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BASIG q1 > exam 5 > Flashcards

exam 5 Flashcards

1
Q

humoral or cell mediated: what is best for extracellular and which is best for intercellular defense

A

humoral : extracellular
Cell mediated: intracellular

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2
Q

what is clonal deletion

A

deleting self reactive B and T cells

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3
Q

what is the precursors for macrophages and some dendritic

A

monocyte

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4
Q

what is langerhan cells and where are they located

A

dendritic cells in skin

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5
Q

list granulcytes

A

NEBM …. nuetrophil, eosinophil, basophil, mast

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6
Q

who is the first responder in cell mediate innate immunity, what do they do

A

PMN luekocytes (nuetrophil)
-they phagocytosis and degranulation and make neutrophil extracellular traps

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7
Q

basophil granules have what?
where are they located

A

histamine and heparin, go through the blood

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8
Q

mast cells granules have what?
where are they located

A

histamine and heparin, found in tissue

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9
Q

the right upper quadrant lymph drains where

A

right lyphatic duct

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10
Q

The thoracic duct drain lymph from what part of the body

A

everywhere except the upper right quadrant because it is drained by right lymphatic duct

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11
Q

name the APC cells

A

dendritic and macrophages B cells

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12
Q

specialized CT is composed of

A

parenchyma (functional part) and stroma (structural part)

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13
Q

the parenchyma has a large amount of what cell

A

lymphocytes

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14
Q

the stroma has what kind of tissue

A

reticular tissue type 3 except the thymus

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15
Q

what shape of cell in HEV

A

simple cuboidal

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16
Q

HEV important role

A

extractivation of lymphocytes from blood to tissue

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17
Q

Difference between primary and seconday lymph organs

A

Primary
- thymus and bone marrow make B & T cells
-B cells stay in bone marrow
-T cells mature in thymus
Secondary
- where immune response occurs
-spleen tonsils lymph nodes

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18
Q

parenchyma in bone marrow is what type of cell
stroma is what kind of tissue

A

parenchyma: hemopoietic cells
stroma: reticular

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19
Q

thymus
stroma is what kind of tissue

A

not reticular but has tight junction

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20
Q

what cells found in the cortex of thymus

A

thymocyte( immature T)
thymic epithelial
macrophage

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21
Q

where is thymocytes selected for immunocompetence

A

in the cortex of the thymus

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22
Q

___% of thymocytes pass selection to become ____ cells or _____ cells

A

__2_% of thymocytes pass selection to become ___helpe cells___ or __cytotoxic t cells__

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23
Q

what is thymic hassalls corpuscles

A

shows where the medulla is in the thymus

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24
Q

Nodules indicate

A

adaptive immune response to antigen - secondary lympoid only not primary

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25
Q

challenged or unchallenged lypmphoid nodules and what does it mean

A

unchallenged - inactive T B cells and APC

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26
Q

challenged or unchallenged lymphoid nodules and what does it mean

A

challenged

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27
Q

red and yellow structure

A

yellow is primary red is secondary

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28
Q

what structure indicates b lymphocyte activation and proliferation

A

secondary lympoid

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29
Q

where are plasma cells and b memory cells made

A

germinal center of the secondary nodule

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30
Q

what does the difuse lyphoid tissue and tonsils survery

A

epithelial barriers

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31
Q

Tonsils are made of what tissue? describe structure and components

A

MALT (mucosa associated lymphoid)
-No cortex or capscle or medulla
-randomy packed B and T lymphocytes
-crypts
-nodules
- epithelium

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32
Q

what tissue

A

MALT

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33
Q

Stroma of a lymphnode is made of

A

reticular CT

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33
Q

what is this and what is ABC

A

A- subcapsular
B-trabecular
C-Medullary

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34
Q
A
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35
Q

what tissue is found in the sinuses of the lymph node sinuses

A

reticular fibers

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36
Q

-The outer cortex of the lymph node is what kind of teritorritory
-the deep cortex is what kind of teritorritory

A

Outer- nodule houses B cell
deep cortex is T cell and HEV extravation

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37
Q

name the blue red and dotted yellow, green
where are T , B and HEV located

A

Yellow dotted: nodule
red: is outer cortex
blue is deep cortex
green: medullary cord
T is in the deep cortex
B is in nodule
HEV is in deep cortex

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38
Q

explain the route of a lymphocyte in lymphnode

A

B T come in through artery, enter lymph node through HEV, T stay in cortex, B cells go to outer cortex and form noduled. APC activate T helper cells. T cells activate B cells to make them into plasma cells (germinal center) . Plasma cell goes to medulallary since and exit efferent vessels

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39
Q

what forms the medullary cord and what does the medullary cord do

A

it is made of parenchyma cells
macrophages, lymphocytes and plasma cells stey here.

