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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
Libman-Sacks endocarditis
Verrucous (warty) deposition on heart valves = fibrin,
26
SLE histology
L-E cell **** | N that are stuffed with lymphocyte it has eaten
27
Discoid lupus SX
1. Discoid rash 2. + ANA 3. + immunoflorescence stain (no other SLE SX)
28
Discoid lupus skin
face and scalp rash (hypopigmented, red around it, looks like burn) Anti- DS DNA = - ANA = +/-
29
Drug induced Lupus SX
1. Arthralgias (joint) 2. ANA + 3. Anti-Histone Ab** 3. immunoflorescence + 4. Discoid rash 5. Hematologic disease (no other SLE SX)
30
Drug induced SL due to and clinical
Mx given to them anti- histone Ab + ANA + red patches around skin on body, arthralgia, fever
31
Drug induced SL linked to
HLA -DR4 | HLA- DR6
32
Sjögren syndrome SX
lacrimal and salivary gland destruction | B and T cells inflammation --> fibrotic destruction
33
Sjögren syndrome SX Clinically
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
34
Sjögren syndrome DX
Anti- RO Anti-LA Anti- SSA, Anti- SSB biopsy lip
35
Sjögren syndrome can lead to
pulmonary fibrosis | Lymphoma from lymphocyte proliferation (swollen gland)
36
Systemic sclerosis (sceroderma) SX
fibrosis in many organs | can be a SX in CREST Syndrome
37
Systemic sclerosis (sceroderma) histology
subcutaneous adipose X in skin CT grows down skin = scerodactaly - > keratonic thick skin on hands = squeezes BVs
38
Systemic sclerosis (sceroderma) can lead to
Raynaud phenomenon : cold X blood necrotic fingers, distal finger bone resorption (white fingers --> black)
39
Systemic sclerosis (sceroderma) GI
``` GERD Esophageal ulceration (lower sphincter X) ```
40
Systemic sclerosis (sceroderma) Renal
renal crisis can happen
41
Systemic sclerosis (sceroderma) pulmonary
HTN pulmonary | fibrosis pulmonary
42
Systemic sclerosis (sceroderma) Immunoflorescence
1. speckled | 2. can have centromeric = CREST syndrome
43
CREST syndrome SX
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)
44
IgG4- related disease SX
1. plasma cells make IgG4 --> stains IgG4 + cells | 2. Fibrosis (scarring to areas)
45
IgG4 related disease 1. submandibular gland 2. bile duct
1. Mickulicz Syndrome | 2. Scerotizing Cholangitis
46
cell mediated transplant rejection
1. Acute cellular rejection | 2. Chronic cellular rejection
47
humoral mediated transplant rejection
1. acute Ab- mediated rejection | 2. chronic Ab- mediated rejection
48
hyperacute rejection
within minutes during surgery (graft turns dark) - from preformed Abs - thrombotic
49
hyperacute rejection usually from
Blood group Ags
50
Acute cellular rejection
T-cell mediated - days to months to years later graft rejection is happening - C4d - stain
51
Chronic cellular rejection
``` **** Arteriosclerosis**** = fibrotic and sclerotic rejection - fibrosis in BVs - glomerular changes - GI fibrosis ```
52
Acute - Ab mediated rejection
C4d complement inflammation | - C4d + stain
53
chronic - Ab mediated rejection
looks like chronic cellular with + C4d stain
54
TX of rejection can cause
1. Polyomavirus, Cytomegalovirus = viral 2. Fungal and bacterial 3. tumors from virus
55
Hematopoietic stem cell transplant | rejection
(can be from chemo or from lymphoma) rejection = does not happen - you get new immune system that can attck you = graft vs host
56
Hematopoietic stem cell transplant | rejection SX
T-cell attack host (in BM, Thymus, liver Transplant) 1. Rash --> desquamation 2. Liver --> jaundice, cholestasis 3. GI --> Bloody D, strictures
57
Bacterial infection from what type of immunodeficiency
B-cell | Innate immune
58
Viral infection from what type of immunodeficiency
B-cell innate immune T-cell
59
fungi, TB, cancer from infection : infection from what type of immunodeficiency
T-cell
60
Primary innate immunodeficiency 4
Leukocyte disorder = N -mediated response 1. defective adherence (LAD) 2. phagocytic function (Chediak Higashi) 3. Superoxide radical production (CGD) 4. complement disorders
61
LAD type 1 deficiency
X B2 integrin helping N anchor
62
LAD type 2 deficiency
X selectin ligand (due to no fucosyl transferase)
63
Chediak Higashi syndrome what happens
Failure of phagolysosomal fusion
64
Chediak Higashi syndrome SX
1. bleeding and bruising easily from platelet dysfunction , 2. albinism (X melanocytes) 3. increased bacterial infections
65
Chediak Higashi syndrome on blood smear
Giant granules in the N
66
Chronic granulomatous disease what happens
X Superoxide production in phagosomes
67
Chronic granulomatous disease SX
1. many M accumulate | 2. Granuloma causes body to wall off the infection since it cant kill it
68
Primary innate immunodeficiency can lead to what
strep, entero, | staph aures
69
Complement immunodeficiency
X MAC C5-C9
70
Complement immunodeficiency can lead to
Neisseria infections especially meningitis
71
Hereditary angioedema
X C1-INH (inhibitor), AD = high complement and kallikrein ----> bradykinin-mediated edema in many places including organs(especially in lips, fingers)
72
C1-INH
regulates complement pathway
73
Primary adaptive immunodeficiency
Lymphocyte maturation disorders
74
Severe combined immunodeficiency (SCID) SX
