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*med3* > Immunology - Basic Immunology > Flashcards

Immunology - Basic Immunology Flashcards

1
Q

what are the 3 barriers to infection?

A

skin/mucous membranes

innate immune system

adaptive immune system

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2
Q

what cells are part of the adaptive immune system?

A

B cells and T cells

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3
Q

what 2 things are unique to the adaptive immune system?

A

specific for the pathogen

memory

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4
Q

what is antigen presentation?

A

APC presents pieces of the pathogen to T cells

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5
Q

how does the immune system keep the adaptive response for the worst pathogens?

A

by using APC’s

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6
Q

what are the 5 subsets of cytokines?

A

chemokine - attracts immune cells (chemotaxis)

interleukins

TNF - can cause tumor death

transforming growth factor (TGF)

interferons - named for interfering with viral replication

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7
Q

what is the cluster of differentiation?

A

CD3, CD4, CD8 - Cell surface molecules used to identify cell types some used as receptor/cell binding

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8
Q

what are the 2 phagocytes of the innate immune system?

A

macrophages

neutrophils

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9
Q

what are the 5 cell types of the innate immune system?

A

phagocytes

complement

NK cells

Eosinophils

mast cells and basophils

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10
Q

how does the innate immune system recognize a molecule as foreign?

A

PAMPs - pathogen associated molecular patterns - present on microbes not on human cells

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11
Q

What is the main pattern recognition receptor used for recognizing a PAMP?

A

TLR - toll like receptors

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12
Q

what cells are TLRs found on?

A

macrophages

dendritic cells

mast cells

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13
Q

what happens when a TLR recognizes a PAMP?

A

the cell the TLR is on secretes cytokines to trigger an inflammatory response

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14
Q

What are 2 important PAMPs?

A

endotoxin (LPS)

peptidoglycan cell wall

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15
Q

what is endotoxin? where is it found?

A

aka LPS - lipopolysaccharide found in gram negative bacteria

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16
Q

what does LPS bind?

A

LPS binding protein - found in plasma - then the complex binds CD14 on macrophages

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17
Q

what TLR does LPS trigger?

A

TLR 4

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18
Q

when LPS binds TLR 4 what cytokines are released from the macrophage?

A

IL-1

IL-6

IL-8

TNF

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19
Q

What does CD14 bind?

A

LPS

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20
Q

what happens when peptidoglycan binds to NOD receptors?

A

cytokines released

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21
Q

what other patterns are recognized by the innate immune system?

A

mannose lipoteichoic acid on gram+ bacteria

dsRNA

unmethylated DNA

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22
Q

what is mannose?

A

a polysaccharide found on bacteria and yeast that binds MBL (mannose binding lectin) activating the lectin pathway of complement activation

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23
Q

_____ are the guardians of innate immunity

A

macrophages

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24
Q

where are macrophages produced?

A

bone marrow as monocytes

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25
Q

what is the name for macrophages that are in different tissues?

  1. liver
  2. CNS
  3. bone
A
  1. kupffer cells
  2. microglia
  3. osteoclasts
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26
Q

when does a monocyte become a macrophage?

A

when it enters the tissue

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27
Q

what are the 3 key functions for macrophages in innate immunity?

A

phagocytosis

cytokine production

antigen presentation

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28
Q

what happens during phagocytosis?

A

macrophage engulfs pathogen into phagosome that fuses with a lysosome that contains deadly enzymes killing the bacteria/virus

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29
Q

what is inside lysosomes that makes them so deadly?

A

Reactive oxygen species (ROS)

Reactive nitrogen intermediates enzymes - proteases, nucleases, lysozymes

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30
Q

what are reactive oxygen species?

A

superoxides produced by NADPH oxidase via respiratory burst leading to the production of hydrogen peroxide (H2O2) and superoxide (O2-)

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31
Q

what are reactive nitrogen intermediates?

A

when NO is reacted with superoxide forming peroxynitrite (ONOO-) which is toxic to bacteria

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32
Q

what do lysozymes do?

