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MOD Exam2 > Immune System Lecture - Singh > Flashcards

Immune System Lecture - Singh Flashcards

1
Q

Autoimmune diseases

A
  1. SLE
  2. Sjögren syndrome
  3. Systemic sclerosis
  4. IgG4-related disease
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2
Q

which lymphocyte can escape apoptosis from self recognition in central tolerance

A

B-cells, –> Receptor editing

T-cells –> Treg cells (if right cell)

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3
Q

which lymphocyte can escape apoptosis from self recognition in peripheral tolerance

A

T cells –> Tregs (anergy, inflammation suppression)

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4
Q

T cell inhibitory R

A

CTLA, PD-1 recognize self ligands and inhibits T-cell to activate
(** virus and cancer cells can have these also)

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5
Q

environmental ways of autoimmune

A
  1. Epitope spreading = damaged tissue release Ag that cells dont know
  2. Molecular mimicry = from infections
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6
Q

Genetics and autoimmune

which haplotype, genes

A 
HLA B27 (haplotype)
PTPN22, NOD2 (genes)
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7
Q

Ankylosing spondylitis

A

degeneration and fusion of vertebrse from inflammation

** HLA B27 susceptibility link

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8
Q

Rheumatoid arthritis linked to

A

PTPN22 gene

= lowers B cell and T cell self tolerance

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9
Q

Crohns Disease linked to

A

NOD2 gene mutation –> X NOD-like R

= Paneth cells in GI CANT kill = accumulation of bacteria

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10
Q

Rheumatic heart disease mechanism

A

molecular mimicry (from STREPTOCOCCUS Ag and MYOCARDIAL Ag)

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11
Q

Oral Lichen Planus mechanism

A

Epitope spread from this disease

  1. Keratosis in oral cavity (T CELLS)
  2. Blistering in secondary pemphigold (B CELLS)
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12
Q

ANA sensitive test

A 
ANA + = autoimmune disease fro several diseases 
1. SLE
2. Sjögren syndrome 
3. Sytemic sclerosis
4. nothing 
ANA - = nothing
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13
Q

testing for SLE after ANA +

A
  1. Anti DS DNA +
  2. Anti Smith +
    (homogenous + speckled)
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14
Q

testing for Sjögrens syndrome after ANA +

A
  1. Anti Ro/SS-A +
  2. Anti La/SS-B +
    (speckled stain - not specific)
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15
Q

testing for Systemic sclerosis after ANA +

A
  1. Anti DNA topoisomerase (Scl-70) + (nucleolar + speckled stain)
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16
Q

SLE
type
mechanism

A

type 3

B-cells and CD4+ cells

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17
Q

SLE environmental influences that can this

A
  1. HLA-DQ family hesitance
  2. X chromosome (female)
  3. UV can burst cells
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18
Q

SLE SX

A
  1. Malar rash = butterfly rash on cheeks by nose

2. abnormal CBC*

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19
Q

CBC on SLE

A
  1. thromcytopenia
  2. leukopenia
  3. hemolytic anemia
  4. arthritis joints
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20
Q

Lupus Nephritis SX

A

kidney lupus

  1. protein in urine, Cr in urine
  2. edema (lost colloid P)
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21
Q

Diffuse Lupus Nephritis (most common lupus nephritis) SX

A

Protein, blood in urine
Ab-Ag deposition in subendothelium (electron microscopy)
cell proliferation of kidney cells

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22
Q

Lupus nephritis on immunoflourescence

A

granular IgG complex staining

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23
Q

skin SLE

A

basal layer of skin degeneration due to complexes = malar rash

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24
Q

heart SLE

A
  1. Libman-Sacks endocarditis (not bacterial just fibrin)

2. Coronary Artery Disease from anti-phospholipid Ab syndrome

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25
Q

Libman-Sacks endocarditis

A

Verrucous (warty) deposition on heart valves = fibrin,

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26
Q

SLE histology

A

L-E cell **

N that are stuffed with lymphocyte it has eaten

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27
Q

Discoid lupus SX

A
  1. Discoid rash
    • ANA
    • immunoflorescence stain
      (no other SLE SX)
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28
Q

Discoid lupus skin

A

face and scalp rash (hypopigmented, red around it, looks like burn)
Anti- DS DNA = -
ANA = +/-

