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Block 1 Week 5 > Plasma > Flashcards

Plasma Flashcards

1
Q

What is plasma?

A
  • the fluid left over after blood cells are removed

- it can clot

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2
Q

What is Serum?

A

-the fluid left after the blood clot (plasma) and cells are removed

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3
Q

The liver and chemical mediators of inflammation?

A
  • liver is systemic source of some

- bacteria induces macrophages to make IL-6; acts on live to produce mediators

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4
Q

Mediators consitituvely produced or regulated?

A

-both; they are constitutively produces at low levels, but when PAMPs are activated, cascade events cause sliver to produce at much higher level

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5
Q

four mediators liver secretes? What are they in response to?

A

1) C-reactive protein (CRP)
2) Mannose-Binding Lectin
3) Serum Amyloid Portein
4) Fibinogen

-in response to systemic IL-6, IL-1, TNF (bacteria infection)

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6
Q

C-reactive protein (CRP)

A
  • CRP binds phosphocholine on bacteria
  • acts as opsonin
  • activates complement
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7
Q

Mannose-binding lectin?

A
  • mannose-binding lectin binds residues on bacterial surfaces
  • acts as opsonin
  • activates complement
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8
Q

What does high levels of CRP in the blood indicate?

A
  • used as diagnostic measure of ongoing inflammation (acute/chronic)
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9
Q

How distinguish self mannose from bacteria?

A

-bacterial mannose is structurally different from how humans make it

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10
Q

What comprises the Pentraxin family?

A

1) CRP: opsonization; complement activation

2) SAP: opsonization, complement activation, binding of mannose/glucose

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11
Q

Serum Amyloid Portein (SAP)

A
  • secreted by liver
  • opsonization,
  • complement activation
  • binding of mannose/glucose
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12
Q

opsonin

A

-a molecule that binds a pathogen, coats it in opsin, and facilitates phagocytosis of the opsin coated pathogen

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13
Q

Opsonization

A
  • the process by which a pathogen (virus, fungi or bacteria) is marked for ingestion and destruction by a phagocyte
  • done by opsonin
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14
Q

What is the benefit of opsonization?

A
  • so phagocytes only need receptors for opsin, and not for each individual type of pathogen
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15
Q

How do CRP/SAP do opsinization?

A
  • CRP and SAP bind microbial cell walls, coating the pathogen and facilitating phagocytosis
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16
Q

Complement

A
  • primary mechanism by which pathogen recognition is immedietly converted into an effective host defense against infection
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17
Q

What are the complement proteins? What form are these proteins typically in?

A
  • numbered C1-C9
  • are present as inactive forms in plasma
  • get activated into proteolytic enzymes that degrade & activate downstream complement components
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18
Q

What do complement proteins trigger?

A
  • trigger cascade amplification of inflammation

- by activating into protelotyc from, that degrade & activate downstream complement components

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19
Q

3 pathways that lead to complement activation

A

1) Classical Pathway
2) MB-Lectin Pathway
3) Alternative Pathway

all three lead to the single pipeline that is the complement pathway activation

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20
Q

Classical pathway, what is it dependent on?

A
  • the first discovered
  • activated by antigens binding to antibody & making a complex
  • dependent on ADAPTIVE IMMUNITY (antibodies)
  • leads to complement activation
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21
Q

MB-Lectin Pathway

A
  • activated by lectin binding to pathogen surfaces

- activated complement pathway

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22
Q

alternative pathway

A

activated by the surface of pathogens

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23
Q

what are the three outcomes of complement activation? Do all 3 happen ALL the time when complement pathway is activated?

A

1) recruitment of inflammatory cells
2) opsonization of pathogens
3) killing of pathogens

YES, once complement activated ALL happen

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24
Q

What is the complement pathway?

A

-complement pathway is a single pipeline having three entry points and three exit points

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25
Q

What is the key step that the 3 complement pathways share? What is the result of this step?

A
  • generation of protease C3 convertase which produces C3b

- once made, there are three outcomes (all happen)

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26
Q

3 outcomes after C3 convertase generation? Where is C3 convertase put?

