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552 Pathophysiology > Immunity > Flashcards

Immunity Flashcards

1
Q

What are some ways that bacteria are classified?

A

gram+/gram-
rods/ spheres
aerobic / anaerobic

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2
Q

What are 2 examples of gram+ bacteria that are spherical and aerobic? How are these bugs distinguished from one another?

A

Staph: in clusters
Strep: in chains and pairs

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3
Q

What are 2 bacteria that are gram +, in rods and anaerobic? How are they distinguished from one another?

A

Clostridium: spore forming
Propionbacterium: non spore forming

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4
Q

What are 2 bacteria that are aerobic, in rods and gram +? How are they distinguished from one another?

A

Bacillus: spore forming
listeria: non spore forming

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5
Q

What is an example of a bacteria that is gram -, in rods, and anaerobic?

A

Bacteroides

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6
Q

What are some examples of gram- bugs, in rods, aerobic, and grow on a complex media?

A 
Legionella
Haemophiulus
Bordetella
Brucella
Campylobacter
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7
Q

What are some examples of gram- bugs, in rods, aerobic and grow on simple media?

A 
Vibrio
Escherichia
Klebsiella
Salmonella
Shigella
Pseudomonas
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8
Q

What is an example of a bug that is gram-, in spheres, and in pairs?

A

Neisseria

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9
Q

Aerobic

A

need O2 for oxidative phosphorylation
no O2= death
find on skin and lungs

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10
Q

Microaerobic

A

Need some O2 but alot of O2 will kill them

GI tract

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11
Q

Facultative anearobic

A

can use O2 if they have it, but can survive w/o it

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12
Q

Obligate anaerobic

A

cannot tolerate O2

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13
Q

Endotoxin

A

from gram - bacteria
release by bacteria after bacterial cell death
i.e. LPS lipopolysaccharide

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14
Q

Exotoxin

A

from gram+ bacteria
secreted from life bacteria
i.e. botulinum toxin, tetanus

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15
Q

How are gram+ and gram- bugs structurally different?

A

determined by cell wall
gram+: has a thick layer of peptidoglycan: stains purple
gram-: thick layer of peptidoglycan & outer membrane: stains pale

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16
Q

Plasmids and what they cause?

A

small piece of DNA: give bacteria super powers (i.e. ability to break down abx)
bacteria can transfer this power to other friends, even it it isn’t in the same species
-can cause abx resistance to spread quickly

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17
Q

All _____________ are intracellular while most __________ are extracellular

A

viruses

bacteria

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18
Q

How specific do host cells need to be for viruses?

A

Very: species specific and cell type specific

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19
Q

How do viruses work?

A

enter cell as viron w/ genetic material and a capsid (shell)
uncoats itself; exposes genetic material which then inserts into host cell DNA or RNA and uses the cell to make its own proteins

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20
Q

What are 2 positive aspects of viruses?

A
  1. gene therapy

2. 5% of our DNA is derived from viruses

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21
Q

What are 2 classifications of fungi? Describe them.

A

Molds: filamentous fungi grow as multinucleate, branching hyphae, forming a mycelium (ringworm)

Yeasts: grow as ovoid or spherical, single cells multiply by budding & division (histoplasma)

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22
Q

Candida albicans

A

fungi found in normal gut flora

causes opportunistic infections: thrush, yeast infections

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23
Q

Aspergillus spp.

A

highly aerobic fungi
cause of respiratory infections
worse in immunocompromised patients
most common nosocomial fungal infection

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24
Q

Tinea

A

general term for skin fungus: dermatophyte
Tinea capitis: head
cruris: groin (jock itch)
pedis: feet (athlete’s foot)

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25
Q

What are the 3 big categories of the innate immune system?

A

Mononuclear phagocytic system
Polymorphonuclear leukocytes/ Granulocytes
Lymphocytes

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26
Q

Monocyte

A

become macrophages when they leave the blood

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27
Q

What are the big players of the mononuclear phagocytic system?

A

macrophages:
Kuppfer: liver
Microglia: brain (don’t want these activated, usually in brain injury or stroke)
Dust cell: lung
Osteoclast: bone (not immune; aggregates of macrophages)

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28
Q

Dendritic cell

A

NOT macrophages; but part of mononuclear phagocytic system
i.e Langerhans cells on skin
“eat and run away”

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29
Q

What types of cells are in the polymorphonuclear leukocyte/granulocyte category

A

Neutrophil: most common WBC (97%)
Basophil
Eosinophil
Mast cell

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30
Q

What is the order of frequency of immune cells from most to least?