A

hydrolyze peptidoglycan in the cell wall of bacteria

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33
Q

what pathogens block phagocytosis?

A

tuberculosis

*** Chediak-Higashi syndrome

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34
Q

how does TB block phagocytosis?

A

modifies phagosome and can no longer fuse with lysosome allowing for TB to proliferate inside the macrophages and evade antibodies in the plasma

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35
Q

how does Chediak-Higashi syndrome block phagocytosis?

A

immune deficiency syndrome causing failure of lysosomes to fuse with phagosomes causing recurrent bacterial infections

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36
Q

someone with chediak higashi syndrome is likely to have recurrent ______ infections

A

bacterial

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37
Q

what are the different “states” of macrophages?

A

resting - debris removal; circulate through the tissues picking up dead/dying tissues

activated (“primed”) - more effective phagocytes/killers

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38
Q

what are the 3 major activators of macrophages via TLRs?

A

LPS from gram neg. bacteria

Peptidoglycan from bacterial cell wall

Bacterial DNA (no methylation)

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39
Q

what other things besides TLRs can activate macrophages?

A

IFN-gamma from T cells & NK cells

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40
Q

How do T-cells activate macrophages?

A

when adaptive immune system and T cells become activated they can then in turn stimulate the macrophages to become more activated

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41
Q

what component of complement are macrophages attracted to?

A

C5a

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42
Q

what are the key surface receptors on macrophages? what do they bind to?

A

CD14 - LPS on gram neg

Fc-R - Fc Ab

C3b-R - C3b (complement)

MHCII - CD4 on TCELLS

B7 - CD28 on TCELLS

CD40 - CD40L on TCELLS

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43
Q

What 3 R’s are needed on a macrophage for it to interact with a T cell?

A

MHC II

B7

CD40

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44
Q

What signals on TCELLS allow for them to interact with macrophages?

A

CD4

CD28

CD40L

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45
Q

what cytokines do macrophages release?

A

IL-1 and TNF-alpha

**** most imp other: IL-6 IL-8 IL-12

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46
Q

IL-1 and TNF-alpha both increase synthesis of what?

A

endothelial adhesion molecules

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47
Q

what do endothelial adhesion molecules do?

A

allow neutrophils to enter inflamed tissue

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48
Q

what does IL-1 do?

A

endogenous pyrogen - causes fever acts on hypothalamus and raises the set point for temp. of the body

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49
Q

what does TNF-alpha do?

A

can cause vascular leak, septic shock

cachectin reduces utilization of fatty acids

kills tumors in animals

can cause intravascular coagulation and DIC

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50
Q

what is a cachectin?

A

inhibits lipoprotein lipase in fat tissue causing decreased utilization of fatty acids

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51
Q

how does TNF kill tumors in animals?

A

causes coagulation and thrombosis in the blood vessels that supply the tumor

remember: in patients with severe infections TNF alpha can cause DIC via intravascular coagulation

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52
Q

IL-6

A

fever stimulates acute phase protein production in liver (CRP)

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53
Q

IL-8

A

attracts neutrophils

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54
Q

IL-12

A

promotes Th1 development (cell-mediated response)

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55
Q

how do neutrophils relate to macrophages?

A

they are the back up cell to macrophages

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56
Q

neutrophils are derived from where?

A

bone marrow

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57
Q

neutrophil granules stain what color w/ Wright stain?

A

pink (eosinophils = red; basophils = blue)

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58
Q

neutrophils are drawn from the blood stream to sites of inflammation by what?

A

macrophages and cytokines

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59
Q

how long to neutrophils circulate to become activated before they die?

A

5 days

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60
Q

when neutrophils enter tissues what is their job?

A

phagocytosis - pink staining granules are lysosomes (bactericidal enzymes)

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61
Q

when macrophages need help who do they call?

A

neutrophils

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62
Q

What are the steps involved in the process by which neutrophils exit the blood stream to enter sites of inflammation?