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29
Q

Drug induced Lupus SX

A
  1. Arthralgias (joint)
  2. ANA +
  3. Anti-Histone Ab**
  4. immunoflorescence +
  5. Discoid rash
  6. Hematologic disease
    (no other SLE SX)
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30
Q

Drug induced SL due to and clinical

A

Mx given to them
anti- histone Ab +
ANA +
red patches around skin on body, arthralgia, fever

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31
Q

Drug induced SL linked to

A

HLA -DR4

HLA- DR6

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32
Q

Sjögren syndrome SX

A

lacrimal and salivary gland destruction

B and T cells inflammation –> fibrotic destruction

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33
Q

Sjögren syndrome SX Clinically

A
  1. dry eyes (sand stuck in eye pain)
  2. dry mouth = xerostomia (X swallow)
  3. root caries : no saliva = bacteria in roots of teeth
  4. white patch in tongue
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34
Q

Sjögren syndrome DX

A

Anti- RO Anti-LA
Anti- SSA, Anti- SSB
biopsy lip

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35
Q

Sjögren syndrome can lead to

A

pulmonary fibrosis

Lymphoma from lymphocyte proliferation (swollen gland)

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36
Q

Systemic sclerosis (sceroderma) SX

A

fibrosis in many organs

can be a SX in CREST Syndrome

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37
Q

Systemic sclerosis (sceroderma) histology

A

subcutaneous adipose X in skin
CT grows down skin
= scerodactaly - > keratonic thick skin on hands
= squeezes BVs

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38
Q

Systemic sclerosis (sceroderma) can lead to

A

Raynaud phenomenon : cold X blood necrotic fingers, distal finger bone resorption (white fingers –> black)

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39
Q

Systemic sclerosis (sceroderma) GI

A 
GERD
Esophageal ulceration (lower sphincter X)
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40
Q

Systemic sclerosis (sceroderma) Renal

A

renal crisis can happen

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41
Q

Systemic sclerosis (sceroderma) pulmonary

A

HTN pulmonary

fibrosis pulmonary

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42
Q

Systemic sclerosis (sceroderma) Immunoflorescence

A
  1. speckled

2. can have centromeric = CREST syndrome

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43
Q

CREST syndrome SX

A
  1. Telangiectasia : capillary dilation red marks on skin
  2. Sclerodactaly (Systemic sclerosis)
  3. Esophageal dysfunction
  4. Raynauds phenomenon (fingers)
  5. Calcinosis : Ca+2 deposits on skin (hard marble skin nodules)
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44
Q

IgG4- related disease SX

A
  1. plasma cells make IgG4 –> stains IgG4 + cells

2. Fibrosis (scarring to areas)

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45
Q

IgG4 related disease

  1. submandibular gland
  2. bile duct
A
  1. Mickulicz Syndrome

2. Scerotizing Cholangitis

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46
Q

cell mediated transplant rejection

A
  1. Acute cellular rejection

2. Chronic cellular rejection

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47
Q

humoral mediated transplant rejection

A
  1. acute Ab- mediated rejection

2. chronic Ab- mediated rejection

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48
Q

hyperacute rejection

A

within minutes during surgery (graft turns dark)

  • from preformed Abs
  • thrombotic
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49
Q

hyperacute rejection usually from

A

Blood group Ags

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50
Q

Acute cellular rejection

A

T-cell mediated

  • days to months to years later graft rejection is happening
  • C4d - stain
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51
Q

Chronic cellular rejection

A 
**** Arteriosclerosis**** 
= fibrotic and sclerotic rejection
- fibrosis in BVs
- glomerular changes
- GI fibrosis
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52
Q

Acute - Ab mediated rejection

A

C4d complement inflammation

- C4d + stain

53
Q

chronic - Ab mediated rejection

A

looks like chronic cellular with + C4d stain

54
Q

TX of rejection can cause

A
  1. Polyomavirus, Cytomegalovirus = viral
  2. Fungal and bacterial
  3. tumors from virus
55
Q

Hematopoietic stem cell transplant

rejection

A

(can be from chemo or from lymphoma)
rejection = does not happen
- you get new immune system that can attck you = graft vs host

56
Q

Hematopoietic stem cell transplant

rejection SX

A

T-cell attack host (in BM, Thymus, liver Transplant)

