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USMLE: step 1 > Path inflammation / FA immunology > Flashcards

Path inflammation / FA immunology Flashcards

1
Q

What is LPS?

A

PAMP present in cell wall of all gram neg bacteria that is recognized by CD14 on macs

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2
Q

What is NFKB?

A

Turned on when TLR is activating turning on acute inflammatory response

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3
Q

What does LTB4 doing?

A

Attract and activate neuts

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4
Q

4 things attracting and turning on macs?

A
  1. C5a
  2. LTB4
  3. IL8
  4. Bacterial products
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5
Q

Function of LTs?

A
  1. Vasoconstrict
  2. Bronchospasm
  3. Vascular perm
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6
Q

What are pericytes?

A

Contract to pull endothelial cells to allow extravasation form capillaries
- Activated by leukotrienes

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7
Q

What activates masts?

A
  1. Trauma
  2. C3/5
  3. IgE cross linking
    * Causes dumpin of histamine = dilation and increased permeability
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8
Q

What do mast cells do after dumping histamine?

A

Several hours later dumb leukotrienes to keep acute response going

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9
Q

How is classical complement path activated?

A

“GM makes classic cars”

IgG / M bound to antigen turn on C1

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10
Q

What is C3b?

A

Opsonin for phagocytosis

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11
Q

What mediates pain?

A
  1. Bradykinin

2. PGE2

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12
Q

Who is fever caused?

A
  1. Macs release IL1 and TNF
  2. Increase COX in perivascular cells of hypothalamus
  3. Increased PGE2 raises temp set point
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13
Q

What upregulates P and E selectin?

A

P: histamine
E: IL1 / TNF

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14
Q

What is sialyl Lewis X?

A

What selectins bind on neuts to slow them down

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15
Q

What binds in adhesions?

A

Integrins on neuts to cellular adhesion molecules

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16
Q

What is leukocytes adhesion deficiency?

A
  • AR defect in CD18 unit of integrins responsible for adhesion
    1. Delayed umbilical separation
    2. Increased neuts
    3. Recurrent bacterial infx w/o puss
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17
Q
  1. Delayed umbilical separation
  2. Increased neuts
  3. Recurrent bacterial infx w/o puss
A

leukocytes adhesion deficiency

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18
Q

2 opsonins?

A

IgG

C3b

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19
Q

What is chediak hegashi?

A
  • AR protein trafficking defect with impaired phagolysosome formation
  • Defect in microtubules
    1. Increased pyogenic infections
    2. Albinism
    3. Neutropenia: microtubule issues
    4. Granules in leukocytes
    5. Neuropathy: cant move nutrients to end of nerve
    6. Defective primary hemostasis
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20
Q
  1. Increased pyogenic infections
  2. Albinism
  3. Neutropenia
  4. Granules in leukocytes
  5. Neuropathy
  6. Defective primary hemostasis
A

Chediak

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21
Q

Oxidative burst?

A
  1. O2 -> O2- (superoxide): via NADPH oxidase
  2. O2- -> H202: via superoxide dismutase
  3. H2O2 -> HOCL: via MPO
    * HOCL kills microbe in phagolysosome
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22
Q

CGD?

A

NADPH oxidase deficiency: cant make O2-

**Catalase positive infx

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23
Q

Why catalase positive in GCG?

A

Catalase destroys the H2O2 bacteria is making preventing CGD cells from using it to make HOCL

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24
Q

Cat pos orgs?

A 
Aureus
Pseudomonas cepacia 
S marcescens 
Nocardia 
Aspergillus
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25
Q

Nitro blue test?

A

Turs blue if person can turn O2 -> O2-

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26
Q

Negative nitro blue test?

A

= CGD

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27
Q

MPO deficiency?

A

Candida infx with normal nitro blue as can make O2- but problem making HOCL

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28
Q

How do macs kill?

A

Mainly oxygen independent with enzymes in secondary granules
**Lysozyme

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29
Q

What do macs release for resolution?

A

IL10
TGF Beta
- Could release IL8 if want more neuts

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30
Q

What is TCR coupled with?

A

CD3 - allows to recognize antigens but only when present in MHC

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31
Q

2nd CD4 signal?

A

APC B7 binds CD28 on CD4 t cell

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32
Q

2 types of CD4s?

A
  1. TH1: help CD8s

2. Th2: help B cells

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33
Q

What does TH1 secrete?

A
  1. IL2: activates and grows CD8s

2. IFN gamma: activates macs

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34
Q

What do Th2s secrete?