X - linked mostly X Tcells = no Bcells (**** can happen from Adenosine Deaminase deficiency ADA)
75
SCID causes what step to not happen
Pro T cell--X--> immature T-cell
76
ADA
common myeloid-lymphoid progenirator ----> pro T cell
77
DiGeorges causes what step to not happen
immature T cell --X--> CD4+ and CD8+ cells
78
SCID
BM transplant
79
DiGeorges other name
22q11 deletion
80
DiGeorges what happens
X T cells , from PP 3 and PP4 problems (thymus, parathyroid, heart, great vessels)
81
DiGeorges SX
1. facial + palatal abnormalies 2. cardiac abnomalies 3. hypercalcemia --> Tetany 4. you can get SCID if complete thymus is gone (can be partial)
82
X - linked agammaglobulinemia happens from
``` 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
X - linked agammaglobulinemia SX
1. high risk for infection after maternal Ab go away = no Igs 2. no opsonization (especially needed for encapsulated bacteria, virus, protozoa
84
Hyper- IgM syndrome
mutation in CD40 (B)-CD40L (T) CD4+ cells CANT help B-cells CLASS SWITCH = Only IgM is present
85
Hyper- IgM syndrome SX TX
1. high infections, (encapsulated, due to no opsonization) | 2. IV-Ig, stem- cell transplant
86
CVID common variable immunodeficiency
hypogammaglobulinemia (NO Igs) | immature B cell --X--> mature B cell
87
CVID can lead to
1. high autoimmune diseases (anemia, thrombocytopenia) | 2. encapsulated bacteria, virus, parasite
88
IgA deficiency SX
1. sinus and resp infections 2. UTI 3. GI infections 4. allergies, autoimmune diseases
89
when do most people realize they are IgA deficient
when having blood transfusion with IgA present = Ab blood reaction = anaphylatic reaction
90
systemic diseases immunodeficiency 2
1. Wiskott Aldrich syndrome | 2. Ataxia Telangiectasia
91
Wiskott Aldrich syndrome happened from | no details
mutation in WASP gene
92
Wiskott Aldrich syndrome SX | no details
1. thrombocytopenia 2. Eczema 3. recurrent infection (low Tcells, low Bcells)
93
Wiskott Aldrich syndrome TX | no details
stem cell transplant
94
Ataxia Telangiectasia happens due to | no details
low IgA + IgG | from ATM mutation --> no DNA repair
95
Ataxia Telangiectasia SX | no details
ataxia Telangiectasia = vascular defects resp, autoimmune, cancer
96
secondary immunodeficiency EX
AIDS from other illness
97
AIDS was discovered how
in LA when 3 men got infections that most immunocompetent dont get (can got weird tumors, neuro problems, infections)
98
AIDS is when
HIV is taking over the body to the point that you get 1. opportunistic infections 2. secondary neoplasms 3. Neurologic manifestations
99
most risky way to get HIV
anal receptive intercourse (since mucosal barrier is so thin) also vaginal intercourse - easier if you have a wound
100
parenteral routes of HIV transmission
IV drug, blood transfusion
101
mother to child HIV
through placenta , milk, birth canal
102
HIV is what type of virus
Retrovirus, Lentivirus = slow action | RNA --> DNA --> protein
103
HIV regions to know 4
1. LTR : initiate transcription 2. gag : encodes viral proteins inside virus 3. env : surface glycoproteins encoding 4. pol : viral enzymes encoding
104
HIV life cycle
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
how does HIV activate its disease
NFkB ----> LTR = kills the T cell CD4+ | *NFkB is supposed to upregulate T cells = hey wake up T cell
106
viral replication occurs where
LN
107
acute retroviral syndrome
first few days of infection mild flu sx
108
after acute retroviral syndrome
AB response, HIV go to LN underground (cant test for HIV between 7-21 days of infection)
109
HIV testing
1. NAT : viral RNA 2. protein Ag p24 3. HIV Ab
110
window period
has been exposed and no + test for about a week (with most sensitive HIV anti-env Ab)
111
what happens after HIV hides in LN
HIV virus RNA lowers to a Viral set point (at this point/peak downward = clinical latency)
112
latency period
T cells are getting killed silently however no real SX
113
CNS of AIDS
CNS toxoplasmosis
114
AIDS is when
WBC is below 200cells/mm3 or an unusual infection
115
Pneumocystic jiroveci (carinii)
fungal, shows someone has AIDS | silver stain shows black stains of fungal yeast
116
Kaposi sarcoma
vascular tumor from HHV8/ KSH8, can defines AIDS | = red lesions patch like
117
B cell lymphoma
from EBV, can define AIDS - hypergammaglobulinemia (many uneffective Abs - low isotype switch
118
cervical cancer
from HPV, can define AIDS
119
HIV and brain
microglia have HIV accumulation = encephalopathy = dementia
120
Amyloid is what
misfolded proteins becoming B-pleaded sheets
121
how do you see amyloid
1. Congo Red stain = bubble gum pink 2. Polarized light = apple green = determines amyloid (take from any tissue like belly fat)
122
what disease has to do with amyloid
myeloma
123
myeloma = acquired mutation
B cell plasma cells get IGs accumulate of light chain = AL amyloid
124
chronic inflammation
M activation makes SAA proteins = AA amyloid
125
hereditary mutation and no other sx
transthyretin --> ATTR amyloid
126
organs that amyloid deposits
kidney, liver , heart
127
kidney amyloid sx
edema, protein in urine
128
heart amyloid sx
dysrhythmias, disrupt electric signaling

MOD Exam2 (8 decks)

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