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USMLE STEP 1 > Immune System > Flashcards

Immune System Flashcards

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USMLE® Step 1 flashcards
1
Q 
Innate Immunity 
Receptor coding?
Response to pathogens is
Memory?
Cells involved?
Molecules involved?
A

Receptors that recognize pathogens are germline encoded
Response to pathogens is fast and nonspecific
No Memory
Neutrophils, Macs, Dendritic Cells, Natural Killer Cells (lymphoid origin)
Complement

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2
Q 
Adaptive Immunity
Innate Immunity 
Receptor coding?
Response to pathogens is
Memory?
Cells involved?
Molecules involved?
A

Receptors that recognize pathogens undergo V(D)J recombination during lymphocyte development
Response is slow on first exposure. Memory response is faster and more robust.
T and B cells
Antibodies

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3
Q 
MHC 
Stands for
Encoded by what gene?
Function 
What does it bind?
A

Major Histocompatibility Complex
Human Leukocyte Antigen (HLA) gene
Presents antigen fragments to T cells and binds TCR

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4
Q 
MHC I
Genes encoding it?
Binds what receptors 
Which cells express it?
Where is antigen loaded
What kind of antigens?
What kind of immunity does it mediate?
What does it pair with and why?
Where is peptide groove?
A

HLA A, B and C
Binds TCR and CD8
All nucleated cells (not RBCs)
Antigen loaded in RER with mostly intracellular peptides
Mediates viral immunity
Pairs with β2 microglobins (aids in transport to cell surface)
Peptide groove in α chain

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5
Q 
MHC II
Genes encoding it?
Binds what receptors 
Which cells express it?
When is antigen loaded
What does it look like?
A

HLA DR, DP and DQ
Binds TCR and CD4
Expressed only on APCs
Antigen is loaded following release of invariant chain in an acidified endosome
α and β chains pair with peptide groove in between

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6
Q

Association with HLA A3

A

Hemochromatosis

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7
Q

Association with HLA B27

A

“PAIR”

Psoriasis, Ankylosing Spondylitis, IBDm Reiter’s syndrome

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8
Q

Association with HLA DQ2/DQ8

A

Celiac

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9
Q

Association with HLA DR2

A

Multiple Sclerosis, Hay Fever, SLE, Goodpastures

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10
Q

Association with HLA DR3

A

DM type 1, Graves’ Disease

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11
Q

Association with HLA DR4

A

RA, DM type 1

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12
Q

Association with HLA DR5

A

Pernicious anemia (B12 deficiency), Hashimoto’s thyroiditis

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13
Q 
Natural Killer Cells
What do they do?
What do they use to do it?
How are they unique?
What molecules enhance their activity?
When are they induced to kill?
A

Induce apoptosis in virally infected cells or tumor cells
Use perforin and granzymes
Only lymphocyte member of innate immune system
“#2, get #12, tell him the boss needs to take out α and β”
Activity is enhanced by IL2, IL12, INFα, INFβ
Induced to kill when exposed to a nonspecific activation signal on target cell +/or to an absence of MHCI on target cell surface

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14
Q

B cells functions

A

Make Abs: opsonize bacteria, neutralize viruses (IgG), Activate complement (IgM and IgG), Sensitize mast cells (IgE)
Allergy (Type I hypersensitivity): IgE
Cytotoxic (Type II hypersensitivity): IgG
Immune Complex (Type III hypersensitivity): IgG
Hyperacute and humorally mediated acute and chronic organ rejection

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15
Q

T cell functions
Generally
CD4
CD8

A

Delayed cell mediated hypersensitivity reaction (IV)
Acute and chronic cellular organ rejection
CD4+ cells help B cells make Ab and produce cytokines to activate other cells of the immune system
CD8+ cells kill virus infected cells directly

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16
Q

Differentiation of T cells
In Bone Marrow
In Thymus
In Lymph Node

A 
In BM: T cell precursor
In T: expresses TCR, CD4 and CD8 and then will switch to only expressing one of the CDs and a TCR
In LN: CD8+ --> cytotoxic T cells
CD4+: if exposed to IL12 --> Th1
if exposed to IL4 --> Th2
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17
Q

Where is there Positive selection in T cell differentiation?

A

In the Thymic Cortex where T cells expressing TCR capable of binding self MHC survive

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18
Q

Where is there Negative selection in T cell differentiation?

A

Medulla where T cells expressing TCR with high affinity for self antigens undergo apoptosis

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19
Q 
APCs
# of signals needed for what?
A

Dendritic cell (Only APC that can activate naive T cell)
Macrophage
B cell
2 signals needed for T cell activation, B cell activation, and class switching

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20
Q

Steps of naive T cell activation

A
  1. Foreign body is phagocytosed by dendritic cell
  2. Foreign antigen presented on MHCII
  3. MHCII + antigen recognized by TCR on Th cell or MHCI + antigen recognized by TCR on Tc cell
  4. Costimulatory signal given by interaction of B7 (DC) and CD28 (T cell)
  5. T cell activated: Th produced cytokines, Tc kills virus infected cells
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21
Q

Steps of B cell activation and class switching

A
  1. Th cell activated
  2. B cell receptor mediated endocytosis
  3. Foreign antigen presented on MHCII
  4. MHCII + antigen recognized by TCR on Th cell
  5. CD40 receptor on B cell binds CD40 ligand on Th cell
  6. Th cell secretes cytokines that determine Ig class switching of B cell
  7. B cell activates and undergoes class switching, affinity maturation, and Ab production
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22
Q

