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Immune > Plasma > Flashcards

Plasma Flashcards

1
Q

What is plasma?

A

Fluid left over after blood cells are removed.

can CLOT

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2
Q

Can plasma clot?

A

Yes plasma can clot

it is the fluid left over after blood cells are removed

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3
Q

What is serum

A

Fluid left after the blood clot and cells are removed

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4
Q

Can serum clot?

A

No the blood clot and cells are removed

no clotting

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5
Q

Which organ synthesize the majority of the plasma? Its a major source of plasma?

A

Liver

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6
Q

Plasma activates what two systems?

A

Activates

1) Factor 12 (hageman factor) activation
2) Complement Activation

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7
Q

Which complement is important to MACs?

A

C5b

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8
Q

Which complement is important for phagocytosis?

A

C3b and C5a (the latter to actually initiate phagocytosis)

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9
Q

Which complements are anaphylatoxins?

A

C3a, C4a, and C5a

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10
Q

Plasmin coverts what complement to its active form?

A

C3 to C3a

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11
Q

What protein activates plasmin?

A

Kallikrein

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12
Q

What are two important functions of plasmin?

A

1) degrades fibrin

2) coverts C3 to C3a

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13
Q

TNF-alpha and IL-1B and IL-6 are cytokines that induce the liver to produce what ?

A

Acute phase proteins

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14
Q

List 5 groups of acute phase proteins?

A

1) serum amyloid protein (SAP)
2) C-reactive protein (CRP)
3 Fibrinogen
4) MBL
5) SP-A and Sp-D

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15
Q

Which acute phase proteins are part of pentraxin family?

A

CRP c-reactive protein

SAP serum amyloid protein

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16
Q

What does pentraxin acute phase protein ‘CRP’ do?

A

opsonization, complement activation

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17
Q

What does pentraxin acute phase protein’SAP’ do?

A

opsonization, complement activation, binding of mannose/galactose

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18
Q

C reactive protein binds to XXX on bacterial surfaces, acting as an opsonin and also activating what?

A

CRP binds to PHOSPHOCHOLINE on bacterial surfaces acting as OPSONIN and also activating COMPLEMENT

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19
Q

MBL binds to mannose residuces on bacteria’s surface acting as an what and also activating what?

A

acting as OPSONIN and activating COMPLEMENT

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20
Q

When the liver is stimulated by TNF, IL-6, and IL-1 what three important acute phase proteins does it produce?

A

C-reactive Protein opsonization, complement activation

Serum amyloid protein (SAP) opsonization, complement activation, and mannose-galactose binding

Fibrinogen helps with clotting

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21
Q

What stimulants does the liver need to produce actue phase proteins CRP, SAP, and fibrinogen?

A

TNF, IL-1, IL-6

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22
Q

High CRP levels in serum are used as a dx measure of what?

A

Ongoing inflammation

BOTH actute and Chronic

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23
Q

CRP and SAP besides opsonizing pathogens, also bind to WHAT to facilitate the WHAT ?

A

CRP and SAP also bind to CHROMATIN and facilitate the CLEARANCE OF DAMAGED CELLS

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24
Q

Your lab test shows high CRP levels in the serum?

A

Ongoing infection can be BOTH ACUTE and CHRONIC inflammation

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25
Q

Complement proteins are present as XXX forms in plasma and are numbered C1-C9?

A

Compelment proteins are present as INACTIVE forms in PLASMA and are numbered C1-C9.

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26
Q

What are 3 pathways to activate complement pathway?

A

Classical Pathway

MB-Lectin Pathway

Alternative Pathway

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27
Q

Describe Classical Pathway

A

Ag:Ab complexes

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28
Q

Describe MB-Lectin Pathway

A

Lectin binding to pathogen surfaces

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29
Q

Describe Alternative pathway

A

Pathogen surfaces

One of 3 pathways that opsonize and kill pathogen

pathway is activated when C3a binds to pathogen

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30
Q

What are the outputs of complement activation?

A

1) Recruit inflammatory cells

2) Opsonize and kill pathogens

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31
Q

What complements are associated with the Classical Pathway?