A
  1. IL4 - Class switch to IgG / E
  2. IL5 - IgA, b cell maturation, Eosinophils
  3. IL10 - Stops Th1
    - Macs also produce IL 10 to end acute inflammation
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35
Q

Second signal for CD8s?

A

IL2 from TH1 CD4

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36
Q

How does CD8 kill?

A
  1. Performing makes hole, granzyme enters, apoptosis occurs via caspase
  2. Fas ligand on CD8 binds FAS on target = apoptosis
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37
Q

How are Caspases activated?

A
  1. Cytochrome C from mitochondria
  2. Fas
  3. Granzyme `
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38
Q

What do naive B cells express?

A

IgM and IgD think, naive MD

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39
Q

How are naive B cells activated?

A
  1. Antigen binds IgM / D: becomes IgM plasma cell

2. B cells presents to CD4 in MHC2, CD40/40L provides second signal: T cell releases IL4/5 allowing isotype switching

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40
Q

Cell that defines granuloma?

A

Epithelioid histiocyte: Mac with pink cytoplasm

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41
Q

Do non caseating granulomas have necrosis?

A

No

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42
Q

DDx non caseating?

A
  1. Beryllium
  2. Crohns
  3. Sarcoid
  4. Foreign material
  5. Cat Scratch
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43
Q

Stellate shaped granuloma?

A

Cat Scratch: non caseating

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44
Q

DDx caseating? How do differentiate types?

A
  1. TB: AFB stain

2. Fungal: GMS stain

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45
Q

How is granuloma formed?

A
  1. Macs present to CD4 in MHCII
  2. Macs release IL2 - > TH1 differentiation
  3. TH1 secreted IFN-gamma -> giant cells and epithelioid histiocytes form macs
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46
Q

What does IL12 do?

A

Released by macs for TH differentiation

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47
Q

Digeorge?

A
  1. T cells deficient: lack of thymus - > viral / fungal
  2. HYPO Ca: no parathyroids
  3. Facial deformities
  4. Cardiac abnormalities
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48
Q

SCID? Causes?

A

Defective cell and Ig immunity

  1. Cytokine recept Defect
  2. Absent MHC II
  3. Adenosine deaminase deficiency: adenosine builds up and is toxic to lymphocytes
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49
Q

What does Adenosine deaminase deficient cuase?

A

SCID

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50
Q

X linked Agammaglobulinemia?

A
  • Zero Ig from disordered B cell maturation
  • Naive cannot become plasma
  • Absent lymph nodes
  • Only seen in boys
  • Bruton tyrosine kinase deficiency
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51
Q

*Bruton tyrosine kinase deficiency

A

Agammaglobulinemia

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52
Q

Presentation of Agammaglobulinemia?

A

A 6 months infx with:

  1. Giardia
  2. Enterovirus
  3. Bacterial
    * only in boys
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53
Q

A 6 month old boy infx with:

  1. Giardia
  2. Enterovirus
  3. Bacterial
A

Agammaglobulinemia

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54
Q

Disease common in IgA deficient?

A

Celiacs

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55
Q

Hyper IgM

A
  • Second 40/40L signal cant be sent
  • Cytokines for class switching cant be made
  • Low IgA / E / G
  • *Recurrent mucosal and pyogenic infx
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56
Q

Wiskott aldrich?

A
  1. Eczema
  2. Thrombocytopenia: petechia
  3. Recurrent infx
    * WASP mutation
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57
Q
  1. Eczema
  2. Thrombocytopenia: petechia
  3. Recurrent infx
    * WASP mutation
A

Wiskott aldrich

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58
Q

C5 - 9 Deficient?

A

Neisseria

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59
Q

C1 inhibitor deficient?

A

Edema of skin and mucosal surfaces especially around eyes

“C1 esterase”

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60
Q

Positive selection?

A

Can you bind MHC and antigen

- If not = death

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61
Q

Negative selection?

A

Do you bind self antigen too strongly?

- Yes = death

62
Q

Where does negative selection occur?

A

Medulla of thymus

63
Q

Autoimmune polyendocrine disease?

A

AIRE mutations

  1. HYPOparathyroid
  2. Adrenal failure
  3. Chronic candida
64
Q

What is AIRE?

A

Responsible for creating self antigens in medullary thymus to test for self reactive T cells

65
Q
  1. HYPOparathyroid
  2. Adrenal failure
  3. Chronic candida
A

Autoimmune polyendocrine disease

66
Q

What is peripheral tolerance?

A
  • If cell recognizes cell in periphery without second signal the immune cell will undergo anergy and shut down
  • *Second signal only present when inflammation
67
Q

What is CD95?