A 
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
NEVER LET MONKEYS EAT BANANAS
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31
Q

What innate immune cells occur primarily in tissue, and not in blood?

A

macrophages
dendritic cells
mast cells

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32
Q

What are the 3 big categories of lymphocytes?

A

B cells
T cells
NK: natural killer cells

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33
Q

B cells: 2 types

A

plasma cells: make antibodies

memory cells: keep copy in case pathogen ever comes back

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34
Q

T cells: 4 types

A

Tc: cytotoxic T cells- CD8
Th1: helper T cells- CD4
Th2: helper T cells-CD4
Memory cells

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35
Q

What is the difference between humoral and cell mediated?

A

humoral: extracellular: all fluid outside cells; eg plasma, interstitial, synovial, mucus etc
cell mediated: intracellular: mostly viral infections

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36
Q

What is the difference btw innate and adaptive immune system?

A

innate: born with
adaptive: respond specifically to pathogens you’ve been exposed to

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37
Q

What are some examples of innate humoral immune responses?

A

humoral: myeloid cells–> immediate response
-neutrophils
-macrophages
-mast cells
-eosinophils
DOES NOT CHANGE
Non-host epitopes (part of protein that the immune cell can attach to)
-bacteria try to limit amount of epitopes

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38
Q

What are some examples of adaptive humoral immune respones?

A

change over time based on specific threats body has encountered

  • B cells (also Th cells, APCs, Antigen presenting cells)
  • produce antibodies that are very specific
  • takes time to develop
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39
Q

What are some examples of innate cell-mediated immune responses?

A

NK cells: natural killer T cells
MHC existence
look for virally infected cells, not specific

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40
Q

What is an example of adaptive cell-mediated immune response?

A

Tc cells: cytotoxic T cells
if the cell is abnormal, it kills it
-specific but slower
MHC1-TCR

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41
Q

Macrophages

A

all over body, waiting for something to happen
responsible for innate response to trauma
-Engulf bacteria and release cytokines (chemical messangers btw cells, usually immune)
-trigger chemokines
-antigen presentation

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42
Q

Cytokines

chemokines

A

Cytokines: “magic fairy dust” released by macrophages
-do whatever they are supposed to do
-act as chemical messengers btw immune cells
-initiate inflammation
Chemokines: triggered by cytokines
-allow neutrophils to come kill bacteria

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43
Q

Dendritic cells

A

antigen uptake in peripheral sites

-antigen presentation in lymph nodes

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44
Q

Neutrophils

A

phagocytosis and activation of bactericidal mechanisms

short lived; become pus when they die

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45
Q

Eosinophils

A

killing of antibody-coated paraistes

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46
Q

Mast cells

A

release granules containing histamine and other active agents

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47
Q

How are cytokines and chemokines involved in inflammation?

A

released by macrophages after bacteria is found

  • they act on vascular wall to increase permeability and cause vasodilation: causes redness, heat, swelling
  • inflammatory cells can now migrate into tissue, releasing inflammatory mediators and cause pain
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48
Q

What happens at the arteriole during inflammation?

A
  • arteriolar constriction
  • transudate leaves: swelling
  • mast cell degranulation: release histamine
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49
Q

What happens at the capillary during inflammation?

A
  • endothelial cell contraction
  • increased vascular permeability
  • plasma proteins and neutrophils leak out
  • platelet aggregation and adhesion
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50
Q

What happens at the venule during inflammation?

A
  • emigration of neutrophils
  • infiltration by macrophages
  • fibrin deposiiont and fibrosis
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51
Q

What plasma systems are activated during acute inflammation?

A

Complement system
clotting system
kinin system

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52
Q

What 3 activities occur as a consequence of cellular injury in the acute inflammation cascade?

A
  1. mast cell degranulation
  2. activation of plasma systems (complement, clotting, kinin)
  3. release of cellular products
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53
Q

What are the s/s of acute inflammation?

A 
Vasodilation: redness, heat
vascular permeability: edema
cellular inflammation: pus
thrombosis: clots
stimulation of nerve endings: pain
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54
Q

During inflammation, what 2 major things do mast cells do?

A
  1. degranulation

2. synthesis of eicosanoids

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55
Q

What pre-formed factors do mast cells degranulate?