A

(5 complements) C1q, C1r, C1s, C4, C2

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32
Q

What complements are associated with the MBL pathway?

A

(5 things) MBL, MASP-1, MASP-2, C4, C2

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33
Q

What compelments are associated with Alternative pathway?

A

(3 things) C3, factor B, Factor D

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34
Q

C3a and C5a are what?

A

Peptide Mediators of INFLAMMATION, and PHAGOCYTE RECRUITMENT

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35
Q

C3b does what?

A

Binds to COMPLEMENT RECEPTORS on PHAGOCYTES

Opsonize pathogens

REMOVAL OF IMMUNE COMPLEXES (important for immune diseases)

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36
Q

Terminal complement components C5b, C6-C9 does what?

A

MAC membrane attack complex, LYSIS of certain pathogens and cells

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37
Q

Can macrophage phagocytosed a MBL complexed bacteria if only the C3b binds to CR1?

A

No it also needs C5a to activate the macrophage to phagocytose via CR1

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38
Q

Peptide mediators of inflammation, phagocyte recruitment?

A

C3a C5a

> Increase vascular permeability
Fluid leakage from blood vessels
Extravasation of IgG and IgM and compement molecules
Migration of macrophages PMN leukocytes
Microbicidal activity of PMNs and macrophages are increased

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39
Q

Early events: which compelment is common to the classical and MBL pathway that needs to be activated for the proteolysis of which two compement?

A

MBL and Classical pathway acts on C1 to activate it so it can cleave C4 and C2 into C4b2b that functions as C3 CONVERTASE

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40
Q

What is made of C3 Convertase?

A

C4b2b from MBL and Classical

C3bBb from Alternative

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41
Q

How is C3 Convertase made?

A

C3 Convertase is made by C1 active form proteolysing C4 and C2 creating C4b2b which is C3 convertase

can be via MBL or CLassical

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42
Q

Which pathway does LPS, Complex polysacchrides, cobra venome stabilize the spontaneous cleavage of WHAT and breakdown of WHat?

A

ALTERNATIVE PATHWAY: LPS, Complex polysacchrides, cobra venome stabilize spontaneous cleavage of C3 (C3b) and FACTOR B (Bb). C3bBb is a C3 convertase

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43
Q

What two complexes are considered as C3 convertases?

A

C4b2b from MBL and CLassical pathway (activated by C1 activated form)

C3bBb from Alternative Pathway

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44
Q

What two things activate the C1 to proteolytically cleave C4 and C2 into C4b2b (C3 convertase)?

A

Classical:

> Ab:Ag:C1

MBL

MBL:Pathogen:C1

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45
Q

MBL directly bind to pathogens and directly activates C1 and thus indirectly initiates the WHAT?

A

indirectly initiates the Classical Pathway

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46
Q

T/F C3 Convertase converts C3 to C3a and Cb

A

True
C3 convertases

MBL/CLassical C4b2b

Alternate 3bBb

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47
Q

C5a and C3a are generated from complement pathway but are also generated via WHAT and WHAT proteases?

A

Plasmin or lysomal proteases

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48
Q

T/F all three pathways MBL, Classical, Alternate can generate C3b.

A

True

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49
Q

C3b from all three pathways can bind to C3 Convertase (C4b2b and C3bBb) to produce C5 convertase (C4b2b3b and C3bBb3b) which cleaves C5 to C5a and C5b. C5b remains attached to complex and forms binding substrate for complement components 1-9. Polymerized WHAT forms a channel in lipid membranes called MAC

A

polymerized C9

MAC allow fluid and ions to enter > LYSIS of pathogens

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50
Q

MAC kills pathogen by

A

allowing FLUID and IONS to enter causing cell LYSIS

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51
Q

Deficiencies that decrease MAC formation cause minor/major immune susceptibilities s?

A

MINOR , suceptibility to Neisseria

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52
Q

decrease MAC formation increase susceptibility to what organism?

A

Neisseria

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53
Q

C3a, C5a, C4a simulate what release from what cells (increases vascular permeability, cause vasodilation), they are called what toxins?

