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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
Nitro blue test?
Turs blue if person can turn O2 -> O2-
26
Negative nitro blue test?
= CGD
27
MPO deficiency?
Candida infx with normal nitro blue as can make O2- but problem making HOCL
28
How do macs kill?
Mainly oxygen independent with enzymes in secondary granules **Lysozyme
29
What do macs release for resolution?
IL10 TGF Beta - Could release IL8 if want more neuts
30
What is TCR coupled with?
CD3 - allows to recognize antigens but only when present in MHC
31
2nd CD4 signal?
APC B7 binds CD28 on CD4 t cell
32
2 types of CD4s?
1. TH1: help CD8s | 2. Th2: help B cells
33
What does TH1 secrete?
1. IL2: activates and grows CD8s | 2. IFN gamma: activates macs
34
What do Th2s secrete?
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
35
Second signal for CD8s?
IL2 from TH1 CD4
36
How does CD8 kill?
1. Performing makes hole, granzyme enters, apoptosis occurs via caspase 2. Fas ligand on CD8 binds FAS on target = apoptosis
37
How are Caspases activated?
1. Cytochrome C from mitochondria 2. Fas 3. Granzyme `
38
What do naive B cells express?
IgM and IgD think, naive MD
39
How are naive B cells activated?
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
40
Cell that defines granuloma?
Epithelioid histiocyte: Mac with pink cytoplasm
41
Do non caseating granulomas have necrosis?
No
42
DDx non caseating?
1. Beryllium 2. Crohns 3. Sarcoid 4. Foreign material 5. Cat Scratch
43
Stellate shaped granuloma?
Cat Scratch: non caseating
44
DDx caseating? How do differentiate types?
1. TB: AFB stain | 2. Fungal: GMS stain
45
How is granuloma formed?
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
46
What does IL12 do?
Released by macs for TH differentiation
47
Digeorge?
1. T cells deficient: lack of thymus - > viral / fungal 2. HYPO Ca: no parathyroids 3. Facial deformities 4. Cardiac abnormalities
48
SCID? Causes?
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
49
What does Adenosine deaminase deficient cuase?
SCID
50
X linked Agammaglobulinemia?
- Zero Ig from disordered B cell maturation - Naive cannot become plasma - Absent lymph nodes - Only seen in boys * Bruton tyrosine kinase deficiency
51
*Bruton tyrosine kinase deficiency
Agammaglobulinemia
52
Presentation of Agammaglobulinemia?
A 6 months infx with: 1. Giardia 2. Enterovirus 3. Bacterial * only in boys
53
A 6 month old boy infx with: 1. Giardia 2. Enterovirus 3. Bacterial
Agammaglobulinemia
54
Disease common in IgA deficient?
Celiacs
55
Hyper IgM
- Second 40/40L signal cant be sent - Cytokines for class switching cant be made - Low IgA / E / G * *Recurrent mucosal and pyogenic infx
56
Wiskott aldrich?
1. Eczema 2. Thrombocytopenia: petechia 3. Recurrent infx * WASP mutation
57
1. Eczema 2. Thrombocytopenia: petechia 3. Recurrent infx * WASP mutation
Wiskott aldrich
58
C5 - 9 Deficient?
Neisseria
59
C1 inhibitor deficient?
Edema of skin and mucosal surfaces especially around eyes | "C1 esterase"
60
Positive selection?
Can you bind MHC and antigen | - If not = death
61
Negative selection?
Do you bind self antigen too strongly? | - Yes = death
62
Where does negative selection occur?
Medulla of thymus
63
Autoimmune polyendocrine disease?
AIRE mutations 1. HYPOparathyroid 2. Adrenal failure 3. Chronic candida
64
What is AIRE?
Responsible for creating self antigens in medullary thymus to test for self reactive T cells
65
1. HYPOparathyroid 2. Adrenal failure 3. Chronic candida
Autoimmune polyendocrine disease
66
What is peripheral tolerance?
- 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
What is CD95?
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
ALPS "Autoimmune lymphoproliferative syndrome"
FAS mutations | - Caspase 10 is also important and can be mutated
69
FAS mutations
ALPS "Autoimmune lymphoproliferative syndrome"
70
How does Treg work?
1. Uses CTLA4 to bind B7 and prevent CD4 activation 2. IL10 3. TGF beta - Limits MHC II
71
Cds of t reg?
CD4 CD25 (IL-2 receptor) FoxP3
72
CD4 CD25 FoxP3
T reg
73
FOXP3 mutation?
``` IPEX syndrome: Immune dysfunction Polyendocrinopathy Enteropathy X linked ```
74
``` IPEX syndrome: Immune dysfunction Polyendocrinopathy Enteropathy X linked ```
FOXP3 mutation
75
What does HLA do?
Code for MHC
76
HLA B27 has strongest association with what?
Ankylosing spondylitis
77
Brief overview of Lupus?
- Ig / antibody complex deposit in tissues activating complement which then damages tissue - Ig is directed against host nuclear material
78
What type of HSR is lupus?
III | ***Destruction of their blood cells is Type II HSR, however
79
Decreased CH50, C4, C4?
SLE
80
Whats responsible for clearing Ig / antigen complexes?
- Complement, if you have complement deficiency, are shown to develop SLE earlier
81
Renal damage seen in lupus?
1. Membranous nephropathy | 2. Diffuse proliferative glomerulonephritis
82
Tests for SLE?
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
Anti Smith?
SLE
84
Anti DSDNA?
SLE
85
What is APA syndrome?