A

Histamine

neutrophil and eosinophil chemtactic factors (attract these types of cells)

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56
Q

What products do mast cells stimulate the synthesis of?

A

Phospholipase A2–> removes arachiodonic acid 9AA) & eicosaphentaenoic acid (EPA) from plasma membrane:

  • Cyclooxygenase–>prostaglandins (cause vascular effects and pain)
  • 5-lipoxygenase–> Leukotrienes (vascular effects)

also makes platelet activating factor (vascular effects and platelet aggregation)

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57
Q

What blocks phospholipse A2 from breaking down the AA and EPA from the plasma membrane

A

steroids

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58
Q

What can be used to block the prostaglandins from the cyclooxygenase pathway?

A

NSAIDS; COX inhibitors
COX-1: multi fx
COX-2: inflammation specific

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59
Q

Describe the nature of leukocyte infiltrates in the inflammatory process, using an MI as example.

A

infarction= ischemic necrosis

  • dead cardiomyoctes trigger inflammatory response
  • edema occurs almost immediately: increased vasc. permeability
  • Neutrophils respond early: ~ 1 day
  • Monocytes come later; convert to macrophages; start repair process
  • replace dead tissue w/ scar tissue
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60
Q

Macrophages can either ________ or __________

A

fight or build

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61
Q

Phagocytosis is a multistep process that involves diffusion of ____________ from a site of injury

A

chemotactic factors

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62
Q

What types of cells are involved in phagocytosis (opsonisation)?

A

macrophage, neutrophils,

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63
Q

How do neutrophils know where to go?

A

Diapedesis: movement of neutrophils through the opened intercellular junctions and into the tissue
From there, they move up the gradient to where there is the highest concentration of chemotactic factors (chemotaxis)

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64
Q

What is chemotaxis signaled by?

A

chemokines

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65
Q

What are the phases of phagocytosis?

A
  1. recognitions: non-host epitopes, bound antibody ( opsonisation) or complement (C3b): neutrophil adheres to the bacteria
  2. engulfment: by extensions of the neutrophil’s membrane (pseudopods)
  3. formation of phagosome: containing bacterium surrounded by neutrophil’s plasma membrane
  4. fusion of lysosomes w/ vacuole to form phagolysosome, lysosomes release their digestive enzymes & production of free radicals
  5. killing and breaking down of bacterium
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66
Q

What needs to be on the bacteria for the neutrophil to attach to it?
What is opsonisation?

A

PAMP: pathogen-associated molecular patterns: something on bacterium that looks different then the host cell;
Ab R: antibody receptor
opsonization: the process by which a pathogen is marked for ingestion and destruction by a phagocyte. Opsonization involves the binding of an opsonin, e.g., antibody, to an epitope on an antigen After opsonin binds to the membrane, phagocytes are attracted to the pathogen.

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67
Q

___________ are associated with the stages of inflammation. They mediate ____________ and the acquired _______________.

A

Cytokines; inflammation; immune response

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68
Q

What are the 4 stages of inflammation?

A
  1. initial response
  2. recruitment of cells
  3. Remove debris
  4. repair and regeneration
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69
Q

What happens in the initial response phase of inflammation?

A

Induce vessel leakage and endothelial adherence molecules

  • first few seconds to minutes
  • swelling starts
  • endothelial adheasion: stops rolling neutrophils at site of injury = first line of defense; very short life span
70
Q

What happens in the recruitment of cells phase of inflammation?

A

neutrophils are stopped close to damage site; diapedesis; and chemotaxis
-signal sent to body to send new neutrophils (bone marrow)

71
Q

What happens in the remove debris phase of inflammation?

A

activate leukocytes; lymphocyte growth; antibody synthesis

72
Q

What happens in the promote and regeneration phase of inflammation?

A

induce fibroblast growth and collagen production

73
Q

What happens if we can’t fix the problem causing acute inflammation?

A

becomes chronic inflammation:
angiogensis: new blood vessels to area
mononuclear cell infiltrates
fibrosis (scar tissues)

74
Q

Hematopoietic stem cells begin where?

A

bone marrow

75
Q

Where do t-cells go?

A

thymus

76
Q

What are the two types of t-cells

A

helper t cells

cytotoxic t cells

77
Q

Where do b cells go?

A

bone marrow

78
Q

T/B cells should not be ____________

A

self reactive

79
Q

Where do t/b cells go to find their antigen?