A

HISTAMINE release from Mast Cells and C3a, C4a, C5a are called anaphylatoxins

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54
Q

Anaphylatoxins are which compelments?

A

C3a C4a C5a

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55
Q

Which complements stimulate histamine release from mast cells?

A

C3a C4a C5a

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56
Q

C5a is a anaphylaxtoxins that stimulates histmaine release form mast cells, but it also activates what pathway in neutrophils and monocytes?

A

The LIPOXYGENASE pathway to produce interleukins and lipoxins

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57
Q

Which complement other than recruiting other immune cells also induce mast cells’ histamine release also activates the LOX pathway of AA in neutrophils and monocytes?

A

C5a

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58
Q

C5a also activates LOX pathway of AA in which two cells?

A

Neutrophils and Monocytes

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59
Q

C5a is also a what for monocytes and MNP leukocytes?

A

C5a is also CHEMOATTRACTANT for monocytes, neutrophils, eosinophils, basophils

60
Q

List 3 functions of C5a?

A
  • like C3a and C4a, it is ANAPHYLAXTOXINS and induces histamine release from mast cells
  • it also activates the LOX pathway neutrophils and monocytes producing interleukins and lipoxins
  • chemoattractant for monocytes, and PMN leukocytes
61
Q

C3b (iC3b is inactive form) act as XXX when fixed to bacterial cell walls and promote which process?

A

C3b act as OPSONINS fixed to bacterial cell wall and PROMOTE PHAGOCYTOSIS in neutrophils and macrophages

62
Q

Neutrophils can phagocytose T/F

A

True

63
Q

In general what if you fail to activate complement?

A

Suceptibilities to FATAL infections

64
Q

If you’re deficient in MAC formation your suceptibility to what rises?

A

deficient in MAC increases susceptibilities to NEISSERIA

65
Q

Deficiencies in C2 and C4 are associated with what disorders such as what because of what?

A

Deficiencies in C2 and C4 lead to AUTOIMMUNE disorders like LUPUS because IMMUNE COMPLEXES CANNOT be efficently CLEARED

66
Q

Deficiency in what leads to increased Suceptibility to Nisseria?

A

MAC deficiency

67
Q

Deficiency in what leads to disorders like LUPUS because it can’t efficently clear away Immune COmplexes?

A

C2 and C4

68
Q

Deficiency in the classical pathway leads to what?

A

Deficiency in C1, C2, C4 of the classical pathway leads to immune complex disease

69
Q

Deficiency in the MBL leads to what?

A

Bacterial infections mainly in childhood

MBL, MASP1, MASP2, C2, C4

70
Q

Deficiency in Alternative Pathway leads to ?

A

Factor D and Factor P deficient

Infection with pyogenic bacteria and NEIsseria spp. NO immune complex disease

71
Q

What causes increased susceptibility with pyogenic bacteria adn Neisseria but NO immune-complex disease?

A

Alternative Pathway

Factor D and Factor P

72
Q

Deficiency leads to immune-complex disease?

A

C1, C2, C4

73
Q

Deficiency leads to bacterial infection mainly in childhood?

A

MBL, MASP1. MASP2, C2, C4

74
Q

C3 deficiency leads to what?

A

infection with pyogenic bacteria and Neisseria sapp and SOMETIMES IMMUNE COMPLEX DIsease

75
Q

C5-C9 deficiency leads to what infection

A

Neisseria Spp. only

76
Q

What deficiency leads to infection with pyogenic bacteria, nisseria spp, and sometimes immune complex disease?

A

C3

77
Q

What leads to to infection with pyogenic bacteria, nisseria spp, but no immune complex disease

A

Factor D and Factor P of alternative pathway

78
Q

What leads to Nisseria spp only?

A

C5-C9

79
Q

Key inhibitory point of complement pathway?

A

C3 and C5

80
Q

How to inhibit C3 and C5?

A

Decay Accelerating Factor (DAF) or by cleaving C3b (Factor 1)

81
Q

What is Factor 1

A

C3b

82
Q

What does CiiNh inhibit?