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40
Q

what are the primary functions of spleen

A

filter blood of ag
remove aged RBC

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41
Q

name yellow and white arrows and tissue or organ is this

A

Spleen
yellow is nodules
white is CT capsule

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42
Q

name the red and white dots
what tissue or organ is this

A

Red dot = red pulp : blood filled caillaries and splenic cords
White dot = white pulp: lymphoid nodules

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43
Q

does spleen filter lymph

A

no

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44
Q

red pulp and white pulp which one is basophillic

A

red pulp is acidophillic
white is basophillic

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45
Q

describe how the filtration of antigen and old rbc

A

In spleen
-Trabecular art
-Central art
-penicillar arteriols
-dump blood into splenic cords of the red pulp
-goes to venous circulation via sinusoidal capillaries

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46
Q

Splenic chords are used for

A

getting rid of RBC

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47
Q

what cell activated White pulp

A

APC

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48
Q

what cell sursounds central arteriole (what organ)

A

T cells spleen

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49
Q

what is this showing. explain the steps

A

white pulp response to ag.
1. APC in the red chored activate T helper in the PALS
2. T helper activate B cceels
3. primary nodules expand &push pals
4. B cells proliferate secondary nodule
5. plasma and memory B cells into sinusoid

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50
Q
A

B - tonsils have epithelium

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51
Q

what is an immunogen

A

an antigent that binds to a receptor and elicits an immune response

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52
Q

whats a hapten

A

small anitgen that binds to receptor with no immune response

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53
Q

whats a mitogen

A

binds to receptor and induce cell division (polyclonal activator)

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54
Q

haptens can turn into _______

A

immunogens when conjugated

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55
Q

explain clincal application hemolytic anemia

A

antibiotic are haptens but they absorb and bind to proteins on RBC surface making an immunogen that make RBC lysis = Jaundice

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56
Q

Tollergen vs immunogen

A

second exposure of immunogen
tollergen reduced immune response
immunogen increases immune response

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57
Q

what Ag is polyclonal activator

A

mitogen

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58
Q

some exotoxins from bacteria acts like a ______ antigen

A

super antigen - type of mitogen

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59
Q

what is an antigenic determinant

A

epitope

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60
Q

what is multivalent antigen vs polyvalent epitope

A

-antigen that has alot of copies of a single epitope

-antigen has different epitopes

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61
Q

the more complex an epitope the _____ he immune response

A

higher

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62
Q

what type of antigen creates polyclonal response

A

polyvalent ag

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63
Q

what is Adjuvants

A

substance that enhances immune response

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64
Q

what are PRR where are they located? Innate or adaptive

A

receptor from innate systme, that recognizes (PAMPS - pathogen associated pattern) NON specific
-located in and out of cell

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65
Q

What are PAMPS

A

pathogen associated patterns binds to PRP or TLR

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66
Q

what are TLR

A

type of PRR, recognize PAMPS leucin rich

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67
Q

what receptors are your adaptive immune

A

BCR and TCR

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68
Q

what is the difference between B cell receptors and T cell receptors

A

B cell-
-membrane bound immunoglobulin on the surface
-receptors can be secreted as antibodies
-bind many types of shapes ag
T Cells
-tcr bind only linear peptride ag displayed on MHC

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69
Q

BCR is specific for ______ ag
TCR is specific for _______ ag

A

single for both

70
Q

TLR are what type of receptor

A

PRR

71
Q

Compliment is part of the of ________ immunity

A

innate humoral immunity

72
Q

what pathway:
antibody to epitopes

A

classical

73
Q

what pathway:
MBL - Mannose

A

Lectin pathway

74
Q

what pathway:
cleaved c3 c3b - pathogen surface

A

allternative

75
Q

what is the convergence point of the three pathways of the compliment response

A

c3 convertase

76
Q

C3b leads to

A

opsonization

77
Q

c5b-9

A

membrane attack complex MAC

78
Q

c3a leads to

A

inflammation, and chemotaxis (a - stands for anaphylatoxins)