A

AKA “FAS” death receptor
- If Immune cell repeatedly binds cells without second signal it will express FASL which binds FAS on same cell causing it to die

68
Q

ALPS “Autoimmune lymphoproliferative syndrome”

A

FAS mutations

- Caspase 10 is also important and can be mutated

69
Q

FAS mutations

A

ALPS “Autoimmune lymphoproliferative syndrome”

70
Q

How does Treg work?

A
  1. Uses CTLA4 to bind B7 and prevent CD4 activation
  2. IL10
  3. TGF beta - Limits MHC II
71
Q

Cds of t reg?

A

CD4
CD25 (IL-2 receptor)
FoxP3

72
Q

CD4
CD25
FoxP3

73
Q

FOXP3 mutation?

A 
IPEX syndrome:
Immune dysfunction 
Polyendocrinopathy 
Enteropathy 
X linked
74
Q 
IPEX syndrome:
Immune dysfunction 
Polyendocrinopathy 
Enteropathy 
X linked
A

FOXP3 mutation

75
Q

What does HLA do?

A

Code for MHC

76
Q

HLA B27 has strongest association with what?

A

Ankylosing spondylitis

77
Q

Brief overview of Lupus?

A
  • Ig / antibody complex deposit in tissues activating complement which then damages tissue
  • Ig is directed against host nuclear material
78
Q

What type of HSR is lupus?

A

III

***Destruction of their blood cells is Type II HSR, however

79
Q

Decreased CH50, C4, C4?

80
Q

Whats responsible for clearing Ig / antigen complexes?

A
  • Complement, if you have complement deficiency, are shown to develop SLE earlier
81
Q

Renal damage seen in lupus?

A
  1. Membranous nephropathy

2. Diffuse proliferative glomerulonephritis

82
Q

Tests for SLE?

A
  1. ANA: sensitive
  2. Anti smith: specific
  3. Anti-DSDNA: specific
    - Good for following reactivity
  4. Anti phospholipid Ig
    a. Cardiolipin - false positive syphillis test
    b. Lupus anticoag - falsely elevated PTT
    c. Anti b2 glycoprotein I
83
Q

Anti Smith?

84
Q

Anti DSDNA?

85
Q

What is APA syndrome?

A
  • Patient has antiphospholipid Ig from lupus AND actually have a hypercoagulable state
  • **Normally patient will not actually have SLE
86
Q

Antihistone Ig?

A

Drug induced SLE

87
Q

Drugs causing SLE?

A
  1. Hydralazine
  2. Procainamide
  3. Isoniazid
    * **Usually goes away if you remove these drugs
88
Q

Death in lupus?

A
  1. Renal failure
  2. Infx
  3. Late atherosclerosis
89
Q

Sjogren?

A
  • AI destruction of lacrimal and salivary glands

- Lymphocyte mediated HSR with fibrosis

90
Q

Sjogren presentation?

A

“Cant chew a cracker, dirt in my eyes”

  1. Dry eyes
  2. Dry mouth
  3. Dental caries
91
Q

Sjogren common association?

A

Rheumatoid arthritis

***RF often seen even if patient is not presenting with RA

92
Q

Serum in sjogren?

A
  1. ANA
  2. Ig against ribonucleoprotein: Anti SS-a / SS-b
  3. RF
93
Q
  1. ANA

2. Ig against ribonucleoprotein

94
Q

Other risks of sjogren?

A
  1. SS-a can cross placenta: congenital heart block or neonatal lupus
  2. B cell lymphoma
95
Q

Lymphocytic sialadenitis?

A
  • Lymphocytes attacking salivary glands on sjogren’s biopsy
96
Q

Other disease causing dry eyes?

A
  1. Amyloid

2. Saroid

97
Q

Sjogren with on parotid bigger than other?

A

B cell lymphoma

98
Q

Whats happening in systemic sclerosis?

A
  • Fibroblast activation = deposition of collagen hardening tissues
99
Q

What is CREST?

A 
Calcinosis
Centromere - Ig against them 
Raynaud's
Esophageal dysmotility 
Sclerodactyly - fibrosis of skin on hands
Telangiectasias
100
Q

Anticentromere Ig?

101
Q

DNA topoisomerase I IG?

A

Diffuse systemic sclerosis

102
Q

ANA with anti U1 ribonucleoprotein Ig?

A

Mixed connective tissue disease

103
Q

Difference between regeneration and repair?

A

Regeneration: replace damaged tissue with tissue itself
Repair: replacement of tissue with scar

104
Q

3 types of tissue based on regeneration?