A

1) C1
2) Hageman Factor (Factor 12)

3) Kallikrein

83
Q

CD59 inhibits what?

A

Mac formation

84
Q

C1 is inhibited by what?

A

CiiNH

85
Q

MAC formation is inhibited by?

A

CD59

86
Q

C3 and C5 are inhibited by what?

A

DAF

or cleaving C3b (factor 1)

87
Q

Hageman Factor is inhibited by?

A

CiiNH which also inhibits Kallikrein and C1

88
Q

Kallikrein is inhibited by?

A

CiiNH which also inhibits Hageman Factor and C1

89
Q

CiiNH deficiencies lead to what?

A

Excessive production of vasoactive mediators > episodic edema in Skin, extremeties, intestinal and laryngeal mucosa

90
Q

Excessive production of vasoactive mediators with episodic edema in skin, extremities, intestinal laryngeal mucsoa is associated with what deficiency?

A

CiiNH

91
Q

What is a spefic mediator of edema in CiiNH deficiency?

A

Bradykinin

92
Q

Bradykinin is a specific mediator of edema in what deficiency?

A

CiiNH

93
Q

Bradykinin is a specific mediator of what?

A

Edema in CiiNH deficiency

94
Q

Besides complemnt activation, Plasma also participates in producing?

A

clotting factors
detection injury
wound repair

95
Q

Activation of Hageman factor (factor 12 of INTRINSIC clotting pathway) is caused by contact with?

A

NEGATIVELY charged surfaces like COLLAGEN and BASEMENT MEMBRANE

96
Q

Activation of Hageman factor is extrinsic/intrinsic clotting pathway?

A

INTRINSIC

97
Q

PRekallikrein activator (factor 12a) converts prekallikrein to what ?

A

activated Prekallikrein activator (factor 12a) activates Kallikrein by transforming Prekallikrein to Kallikrein

98
Q

Bradykinin causes what?

A

CONTRACTION OF SMOOTH MUSCLE

increases vascular permeability

dilation of blood vessels

pain

99
Q

What causes vascular permeability, smooth muscle contraction, dilation of blood vessels, and pain

A

Bradykinin

100
Q

What activates prekallikrein to Kallikrein

A

Prekallikrein activator (12a)

101
Q

HMWK high molecular weigh kinongen is a cofactor to what?

A

Factor 12 hageman factor along with NEGATIVELY CHARGED surfaces like collagen and basement membrane and activated platelets to turn into Factor 12a

102
Q

HMWK is a cofactor to what?

A

promoting the activation of factor XII

103
Q

what is the cofactor to promoting the activation of factor XII?

A

HMWK kinogen

104
Q

What else besides HMWK acts as a potent activator of the Hageman factor?

A

Kallikrein

105
Q

List 3 functions of Kallikrein

A

> convert C5 into C5a
Activator of Hageman Factor
activates Plasminogen to Plasmin

106
Q

How do you inactivate Bradykinin?

A

Kininase in the PLASMA or Angiotensis-converting enzyme when it goes thru the LUNG

107
Q

Intrinsic clotting pathway?

A

> liver produces Hageman factor

> inactivated form circulates in plasma until activated by TISSUE DAMAGE

108
Q

Liver produce Hageman factor which circulate in inactive form in plasma until it encoutners tissue damage?

A

Intrinsic clotting pathway

109
Q

Extrinsic clotting pathway

A

TISSUE FACTOR from damaged endothelial cells, microparticles, innate immune cells, and or platelets

110
Q

Tissue factor from damaged endothelial cells, microparticles, innate immune cells, and or platelets.

A

Extrinsic clotting pathway

111
Q

Difference between intrinsic and extrinsic clotting pathways?

A

intrinsice: Hageman factor produce by the liver circulates in plasma in inactive form until its activated by damaged tissue

Extrinsic: TF from damaged EC cells, microparticles, innate immune cells, and or platelets
TISSUE FACTOR

112
Q

Extrinsic/Intrinsic pathway coverages at where?

A

Factor 10, or Factor X

113
Q

What coverts prothrombin to thrombin?

