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PBD1 > Chapter 6 > Flashcards

Chapter 6 Flashcards

1
Q

NK T cells

A

recognize glycolipids displayed by MCH like molecule CD1

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2
Q

CD40

A

expressed on B cells

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3
Q

NK cells

A

express CD16 and CD56

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4
Q

CD16

A

on NK cells
FcR for IgG
Ab dependent cell mediated cytotoxcity (ADCC)

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5
Q

NKG2D

A

family which activates NK cells

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6
Q

CD94 family of lectins

A

inhibit NK cells

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7
Q

cytokines which stimulate NK cell proliferations

A

IL2, 15

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8
Q

cytokines which stimulate NK activation

A

IL12, also stimulated the release of IFN-y

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9
Q

Class I HLA

A

A,B,C
heterodimer of polymorphic alpha (heavy) chain and non-polymorphic beta 2-microglobulin chain
Alpha divided into 1,2,3
alpha 1 and 2 make polymorphic peptide binding cleft
display internal Ags like viruses

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10
Q

Class II HLA

A

P,Q,R
dimer of alpha and beta chains, both polymorphic
alpha 1 and beta 1 create polymorphic peptide binding cleft
present extracellular stuff that has been internalized and processed like bacteria

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11
Q

activated CD4 cells

A

secrete IL2 and express high affinity IL2Rs
IL2 acts as GF in autocrine loop
display CD40L which bind CD40 on B cells and Macrophages

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12
Q

TH1

A

secrete IFN-y

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13
Q

TH2

A

secrete IL4 -> B cells -> IgE plasma cells and IL 5 -> Eos

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14
Q

TH17

A

IL17- neutraphils and monocytes

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15
Q

class switching

A

induced by IFN-y and IL4

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16
Q

Type I hypersensativity reaction

A 
aka immediate hypersensitivity
TH2,IgE -> mast cells -> inflammation
occurs w/in minutes
allergies
systemic or local
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17
Q

initial reaction in type I

A

vasodilation, vascular leakage, smooth m contraction, glandular secretions

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18
Q

late phase reaction in type I

A

begins in 2-24 hours, can last for days
infiltration of Eos, neturophils, basophils, monocytes, and CD4 cells -> tissue damage
IL3,5, GM-CSF all promote survival of eos
IL5 most potent stimulator of eos

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19
Q

secretagoges of mast cells

A

IgE, C5a, C3a, codeine, morphine, adenosine, mellitin, heat, cold, sunlight

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20
Q

leukotrienes

A

C4,D4- most potent vasoactive and spasmotic agents

B4-chemotactic for neutrophils, eos, and monocytes

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21
Q

extreme temperature or exercise hypersenativites

A

not mediated by TH2 or IgE

non-atopic allergy

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22
Q

Type II hypersensativity

A

aka Ab mediated

transfusion reactions, hemolytic disease of newborn, autoimmune hemolytic anemia, drug reactions (haptens)

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23
Q

type III hypersensativity

A

aka immune complex mediated
elicit inflammation at site of deposition
systemic immune complex disease
acute serum sickness

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24
Q

morphology of type III

A

acute necrotizing vasculitis
intense neutrophil infiltration
fibrinoid necrosis

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25
Q

type IV

A

aka T cell mediated

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26
Q

APC released IL12

A

induced CD4 to become TH1

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27
Q

What cytokines released from APC induces TH17

A

IL1,6,23 and TGF beta

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28
Q

CD8 mediated type IV

A 
autoimmune following viral infections
graft rejection
tumor rejection
kills with perforins and granzymes
releases IFN-a
tuberculin reaction, contact dermatitis
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29
Q

3 requirements of autoimmune disease

A

presence of immune reaction specific for a self Ag or self tissue
evidence that reaction is not secondary to tissue damage, but is primary pathology
absence of another well defined cause

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30
Q

AIRE

A

critical for negative selection to occur in thymus for central tolerance

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31
Q

Treg cells

A

express CD25

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32
Q

FOXp3 mutations

A

IPEX

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33
Q

PTPN-22

A

tyrosine phosphatase

rheumatoid arthritis and DMI

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34
Q

NOD2

A

chrons disease

cytoplasmic sensor of microbes

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35
Q

IL2R-CD25, and IL7R

A

MS

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36
Q

Epitope spreading

A

when cell injury releases previously immune privileged self Ags

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37
Q

SLE

A

woman 9-1
2-3x higher in black and hispanic
arises in early 20s-30s

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38
Q

ANAs in SLE

A

dsDNA
histones (drug induced)
non-histone proteins bound to RNA
Abs to nuclear agents