79
Q

C4b

A

opsonization

80
Q

factor 1 degrades what, how does the cleaved products act

A

c3b and c4b, can still function as opsons but no amplication of enzyme cascade

81
Q

what does c5 convertase do

A

turns c5 to c5a (chemotaxis, inflammation) and c5b (Membrane attack lysis)

82
Q

what is Hereditary angio edema HAE

A

deficiency in CN INH (C1inhibitor)…. increased concentration of c3a C5a and thus excessive selling
-tx with recombinant C1INH

83
Q

what is the C1 inhbitor

A

C1INH

84
Q

what is paroxymal noctural hemoglobinuria

A

deficiency in DAF and CD59 on RBC . CD59 inhibits MAC
DAF inactivates c3 convertase
leads to c3 convertase always on and MAC formation
causing
meolytic enemia

85
Q

what does DAF do

A

inactivates c3 convertase

86
Q

what does CD59 do

A

inhibits MAC

87
Q

cells in acute and chronic inflammation

A

ACUTE: neutrophils
CHRONIC: macrophages lymphocytes

88
Q

vaso dilation is key feature of

A

innate response

89
Q

Name inflamation mediators (plasma derived)

A

-compliment (c5a c3a chemotaxis)
-coagulation factors
-kinins

90
Q

what is arachidoonic acid and where is derived and made

A

-cell derived inflammation mediator
-from wbc and injured cells
-vasodilator that fx with fever and pain

91
Q

What releases NO
what releases cytokines

A

NO: endothelial
Cytokines: Macrophages

92
Q

what is a inflammasome

A

reguates cytokine release
-cleaves pro-forms into active cytokines which matures IL1 IL18
** novel target for anitinflammatory therapy

93
Q

what is acute phase protein

A

cytokines make liver realease these proteins causing a 25% increase in inflamation RBC to sediment fast and increased ESR and CRP

94
Q

What is CRP

A

most sensitie acute phase protein
useful marker to show how bad inflammation including course
-activates complement
-stimulates release of cytokines from phagocytes

95
Q

what mediates exravastion

A

CAMS
-selectins
-integrins

96
Q

explain process of extravation

A
  1. rolling adhesion
    wbs attatched to endothelial cells via selectins
    2.stable adhesion (stop them at site of infection)
    wbc attatched to endothelial cells via integrins
97
Q

describe expression difference of integrins and selectins

A

selectins always expressed
integrins espression increased by inflammatory mediators

98
Q

what is the hallmark of chronic inflammation

A

infiltration of tissues with mononuclear cells
-monocytes macrophages and lymphocytes

99
Q

What is M2 cells

A

macrophages that clean up coes form monocyte

100
Q

what is granuloma

A

happens in chronic infection
- macrophage turns to epithliod cell
-surrounded by T and Fibroblasts
-has necrotic center
-can cause re-infection

101
Q

Valley fever clinical relavence

A

granuloma
happens in chronic infection
- macrophage turns to epithliod cell
-surrounded by T and Fibroblasts
-has necrotic center
-can cause re-infection

102
Q

How does NSAIDS work

A

block prostogladins and thromboxane that came from arachidonic acid (which is a cell derived mediator)
-so limit vasculatory permeability

103
Q

how does corticosteroids

A

basically decreased everything so immuno supressed

104
Q

How does Anti-TNF nuetralizing agent work

A

binds to TNF-a
blocks it from going to receptor at site of infection

105
Q

Anti CAM antibodies

A

blocks integrin ICAM interaction preventing extravation

106
Q

When does CT/scar occur

A

-ecm damaged
-stem cells lost
-tissue lacks proliferative regen capabilities
HEART

107
Q

what two supplements are needed for scarring and why

A

VIT C
COPPER
- both for cross linking of collagen formation

108
Q

what are Libile cells, list examples

A

HIGH PROLIFERATIVE CELLS
-epithelium in skin (stem cells @ basal layer) GIT (@crypts)
-Bonemarrow - (hematopoetic stem cells)
-corneal epithelium - (@limbus)