A

1) inflammation
2) Phagocytosis
3) Lysis of Microbe

C3 convertase is deposited onto the microbe

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27
Q

C5A/C3a

A
  • peptide mediators of inflammation
  • promote phagocyte recruitment
  • heavily involved with inflammation/anaphalaxsis
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28
Q

phagocytosis pathway steps after C3B generation? what pathways help with this outcome?

A

1) opsinozation of pathogens by addition of C3b coat
2) C3b binds to phagocyte
4) removal of immune complexes

*alternative & MBL pathway?

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29
Q

C3b

A
  • activated by generation of C3 convertase
  • binds to C3b receptors on phagocytes
  • opsinozation of pathogen
  • removal of immune complexes
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30
Q

lysis pathway steps after C3B generation? specific effectors used & their function?

A

1) C3b produces terminal complement components
2) these form the Membrane-Attack complex (MAC)
3) MAC causes lysis of certain pathogens & cells

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31
Q

MAC complex?

A
  • a pore that goes into pathogen, pathogen guts leak out & pathogen lysed/dies
  • allows fluid and ions to enter, causing cell lysis of pathogens
32
Q

How C5A/C3a promote inflammation?

A
  • cause vascular permeability/edema, icnrease cell adhesion moelcuels on vascualature which facilitate immune cells in blood to leave blood
  • promote phagocyte recruitment
33
Q

Does deficiencies leading to decreased formation of MAC cause major immune susceptibilities?

A 
No
-is primarily increased susceptibility to only one class of organisms, Neisseria
34
Q

the single common wayC3a, C5a, C4a amplify inflammation?

A

all 3 cause histamine release from mast cells; increase vascular permeability, cause vasodilation

35
Q

2 unique ways C5a amplify inflammation?

A

1) C5a activates lipoxygenase pathway of AA in neutrophils and monocytes
2) C5a a chemoattractant for monocytes, neutrophils, eosinophils, basophils

36
Q

1 unique way C3 amplify inflammation?

A

C3 acts as opsonins when fixed to bacterial cell walls and promote phagocytosis by macrophages and neutrophils

37
Q

anaphylatoxins

A

when histamine is stimulated to release from mast cells (increase vascular permeability, cause vasodilation)

38
Q

What if fail to activate complement?

A

1) Increased susceptibilities to fatal infections
2) Deficiencies associated with decreased MAC formation
3) Deficiencies in C2 and C4

39
Q

Deficiencies in C2 and C4 cause susceptibility to what?

A

associated w/ autoimmune disorders (lupus) cuz immune complexes can’t be efficiently cleared

40
Q

how regulate C3 & C5?

A
  • is key inhibitory point
  • DAF or other host proteins increase decay rate of these two proteins
  • by proteolytically cleaving C3b (factor I)
  • to stop inflammation progression
41
Q

how inhibit C1

A
  • plasma protein C1 inhibitor (CiiNH) binds C1 & interferes with its enzyme activity
  • CiiNH also inhibits Hageman Factor, Kallikrein & lectin as well
42
Q

how inhibit MAC?

A

Several other host molecules inhibit MAC formation

43
Q

What if you fail to inhibit the complement system C1?

A
  • causes deficiencies in CiiNH

- lead to excessive production of vasoactive mediators causing episodic edema (fluid accumulation)

44
Q

Specific mediator of edema in CiiNH deficiency?

A

bradykinin

45
Q

2 possible activation pathways of chemical mediators in plasma?

A

1) Factor X11 (Hageman factor) activation

2) Complement Activation

46
Q

Factor X11 (Hageman factor) activation and complement Activation

A

-can acitvate part of complement cascade & activate C3a to get anaphylaxis activation

47
Q

Kinin system:

A
  • enzymatic cascade triggered by tissue damage

- causes inflammation

48
Q

Hageman factor (factor XII) & activation? What does it produce after activation?

A
  • factor XII of intrinsic clotting pathway
  • activation caused by contact w/ negatively charged surfaces (collagen & basement membrane)
  • once activated produces Prekallikrein activator (factor XIIa
49
Q

Prekallikrein activator (factor XIIa)?

A

-Prekallikrein activator produced by Hageman factor & converts inactive form of prekallikrein into the active protease: Kallikrein

50
Q

How get negatively charged surfaces for Hageman factor to react to?

A

-due to tissue damage exposing the collagen/basement membrane

51
Q

What does active protease Kallikrein do?

