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Path3 > Immunity > Flashcards

Immunity Flashcards

1
Q

3 examples of type 1 mediated reactions

A

asthma
hives
allergic rhinitis

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2
Q

Ig__ in type 1

A

Ige

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3
Q

most important cells in Type 1

A

mast cells, eosinophils

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4
Q

primary reaction in Type 1 is from

A

preformed mediators

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5
Q

secondary reaction in Type 1 is from

A

synthesized mediators

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6
Q

type II is

A

direct attack on cell/tissues by antibodies

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7
Q

6 examples of type II

A 
hemolytic anemia
erythroblastosis fetalis
Goodpasture syndrome
Myesthenia Gravis
Rheumatic Fever
Grave's Disease
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8
Q

Type II involves

A

complements

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9
Q

type 3 is

A

damage secondary to deposition of immune complexes (igg-ag)

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10
Q

4 examples of type III

A

glomerulonephritis
serum sickness
polyarteritis nodosa
Arthus reaction

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11
Q

type III also involves

A

complements

neutrophils!

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12
Q

type IV is

A

t cell and macrophage mediated

delayed type hypersensitivity

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13
Q

most important cells of type IV

A

cytotoxic T cells

macrophages

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14
Q

hyperacute rejection

A

few minutes–>hour

throbmobosis and vessel attack

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15
Q

acute reject

A

days–>weeks
host becomes sensitized to donor tissue
cellular and antibody mediated
vasculitis, parenchymal attack and damage

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16
Q

chronic rejection

A

mixed mechanism with many macrophages, T cells and plasma cells
–extensive and longstanding damage and FIBROSIS to graft

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17
Q

anaphylatoxins

A

C3a, C5a

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18
Q

Type I mechanism

A

antigen–>DC processing–>DC stimulates TH2 cell–>helper T cell stimulates B cell–> can turn into plasma cell that makes IgE –> bind to FcRe on Mast cells

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19
Q

IL involved in Hay fever

A

IL4

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20
Q

cross linking

A

when Ag brings 2 IgEs close together, stimulating a signal across the mast cell membrane

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21
Q

two phases of anaphylactic rxns

A

immediate/initial response (5 min-1 hr)

delayed/secondary response (2hrs - days)

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22
Q

immediate response involves

A

IGe binding to mast cell and releasing preformed mediators

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23
Q

4 tissue events in immediate/initial responses

A
  • vasodilation & vascular congestion (histamine mediated)
  • vascular leakage= edema
  • smooth muscle contraction
  • glandular secretion
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24
Q

clinical response to secondary response

A

coughing
chest tightness
mucous after original exposure

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25
Q

3 tissue events due to secondary response

A
  • tissue infiltraton by eosinophils, basophils, neutrophils, some T cells
  • tissue injury
  • mucosal damage and remodeling
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26
Q

primary mediators of secondary response

A
  • leukotrienes
  • prostaglandins
  • platelet activating factor (PAF)
  • cytokines
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27
Q

eosinophilic contribution

A

PAF acether–> LTC4 & 15 HETE
- mucous secretion & epithelial desquamation
Cationic/Neutrotoxic Protein–>Peroxidase & Arylsulphatase
- Major basic protein–> Mast cell degranulation & epithelial desquamation

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28
Q

3Localized Type 1 rxns

A

1) severe urticaria- massive degranulation in response to cold or heat
2) atopic keratoconjunctivitis- eye will become puffy and get corneal edema that extends into slclera
3) asthma

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29
Q

pathogenesis of asthma

A

1) epithelial cells killed off and have to be replaced–> myofibroblasts thicken basement membrane
2) smooth muscle cells hypertrophy
==> tissue damage and matrix remodeling

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30
Q

hemolysis through mismatched blood transfusion

A

type 2 rxns

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31
Q

2 mechanisms of hemolytic transfusion rxns

A

1) acute- premade antibodies–cells lyse due to complement very rapidly
2) delayed- no preexisting Abs- made as transfused Abs degrade by natural causes– attacking remaining live cells

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32
Q

Mac complex

A

attaches to cell surface and creates pores in it

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33
Q

c3b

A

opsonin for Macrophages that phago the fragmented RBC

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34
Q

best Ig for hemolytic RBC

A

iGM (because relies on complement)

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35
Q

Good Pasture’s Disease

A

auto-antibody against collagen Type IV in basement membrane in glomeruli (not tubule) and alveolar walls
clinical- hemoptysis and renal failure

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36
Q

where does rheumatic fever come from?