109
Q

what are stable cells, list examples

A

MIN PROLIFERATIVE
-liver
-kidney
-pancreas

110
Q

what are permanent cells, list examples

A

NO PROLIFERATION
-nuerons
-cardiac
-skelatal
-lens

111
Q

Transforming GF (TGF -beta)

A

collagen formation via stimulation of fibroblast

112
Q

Vascular Endothelial GF (VEGF)

A

-vascular permeability
-important for angiogen
-key in granulation

113
Q

Platelet Derived GF (PDGF)

A

-angiogenesis

114
Q

Fibroblast BF (FGF)

A

angiogen
wound contraction

115
Q

what growth factor and cells is important for wound contraction

A

FGF and myofibroblasts

116
Q

What growth factors for angiogen

A

VEGF
FGF
PDGF

117
Q

what is the hallmark of tissue healing

A

granulation

118
Q

what cells found in granulation?
when does granulation start and peaks?

A

macrophage inflammatory cells and fibroblasts
starts at day 3
Peak at 5 -7 days

119
Q

when does ecm deposition occur?
what is ECM?
When does it start and end?

A

collagen synthesis TGF beta, PDGF, FGF
start 3-5 days
ddense collagen pale is 1 month

120
Q

what are MMPs

A

matric metalloproteinases
- breakdown ECM

121
Q

what is myofibroblast

A

it causes wound contraction

122
Q

explain various times of wound strengthing

A

-end of 1 week : 10 tensile strength

-2 mo increase of ensil due to type 3 collagen increase
-synthesis stops for stucture modification of collagen fibers type 1 collagen

-end of 3 months: PLATUE maximum tensile strength 70-80% normal

123
Q

Difference of first and second intention healing

A

-first is bringing edges together like suture very little scar
ONLY epithelial layer
-second is not being able to close more inflammation large scar

124
Q

Gluco-corticosteroids role in wound healing

A

hormone delays healing… causes weak scar
- decrease inflammatory response….
inhibit TGF-Beta which inhibits collagen synthesis
weak scar

125
Q

Compare contrast keloids and hyper trophic scar

A

-both dues to excess formation of collagen
-Keloids
goes out side boundary of wound
does ot regress
recur after surgical resection
genetic predisposition

-Hypertrophic scar
stays in boundries in wound
regresses

126
Q

Fibrosis occurs where

A

parenchymal organ

127
Q

Keloids is made of what

A

collagen 3

128
Q

contraction of large surface wounds is due to what cell

A

myofibroblasts

129
Q

what do you need to know about this image

A
130
Q

what do you need to know about this image

A
131
Q

what enzymes responsible for would repair

A

MMPs

132
Q

what cell is pattern recognition receptors found

A

they are receptors on phagocytes

133
Q

Name two types of PRR receptos and what they do

A

-PAMPS receptors
(pathogen associated molecular pathogens…)
-Opsonin receptors

134
Q

difference oxygen dependent and oxygen independent digestion

A

done by phagocytes
OXYGEN INDEPENDENT
-proteolytic enzyme

OXYGEN DEPENDENT
-uses reactive oxygen intermediates ROIS and Reactive nitrogen species (RNS)

135
Q

explain clinical relavence. whats left and right?

A

Granulomatous disease X linked —–defect in production of NADPH
-meaning inefficient killing
-granuloma formation
-right enzyme activity
-left no enzyme

136
Q

APC activate what cell

A

T helper and cytotoxic t cells via t cell recepetor

137
Q

MHC1
stucture:
type of antigen - exo or exracellular
or endogenous/ intracellular:
Cells that express this:
T cell subset that will bind:
HLA gene:
Gene expression:

A

MHC1
stucture: 1 variable alpha and one non variable B2 microglbulin
**type of antigen - exo or exracellular
or endogenous/ intracellular: ** endogenous - cytoplasmic peptides
intracellular
Cells that express this: all nucleated cells
T cell subset that will bind: Tc cd-8
HLA gene: HLA-A HLA-B HLA-C
Gene expression: poly morphic (different allels for each gene) polygenic three genes for each class

