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Pathophysiology Spring 16 > Inate and humoral immunity > Flashcards

Inate and humoral immunity Flashcards

1
Q

megakaryocytes (platelets) are not part of immune system, but participate in ___________

A

inflammation

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2
Q

what cells are NOT typically found in tissues

A

macrophages
dendritic cells
mast cells

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3
Q

Cytotoxic T cell

A

CD8- MHC1

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4
Q

Helper T

A

CD4- MHC2

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5
Q

cells in inmate humoral (extracellular immunity)

A

myeloid cells - neutrophils, macrophages, mast cells, eosinophils

non host epitopes- protein that is not part of our immune system, ex- on bacteria

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6
Q

changes over time based on what the body encounters

B-cells, antibodies, T-helper, APC’s

produce antibodies that are very specific- takes time

A

Adaptive humoral immunity

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7
Q

NK cells, MHC existence

A

innate- cell mediated immunity

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8
Q

cytotoxic t cells- if it sees an abnormal cell it kills it

A

cell mediated adaptive immunity

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9
Q

what cells are all over the body and wait for something to happen, they are responsible for the innate response

A

macrophages- they also recognize the possibility of bacteria

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10
Q

engulfs bacteria and releases CYTOKYNES

A

macrophages

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11
Q

Messenger among immune cells- innate inflammation

A

cytokines

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12
Q

cytokines trigger ________ that allow neutrophils that have been circulating blood to come and engulf bacteria

A

chemokynes

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13
Q

INFLAMMATION:

Cell injury or pathogenic invasion causes the activation of ________________ , __________ , __________ which activates the 1)____________, 2)____________, and 3)______________ responses

A

plasma systems, release of cellular products, mast cell degranulation

  1. compliment
  2. clotting
  3. Kinin
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14
Q

INFLAMMATION:

redness and heat

A

vasodilation

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15
Q

INFLAMMATION:

cellular infiltration

A

pus

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16
Q

INFLAMMATION:

thrombosis

A

clots

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17
Q

INFLAMMATION:

stimulation of nerve endings

A

pain

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18
Q

INFLAMMATION:

histamine release and chemotactic factors attract neutrophils + eosinophils

A

mast cell degranulation

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19
Q

INFLAMMATION:

prostaglandins, prostacyclins, leukotrienes and thromboxjnes

have inflammatory in immune functions

A

4 families of ecosinoids

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20
Q

removal of arachidonic acid + EPA from plasma membrane

A

Phosposlipase A2 - a biologic mediator synthesized from mast cells

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21
Q

converta arachidonic acid to prostaglandins, prostacyclins and thromboxane

A

Cyclooxygenase a biologic mediator synthesized from mast cells

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22
Q

blocked by steroids

A

phospholipase A2

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23
Q

blocked by COX-1 inhibitors - ASA, ibuprofen and selective cox II inhibitors like vioxx and celebrex

A

cyclooxygenase

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24
Q

what is the timeline of leucocyte infiltrates in inflammatory reactions such as ischemic necrosis/ infarction?

A
  1. immediate edema
  2. day one- neutrophils peak neurtrophilic infiltrates and congested blood vessels
  3. monocytes peak later, day 2, come into tissue and cover to macrophages to start repair
  4. repair process- repair damaged tissue with scar tissue
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25
Q

Scar tissue in cardiac ischemia is ____________ and results in ____________.

A

non contractile

loss of function

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26
Q

Initial steps of phagocytosis include adherence of neutrophils to the vessel wall (__________) retraction of ________________(vascular permeability), and movement of neutrophils through the vascular spaces (___________), the cells move up the gradient by ____________.

A

pavementing, endothelial cells, diapedesis,chemotactic factors

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27
Q

adherence of neutrophils is optimized by

A

antibody and opsonins

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28
Q

opsonins bid to

A

epitopes

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29
Q

engulfment into

A

phagocytotic vacuole or phagocyte

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30
Q

after a bacteria is engulfed the phagosomes are fused by…

A

lysosomes- which will produce reactive oxygen species hydrogen peroxide and superoxide to kill the microorganism

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31
Q

seconds to minutes- swelling vessel leakage, ENDOTHELIAL ADHESION

INTEGRINS & SELECTINS

A

Initial cytokyne response

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32
Q

stops rolling neutrophils, first line of defense

A

initial cytokyne response

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33
Q

Histamine, kinins, leukotriens, prostaglandin, IL-1 snf TNF

A

initial cytokyne response

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34
Q

neutrophils that are stopped by damage, diapedesis, chemotaxis, send signals to more cells