A

secondary lymphoid organs (lymph nodes)

80
Q

Once the t/b cells find their antigen they go through ______ and ________.

A

clonal selection and clonal proliferation

81
Q

When are t/b cells considered active?

A

when they find their antigen

82
Q

What happens if naive t/b cells don’t find their antigen?

A

they die

83
Q

Somatic hypermutation

A
  • b cells under go this as they replicate
  • daughter b cells that bind better continue to expand, daughters that bind worse are discarded
  • results in extremely specific b cells
84
Q

T/F: T-cells also undergo somatic hypermutation.

A

False

85
Q

T/F: T and B cells both make memory cells.

A

True

86
Q

What are examples of primary lymphoid tissue?

A

thyroid and bone marrow

87
Q

What ares of the body do not have lymph?

A

brain, kidney, and bone

88
Q

What are some examples of secondary lymphoid tissue?>

A

lymph nodes, spleen, MALT (mucosal), GALT (gut)and BALT (bronchial)

89
Q

Where are peyer’s patches found?

A

ileum of small intestines

90
Q

What is an epitope?

A

-part of antigen that t/b cell will actually bind to

91
Q

The more epitopes a bacteria has, this ________ chance a b cell will react to it.

A

increase

92
Q

Epitopes are almost always a ________.

A

protein

93
Q

B-cells are _______ but ______.

A

specific but slow

94
Q

The constant region of the antibody determines what?

A

antibody class

95
Q

IgM

A
  • largest
  • first to appear
  • spleen is the major site
96
Q

IgG

A
  • most common in the blood

- 4 subclasses of IgG

97
Q

IgE

A

allergies, found in tissues bound to mast cells

98
Q

IgA

A

secreted in GI tract, GU tract, resp tract

99
Q

Opsonization

A
  • process by which a pathogen is marked for ingestion and destruction by antibodies
  • greatly increases efficiency of phagocytosis
100
Q

How are parasitic worms killed?

A

-worm is too big for ingestion so eosinophil degranulates to degrade it

101
Q

T/F: A given B cell makes only 1 specific antibody

A

true

102
Q

You do NOT want b-cells to be _____

A

self-reactive

103
Q

Negative selection

A

keep the b-cells that don’t bind with self antigen

104
Q

Primary exposure

A
  • delayed response while naive b-cells look for antigen
  • always start as IgM
    i. e. flu shot
105
Q

Secondary exposure

A
  • much quicker
  • bigger response
  • mostly from IgG (possibly IgA or IgE)
  • this is how vaccines work
106
Q

Peyers Patches

A
  • gut associated lymphoid tissue
  • antigen is imported from lumen and presented to t/b cells
  • plasma cells produce antibody that is secreted into the lumen - neutralized pathogens
107
Q

What immunoglobin can cross the placenta?

A
  • IgG
  • protects fetus from pathogens
  • relies on IgG
108
Q

Breastfeeding

A
  • IgG and IgA will be given to baby in milk
  • provides protection against pathogens in GI tract
  • bottle fed baby more likely to get infections
109
Q

B lymphocytes may become plasma cells that produce free floating __________

A

antibodies

110
Q

What are the 2 types of T lympocytes? Which one is part of the adaptive immune system?

A

helper: phagocytosis
cytotoxic: lysis of infected cell (adaptive)

111
Q

What is the clonal diversity phase of T/b cells?

Where do they reside?

A

lymphoid stem cells from the marrow migrate to central lymphoid organs and differentiate (thymus=T cells, regions of marrow=b cells)
these cells are IMMUNOCOMPETENT, naive and have never encountered foreign antigens.
They migrate to secondary lymphoid organs (spleen, nodes) until antigen comes along

112
Q

What happens when a T/B cell finds its antigen?

A

They become active

go through clonal selection and clonal proliferation—clonal expansion

113
Q

What do B cells undergo that T cells don’t

A

somatic hypermutation
Daughter B cells that bind better to antigens continue to expand and ones that don’t die
=extremely specific B cells

114
Q

What are primary and secondary lymphoid tissue?

A

Primary: thymus; bone marrow
Secondary: lymph nodes, speleen, MALT & GALT & BALT

115
Q

Describe the structure of an antibody

A

Y shaped: 2 identical light (L) & 2 identical heavy (H) chains held together by disulfide bonds

  • constant and variable regions:
    constant: same for each antibody class
    variable: differs from antibody to antibody
116
Q

Antibodies always start as _____. Then they change based on _________

A

IgM

where they are needed

117
Q

Generally, where do you find:
IgG
IgA
IgE

A

IgG: blood
IgA: secreted
IgE: mucosa

118
Q

An antigen attaches to the ________ part of an antibody.