- Patient has antiphospholipid Ig from lupus AND actually have a hypercoagulable state * **Normally patient will not actually have SLE
86
Antihistone Ig?
Drug induced SLE
87
Drugs causing SLE?
1. Hydralazine 2. Procainamide 3. Isoniazid * **Usually goes away if you remove these drugs
88
Death in lupus?
1. Renal failure 2. Infx 3. Late atherosclerosis
89
Sjogren?
- AI destruction of lacrimal and salivary glands | - Lymphocyte mediated HSR with fibrosis
90
Sjogren presentation?
"Cant chew a cracker, dirt in my eyes" 1. Dry eyes 2. Dry mouth 3. Dental caries
91
Sjogren common association?
Rheumatoid arthritis | ***RF often seen even if patient is not presenting with RA
92
Serum in sjogren?
1. ANA 2. Ig against ribonucleoprotein: Anti SS-a / SS-b 3. RF
93
1. ANA | 2. Ig against ribonucleoprotein
Sjogren
94
Other risks of sjogren?
1. SS-a can cross placenta: congenital heart block or neonatal lupus 2. B cell lymphoma
95
Lymphocytic sialadenitis?
- Lymphocytes attacking salivary glands on sjogren's biopsy
96
Other disease causing dry eyes?
1. Amyloid | 2. Saroid
97
Sjogren with on parotid bigger than other?
B cell lymphoma
98
Whats happening in systemic sclerosis?
- Fibroblast activation = deposition of collagen hardening tissues
99
What is CREST?
``` Calcinosis Centromere - Ig against them Raynaud's Esophageal dysmotility Sclerodactyly - fibrosis of skin on hands Telangiectasias ```
100
Anticentromere Ig?
CREST
101
DNA topoisomerase I IG?
Diffuse systemic sclerosis
102
ANA with anti U1 ribonucleoprotein Ig?
Mixed connective tissue disease
103
Difference between regeneration and repair?
Regeneration: replace damaged tissue with tissue itself Repair: replacement of tissue with scar
104
3 types of tissue based on regeneration?
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
Marker of HSC?
CD34
106
Which are the permanent tissues?
1. Neurons 2. Skeletal muscle 3. Myocardium
107
Initial phase of repair?
Granulation tissue: 1. Fibroblasts deposit type III collagen 2. Capillaries bring nutrients 3. Myofibroblasts: contract wound
108
End game of granulation tissue?
Forming scar
109
Difference in collagen in scar and granulation?
Type III collagen replaced with I in scar
110
Types of Collagen?
Type I: bone, scars Type II: Cartilage "Car'two'lage" Type III: Vessels, granulation tissue, embryo Type IV: Basement membranes
111
How is Type III replaced with one?
Collagenase that needs zinc as cofactor
112
TGF alpha? Beta?
Alpha: epithelial and fibroblast growth factor Beta: Inhibits inflammation, fibroblast growth factor
113
PDGF?
Growth factor of: 1. Endothelium 2. Smooth muscle 3. Fibroblast
114
FGF?
1. Angiogenesis | 2. Skeletal development
115
Primary vs. secondary intention?
Primary: wound brought together = minimal scar Secondary: not brought together, granulation fills wound - Myofibroblasts pull sides together
116
Deficiencies impacting collagen?
1. Vitamin C: required for hydroxylation / cross linking ` 2. Copper: needed for lysyl oxidase 3. Zinc
117
Dehiscence?
Rupture of wound during healing
118
What is excess in keloid?
Type III collagen
119
Artery to liver?
Celiac
120
What is IgM important for?
- Encapsulated bacteria, IgM is main Ig of spleen
121
What part of MHC is antigen bound on?
Beta 2 subunit
122
What encodes for MHC1?
HLA-A, B, C
123
What encodes MHC2?
HLA DP, DQ, DR
124
HLA-A3?
Hemochromatosis
125
B27?
``` PAIR Psoriasis Ankylosing spondylitis IBD Reiters syndrome ```
126
DQ2/8?
Celiacs
127
DR4?
RA
128
What does IL12 promote?
TH1 to stimulated B cells
129
What does IL4 promote?
TH2, allergy IgE response
130
CD3/4/25?
T reg secreting IL10/TGF beta to suppress immune system
131
What does mac release once stimulated by CD4?
TNF-a, TH is releasing IFN-gamma back on bac
132
IL6?
IgG class switching
133
VDJ rearrangement?
Process by which body rearranges antigens to create diversity
134
Ig crossing placenta?
IgG
135
Which IL induces acute phase reactants?
IL1 activates IL6 causing liver to release reactants
136
Which is complement important for?
Gram negative
137
C1 esterase inhibitor?
Normally inhibits complement: without you get C5/3a dilating face causing edema and constriction bronchioles causing wheezing
138
What does decay accelerating factor deficiency cause?
PNH
139
HOT T BONE stEAk
``` 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
IL8?
Cleanup on aisle 8 | - Wraps up immune response
141
IL10
Pro TH2 | Anti TH1 "IL10 makes TH1, zero"
142
IL12?
Pro TH1, think the 1 comes first in 12
143
Interferon A/B?
Inhibit viral protein synthesis
144
Interferon gamma?
Increased MHC1 expression
145
Cell marker for NK cell?
CD 56
146
CD56?
NK cell
147
Most common cause of anaphylaxis in blood transfusion?
Selective IgA deficiency
148
Decreased plasma cells and Ig?
CVID
149
Recurrent TB infx?
IL12-r deficiency
150
Allograft?
Same species but not related

USMLE: step 1 (15 decks)

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