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39
Q

nuclear florescent- homogenous/diffuse

A

Abs to chromatin, histones, maybe DNA

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40
Q

nuclear florescent- rim/peripheral

A

Abs to DNA

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41
Q

nuclear florescent- speckled pattern

A

most common, least specific

DNA nuclear constituents

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42
Q

nuclear florescent- nuclear pattern

A

RNA Abs

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43
Q

Other Abs in SLE

A

smooth m, RBCs, platelets, lymphocytes

despite Abs to coagulants are in hypercoagulant state

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44
Q

genetics of SLE

A

HLA-DQ
deficiencies in C3,4 fail to remove ICs
deficiencies in C1q fail to phagocytosis apoptotic cells

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45
Q

drugs that induce SLE

A

hyralazine, procainamide, d-pencillamine, isoniazid
HLA-DR4
Abs to histone

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46
Q

mechanism of tissue injury in SLE

A

Type III

nuclei damaged cells exposed to ANAs -> LE bodies -> engulfed by phagocytes -> LE cells

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47
Q

morphology of SLE

A

fibrinoid necrosis

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48
Q

type I and II lupus nephritis

A

minimal mesangial and mesangial proliferative
10-25%
mesangial cells proliferate and IC deposition involving glomerular capillaries

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49
Q

type III lupus nephritis

A 
focal proliferative glomerulonephritis
20-35%
less then 50% glomeruli involved
glomeruli have crescent formation
fibrinoid necrosis
proliferation of endothelium and mesangial cells
infiltrating leukocytes, eos 
intercapillary thrombi
deposits primarily subendothelial
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50
Q

type IV lupus nephritis

A 
diffuse proliferative glomerulonephritis
35-60%
entire glomerulus affected
acutely injured and chronically scarred
most severe
definitely symptomatic 
deposits primarily subendothelial
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51
Q

type V lupus nephritis

A 
membranous glomerulonephritis
diffuse thickening of capillary walls
10-15%
severe proteinuria
may occur concurrently w/another class
deposits primarily subepithelial
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52
Q

skin SLE

A

facial erythema in butterfly area
uticaria, maculopapular lesions, and ulcers
photosensitive
vasculitis w/fibrinoid necrosis

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53
Q

joints SLE

A

non-erosive synovitis w/little to no deformity

effusions common

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54
Q

CNS SLE

A

Abs against synaptic membrane proteins

non-inflammatory occlusion of small vessels due to intimal proliferation

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55
Q

pericarditis or serosal involvement SLE

A

acute, subacute, or chronic
acute- fibrous exudate
chronic- thickened, opaque, shaggy fibrous tissue

56
Q

CV SLE

A

damage to any layer of the heart
pericardial involvement 50%
myocarditis less common, but causes resting tachycardia
valvular abnormalities (mitral and aortic), thickened on both superior and inferior surface

57
Q

spleen SLE

A

slenomegaly, capsular thickening, follicular hyperplasia

central penicilliary aa show intimal and smooth mm hyperplasia

58
Q

lungs SLE

A

pleuritis in 50% and pleural effusions

sometimes chronic interstitial fibrosis and secondary pulmonary HTN

59
Q

chronic discoid lupus erythmatosus

A

skin maifestations mimic SLE, but systemic manifestations are rare
about 35% ANAs, but rarely against DNA

60
Q

subacute cutaneous lupus erythmatosus

A 
primarily skin 
different from discoid b/c: 
rash widespread superficial, non-scarring
mild to systemic symptoms of SLE
Abs to SS-A Ag
HLA-DR3
61
Q

Sjogren syndrome

A 
dry eyes, dry mouth due to destruction of lacrimal and salivary glands
when isolated (primary) called sicca syndrome, usually w/other autoimmune conditions (secondary)
62
Q