  1. Rash –> desquamation
  2. Liver –> jaundice, cholestasis
  3. GI –> Bloody D, strictures
57
Q

Bacterial infection from what type of immunodeficiency

A

B-cell

Innate immune

58
Q

Viral infection from what type of immunodeficiency

A

B-cell
innate immune
T-cell

59
Q

fungi, TB, cancer from infection : infection from what type of immunodeficiency

A

T-cell

60
Q

Primary innate immunodeficiency 4

A

Leukocyte disorder = N -mediated response

  1. defective adherence (LAD)
  2. phagocytic function (Chediak Higashi)
  3. Superoxide radical production (CGD)
  4. complement disorders
61
Q

LAD type 1 deficiency

A

X B2 integrin helping N anchor

62
Q

LAD type 2 deficiency

A

X selectin ligand (due to no fucosyl transferase)

63
Q

Chediak Higashi syndrome what happens

A

Failure of phagolysosomal fusion

64
Q

Chediak Higashi syndrome SX

A
  1. bleeding and bruising easily from platelet dysfunction ,
  2. albinism (X melanocytes)
  3. increased bacterial infections
65
Q

Chediak Higashi syndrome on blood smear

A

Giant granules in the N

66
Q

Chronic granulomatous disease what happens

A

X Superoxide production in phagosomes

67
Q

Chronic granulomatous disease SX

A
  1. many M accumulate

2. Granuloma causes body to wall off the infection since it cant kill it

68
Q

Primary innate immunodeficiency can lead to what

A

strep, entero,

staph aures

69
Q

Complement immunodeficiency

A

X MAC C5-C9

70
Q

Complement immunodeficiency can lead to

A

Neisseria infections especially meningitis

71
Q

Hereditary angioedema

A

X C1-INH (inhibitor), AD
= high complement and kallikrein —-> bradykinin-mediated edema in many places including organs(especially in lips, fingers)

72
Q

C1-INH

A

regulates complement pathway

73
Q

Primary adaptive immunodeficiency

A

Lymphocyte maturation disorders

74
Q

Severe combined immunodeficiency (SCID) SX

A

X - linked mostly
X Tcells = no Bcells
(** can happen from Adenosine Deaminase deficiency ADA)

75
Q

SCID causes what step to not happen

A

Pro T cell–X–> immature T-cell

76
Q

ADA

A

common myeloid-lymphoid progenirator —-> pro T cell

77
Q

DiGeorges causes what step to not happen

A

immature T cell –X–> CD4+ and CD8+ cells

78
Q

SCID

A

BM transplant

79
Q

DiGeorges other name

A

22q11 deletion

80
Q

DiGeorges what happens

A

X T cells , from PP 3 and PP4 problems (thymus, parathyroid, heart, great vessels)

81
Q

DiGeorges SX

A
  1. facial + palatal abnormalies
  2. cardiac abnomalies
  3. hypercalcemia –> Tetany
  4. you can get SCID if complete thymus is gone (can be partial)
82
Q

X - linked agammaglobulinemia happens from

A 
X BTK (Bruton tyrosine kinase) gene on X chromosome 
* Pre B-cell (IgM)--X--> immature B-cell (IgM + IgD)
= light chains cant be rearranged ****
83
Q

X - linked agammaglobulinemia SX

A
  1. high risk for infection after maternal Ab go away = no Igs
  2. no opsonization (especially needed for encapsulated bacteria, virus, protozoa
84
Q

Hyper- IgM syndrome

A

mutation in CD40 (B)-CD40L (T)
CD4+ cells CANT help B-cells CLASS SWITCH
= Only IgM is present

85
Q

Hyper- IgM syndrome SX TX

A
  1. high infections, (encapsulated, due to no opsonization)

2. IV-Ig, stem- cell transplant

86
Q

CVID common variable immunodeficiency

A

hypogammaglobulinemia (NO Igs)

immature B cell –X–> mature B cell

87
Q

CVID can lead to

A
  1. high autoimmune diseases (anemia, thrombocytopenia)

2. encapsulated bacteria, virus, parasite

88
Q

IgA deficiency SX

A
  1. sinus and resp infections
  2. UTI
  3. GI infections
  4. allergies, autoimmune diseases
89
Q

when do most people realize they are IgA deficient

A

when having blood transfusion with IgA present = Ab blood reaction
= anaphylatic reaction