A

cytokine response causing recruitment of cells

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35
Q

activation of leukocytes, lymphocyte growth, antibody synthesis

A

cytokyne response causing removal of debris

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36
Q

induce fibroblast growth and collagen production

A

cytokyne respons to promote regenteration and repair

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37
Q

granulocyte colony stimulating factor

A

cytokine response causing recruitment of cells

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38
Q

platelet derived growth factor (PDGF)

A

cytokyne respons to promote regenteration and repair

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39
Q

Fibroblast growth factor (FDG)

A

cytokyne respons to promote regenteration and repair

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40
Q

Tumor Necrosis factor TNF

A

is active in all four stages of cytokine involvement with inflammation

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41
Q

there results of chronic inflammation

A
  1. angiogenesis
  2. mononuclear cell infiltrate
  3. SCAR formation
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42
Q

loss of function

A

fibrosis

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43
Q

mediators, neutrophil recruitment, swelling

A

acute inflamation

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44
Q

clearance of injurious stimuli, clearance of mediators and acute inflammation cells, replacement of injured cells, normal function

A

resolution

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45
Q

when b and t cells find an antigen

A

they are activated- clonal selection leads to clonal proliferation and expansion.

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46
Q

somatic hypermutation

A

activated b cells

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47
Q

produce free floating antibodies

A

b cells that become plasma cells

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48
Q

do NOT undergo somatic hypermutation

A

T-cells

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49
Q

____________ help ___________ to mature

A

helper T cells

naive b cells

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50
Q

cytotoxic T cell

A

adaptive immunity

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51
Q

NK cells

A

Innate immunity

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52
Q

bone marrow, thymus

A

primary lymphoid tissue

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53
Q

lymph nodes

A

2ndarey lymphoid tissue - none in brain, kidneys or bones

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54
Q

lymph from brain drains to

A

cervical lymph nodes

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55
Q

Mucosal/ gut associate lymph tissues

A

MALT/GALT
pyers patches ilium of small intestine
tonsils and adenoids

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56
Q

BALT

A

in lungs, bronchial associated lymph tissue

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57
Q

antigenic determinants that B or T cell bind to

A

Epitopes - the more epitopes the more the chance of binding

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58
Q

antigen binding domain

A

variable region

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59
Q

determines antibody class

A

constant region

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60
Q

antibody most common in blood

A

IgG

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61
Q

only antibody that can cross placenta

A

IgG

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62
Q

all antibodies start as these

A

IgM or IgD

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63
Q

pentamer

A

IgM

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64
Q

monomer

A

IgD, IgE, IgG

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65
Q

antibody of allergies found tin tissues and bound to mast cells

A

IgE

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66
Q

causes allergic Rhinitis

A

IgE

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67
Q

secreted in GI tract, genital and urinary tract and respiratory tract

A

IgA

68
Q

J chain

A

IgA

69
Q

class switch

A

antibodies start as IgM and switch to IgE, IgG, IgA

70
Q

the antibody variable binding region bind to and epitome in a specific ares, then epitope can be_________

A

present on your cells

71
Q

has a receptor for a CONSTANT region

A

macrophages- for opsonization, they look for bacteria and viruses

72
Q

parasites

A

eosinophils- worm too big , eosinophils degranulate and spill out enzymes

73
Q

have one specific antibody antibody, if it becomes ACTIVATED, it will produce that antibody

A

b cells

74
Q

takes deal and area that codes for that variable region and rearranges it/chops out parts

A

b cell recombination

75
Q

__________ cells check to be sure B-Cell is not self reactive using __________.

A

nurse cells- if b cell responds they die= self reactive

Negative selecton

76
Q

have and antibody on surface, but have not found antigen

A

naieve b cells

77
Q

every generation binds more specifically

A

somatic hypermutation

78
Q

if a nurse cell throws self antigen at a b cell and it does not bind what is it?

A

it becomes an immunocompetent naive B cell via negative selection

79
Q

Immunoglobulin used in parasitic infection

A

Pieces of dead worm bind to naive B cell

Clonal selection, expansion and hyper proliferation

Class switch to IgE- constant region can bind to MAST CELLS,

next exposure MAST cell releases eosinophil chemotactic factors

IgE Variable region will bind to another worm attract eosinophils and degrade worm

80
Q

what generates the primary and secondary immune response

A

IgM is primary, then a class switch to IgG, next exposure IgG takes over MUCH quicker

81
Q

secretory immune response

A

IgA

82
Q

GALT________________

antigen passes through M cell (intestinal lumen) and presents to B and Helper t cells

plasma cells produce ________________.