A

Group A beta hemolytic streptococcal infection (Ab that clear infection start attacking self-antigen)

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37
Q

subsets of rheumatic fever

A

endocarditis

myocarditis

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38
Q

endocarditis

A

vegetations form on valves with fibrin/platelet aggregates

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39
Q

myocarditis

A

Aschoff bodies (areas of inflammation within heart CT that become granulomatous when fully developed)

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40
Q

Grave’s Disease

A

anti-receptor antibodies can cause autoimmune overstimulation or receptor blockade
(TSH on TSH R)

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41
Q

Myasthenia Gravis

A

AchR antibody binds and destroys receptor

–weakness in muscles as day progresses

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42
Q

Local Type III rxns

A 
arthus rxn
vasculitis
glomerulonephritis
arthritis
pneumonitis
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43
Q

systemic type III rxns

A

serum sickness
SLE
drug rxns

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44
Q

key damage cell in Type III

A

neutrophil!

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45
Q

deposited complexes form

A
  • complement cascade

- platelet activation (Hageman factor)

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46
Q

platelet activation results in

A
  • microthrombi formation–>occlude small vessels–>potential ischemia if extensive
  • hageman factor (f XII of coagulation cascade)–>activation of kinins–>vasodilation and edema
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47
Q

glomerulonephritis caused by

A

different streptococcus from that causing rheumatic fever

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48
Q

why do streps localize to glomeruli

A

charge- complexes have specific charge that allows them to cross the vascular membranes and enter blood vessel lumen

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49
Q

serum sickness

A

following diptheria horse antitoxin, pts develop arthritis, skin rash, and fever

formation of anti-horse Ig antibodies then form complexes that get stuck places

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50
Q

main types of cells in type IV

A

t cells
macrophages
APC

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51
Q

types of type Iv HS

A

1) Delayed type- CD4+
2) T cell mediated- CD8+
3) Rejection of transplanted organ- CD4/8/ antibodies

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52
Q

what almost always results in DTH

A

virally induced inflammation

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53
Q

detrimental cell products in type IV

A 
TNFa/b
IL1
superoxides
NO
hydroxyl radicals
neuron toxins
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54
Q

beneficial cell products

A

TGFb
Growth & Trophic Factors
GM-CSF

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55
Q

prototype DTH

A

TB granuloma

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56
Q

what type of cells participate in allograph rejection

A

CD4 and CD8

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57
Q

hyperacute rejection

A

moments-48 hrs
Ab rxn at endothelium

  • rapid thrombosis of vessels and organ death
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58
Q

acute rejection does NOT mean___ and is mediated by

A

neutrophils

- t cells

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59
Q

2 types of acute rejection

A

acute cellular- CD4/CD8, lymphocytes, macrophages

acute humoral-
anti-graft antibodies

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60
Q

chronic rejection

A

months to years
chronic vasculitis, intimal fibrosis, obliteration of lumen–>organ ischemia, interstitial mononuclear cell infiltrates–>organ atrophy

61
Q

2 mechanisms to initiate rejection

A
  • cellular: Tc attack cells with foreign MHCI

- humoral- Th cells recognize foreign MHCII and stim Tc and B cells–>B cells make plasma cells to make Ab

62
Q

direct vs indirect antigen presentation

A

direct- APC from donor in graft

Indirect- APC is dead and host cell presents

63
Q

acute kidney rejection

A

congested
swollen
hyperemic

64
Q

chronic rejection

A

shrunken
scarred
severely damaged kidney

65
Q

graft atherosclerosis

A

chronic graft rejection secondary toe xtensive damage to endothelium and artery wall