A

Rolling

Crawling (tight binding)

Transmigration

Migration to site of inflammation

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63
Q

What is “Rolling”

A

neutrophils that are circulating in the blood start to slow down when they get near sites of inflammation and roll along the blood vessel using their selectin ligands to bind the endothelium of the blood vessel

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64
Q

what carbohydrate is known to be in the selectin ligand on neutrophils?

A

Sialyl-Lewis X

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65
Q

What 2 processes is Sialyl-Lewis X involved in?

A

neutrophils bind to endothelium during rolling

sperm cells bind to eggs for fertilization

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66
Q

What do the selectin ligands on neutrophils bind to?

A

E-selectin or P-selectin on endothelial cells causing them to roll

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67
Q

what is “crawling”

A

tight binding integrin on neutrophils

binds ICAM on endothelial cells

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68
Q

what is “transmigration”

A

neutrophils bind PECAM-1 between endothelial cells and they go across the endothelium into tissues

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69
Q

what chemokines are use to attract neutrophils to the site of inflammation?

A

C5a

IL-8

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70
Q

neutrophils are always circulating with ______ on their surface but usually nothing is there to bind to it but with an infection ____&______ which stimulates the expression of _____ on the surface of endothelial cells; neutrophils bind to the selectin and begin to roll along the endothelium for crawling to occur the neutrophil has to express _______ which is triggered by ____ or ____and then _____ can bind _____ on endothelial cells

A

selectin ligand

IL-1 & TNF-alpha

selectin

integrin

LPS

C5a

integrin

ICAM

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71
Q

what is always present on endothelial cells?

A

ICAM

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72
Q

what stimulates the expression of selectin on the surface of endothelial cells?

A

IL-1 and TNF-alpha secreted by macrophages

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73
Q

what stimulates the expression of integrin

A

LPS

C5a

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74
Q

what are the 2 groups of neutrophil granules?

A

small granules (specific or secondary)

larger (azurophilic or primary)

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75
Q

what are the small granules (specific/secondary) of neutrophils and what do they do?

A

enzymes - alkaline phosphatase, collagenase, lysozyme, lactoferrin

fuse with phagosomes to kill pathogens

can be released in extracellular space

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76
Q

patients with certain leukemias have a low alkaline phosphatase score, what does this mean?

A

that they have neutrophils in their blood stream but very low levels of alkaline phosphatase (seen in CML)

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77
Q

what are the larger granules (azurophilic/primary) of neutrophils? what do they do?

A

contains enzymes - acid phosphatase, myeloperoxidase

they only fuse with phagosomes

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78
Q

what does acid phosphatase do?

A

degrades protein in an acidic environment

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79
Q

what does myeloperoxidase do?

A

important for respiratory burst that kills bacteria

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80
Q

what are band forms of neutrophils?

A

immature neutrophils that have a “band like” nucleus seen in plasma during bacterial infections when the BM is being driven to produce more neutrophils

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81
Q

if a lot of band forms are present what is it called?

A

left shift = infection & inflammation

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82
Q

Do neutrophils present Ag?

A

NO

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83
Q

what do neutrophils do?

A

phagocytosis ONLY

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84
Q

macrophage vs neutrophil

A

both can do phagocytosis but only macrophages are APCs too.

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85
Q

what are the chemotaxis for neutrophils?

A

IL-8 from macrophages

C5a from complement

86
Q

what antibody is a major opsonin for neutrophils?

A

IgG is the only antibody that binds to neutrophils

87
Q

how does IgG “tag” neutrophils?

A

neutrophils have R for the Fc portion of the IgG Ab

88
Q

what is an opsonin?

A

substances that bind to a foreign invader and increase the likelyhood of being picked up for phagocytosis (i.e. IgG on neutrophils)

89
Q

complement is part of the _____ immune system

A

innate

90
Q

complement proteins are produced where?

A

in the liver

91
Q

what is the most abundant complement protein?

A

C3

92
Q

what is special about C3?

A

it’s essential for all the pathways of complement activation

93
Q

what is the alternative complement pathway?

A

a frequent, spontaneous conversion of C3 to C3b via hydrolysis

94
Q

what does C3b bind to?