A macrophage attaches to the _________ part of an antibody.

A

variable

constant

119
Q

If a B cell can’t find its antigen what happens?

What happens if it does fine its antigen?

A

It dies

It replicates

120
Q

Everytime a B cell replicates, what happens?

A

the DNA that codes for the binding domain mutates

121
Q

How are self-reacting B cells weeded out?

A

nurse cells throw self-antigens at the them, if the b cell responds it is killed

122
Q

Describe the IgE mediated destruction of parasites

A

pieces of dead worm bind to naive B cell
The B cell undergoes clonal expansion, selection, proliferation
It becomes a IgE
IgE can bind to mast cell
The mast cell degranulates and releases eosinophil factor that attracts eosinophils
IgE variable region binds to worm
Eosinophils degrade the worm

123
Q

What does a high # of eosonophils indicative of?

A

parasitic infection

124
Q

What is an example of primary and secondary exposure in medicine?

A

vaccinations: inject antigens, train B cells against them, create memory cells that spring to action if antigen is ever encountered again

125
Q

What is an MHC?

A

Major Histocompatibility Complex: T cell receptor

-cell that presents an antigen to a T cell

126
Q

How is a T cell different from a B cell?

A

T cell has a variable binding site (like B cell), but only 1 binding site (B cell has 2)
T cell needs its antigen handed to it (B cell goes around searching for its antigen)

127
Q

What 3 things does a T cell need to bind to its antigen?

A
  1. proper antigen
  2. correct TCR (receptor on T cell)
  3. MHC
128
Q

How many MHCs are there? Where do you get them from? How many do you share w/ your sibling?

A

12: 6 from each parent

share 6 w/ sibling (typically)

129
Q

What is the structure of Class I MHC?
Where are they found?
What are the 3 different types?

A

structure: single transmembrane chain (alpha) complexed w/ a B2 microglobulin

Found on all nucleated cells and platelets

3 types: HLA-A HLA-B HLA-C

130
Q

What is the structure of Class II MHC?
Where are they found?
What are the 3 different types?

A

structure: 2 transmembrane chains (alpha and beta)
found: B cells, APCs, and some epithelial cells
types: HLA-DP, HLA-DQ, HLA-DR

131
Q

What does MHC-1 react with?

What does MHC-II react with?

A

I: cytotoxic T cells (CD-8)
II: helper T cells (CD-4)

132
Q

If a T cell reacts with an MHC-I, what has most likely infected the cell? What will happen to the infected cell after the T cell binds to the antigen?

A

virally infected, or cancer: the cell is making a foreign protein
The T cell will signal the MHC to die, or kills it

133
Q

If a T cell reacts with an MHC-II, what type of protein is the antigen made out of? What will the T cell do?

A

antigen is exogenously derived, i.e. macrophage has ingested something foreign

Don’t want to kill macrophage; T cell will signal for help (don’t need to know further than this)

134
Q

What decides if a transplant organ will be rejected?

A

MHCs/HLAs (same thing)

135
Q

What are examples of APCs?

A

APC= Antigen Presenting cells
macrophages
dendritic cells
B lymphocytes

136
Q

For MHC-IIs, what type of helper T cells respond to B-cells? macrophages?

A

B-cells: TH2

macrophages: TH1

137
Q

If a T cell meets a macrophage w/ a foreign antigen, what does the T cell tell the macrophage to do?

A

Activates the macrophage and makes it more aggressive and phagocytotic
-essentially the T cell tells the macrophage to ramp up what it is already doing

138
Q

If a T cell meets a B cell w/ a foreign antigen, what does the T cell tell the B cell to do?

A

T cell will activate the B cell–> leads to clonal selection, proliferation, expansion, etc.

139
Q

What happens if a self-reactive B cell finds an antigen? Why is this mechanism good?

A

no T cell would recognize it and B cell wouldn’t go any further
This is a second checkpoint to avoid autoimmune problems

140
Q

Where does T cell development occur?

A

thymus

141
Q

What is the analogy for how T cells develop that Dr. Garman gave us?

A

You want to date someone that likes you but isn’t a stalker

142
Q

Describe positive selection of T cells.