A
  1. Labile: constantly regenerating -> bowel, marrow, skin
  2. Stable: Quiescent but can reenter cycle
    - Liver: can grow back if resected
    - Occurs via compensatory hyperplasia
  3. Permanent: do no regenerate
105
Q

Marker of HSC?

106
Q

Which are the permanent tissues?

A
  1. Neurons
  2. Skeletal muscle
  3. Myocardium
107
Q

Initial phase of repair?

A

Granulation tissue:

  1. Fibroblasts deposit type III collagen
  2. Capillaries bring nutrients
  3. Myofibroblasts: contract wound
108
Q

End game of granulation tissue?

A

Forming scar

109
Q

Difference in collagen in scar and granulation?

A

Type III collagen replaced with I in scar

110
Q

Types of Collagen?

A

Type I: bone, scars
Type II: Cartilage “Car’two’lage”
Type III: Vessels, granulation tissue, embryo
Type IV: Basement membranes

111
Q

How is Type III replaced with one?

A

Collagenase that needs zinc as cofactor

112
Q

TGF alpha? Beta?

A

Alpha: epithelial and fibroblast growth factor
Beta: Inhibits inflammation, fibroblast growth factor

113
Q

PDGF?

A

Growth factor of:

  1. Endothelium
  2. Smooth muscle
  3. Fibroblast
114
Q

FGF?

A
  1. Angiogenesis

2. Skeletal development

115
Q

Primary vs. secondary intention?

A

Primary: wound brought together = minimal scar
Secondary: not brought together, granulation fills wound
- Myofibroblasts pull sides together

116
Q

Deficiencies impacting collagen?

A
  1. Vitamin C: required for hydroxylation / cross linking `
  2. Copper: needed for lysyl oxidase
  3. Zinc
117
Q

Dehiscence?

A

Rupture of wound during healing

118
Q

What is excess in keloid?

A

Type III collagen

119
Q

Artery to liver?

120
Q

What is IgM important for?

A
  • Encapsulated bacteria, IgM is main Ig of spleen
121
Q

What part of MHC is antigen bound on?

A

Beta 2 subunit

122
Q

What encodes for MHC1?

A

HLA-A, B, C

123
Q

What encodes MHC2?

A

HLA DP, DQ, DR

124
Q

HLA-A3?

A

Hemochromatosis

125
Q

B27?

A 
PAIR
Psoriasis 
Ankylosing spondylitis
IBD
Reiters syndrome
126
Q

DQ2/8?

127
Q

DR4?

128
Q

What does IL12 promote?

A

TH1 to stimulated B cells

129
Q

What does IL4 promote?

A

TH2, allergy IgE response

130
Q

CD3/4/25?

A

T reg secreting IL10/TGF beta to suppress immune system

131
Q

What does mac release once stimulated by CD4?

A

TNF-a, TH is releasing IFN-gamma back on bac

132
Q

IL6?

A

IgG class switching

133
Q

VDJ rearrangement?

A

Process by which body rearranges antigens to create diversity

134
Q

Ig crossing placenta?

135
Q

Which IL induces acute phase reactants?

A

IL1 activates IL6 causing liver to release reactants

136
Q

Which is complement important for?

A

Gram negative

137
Q

C1 esterase inhibitor?

A

Normally inhibits complement: without you get C5/3a dilating face causing edema and constriction bronchioles causing wheezing

138
Q

What does decay accelerating factor deficiency cause?

139
Q

HOT T BONE stEAk

A 
IL1 "HOT"
- Heat: pge2 release from hypothalamus fever
IL2 "T"
- T cell activation
IL3 "Bone"
- Increased bone marrow production 
IL4 "E"
- IgE
IL5 "A"
- IgA
140
Q

IL8?

A

Cleanup on aisle 8

- Wraps up immune response

141
Q

IL10

A

Pro TH2

Anti TH1 “IL10 makes TH1, zero”

142
Q

IL12?

A

Pro TH1, think the 1 comes first in 12

143
Q

Interferon A/B?

A

Inhibit viral protein synthesis

144
Q

Interferon gamma?

A

Increased MHC1 expression

145
Q

Cell marker for NK cell?

146
Q

CD56?

147
Q

Most common cause of anaphylaxis in blood transfusion?

A

Selective IgA deficiency

148
Q

Decreased plasma cells and Ig?

149
Q

Recurrent TB infx?

A

IL12-r deficiency

150
Q

Allograft?

A

Same species but not related

USMLE: step 1 (15 decks)

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