A

amino and hydroxyl groups that are commonly seen on the surface of pathogens

95
Q

what happens if C3b doesn’t find anything to bind to?

A

it is rapidly destroyed

96
Q

how does C3b become stabilized?

A

binds to an amino or hydroxyl group

97
Q

what happens once C3b becomes stabilized?

A

it leads to formation of MAC

98
Q

what complement proteins form the MAC?

A

C5b C6 C7 C8 C9

99
Q

How does C3b lead to the formation of MAC?

A

C3 is hydrolyzed to C3a and C3b then C3b cleaves C5 into C5a and C5b

100
Q

What does the MAC do?

A

forms pores in bacteria leading to cell death

101
Q

what are the 2 key roles of NK cells in innate immunity?

A

kill human cells infected by viruses

produce INF-gamma to activate macrophages

102
Q

What is MHC I?

A

surface molecule of most human cells that presents antigen to CD8 Tcells and activates adaptive immunity against intracellular pathogens

103
Q

why do NK cells destroy human cells without MHC I?

A

because some viruses can prevent MHC I from coming to the surface so if it is not there then the cell must be infected with a virus and will be destroyed

104
Q

what are the 2 important surface molecules on NK cells?

A

CD16

CD56

105
Q

CD16 binds ___ of ____ antibodies.

A

Fc IgG (this causes enhanced activity of NK cells)

106
Q

How do NK cells perform ADCC?

A

through CD16 binding of the Fc portion of IgG that NK cells perform ADCC

107
Q

what is ADCC?

A

antibody dependent cell-mediated cytotoxicity - the process by which the innate and adaptive immune systems work together to kill a pathogen.

108
Q

what is CD56?

A

aka NCAM - neural cell adhesion molecule

****used as a marker for NK cells

expressed on surface of NK cells

also found in brain and NMJ

aids in binding to other cells

109
Q

what is a useful marker to identify NK cells?

A

CD56

110
Q

ADCC- in this process _____ which are produced by _____ of the ____ immune system coats a pathogen or cell and the pathogen is then destroyed by immune cells in a ______ process with cells from the _____ immune system like ____ & _____.

A

antibodies

B cells

adaptive

non-phagocytic

innate

NK cells

Eosinophils

111
Q

What cells commonly use ADCC to kill a pathogen?

A

NK cells

Eosinophils

112
Q

What are the steps of ADCC?

A

Ab binds Ag on the surface of target cells

CD16 on NK cells binds Fc of IgG antibody

NK cell degranulates causing death of the cell

113
Q

how do NK cells kill pathogens with ADCC?

A

IgG binds to pathogen-infected cells

CD16 on NK binds Fc of IgG and NKC kills cell

114
Q

how do eosinophils kill pathogens with ADCC?

A

IgE binds to pathogens - especially large parasites **

eosinophils bind Fc of IgE & toxic enzymes are released onto the parasite

115
Q

What antibody class can bind to pathogens like a large parasite?

A

IgE

116
Q

NK cells … do/do not?

  1. come from the same lineage as Tcells and Bcells
  2. Have memory
  3. require antigen presentation by MHC
  4. mature in the thymus
A
  1. Do - they are all lymphocytes
  2. Do not
  3. Do not
  4. Do not
117
Q

what is similar among eosinophils, mast cells, and basophils?

A
  1. all contain granules with destructive enzymes
  2. all can be activated/triggered by IgE antibodies
  3. important for defense against parasites (helminths)
  4. release of toxic substances kill parasite
  5. main medical relevance is in allergic disease
118
Q

Eosinophil granules appear what color with Wright stain? why are they this color?

A

red

one of the contents within the granules is major basic protein which has a positive charge that picks up the negatively charged eosin dye in the Wright stain

119
Q

what are the discharge contents (cytotoxic enzymes) that are released from eosinophils to kill parasites?

A

MBP = major basic protein

ECP = eosinophilic cationic protein

EPO = eosinophil peroxidase

EDN = eosinophil-derived neurotoxin

120
Q

what are eosinophils designed to do?

A

discharge contents onto parasites

121
Q

What takes care of pathogens that are too big to be phagocytosed?