90
Q

systemic diseases immunodeficiency 2

A
  1. Wiskott Aldrich syndrome

2. Ataxia Telangiectasia

91
Q

Wiskott Aldrich syndrome happened from

no details

A

mutation in WASP gene

92
Q

Wiskott Aldrich syndrome SX

no details

A
  1. thrombocytopenia
  2. Eczema
  3. recurrent infection (low Tcells, low Bcells)
93
Q

Wiskott Aldrich syndrome TX

no details

A

stem cell transplant

94
Q

Ataxia Telangiectasia happens due to

no details

A

low IgA + IgG

from ATM mutation –> no DNA repair

95
Q

Ataxia Telangiectasia SX

no details

A

ataxia
Telangiectasia = vascular defects
resp, autoimmune, cancer

96
Q

secondary immunodeficiency EX

A

AIDS from other illness

97
Q

AIDS was discovered how

A

in LA when 3 men got infections that most immunocompetent dont get
(can got weird tumors, neuro problems, infections)

98
Q

AIDS is when

A

HIV is taking over the body to the point that you get

  1. opportunistic infections
  2. secondary neoplasms
  3. Neurologic manifestations
99
Q

most risky way to get HIV

A

anal receptive intercourse (since mucosal barrier is so thin)
also vaginal intercourse
- easier if you have a wound

100
Q

parenteral routes of HIV transmission

A

IV drug, blood transfusion

101
Q

mother to child HIV

A

through placenta , milk, birth canal

102
Q

HIV is what type of virus

A

Retrovirus, Lentivirus = slow action

RNA –> DNA –> protein

103
Q

HIV regions to know 4

A
  1. LTR : initiate transcription
  2. gag : encodes viral proteins inside virus
  3. env : surface glycoproteins encoding
  4. pol : viral enzymes encoding
104
Q

HIV life cycle

A
  1. binds to CD4+ (gp120)
  2. gp41 used to fuse into cell and ejects into RNA
  3. makes DNA that is inserted into genome
  4. LTR initiated transcription of HIV RNA
105
Q

how does HIV activate its disease

A

NFkB —-> LTR = kills the T cell CD4+

*NFkB is supposed to upregulate T cells = hey wake up T cell

106
Q

viral replication occurs where

A

LN

107
Q

acute retroviral syndrome

A

first few days of infection mild flu sx

108
Q

after acute retroviral syndrome

A

AB response, HIV go to LN underground (cant test for HIV between 7-21 days of infection)

109
Q

HIV testing

A
  1. NAT : viral RNA
  2. protein Ag p24
  3. HIV Ab
110
Q

window period

A

has been exposed and no + test for about a week (with most sensitive HIV anti-env Ab)

111
Q

what happens after HIV hides in LN

A

HIV virus RNA lowers to a Viral set point (at this point/peak downward = clinical latency)

112
Q

latency period

A

T cells are getting killed silently however no real SX

113
Q

CNS of AIDS

A

CNS toxoplasmosis

114
Q

AIDS is when

A

WBC is below 200cells/mm3 or an unusual infection

115
Q

Pneumocystic jiroveci (carinii)

A

fungal, shows someone has AIDS

silver stain shows black stains of fungal yeast

116
Q

Kaposi sarcoma

A

vascular tumor from HHV8/ KSH8, can defines AIDS

= red lesions patch like

117
Q

B cell lymphoma

A

from EBV, can define AIDS

  • hypergammaglobulinemia (many uneffective Abs
  • low isotype switch
118
Q

cervical cancer

A

from HPV, can define AIDS

119
Q

HIV and brain

A

microglia have HIV accumulation = encephalopathy = dementia

120
Q

Amyloid is what

A

misfolded proteins becoming B-pleaded sheets

121
Q

how do you see amyloid

A
  1. Congo Red stain = bubble gum pink
  2. Polarized light = apple green = determines amyloid
    (take from any tissue like belly fat)
122
Q

what disease has to do with amyloid

A

myeloma

123
Q

myeloma = acquired mutation

A

B cell plasma cells get IGs accumulate of light chain = AL amyloid

124
Q

chronic inflammation

A

M activation makes SAA proteins = AA amyloid

125
Q

hereditary mutation and no other sx

A

transthyretin –> ATTR amyloid

126
Q

organs that amyloid deposits

A

kidney, liver , heart

127
Q

kidney amyloid sx

A

edema, protein in urine

128
Q

heart amyloid sx

A

dysrhythmias, disrupt electric signaling

MOD Exam2 (8 decks)

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