A

Peyers patches

IgA that is secreted into the lumen to neutralize pathogens

83
Q

before birth fetus relies on _____ for immune protection because they have NO _____________ . it protects the fetus from pathogens and toxins

A

Maternal IgG, Adaptive immune system

84
Q

in the fetus, their do not have ___________, but the ____________ system is working

A

Adaptive immune system,

Innate system is functional

85
Q

what happens to fetal IgG after birth?

A

no longer receiving maternal IgG, and it slowly decline, the baby will begin to produce their ow IgG and it will develop its ADAPTIVE immune system with exposure to antigens

86
Q

provides protection for GI tract

bottle fed = more likely to get GI infections

A

IgG and IgA present in breast milk

87
Q

location of TCR

A

always on the surface of t cell, never released/free floating, unlike antibodies

88
Q

t cell antigen presentation

A

always on another cell always on an MHC

89
Q

always present SELF antigen

A

MHC I

90
Q

useful for virally infected cell

A

MHC I

91
Q

Present to Cytotoxic CD 8 Cells

A

MHC I

92
Q

kills the cell the antigen is presented on

A

Cytotoxoc CD8 cell,

exception = herpes- cannot kill neurons

93
Q

Present foreign antigen

A

MHC II

94
Q

present to helper T

A

MHC II

95
Q

if a macrophage ingests a necrotic cell and it is presented to a helper T what will happen?

A

the helper t will not react because the antigen is NOT FOREIGN

96
Q

MHC are most important in ___________

A

Transplants 6 from mon and 6 from dad

97
Q

HLA- A,B, C

A

MHC I

98
Q

HLA- DP, DQ, DR

A

MHC II

99
Q

protein cut up and presented on MHCII

A

endogeneous;

cancerous

virally infected

100
Q

protein cut up and presented on MHC II

A

EXongenous:

presented by professional APC

101
Q

Professional APC that present to helper T cells

A

b cells
macrophages
dendritic cells

102
Q

what activates the b cell?

A

b-cell presents to helper t and it says it is foreign, so the b cell starts to produce antibodies- Macrophage much more aggressive and phagocytotic

103
Q

checkpoints to avoid autoimmune diseases

A
  1. Nurse cells throw self antigen at b cells

2. B-cell must present the antigen to T helper cells to be activated

104
Q

undergoes BOTH positive and negative selection

A

T-cells

105
Q

keep the ones that bind

A

positive selection must be interested

106
Q

get rid on the ones that bind too much or too tightly

A

negative selection - can’t be a stalker

107
Q

placenta/fetus

testes/ovaries

eyes

brain

thymus

A

Immune privileged sites- T cells cant go here!

108
Q

b-cells to undergo clonal expansion- find antigen

enlarged with infection

A

Germinal center in cortex of lymph node

109
Q

t cells undergo clonal expansion

nearest to the infection site = first to respond and most swollen

A

Pericortical area, between cortex and medulla of lymph node

110
Q

a dendritic cell will capture antigens in _________and then _________ to the ________ where it will present to __________cell.

A

tissues

migrate

lymph node

naive helper t-cell

111
Q

Check MHC and kills if anything is wrong

A

NK cells

112
Q

NK cells are reluctant to kill

A

Neurons

113
Q

Activate the T-Helper independent of TCR antigen specificity

irreversibly bind

Cause MASSIVE up regulation of immune response system wide

A

Super antigens which cause anaphylaxis

114
Q

reaction of immune system worse than the problem it is fighting

A

hypersensitivity

115
Q

IgE mediated

A

Type I hypersensitivity

116
Q

Mast cells degranulate when they see antigen causing inflammation

A

Type I hypersensitivity

117
Q

allergic rhinitis
asthma
anaphalaxis

A

Type I hypersensitivity- allergy

auto and allo rare

118
Q

Free and antigen

Bound and fixed antibody

A

Type I hypersensitivity

119
Q

Mast cells and basophils have antibody attached

A

Type I hypersensitivity

120
Q

antigen must come to immune cells

A

Type I hypersensitivity

121
Q

IgG mediated hypersensitivity

A

Type II hypersensitivity

Type III hypersensitivity

122
Q

Antigen always FIXED on intrinsic tissues

Antibody free and binds to our cells to cause immune response

A

Type II hypersensitivity

123
Q

Self reactive B- Cells are a key feature

A

Type II hypersensitivity- autoimmune diseases

124
Q

Blood transfusion reaction- blood type mismatch, recipient immune cells attack donor blood resulting in hemolysis