A

eosinophils w/ IgE

122
Q

_____ are important in allergic disease

A

eosinophils

123
Q

eosinophils are…

activated by ____ antibodies

stimulated by ___

from ___ cells

A

IgE (ADCC)

IL-5

Th2

124
Q

Patients with a helminth infection will have a high or low eosinophil count?

A

high

125
Q

mast cell and basophil granules appear what color with Wright stain?

A

blue

126
Q

where are basophils found?

A

bloodstream

127
Q

where are mast cells found?

A

tissues

128
Q

mast cells and basophils can both bind what?

A

Fc portion of IgE antibody

129
Q

what happens when IgE molecules are cross-linked by a pathogen?

A

degranulation of the cell releasing histamine & enzymes (peroxidases & hydrolases)

130
Q

what does histamine do to blood vessels

A

vasodilation

131
Q

what are the components of innate immunity?

A

phagocytes - macrophages/neutrophils

complement

NKC

eosinophils

mast cells/basophils

132
Q

what are the cellular components of adaptive immunity?

A

T cells

B cells

133
Q

what do CD4+ Tcells and CD8+ Tcells do?

A

CD4+ produces cytokines

CD8+ destroys infected human cells

134
Q

what is the function of B cells?

A

produce antibodies

135
Q

how are the innate and adaptive immune systems inter-related?

A

cytokines from innate system activate cells in the adaptive immune system and vice versa and the innate immune system (macrophages) will present antigen to T cells to activate the adaptive immune system

136
Q

Dendritic cells … are called what if they are in the skin? do what?

A

Langerhans cells present antigen - pick up antigen from skin and mucosal membranes and migrate to the lymph nodes where they activate T cells

137
Q

What cell type is the “go-between” the innate and adaptive immune systems?

A

dendritic cell - essentially calls to the adaptive system for help because the innate is being over powered while the innate system is trying to fight the pathogen the dendritic cell picks up some antigen and activates T-cells with it to come and help

138
Q

what cells are granulocytes?

A

Mast cells

eosinophils

basophils

neutrophils*** most predominant type; usually the one being tested for

139
Q

What 2 lineages do agranulocytes come from?

A

lymphocytes - NKC/T cell/B cell

monocytes - macrophages

140
Q

Why is it weird that NK cells are lymphocytes?

A

bc they are part of the innate immune system and B/T cells are adaptive

141
Q

multipotent hematopoietic stem cell differentiates into what 2 progenitor cells?

A

common myeloid progenitor

common lymphoid progenitor

142
Q

common myeloid progenitor can become what 3 things?

A

megakaryocyte –> thrombocytes erythrocytes myeloblast –> granulocytes

143
Q

what does the common lymphoid progenitor cell differentiate into?

A

NK cell (large granular lymphocyte)

small lymphocyte = B lymphocyte & T lymphocyte

144
Q

what do B lymphocytes become?

A

plasma cell

145
Q

what do plasma cells produce?

A

antibodies

146
Q

what are the phases of the bacterial growth curve?

A

lag

growth

stationary

death

147
Q

what happens in the lag phase of the bacterial growth curve?

A

culture has been inoculated with a certain # of bacteria but there is no growth in the # of bacteria there can be growth in size - increasing the number of proteins, taking up some of the nutrients but they haven’t yet started to divide

148
Q

what is lymph? where does it end up?

A

interstitial fluid from tissues that drains into the lymphatic system, circulates through lymph nodes and eventually drains into subclavian veins

149
Q

why is It important for lymph to circulate through the lymph nodes?

A

important for activating the immune system in response to pathogens that may be present in the tissue the lymph came from

150
Q

what are primary lymphoid organs? where are they located?

A

sites of lymphocyte formation - B & T cells

bone marrow

thymus

151
Q

what are secondary lymphoid organs? where can they be found?

A

site where B & T cells proliferate in response to infection

lymph nodes

spleen

peyer’s patches

tonsils

152
Q

what are the layers of a lymph node?

A

cortex (outermost)

paracortex

medulla

153
Q

how do lymph nodes work to activate an immune response?