Sjogren syndrome pathogenesis

A 
CD4 and some B cells
75% have rheumatoid factor
80% of ANAs
Abs against SS-A, SS-B 
May be triggered by viral infection of salivary gland
63
Q

systemic sclerosis/sclerederma

A

primarily skin, but GI, kidneys, heart, mm, lungs

progressive interstitial and perivascular fibrosis

64
Q

diffuse sclerederma

A

widespread involvement at onset w/rapid progression

65
Q

limited sclerederma

A

skin, often confined to finger and extremities

CREST

66
Q

CREST

A

calcinosis, raynauds phenomenon, esophageal dysmotility, sclerodactyly, and telangiectadia

67
Q

eitology of sclerederma

A

CD4 response to unknown Ag in skin -> cytokines -> inflammation -> fibroblasts
ANAs: DNA topoisomerase (usually have pulmonary fibrosis) Anticentromere Ab (CREST)

68
Q

Sclerederma- skin

A 
edema w/CD4 cells
eos
capillaries and small aa have thickening of BM 
subcutaneous calcifications (CREST)
claw fingers and masked face
tips of fingers auto-amputate
69
Q

sclerderma GI

A

90%
progressive atrophy and replacement of mm w/collagens
most severe in esophagus -> GERD
loss of villi -> malnourished

70
Q

sclerederma MSK

A

inflammation of synovium
hypertrophy and hyperplasia of synovial soft tissues
rare joint destruction

71
Q

sclerederma kidneys

A

66%
interlobular aa show intimal thickening -> concentric proliferation of intimal cells
not always associated w/HTN, if HTN present usually die from renal failure

72
Q

sclerederma lungs

A

50%

pulmonary HTN and interstitial fibrosis

73
Q

sclerederma heart

A

pericarditis w/effusions and myocardial fibrosis

thickening of intramyocardial arterioles

74
Q

clinical features of sclerederma

A

female:male 3:1
50s-60s
blacks

75
Q

mixed CT diseases

A

clinical features mix of SLE, sclerederma, and polymyositis
increased Abs to ribonucleoprotein
modest renal involvement

76
Q

polyarteritis nodosa

A

necrotizing inflammation of walls of vessels

non-infectious vasculitis

77
Q

T cell mediated rejection of transplants

A

destruction of graft cells CD8

delayed hypersensativity CD4

78
Q

Ab mediated rejection of transplants

A

humoral rejections
must have preformed Abs to graft HLA
previous organ rejection, mulitparous women, prior blood transfusions
hyperacute reaction, rarely happens b/c check for Abs to donor HLA
if does occur usually vascular damage -> rejection vasculitis

79
Q

hyperacute rejection of kidney

A

w/in min
rapidly cyanotic, mollted, flaccid, scant bloody urine
Ig and C’ on vessel walls
neutrophils
fibrinoid necrosis of vessles, coagulative necrosis of kidney walls

80
Q

acute rejection of kidney

A

w/in days or suddenly months/years later due to termination of immunosupressent therapy

81
Q

acute rejection of kidney- cellular reaction

A

interstitial mononuclear infiltrate and edema
renal failure
CD4&8
responds well to immunosupression
cyclosporine immunosupressent, but nephrotoxic, so must balance

82
Q

acute rejection of kidney- humoral reaction

A 
rejection vasculitis
anti donor Abs
extensive necrosis of renal parenchyma
depotstion of CD4
treat w/B cell depleting agents
83
Q

chronic kidney injection

A

progressive renal failure over 4-6 months
vascular changes, interstitial fibrosis, tubular atrophy
glomeruli scar w/duplication of BM

84
Q

methods increasing graft survival

A
  • HLA matching
  • immunosupression- cyclosporine blocks NFAT, proteins which bind B7 costimulators (at risk for EBV, lymphomas, HPV, squamous cell carcinoma, KS)
  • donor specific tolerance therapies
85
Q

transplantation of hematopoietic cells

A

BM2 specific

GVH disease

86
Q

acute GVH disease

A

days-weeks
immune system, skin, liver, GI
generalized rash -> desquamation
destruction of small bile ducts -> jaundice
GI ulcers
infected tissues have decreased lymphocytes

87
Q

chronic GVH disease

A

extensive cutaneous injury (looks like sclerderma)
liver disease and jaundice
GI and esophageal constrictions

88
Q

x-linked/brutons gammaglolinemia

A

failure of pre-B cell to mature b/c cannot form light chain
mutation in cytoplasmic tyrosine kinase (Btk)
primarily males
B cells absent or decreased, germinal centers underdeveloped
T cell mediated reactions normal
replacement therapy w/Igs may reach adulthood