66
Q

acute GVH

A

initially limited to endothelium of skin, GI tract, and liver

67
Q

chronic GVJ

A

multiple organs show significant damage

68
Q

positive selection

A

thymocyte must recognize through the TCR an MHC/peptide above a certain affinity threshold

69
Q

negative selection

A

deletion happens when affinity is too high

70
Q

3 mechanism of peripheral tolerance

A

1) anergy- shut off t cells via CTLA4
2) Tregs
3) clonal deletion by activation-induced cell death

71
Q

main mechanism that shapes repertoire

A

negative selection

72
Q

5 mechanisms of autoimmunty

A

1) molecular mimicry
2) escape of autoreactive clones
3) release of sequestered antigen
4) epitope spreading- more and more antigen released by more and more tissue damage
5) polyclonal B activation

73
Q

PTPN22

A

most freq implicated
-Rheumatoid arthritis, T1DM

encodes a protein tyrosine phosphatase
-defective copy- out of control tyrosine kinases in lymphocytes–>lnger phos & activation of proteins

74
Q

NOD2

A

Crohn’s disease

encodes a cytoplasmic sensor of microbes
-defective copy–>poor at sensing microbes–>increase in tissue invasion by microbes–>chronic inflammation

75
Q

cytokine receptor genes

A

IL2Ra (CD25) and IL7Ra
associated w/ MS

may control maintenance or dev. of tregs

76
Q

2 mechanisms of environmental triggers of autoimmune flare ups

A

adjuvant effect

molecular mimicry

77
Q

polyclonal b cell activation

A

increase production of autoantibodies (EBV, HIV)

78
Q

t regs are

A

CD4+ CD25+

79
Q

CD25

A

low affinity IL2 Receptor (alpha)
aka Tac antgien
–expression rapidly increases upon T cell activation

tends to be overexpressed in autoimmunity

80
Q

how are CD4CD25 cells generated

A
  • from thymus )high avidity)
  • from regular t cells in periphery

**regulated by FoxP3

81
Q

IPEX

A

x linked disease that is due to defect in FoxP3

–characterized by neonatal DM, enteropathy, endocrinopathy

82
Q

what cytokines are req for tregs to suppress other cells

A

IL10, TGFb

83
Q

general features of autoimmune disease

A

progressive- sporadic relapses/remissions

epitope spreading (tissue damage releases self antigens and exposes previously hidden epitopes)

84
Q

TH1 autoimmune disorder contains

A

macrophage rich inflammation

85
Q

TH17 autoimmune disorder contains

A

neutrophil rich

86
Q

type 1 diabetes mellitus

A

t cells reacting to beta cells in islets

often preceeded by dev of anti-insulin antibodies

major targets include insulin and GAD

87
Q

clinical manifestations of lupus

A

Malar Rash
Libman Sacks
Retinal Damage (vasculitis–>arterial occusion)

88
Q

Malar Rash

A

liquefactive degeneration of the basal layer of the epidermis and edema at the dermo-epidermal junction
igg deposits

89
Q

Libman Sacks

A

sterile, inflmmation-free valve vegtations associated with SLE

90
Q

immunological pathology of SLE

A

failed self tolerance-cant eliminate b cells, CD4 cells

abnormal rxn of TLr to self DNA/RNA rather than viral RNA (mediated by IFN1)

91
Q

environmental factors that influence sLe

A

UV exposure
sex hormones (esp during reproductive years)
drugs

92
Q

rheumatoid arthritis

A

chronic systemic inflammatory disease affecting many organs but main target is joint (non-suppurative proliferative/inflam synovitis)