A

infection in a tissue –> lymph drains from the site of infection towards the lymph node –> dendritic cells in the lymph carry processed Ag on MHC I/II to present to the B & T cells when the lymph reaches the lymph node there is also free Ag in the lymph that gets picked up by APC’s waiting in the lymph node many B & T cells waiting for matching Ag => this results in an adaptive immune response

154
Q

what is the first layer of the lymph node that the lymph encounters? what happens there?

A

follicle of the cortex; B-cell activation

155
Q

where does all of the immune system action in the cortex of a lymph node happen?

A

lymphoid follicle

156
Q

what special cells are in the follicle of the cortex in the lymph node that help activate B cells?

A

follicular dendritic cells

157
Q

how do follicular dendritic cells differ from tissue dendritic cells?

A

they are residents of the lymph node

158
Q

how do follicular dendritic cells help to activate B cells?

A

they have surface R’s that bind complement-Ag complexes this makes it easy for the B cells to cross link and become activated

159
Q

What are follicular dendritic cells a reservoir for?

A

HIV early after infection large amounts of HIV particles seen in FDCs

160
Q

what cell is an important part of the pathophysiology of HIV?

A

follicular dendritic cells

161
Q

what are the 2 types of lymphoid follicles?

A

primary follicles - inactive, contain follicular dendritic cells and B cells

secondary follicles - “germinal center”

162
Q

what are secondary lymphoid follicles?

A

what you see during inflammation and infection aka germinal centers

163
Q

what takes place in germinal centers?

A

B cell growth and differentiation

B cell class-switching –> secrete different types of Ab’s nearby helper T cells can bind Ag and stimulate more growth from the B cells

164
Q

what are the 2 key features of the paracortex layer of a lymph node?

A

contain T cells that can be activated by dendritic cells presenting Ag

contain high endothelial venues

165
Q

what are vessels of the paracortex that allow B and T cells into the node?

A

high endothelial venules

166
Q

what are high endothelial venules? where can you find them?

A

venules that come after the capillaries in the lymph nodes, peyers patches, and tonsils they have spaces between cells of their endothelium so the B and T cells can squeeze through to exit the blood stream and enter the lymph nodes

167
Q

how to B and T cells that come from the bone marrow and thymus exit the blood stream to localize into the lymph nodes throughout the body?

A

gaps between cells of high endothelial venules

168
Q

what layer of lymph nodes becomes engorged during an immune response to give a person “swollen glands”?

A

paracortex

169
Q

the paracortex layer of lymph nodes will be underdeveloped in patients with what?

A

T-cell deficiency disorders (i.e. - DiGeorge)

170
Q

why is the paracortex underdeveloped in rare T-cell deficiency disorders?

A

there are no T cells to make up that portion of the lymph node

171
Q

what part of the lymph node do T-cells live?

A

paracortex

172
Q

the medulla of the lymph node has what 2 parts?

A

sinuses aka cavities

chords - tissue between cavities

173
Q

what is the function of medullary sinuses of a lymph node?

A

house macrophages that filter lymph and phagocytose any invaders

174
Q

what is the function of medullary chords of a lymph node?

A

contain plasma cells secreting antibodies

175
Q

What does the spleen do?

A

filters BLOOD ONLY

all blood elements can enter - no high endothelial venules/selective entry

176
Q

where in the body is the spleen located?

A

LUQ

177
Q

what happens when blood gets to the spleen?

A

it enters from the splenic artery and then percolates through the white pulp and then through the red pulp then out through the splenic vein

178
Q

what 3 structures are found in the white pulp of the spleen?

A

follicles

PALS

marginal zone

179
Q

what is the most important structure in the red pulp of the spleen?

A

sinusoids

180
Q

what happens in the white pulp of the spleen?

A

blood is exposed to B and T cells which can be activated if Ag is present macrophages for phagocytosis

181
Q

what happens in the red pulp?

A

blood gets filtered through the sinusoids 30-40% of all platelets are stored

182
Q

why are the sinusoids in the red pulp of the spleen important?