89
Q

x-linked gammaglolinemia at risk for

A

recurrent respiratory infections (staph, strep, flu)
susceptible to enteroviruses (echovirus, poliovirus, coxsackevirus) and giardia
at risk for arthritis, dermatomyositis

90
Q

common variable immunodeficeny

A

group of disorders
hypogammaglobunemia, usually all, sometimes just IgG
sporadic and inherited
normal B cell number, but cannot become plasma cells
BAFF, ICOS weakly implicated
both sexes equally
onset childhood/adolescence
germinal center hyperplastic due to loss of IgG feedback

91
Q

common variable immunodeficiency at risk for

A

recurrent sinolulomary pyrogenic infections and hypersensativites
at risk for autoimmune conditions and gastric cancer

92
Q

isolated IgA deficency

A 
1/600 people of european descent
familial or acquired
usually asymptomatic
mucosal defenses weakened 
increase in respiratory allergies and at risk for autoimmunity
react to IgA as foreign -> shock 
BAFF
93
Q

hyper IgM syndrome

A

make IgM, but no other Igs
T cells cannot deliver signals to B cells and macrophages
70% have x-linked form due to CD40L mutation, the rest autosomal recessive mutations in either CD40L or activation induced deanimase
normal # of T and B cells

94
Q

hyper IgM syndrome at risk for

A

autoimmune hemolyitic anemia, thrombocytopenia, and neutropenia

95
Q

DiGeorge syndrome

A

T cell deficiency due to failure of 3rd and 4th phayngeal pouches to form thymus and PT
tetany, congenital heart defects, abnormal facies, not familial, deletion of 22q11

96
Q

severe combined immunodeficiency syndrome (SCID)

A

lots of syndromes all have defects in both humoral and cellular immunity
prominent thrush in infants
failure to thrive
maternal IgG attack -> GVH disease -> morbilliform rash
with BM transplant will die w/in a year
lymphoid tissue hypopastic

97
Q

x linked SCID

A

50-60%
mostly boys
mutation in common y-chain of cytokine Rs
thymus has lobules of undifferentiated epithelium
gene therapy has been successful, but seem to develop T cell leukemias

98
Q

autosomal recessive SCID

A

deficiency of ADA- accumulations of deoxy-STP -> toxic to dividing lymphocytes -> Hassels corpuscles
mutations in recombinase activating gene
JAK3- Kinase associated w/T cell AgRs

99
Q

Bare lymphocytes sydrome

A

occurs in SCID

don’t express MCH II

100
Q

Wiskott-Aldrich syndrome/Immunodeficiency w/thrombocytopenia and eczema

A

x linked recessive, thrombocytopenia, eczema, recurrent infections, early death
thymus normal, but progressive depletion of T cells
Do not make Abs to polysacharride Ags and respond poorly to protein Ags
Low IgM
normal IgG
high IgE, and IgA
at risk for B cell lymphomas
WASP gene
BM transplant

101
Q

C2,C1,C4 deficincies

A

ususally no increased risk of infection, but at risk for SLE-like disease

102
Q

deficiencies in alternative C’ pathway

A

rare
properdin
factor D
recurrent pyrogenic infections

103
Q

C3 deficiencies

A

affect both alternative and classical pathways

severe risk of recurrent pyrogenic infections and increased risk of IC mediatd glomerulonephritits

104
Q

C5-9

A

loss of MAC at risk for neisserial infections

105
Q

deficiency in C1 inhibitor

A

herediatary angioedema
loss of inhibition of C1, XII, Kallikrein system
treated w/C1 inhibitor from human plasma

106
Q

paroxysmal nocturnal hemoglobinuria

A

cannot form decay accelerating factor of CD59 which regulate C’
factor H mutations underlie about 10% of hemolytic uremic syndromes

107
Q

HIV viral core contains

A 
major capsid protein p24
nucelocapsid protein p7/p9
2 copied of genomic RNA
3 viral enzymes (protease, reverstranscriptase, integrase)
surrounded by p17
108
Q