138
Q

MHC2
stucture:
type of antigen - exo or exracellular
or endogenous/ intracellular:
Cells that express this:
T cell subset that will bind:
HLA gene:
Gene expression:

A

MHC2
stucture: variable alpha and B2 microglbulin
**type of antigen - exo or exracellular
or endogenous/ intracellular: ** exogenous
extracellular
Cells that express this: APC
T cell subset that will bind: Th CD-4
HLA gene: HLA-DP HLA-DQ HLA-DR
Gene expression:
poly morphic (different allels for each gene) polygenic three genes for each class

139
Q

Each person has how many haplotypes?

what is a haplotype

A

2 haplotypes

HLA haplotype is a set of hc alleles

140
Q

Cytosolic pathway
what MHC and explain process

A

MHC 1 for Tc cells
* breakdown endoenous protein in cytosol via proteosomes
* TAP transporter to RER membrane
* synthesize mhc 1 and processing protein in REER
* peptide goes in cleft
* MHC and peptide go to cell membrane for cytotoxic cells to recognize on CD8 receptor

141
Q

Endocytic pathway
what MHC and explain process

A

MHC 2 for Th
* lysosomal degradation of endocytosed antigen
* sythesis of MHC 2 and invariant chain Ii in RER
* degrade Ii from binding cleft
* HLA DM helps load exogenous peptde into MHC 2 cleft
* go to cell membrain for Th cells with cd4

142
Q

What is TAP deficiency

A

They have a reduced MHC 1 meaning reduction of cd8 t cll muturation and function

143
Q

what cell can cross present and what receptors do they present

A

Dendritic for tumor cells MHC 1 and MHC 12

144
Q

what is recognition phase and what is effector phase

A

2 phases of antibodies - humoral immunity
recognition: membrane bound antibodies B cell receptors
effector: secreted by effector B cells (plasma cells)

145
Q

Ch Cl Vh Vl what are they

A

Ch Cl they are the constant region
Vh VL are the variable region

146
Q

what region is responsible for antigen binding

A

both heavy and light chain variable region

147
Q

what region is responsible for isotype of antibody

A

contant region of the heavy chain only

148
Q

signaling portion of the bcr

A

Igalpha Igbeter

149
Q

What is antiserum

A

serm that have alot of antibodies

150
Q

what type of anitbodies activate classical pathway of compliment

A

IgM IgG

151
Q

what region of antibody is needed for opsonization

A

Fc

152
Q

what are the two andibodies used for antibody dependent cell mediate cytotoxicity

A
  • IgG sits on the surface of the cell and NK kill it
  • IgE on helminth and eosinophil kill it
153
Q

what two antibodies cross link degranulation happens

A

IgE

154
Q

what two antibodies have J chain

A

IgM pentamer and IgA dymer

155
Q

IgA

A

in Tears and breast milk and saliva external secretion

156
Q

IgD

A

activates Basophils and mast cells, membrane bound

157
Q

IgE

A

against worms and allergic reaction

158
Q

IgG

A

secreated by plasma cells and can cross placenta

159
Q

IgM

A

may attach to surface of B cell or secreted into blood. EARLY STAGE immunity

160
Q

what cell is the first antibody secreted during primary response what percent is in serum

A

5-10% IgM

161
Q

Ab secreted suring memory response what percent is in serum

A

IgG 8-%

162
Q

which illicites a stronger immune response linear or folded

A

folded

163
Q

what INF stimulates NK cells
is it innate or adaptive

A

beta, innate

164
Q

what inf stimulates nuetrophyl

A

gama

165
Q

what cell is hallmark for chronic inflammation

A

macrophages

166
Q

what do INF1 alpha and beta do

A

antiviral
rnase
viral replication halted
NK activity
increase MHC1 expression

167
Q

name granules of nk cells

A

perforin - makes pore
granzyme - induce apoptosis

168
Q

do cytokines regulate innate or adaptive

A

both

169
Q

what is NF-kb

A

inflammation transcription factor

170
Q

what is IRF-3

A

transcription factor that is antiviral, makes cell release INF alpha aand beta

171
Q

what is IL12

A

macrophage secrete it cause they cant digest microorganism. this activates NK cells

172
Q

what is INF y (gama)

A

secreted by NK cells to microbicidal activity to macrophages

173
Q
A

BASIG q1 (11 decks)

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