A

T cells must interact with one type of MHC; if it can’t then it will never bind.
This is how it will decide if it will become a CD8 or CD4 cell

143
Q

During positive selection of T cells, are Th1 and Th2 cells differentiated yet?

A

no

144
Q

Describe negative selection of T cells.

A

cell presents self-antigen; if it binds too tightly, we get rid of it (stalker)
-remove self reactive T cells

145
Q

If a T cell passes both positive and negative selection in the thymus, what does it do then?

A

T cell leaves thymus as mature naive T cell

146
Q

What is an immune privileged site? What are some examples?

A 
somewhere that T cells don't go
Placenta/fetus
Testes, ovaries
Eyes
Brain
Thymus
147
Q

In lymph nodes, what occurs in the germinal centers located in the cortex?

A

B cells undergo clonal expansion
become enlarged/swollen when there is an infection because they become full of B-cells that have their antigens and are under going clonal exapnsion

148
Q

Where in the lymph nodes, do T cells undergo clonal expansion?

A

paracortical area: btw cortex and medulla

149
Q

Describe the role of dendritic cells in capturing antigens.

A

“they grab a small piece of antigen and run away”

  • Immature dendritic cell picks up antigen in tissue and phagocytoses it (releases cytokines)
  • after it meets antigen, it becomes mature and migrates to regional lymph node and presents the antigen to an immunocompetent T cell
150
Q

What is the analogy that Dr. Garman gave us to describe natural killer cells?

A

“Illiterate Gestapo”

151
Q

Describe how NK cells work. What do they check for?

A

check for MHC-I and accompanying surface proteins to make sure they look ok
-if MHCs are not there, too few, mutated or accompanying proteins not there: NK will kill that cell

152
Q

MHCs are found on all ___________________ cells including leukocytes

A

nucleated

153
Q

What do superantigens bind to? Is this reversible or irreversible?

A

binds random Th-cells w/ random MHC II cell

irreversible

154
Q

Superantigens activate Th cells___________ of the TCR antigen specificity.

A

independently: they don’t fit into the receptor site, but still activate it
- This causes an over active immune response

155
Q

What syndrome is an example of a superantigen?

A

TSST

156
Q

How many types of hypersensitivities are there?

A

4: I-IV

157
Q

Type I hypersensitivity are mediated by _________. They mainly mediate _____________ & _____________

A

IgE

allergies and anaphylaxis

158
Q

What is the main symptom of type I hypersensitivities?

A

Mast cells are activated by IgEs: inflammation

VASCULAR PERMEABILITY & increased blood flow–> edema

159
Q

Type II hypersensitivities are mediated by _____ which cause _________ to bind to our cells and cause immune response.

A

IgG (antibody of blood)

antibodies

160
Q

What are some examples of Type II hypersensitivities?

A

blood transfusion reaction
hemolytic disease of newborn
Graves disease
Myasthenia Gravis

161
Q

Type III hypersensitivities are mediated by _________ and occur when too much antigen and antibodies build up and form __________

A

IgG

immune complexes

162
Q

What happens when immune complexes form?

A

they start sticking on blood vessels and cause vascular damage

163
Q

What are some examples of Type III hypersensitivities?

A

Systemic lupus erythematous
necrotizing vasculitis
serum sickness

164
Q

Type IV hypersensitivities are mediated by ____________

A

T cells (cytotoxic, Th1, or Th2)

165
Q

What are some examples of Type IV hypersensitivities?

A

transplant rejection
Hashimoto’s thyroiditis
DM I
poison ivy

166
Q

What are 3 sources of antigens? What kind of antigen does each type of hypersensitivity usually react with.

A

Allergy
Autoimmunity (self antigen)
Alloimmunity (some one elses antigens)

Type I: mostly allergy
Type II: mostly autoimmune; some alloimmunity
Type III: auto and alloimmunity
Type IV: all 3

167
Q

What 2 things do you need to acquire an autoimmune disease?

A

genetic predisposition (usually HLA linked) & environmental trigger

168
Q

w/ lupus (SLE), ____________ antibodies are produced that work against double stranded _______

A

antinuclear

DNA

169
Q

When does SLE affect DNA?

A

During necrosis, when cells release DNA the antibodies bind to it and form immune complexes and we get vasculitis

170
Q

What demographic of people are most likely to get SLE? What organ failure is a big risk for SLE?

A

African Americans in US are 8x more likely; F>M in their young 20s

Kidney failure

552 Pathophysiology (5 decks)

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