HIV p24

A

target for Abs used in early diagnosis

109
Q

HIV viral envelope

A

gp120, and gp41

110
Q

pathogenesis

A

binds to CD4R
gp120 must bind to coRs CCR5 or CXCR4
binding initiates conformation change so fusion peptide on gp41 can insert into cell membrane and viral core can enter

111
Q

APOBEC3G

A

found in naive T cells
will mutate viral DNA
inactivated when T cell matures

112
Q

HIV in macrophages

A

can replicate in non-dividing macrophages due to HIV1 vpr gene
serve as reservoirs
have impaired microbicidal activities, decreased chemotaxis, decreased secretion of IL2, inappropriate secretion of TNF and poor APC ability

113
Q

HIV and DCs

A

present HIV to T cells

follicular- store HIV on surface FcRs sere as reservoir

114
Q

polyclonal activation of B cells

A

germinal center hyperplasia
BM plasmocytosis
hyperglobulinemia
circulating ICs
HIV -> high levels of IL6 -> proliferation of B cells
must affect B cells b/c cannot mount T independent B cell immuno response

115
Q

acute retroviral syndrome

A

40-90% of patients
3-6 weeks after infection
resolves in 2-4 weeks
number of virons present at this point indicative of prognosis

116
Q

candiasis

A

most common fungal infection in HIV, may mark transition into AIDs

117
Q

opportunistic infections

A

candiasis, cytomegalovirus, TB, cyptococcus, toxoplasmagondii, papovirus JC, mycobacteria, herpes, histoplasma capsulatum

118
Q

Kaposi Sarcomas

A 
vascular tumor very rare, except in AIDs
most common AIDs neoplasm
KS herpesvirus 
increased IL6 and VEGF
rare B cell lymphomas caused by KSHV or castelmens disease
119
Q

early stage HIV morphology

A

follicular hyperplasia
primary B cell areas
HIV particles in germinal center on DC cells
viral DNA in CD4 cells
B cell hyperplasia in BM -> rouleaux due to hypergammaglobulinemia

120
Q

HIV disease progression morphology

A

follicles depleted
germinal cells hyalinized
depletion in spleen and thymus

121
Q

AL

A

amyeloid light chain
derived from Ig light chain produced in B cells
lamda light chain or their fragments, sometimes kappa chain
plasma cell tumors

122
Q

AA

A

amyeloid associated
derived from unique non-Ig protein from liver
cleaved from serum amyloid associated proteins (SSA)
associated w/chronic inflammation, therefore called secondary amyoids

123
Q

A beta amyloid

A

from beta amyloid precursor proteins

alzheimers

124
Q

transthyretin TTR

A

normal serum protein binds and transports thyroxine and retinol
mutant form deposited in familial amyloid polyneuropathies
senile systemic amyloidosis- non mutated form in heart of old people

125
Q

beta 2 microglobulin

A

component of MHC I

amyloid fibril subunit Abeta2m

126
Q

other amyeloids

A

prions, serum amyloid P, proteoglycans, GAGs

127
Q

primary amyeloidosis

A

usually AL
usually systemic
many have plasma cell dyscaria (cancer)

128
Q

Bence-jones proteins

A

Ig light chains

often excreted in urine in primary amyloidosis

129
Q

reactive systemic ameyloidosis

A

secondary
usually have rheumatoid arthritis
heroin users
AA

130
Q

Hemodialysis associated amyloids

A

deposistion of beta 2 microglobulins
increased concentration in renal disease, but not filtered by dialysis membranes
can cause carpal tunnel

131
Q

familial mediterranean fever

A 
heredofamilial amyeloids
autoimmune inflammatory disease
increased IL1
protein pyrin
AA
132
Q

other familial amyloids

A

are usually TTR mutations

133
Q

kidney amyloids

A

most common and most serious
kidneys shrink due to ischemia
primary deposits are in glomeruli
uneven widening of BM

134
Q

spleen amyloids

A

2 patterns

  • deposits limited to splenic follicles -> tapioca like granules -> sago spleen
  • walls of splenic sinuses and CT framework of red pulp -> lardaceous spleen
135
Q

liver amyloids

A

hepatomegaly
in space of disse, hepatic parenchyma, and sinusoids
normal liver function usually preserved

136
Q

heart amyloids

A

can be enlarged and firm, but usually normal appearance
pressure atrophy of myocardium
if subendocardial deposits -> electrical issues

PBD1 (6 decks)

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