vascular wall duing stasis

59
Q

rolling-adhesion-extravasation occurs by

A

modulating various adhesion molecules on the surface of endothelial cells and leukocytes

60
Q

rolling-adhesion-extravasation is mediated by

A

secreated or formed inflammatory mediators

61
Q

rolling-adhesion-extravasation strategies are to

A

increase the number of receptors and increase affinity of receptors for ligands

62
Q

endothelium molecules

A 
p-selectin, 
e-selectin, 
ICAM-1, 
VCAM1, 
CD 34/GlyCam, 
CD31
63
Q

P-selectin

A

sialyl-lewis X and PSGL-1 (rolling: N, M, L)

64
Q

E -selectin

A

sialyl-lewis X (rolling adhesion: N, M, L)

65
Q

ICAM - 1

A

CD11/18 (beta2 integrins, aka LFA1 and Mac-1) (adhesion, arrest and transmigration: all leukocytes)

66
Q

Vcam-1

A

VLA4 (alpha4beta1) (integrins) and LPAM-1(alpha4beta7) (adhesion E,M,L)

67
Q

CD-34/GlyCam

A

L-selectin (rolling; lymphocyte homing: L)

68
Q

CD31 (PECAM)

A

CD31 (transmigration:all)

69
Q

Selectins

A

have an extracellular sugar binding domain similar to lectins. They bind sialyated oligosaccharides

70
Q

knock out L selectin

A

poorly formed LNs and few t cells

71
Q

knock out either E or P selectin

A

mind effects bc the other compensates

72
Q

knock out both e and p selectin

A

severe effects

73
Q

immunoglobulin like molecules

A

ICAM-1, VCAM-1 (both bind integrins on leukocytes)

74
Q

integrins

A

transmembrane heterodimer glycoproteins with alpha and beta chains

75
Q

beta 2 integrins

A

LFA1 and MAC1 (bind ICAM1)

76
Q

beta 1 integrins

A

VLA4 and LPAM1 (bind to VCAM1)

77
Q
  1. histamine, thrombin and PAF induce
A

the redistribution of P-selectin from intracellular sotres (weible-palade bodies) to the surface (takes minutes)

78
Q
  1. Tnf and IL1 induce
A

the synthesis of E-selectin ICAM1, VCAM1 (takes 1-2 hours)

79
Q

3.luekocyte specific chemokines alter

A

conformation of LFA-1 and MAC-1 increasing the affinity of binding to ICAM 1.
requires ICAM1 and synthesis of chemokines by othercells (late response)

80
Q
  1. early endothelial activation i.e.
A

rolling (selectins and sialyl-lewis X)

81
Q
  1. later synthesis of
A

endothelial adhesion molecules and increased affinity of LFA1 and MAC1 –firm adhesion

82
Q
  1. CD31, ICAM and integrins result in
A

transmigration

83
Q

genetic deficiency called leukocyte adhesion deficiency type 1 (LAD1)

A

def in LFA1 and Mac

84
Q

LAD2

A

def in sialyl-LewisX - big problem with leukocyte accumulation

85
Q

antibidies to adhesion molecules can block inflammation like

A

Natalizumab

86
Q

natalizumab

A

humanized monoclonal AB to VLA4 (alpha4beta1interin) to treat MS

87
Q

negative effect of natalizumab

A

bind up all the vla4? So no adhesion of leukocytes

Pathology (26 decks)

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