A

-Kallikrein cleaves high molecular weight kininogen to produce bradykinin

52
Q

What does Bradykinin do?

A

-Bradykinin increases vascular permeability, causes contraction of smooth muscle, dilation of blood vessels & pain

53
Q

What other function does high molecular weight kininogen (HMWK) cofactor do?

A

-acts as a co-factor promoting the activation of Factor XII (Hageman Factor)

54
Q

What other function does high Kallikrein do?

A

1) activator of Hageman factor,

2) directly converts factor C5 to activated C5a which is the inflammatory response in the compliment pathway

55
Q

inactivation of of Bradykinin?

A

1) activation of of Bradykinin is short lived so is partially self regulating
2) inactivated by Kininase in the plasma
3) inactivated by angiotensis-converting enzyme when passes through lung

56
Q

Two types of clotting pathways?

A

1) Intrinsic clotting pathway

2) Extrinsic clotting pathway

57
Q

Intrinsic clotting pathway

A

-damage to blood vessel causes cascade of clotting factors and activation of Hagemen factor (XII)

58
Q

Extrinsic clotting pathway

A
  • tissue damage outside blood vessel causes tissue thromboplastin release & activation of Hagemen factor (XII)
59
Q

2 pathways that can transpire after Hageman factor activation?

A

Factor X11 (Hageman factor activation)–> Factor XIIa–>

1) Kinin cascade
2) Clotting cascade

60
Q

Clotting cascade initiation?

A

1) inactive factor X
2) active factor X
3) cleaves pro-thrombin–>thrombin
4) thrombin activated fibrinogen to fibrin
5) Factor XIII converts fibrin into blood clot

61
Q

thrombin roles? (x2)

A

1) generate fibrin from fibrinogen to make blood clot

2) promotes proinflammatory activation of multiple cells by activating their PARs (protease activated receptors)

62
Q

Fibrinolytic pathway?

A
  • pathway that counterbalances clotting

- activates enzymes that cleave & solubilize fibrin via the kinin cascade

63
Q

How Fibrinolytic pathway work?

A

1) Kallikrein (from kinin cascade) acts to activate plasminogen into plasmin, 2) plasmin degrades fibrin and reverses clotting

64
Q

2 roles of plasmin?

A

1) converts complement C3 to active C3a which causes inflammatory pathway
2) degrades fibrin and reverses clotting

65
Q

Nitric Oxide and Free Radical Production are?

A
  • inducible responses in the vicinity of the vasculature

- also occurs during local inflammatory responses within tissues

66
Q

Nitric Oxide (NO)

A

1) Is a potent vasodilator
2) reduces platelet aggregation
3) inhibits mast cell inflammation
4) is microbicidal

67
Q

How NO generated?

A

-from L-Arginine by the enzyme nitric oxide synthase (NOS)

68
Q

what are the three forms of NOS?

A

1) eNOS =endothelial NOS: calcium dependent
2) nNOS = neuronal NOS: calcium dependent
3) iNOS = inducible NOS: calcium independent-activity is regulated by transcriptional regulation. Expression induced by TNF and other pro-inflammatory cytokines

69
Q

eNOS

A

=endothelial NOS

  • calcium dependent
  • consittuviely made, but need high levels of Ca to be active
70
Q

nNOS

A

=neuronal NOS

- calcium dependent

71
Q

iNOS

A

= inducible NOS

  • calcium independent; active as soon as made
  • activity is regulated by trxn regulation
  • expression induced by TNF and other pro-inflammatory cytokines
72
Q

What does NO contribute to?

A

-both active pathogen defense and resolution of inflammation!

73
Q

Oxygen derived free radicals

A
  • released from leukocytes after exposure to:
    1) microbes,
    2) chemokines & cytokines
    3) immune complex encounter
    4) following phagocytic challenge
74
Q

oxygen derived free radical production dependent on?

A

-activation of NADPH oxidative system

75
Q

What are the major reactive oxygen species produced?

A

-Superoxide anion production, hydrogen peroxide and hydroxyl radical

76
Q

what do reactive oxygen species interact with?

A
  • NO to produce cytotoxic reactive nitrogen intermediates

- means that NO aren’t intrinsically bad, just their combination w/ ROS is really bad

Block 1 Week 5 (8 decks)

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