93
Q

microscopic of RA

A

synovial hypertrophy with formation of villi

subsynovial tissue containg dense lymphoid aggregate

94
Q

environmental associatins with RA

A

infectious agents, but one agent has not been specifically implicated

citrullinated proteins (arginine–>citruline)- can be seen in lung of smokers

95
Q

immunological factors of RA

A

CD4+ t cells with TH17 and TH1 appear early

96
Q

80% of patients with RA have

A

rheumatoid factor-typically igm

autoanitbodies to Fc portion of IgG

NOT cause of disease but marker of disease

97
Q

anti-CCP

A

antibody to citrullinated peptides

produced at sites of inflammation

98
Q

clinical success with RA and

A

TNFa antagonists

99
Q

primary vs secondary ids

A

primary-genetically determined

secondary-acquired

100
Q

xlinked primary iDs

A

xla
hyper igm
scids
wiskott-aldrich syndrome

101
Q

autosomal primary ids

A

dominant -
C1 inhibitor deficiency

recessive-
digeorge syndrome
scids

102
Q

molecular primary ids

A

isolated iga deficiency

common variable immunodeficinecy

103
Q

secondary ids

A

iatrogenic

hiv

104
Q

humoral deficiencies

A
  • XLA
  • common variable immunodeficinecy
  • isolated iga deficiency
  • hyper igm syndorme
105
Q

XLA

A

failure of b cell precursors to develop into mature b cells–> decrease to absent b cells–>deficiency of igg

t cells are still intact so increase risk of autoimmune

106
Q

what are pts with xla susceptible to?

A 
bacterial infection
-- haemophilus, strept, staph
enteroviral
--echovirus, poliovirus, coxsackie
severe intenstinal giardiasis (parasite normally resisted by iga)
--giardia lamblia
107
Q

etiology of xla

A

mutation on Btk gene on x chrome–>req for signal transduction necessary for ig light-chain rearrangement and b cell maturation–>mutation removes maturation signal

108
Q

treatment xla

A

ivig

109
Q

common variable immunodef

A
  • hypogammaglobulinemia

- normal number of b cells, but cant turn into plasma

110
Q

differentiating brutons and CVI

A
  • CVI affects both geneders equally

- CVI has later onset

111
Q

isolated iga def

A

low levels iga–>increase risk resp and gi and uti

112
Q

hyper igm syndrome

A

defect in Th cells ability to deliver activiating signals to b cells for class switching

most are xlinked with mutation in gene encoding CD40L (CD154)

113
Q

cellular deficiencies

A

digeorge syndrome

114
Q

digeorge syndrome

A
  • failure of 3rd and 4th pharyngeal pouches to develop during embryogenesis (no thymus, no pth)
  • loss of t cell mediated immunity
115
Q

clinical manifestations digeorge

A

tetany (no PTH–>noCa2+), congenital heart defects, abnormal facia appearance

116
Q

genetic manifestation of digeorge

A

22q11 deletion

117
Q

infections associated with t cell defects

A

bacterial sepsis
viruses- cmv, epistein-barr, severe varicella, chronic respiratory and intestina infection
fungi/parasites- candida

118
Q

overlap syndromes

A

SCID
Wiskott-Aldrich Syndrome
Complement Deficiencies

119
Q

SCID cellualr level

A
  • lymphopenia (low absent T/B cells)

- hypogammaglobulinemia

120
Q

etiology of scid is

A 
variable!
cytokine recepto def: impacts t cell dev (x linked)
ADA def (autosomal recessive) -- cant remove excess purines (accum of toxic derivatives)
121
Q

WAS genetics

A

x linked recessive mutation of XP11.23 Was protein

–from a family of membrane receptor signal proteins

122
Q

WAS presentation

A

thrombocytopenia (dec platelets)
eczema
immune defiency

123
Q

WAS at cellular level

A
  • low igm, normal igg, high iga & ige
  • do not make antibodies to polysacch antigens and poor antibodies to protein antigens
  • progressive t lymph depeletion
124
Q

Rx WAS

A
  • bone marrow transplant to cure

- platelet transfusion support before that

125
Q

compliment deficiencies

A

C2 def.
C3 def.
C5-9 def.
C1 inhibitor

126
Q

C2 def

A

does not result in an increased risk of infection (alternative C pathway compensates), but there is an increased risk of SLE like autoimmune disease

most common

127
Q

C3 deficiency

A
  • required for function both classic and alt pathways

- increased risk of serious bacterial infection

128
Q

C5- 9 Deficiency

A

cannot form MAC involved in lysis of organisms

-increased suceptibility to Neisseria infection, as this bacteria’s thin cell walls make it susceptible to MAC