A

they get rid of old RBCs - why the red pulp is red

183
Q

the marginal zone of the white pulp in the spleen is important for what?

A

house macrophages to remove debris

house DCs to process Ag

184
Q

follicles of the white pulp in the spleen contain what?

A

B cells - similar to follicles of the lymph nodes

185
Q

Where are T-cells found in the spleen?

A

periarteriolar lymphocyte sheath PALS

186
Q

periarteriolar lymphocyte sheath

A

PALS part of the white pulp in the spleen that houses T-cells for them to respond to Ag’s present in the blood

187
Q

red pulp is lined by vascular ________.

A

sinusoids

188
Q

sinusoids of the spleen have an open _______.

A

endothelium; allows cells to pass in and out

189
Q

sinusoids of the spleen exit into _____ ______.

A

splenic chords

190
Q

splenic chords contain ______.

A

macrophages

191
Q

what is unique about the macrophages in the sinusoids of the spleen?

A

their main job is to get rid of dead and dying RBCs; this is how hold RBC’s exit the circulation

192
Q

barrel hoop membrane

A

thin basement membrane that surrounds the cells of the sinusoids

193
Q

splenic dysfunction puts you at risk for what kinds of infections?

A

bloodstream infections from encapsulated organisms

194
Q

why is there an increased risk of infection from encapsulated organisms associated with splenic dysfunction?

A

loss of marginal zone macrophages results in decreased phagocytosis of encapsulated organisms

loss of opsonization results in decreased: IgM and IgG against capsules

IgG opsonization

complement against encapsulated bacteria

C3b opsonization

195
Q

if encapsulated organisms can resist phagocytosis, how do we get rid of them?

A

macrophage phagocytosis & complement

organism is tagged with IgG –> activate complement which can directly kill the bacteria

complement also creates C3b which attracts macrophages to phagocytose the bacteria

196
Q

why is there less IgM and IgG as a result of splenic dysfunction?

A

loss of splenic B cells

197
Q

what bugs cause infection in ppl with splenic dysfunction?

A

Strep. pneumo

H. flu type B

Neisseria meningitidis

less common:

S. pyogenes

E. coli

salmonella

RBC infections - malaria, babesia

198
Q

what is the most common pathogen to cause sepsis in a patient with splenic dysfunction

A

strep pneumo death in >50% of patients

199
Q

what are 2 common reasons for splenic dysfunction?

A

splenectomy

functional asplenia

200
Q

what are the reasons someone might have a splenectomy?

A

trauma

ITP

hereditary spherocytosis

201
Q

Why would a splenectomy treat ITP?

A

ITP causes increased phagocytosis of platelets which happens in the spleen so if it is removed they won’t be destroyed and the platelet count will rise

202
Q

Why would a splenectomy treat hereditary spherocytosis?

A

less destruction of RBCs minimizes anemia

203
Q

people with what kind of anemia will have functional asplenia?

A

sickle cell anemia

they have so many abnormal red cells that their spleen is often damaged from trying to consume and remove all of them and as a result they are functionally asplenic and at risk for encapsulated bacterial infections

204
Q

what are the characteristic peripheral blood smear findings in a patient that has had a splenectomy?

A

Howell-Jolly bodies

Target cells

205
Q

Howell-Jolly bodies

A

some RBCs leave the marrow with nuclear remnants still present inside the cell which are normally cleared by the spleen

no spleen = nuclear remnants not cleared

206
Q

what causes target cells

A

too much surface area/membrane or too little volume of the RBC

207
Q

target cells are indicative of what 3 things?

A

splenic dysfunction

liver disease (too much surface area of RBC)

hemoglobin disorders (too little volume in RBC)

208
Q

why do you get target cells post-splenectomy?

A

there is always a small amount that are usually cleared by the spleen so the number of target cells will increase

209
Q

splenectomy is associated with what blood disorder?

A

thrombocytosis - failure of spleen to remove and store platelets

210
Q

T cells can only recognize what?

A

Peptides presented by an APC

211
Q

p

A

*med3* (21 decks)

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