A

Activated factor X

114
Q

Factor X activated coverts what

A

Prothrombin to thrombin

115
Q

Thrombin converts what to what?

A

Fibrinogen to fibrin

116
Q

Fibrinogen to fibrin is coverted by

A

Thrombin

117
Q

Fibrin is converted by blood clot by

A

Factor 13

118
Q

Factor 13 converts

A

fibrin to blood clot

119
Q

Chemical released from injury site and by contact with underlying collagen, Platelets are activated and become

A

spiked and stick to each other and the wound site

120
Q

Initial platelets are activated by

A

Chemical released from injured cells and contact with broken collagen

121
Q

Bound platelets do what?

A

Release chemicals that activate and attract other platelets

122
Q

In coagulation fibrinogen is converted to fibrin, which form what?

A

Fibrin forms a mesh that traps more platelets and RBC producing clots

123
Q

Steps of clotting

A

1) injury
2) vascular spasm, smooth muscle contracts to prevent blood loss
3) Platelet plug formation
4) coagulation fibrin form mesh trap more platelets and rbc

124
Q

Chemokines and PG both use what receptors?

A

GPCR

125
Q

Besides generating fibrin, thrombin promotes proinflammatory activation of cell by activating their?

A

Protease activated receptors

126
Q

How does factor 12a counterbalance clotting?

A

ACleaves Fibrin via kinin cascasde by Plasmin

127
Q

Plasmin coverts what compelments?

A

C3 to C3a and (C5)

128
Q

Kallikrein activates what ?

A

Kallikrein activates plasminogen to plasmin

129
Q

Plasmin does what?

A

Covernts C3 to C3a and cleaves Fibrin

130
Q

Describe the effects of NO?

A

> reduce leukocyte adhesion
reduce platelets adhesion
vascular smooth muscle relaxation
vasodilation

131
Q

What reduces:

1) leukocyte adhesion
2) Platelets adhesion
3) vasodilation
4) relaxation of vascular smooth muscle

A

NO Nitric Oxide

132
Q

NO is generated from what a.a via what enzyme?

A

L-Arginine by enzyme nitric oxide synthase (NOS)

133
Q

NOS generates what from L-Arginine?

A

Nitric Oxide

134
Q

List 3 types of NOS enzymes?

A

eNOS= endothelial NOS calcium dependent

nNOS= neuronal NOS, calcium dependent

iNOS = inducible NOS, calcium INDEPENDENT

  • regulated by transcription
  • induced by TNF and other cytokines
  • in MACROPHAGES
135
Q

What NOS enzyme is calcium dependent?

A

eNOS

nNOS

neuronal and endothelial NOS

136
Q

Which NOS enzyme is calcium INDEPENDENT?

A

iNOS in macrophages which are regulated by transcription.

iNOS’s expression is induced by TNF and other cytokines

137
Q
  • List 4 things NO do?
A

1) potent vasodilator
2) reduces platelet aggregation
3) inhibits MAST cells inflammation
4) is microbial

138
Q

No contributes to both

A

ACTIVE pathogen defense and RESOLUTION of inflammation

139
Q

What participates in ACTIVE pathogen defense and RESOLUTION of inflammation?

A

Nitric Oxide

140
Q

What reduces platelet aggregation, potent vasodilator, microbial, and inhibits mast cell inflammation?

A

Nitric Oxide

141
Q

Oxygen derived free radicals released by leukocyte is dependent upon?

A

activation of NADPH oxidative system

142
Q

Species of Oxygen Derived free redicals?

A

Superoxide anion production, Hydrogen Peroxide, hydroxy radical

143
Q

What interacts with superoxide anion, hydroxyl radiacal, hydrogen peroxide to produce reactive nitrogen intermediates?

A

Nitrogen Oxide

144
Q

What interacts with Nitrogen Oxide to produce reactive nitrogen intermediates?

A

superoxide anion, hydrogen peroxide, and hydroxyl radical

145
Q

What is dependent on oxidative NADPH system from activation?

A

Oxygen derived free radicals released by leukocyte after exposure to microbes, chemokines, cytokines, immune complex, phagocytic challeng

Immune (6 decks)

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