129
Q

C1 inhibitory deficiency

A

hereditary angioedema
- episodic edema of skin and mucosa surfaces due to stressor trauma

stressor trauma–>unregulated C1 Hageman factor, kallikrein and Plasmin–>mast cell degran and vasoactive peptide release

130
Q

Iatrogenic disorders due to

A

Chemotherapy, immunosuppressive therapy
–bone marrow becomes less cellular and more fatty

underlying medical conditions
-cancer, diabetes, renal disease, infection

131
Q

HIV structure

A

spherical and contains an electron-dense, cone-shaped core surrounded by a lipid envelope derived from the host cell membrane

132
Q

virus core contains

A

1) major capsid protein p24
2) nucleocapid protein p7/p9
3) two copies of genomic RNA
4) three viral enzymes

133
Q

three viral proteins of HIV

A

protease
reverse transcriptase
integrase

134
Q

p24

A

most readily detected viral antigen and is target for antibodies that are used for the diagnosis of HIV infection in the widely used enzyme-linked immunosorbent assay

135
Q

2 glycoproteins on viral envelope

A

gp120, gp41

critical for hib infection of cells

136
Q

HIV genome

A

RNA–> gag, pol, env

–>translated into large precursor protein that are cleaved by viral protease–> mature proteins

137
Q

targets of highly effective anti-hiv1 drugs

A

protease

inhibit formation of mature viral proteins–>not curative, but suppress viral load

138
Q

primary infection of HIV

A

virus enters blood or mucosal tissues–>infects t cells, DC, and MO–>carry it to lymphoid tissue–>viremia

139
Q

mechanism of infection of HIV

A

gp120 binds CD4 R and chemokine coreceptors on t cell, monocyte macrophage, or DC–>confirmational change in gp41 that allows fusion of virus with host cell–>viral core enters cytoplasm of host cell–> lipid envelope surrounds capsids derived from host membrane–>viral particles bud

140
Q

mechanisms of ID in HIV

A
  • direct, cytopathic effect of replicating virus
  • colonization of lymphoid tissue leading to progress destruction
  • chronic activation of uninfected cells leading to activation induced cell death
  • klling of infected cells by cytotoxic t lymphocytes
141
Q

3 phases of HIV infection

A

1) acute retroviral syndrome
2) middle, chronic phase
3) clinical AIDS

142
Q

acute retroviral syndrome

A
  • infection of CD4+ t cells (expresse CCR5)
  • mucosal infection–> dissemination of virus & dev of host immune response
    -CD8+ t cells- initial containment (kill Cd4) –>drop in viremia
    ==> end of acute phase reflects equil. between virus and host response (patient can be stable for several years)
143
Q

middle chronic phase

A

asymptomatic–” clinical latency period”

  • replicate and destroy cells in lymph nodes and spleen
  • majority of circulating CD4+ t cells do not have disease, but since ones made in lymph nodes are being destroyed, level of t cells is steadily declining
144
Q

clinical AIDs

A
  • breakdown of host defense, dramatic increase in plasma virus, severe
  • long-lasting fever, fatigue, weight loss, diarrhea
  • after a period of time, opportunistic infections, secondary neoplasms, clinical neurologic disease emerge
145
Q

when and how does HIV evade host immune system?

A

chronic phase

  • virus has glycan shield -prevents antibody binding
  • pt mutations, insertions, deletions–>alter position of sugars–> ever-changing disguise
146
Q

when is seroconverstion first detected?

A

3-7 weeks post-exposure

147
Q

considered to have aids when

A

<200 cells/ul

148
Q

category B conditions

A
  • oroopharyngeal candida (thrush)
  • vulvovaginal candidiasis (yeast infecton)
  • pelvic inflammatory disease
  • hairy, leukoplakia, oral-cancer
  • idiopathic thrombocytopenic purpura
  • peripheral neuropathy
  • herpes zoster (shingles)
149
Q

category C indicator conditiosn

A
  • active CMV in lungs
  • mycobacterium avium-intracellulare infection of lymph nodes in
  • toxoplasmosis of brain
  • lung infection with pneumocystis carinii
  • kaposi sarcoma lesion

Path3 (11 decks)

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