A

Type II hypersensitivity - alloimunity

125
Q

Hemolytic disease of the newborn

A

Type II hypersensitivity

126
Q

Rh - MOM with Rh+ FETUS, mom makes IgG (Anti Rh+ antibodies)

Baby born with ANEMIA because RBC’s are destroyed by fetal immune system

A

Hemolytic disease of the newborn- alloimunity

127
Q

Graves disease

A

Type II hypersensitivity - autoimmune

128
Q

antibody binds to TSH receptors Produce lots of T3 and T4

A

Graves disease

129
Q

Myasthenia Gravis

A

Type II hypersensitivity - autoimmune

130
Q

antibody binds to Ach receptor on muscle and destroys receptors

A

Myasthenia Gravis

131
Q

Rheumatic fever

A

Type II hypersensitivity- antibodies against heart and CNS

132
Q

Exongenous or Endogenous FREE antigen

FREE antibody

A

Type III hypersensitivity

133
Q

formation of free immune complexes

A

Type III hypersensitivity

134
Q

found in circulation or tissue fluids

A

Type III hypersensitivity

135
Q

immune complexes result from

A

phagocytes not able to keep up with destruction of immune complexes

136
Q

when immune complexes start sticking to vessels the cause

A

vascular damage

137
Q

Systemic lupus Erythematous

A

Type III hypersensitivity - autoimmune

138
Q

Necrotizing vasculitis

A

Type III hypersensitivity - autoimmune

139
Q

serum sickness- antigen in blood that host reacts with

A

Type III hypersensitivity - aloimmune

140
Q

T cell mediated hypersensitivity

three types- cytotoxic, helper T1 and T2

A

Type IV hypersensitivity

141
Q

transplant rejection- body rejects foreign tissue

A

Type IV hypersensitivity - Alloimunity

142
Q

hashimotos thyroiditis

A

Type IV hypersensitivity - Autoimmune

143
Q

type I diabetes- kills pancreatic beta cells that price insulin

A

Type IV hypersensitivity - autoimmune

144
Q

Poison ivy

A

Type IV hypersensitivity - Allergy

145
Q

allergens, foods, pollen

A

environment

146
Q

self antigen

A

autoimmune

147
Q

another person, transplants, blood products, pregnant, animal, toxin

A

alloimunity

148
Q

wheat allergy

A

Type III hypersensitivity- allergy

149
Q

Hyperacute graft rejection

A

Type II hypersensitivity - alloimunity

150
Q

need environmental trigger + genetic predisposition (wrong HLA)

A

Autoimmune disease

151
Q

type III hypersensitivity, butterfly rash, anti-nuclear antibodies against DNA, cell damage and necrosis, immune complexes, vasculitis, kidney failure is a high risk

A

Systemic lupus Erythemotosus

152
Q

environmental trigger for lupus

A

UV radiation - IgG

153
Q

lymph nodes completely empty

A

SCID

154
Q

lymph node with no germinal centers

A

X-linked -agammaglobulinemia

155
Q

lymph node with empty inner cortex- t cells absent

A

Digeorge syndrime

156
Q

SCID, Agammaglobulinemia, Digeorge syndrome

A

primary lymphoid (B and T cells) immunodeficiency

157
Q

Chronic granulomatous disease

A

primary meyloind immunodeficiency

158
Q

No B or T cells

adenasine deaminase

A

SCID

159
Q

without immunoglobulin in blood

No B-cells = No immunoglobulins

Cellular reaction but no humoral reaction

A

X-linked agammaglobulinemia

160
Q

No thymus = NO T-cell development

during development of pharyngeal arches- also have facial deformities because that develops with pharyngeal arch

A

DiGeorges Dyndrome

161
Q

Infects CD4

A

HIV

162
Q

drug that prevents virus from entering CD4 cell

A

entrance inhibitoe

163
Q

stops all reverse transcriptase, will not effect us because we do not have

A

Revers transcriptase inhibitor

164
Q

prevents intigration of viral DNA with our DNA

A

integrase inhibitor

165
Q

inhibit HIV proteases but not our own

A

protease inhibitors

166
Q

HIV causes a loss of __________ cells, central to activating _________ cells

A

CD4 and helper

activating B cells

167
Q

can’t make oxidative burst to make hydrogen peroxide to kill bacteria.

phagocyte cannot kill bacteria

lots of bacterial infections, no effect on viral infections

A

Chronic granulotomas disease

Pathophysiology Spring 16 (9 decks)

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