Th1
What do they secrete
What do they activate
What inhibits them

A

Secretes INFγ
Activates Macs
Inhibited by IL4 and IL10 from Th2

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23
Q

Macrophage-Lymphocyte interaction

A

Activated lymphocyte –> INFγ –> Macs –> IL1 and TNFα –> lymphocytes

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24
Q

Th2
What do they secrete
What do they activate
What inhibits them

A

Secrete IL4, IL5, IL10, IL13
Recruit eosinophils for parasite defense, promote IgE production by B cells
Inhibited by INFγ from Th1

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25
Q 
Lymph Node
What is it?
Afferents?
Efferents?
Encapsulated? 
Function
A 
Secondary Lymphoid Organ
Many afferents 
1 or more efferents
Encapsulated w/ trabeculae 
Filtration by Macs, storage, activation of B and T cells, Ab production
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26
Q

Lymph Node Follicle
Location
Function
Primary vs Secondary

A

Outer cortex
B cell localization and proliferation
Primary: dense and dormant
Secondary: pale central germinal centers and are active

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27
Q

Lymph Node Medulla

What does it consist of?

A

Medullary cords: closely packed lymphocytes and plasma cells
Medullary sinuses: Communicate with efferent lymphatics and contain reticular cells and Macs

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28
Q 
Paracortex 
Location
What does it house?
What does it contain?
What happens in an extreme cellular response?
Disease?
A

Between follicles and medulla
T cells
High endothelial venules through which T and B cells enter from blood
In extreme celular response, becomes enlarged
Not well developed in DiGeorge Syndrome

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29
Q

Lymph Drainage of Upper limb and lateral breast

A

Axillary

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30
Q

Lymph Drainage of Stomach

A

Celiac

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31
Q

Lymph Drainage of Duodenum and Jejunum

A

Superior Mesenteric

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32
Q

Lymph Drainage of Sigmoid Colon

A

Colic –> Inferior Mesenteric

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33
Q

Lymph Drainage of lower rectum and anal canal above pectinate line

A

Internal Iliac

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34
Q

Lymph Drainage of Anal Canal Below Pectinate Line

A

Superficial Inguinal

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35
Q

Lymph Drainage of Testes

A

Superficial and Deep Plexuses –> Para-Aortic

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36
Q

Lymph Drainage of Scrotum

A

Superficial Inguinal

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37
Q

Lymph Drainage of Thigh

A

Superficial Inguinal

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38
Q

Lymph Drainage of Lateral Side of Dorsum of the foot

A

Popliteal

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39
Q

What does Right Lymphatic Duct drain?

What does Thoracic Duct drain?

A

Right arm, right chest, Right half of head

Everything else

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40
Q

Sinusoids of the Spleen
What are they?
What are found nearby

A

Long Vascular Channels in red pulp with fenestrated “barrel hoop” basement membrane
Macrophages found nearby

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41
Q

Where are T cells in the spleen?

A

Periarterial lymphatic sheath (PALS) w/in white pulp

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42
Q

Where are B cells in the spleen?

A

Follicles w/in white pulp

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43
Q

What do macrophages do in the spleen?

A

Remove encapsulated bacteria

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44
Q

Splenic Dysfunction
Pathway
What are pts susceptible to?

A

↓ IgM –> ↓ Complement activation –> ↓ C3b opsonization –> ↑ susceptibility to encapsulated organisms
“SHiNE SKiS”
Strep pneumoniae, Haemophilis influenza type B, Neisseria meningitidis, Salmonella, Klebsiella pneumoniae, Group B Strep, E coli

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45
Q

Blood of pt post Splenectomy

A

Howell Jolly Bodies, Target Cells, Thrombocytosis

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46
Q 
Thymus 
Function 
Encapsulated 
Development 
Origin of lymphocytes
A

Site of T cell differentiation and maturation
Encapsulated
From epithelium of 3rd Branchial pouches
Lymphocytes of mesenchymal origin

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47
Q

Thymus Cortex
Appearance
Kind of T cells there?
Kind of selection

A

Dense
Immature T cells
Positive selection (MHC restriction)

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48
Q 
Thymus Medulla 
Appearance 
Kind of T cells there?
Histo
Kind of selection
A

Pale
Mature T cells
Epithelial Reticular cells containing Hassall’s Corpuscles
Negative Selection (nonreactive to self)

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49
Q

Cytotoxic T cells
Function
What doe they release
Markers

A

Kill virus-infected cells, Neoplastic, and donor graft cells by inducing apoptosis
Release cytotoxic granules containing preformed proteins (Perforin, Granzyme, Granulysin)
CD8

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50
Q

Perforin
Granzyme
Granulysin

A

Perforin: Helps deliver the content of granules to target cells
Granzyme: Serine Protease activates apoptosis inside target cells
Granulysin: Antimicrobial, induces apoptosis

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51
Q

Regulator T cells
Function
Markers
What doe they produce?

A

Help maintain specific immune tolerance by suppressing CD4 and CD8 T cells
CD3, CD4, CD25 (α-chain of IL2 receptor)
IL10 and TGFβ

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52
Q

What part of Ab recognizes Ag

A

Variable portion of L and H chains

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53
Q

Function of Fc portion of IgM and IgG

A

Fix complement

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54
Q

Composition of Fc and Fab fractions Re H and L chains

A

H contributes to both Fc and Fab

L contributes only to Fab

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55
Q

Fab functions

A

Ag binding fragment

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56
Q 
Fc portion 
What is it?
Which end of the protein?
Function 
Side chains 
What does it determine?
A 
Constant portion
Carboxy terminal
Complement binding @ CH2 (IgM and IgG only)
Carbohydrate side chains 
Determine isotype (IgM, IgD...)
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57
Q

How is Ab diversity generated?

A

Light chain undergoes random VJ recombination
H undergoes random VDJ recombination
Random combination of H and L chains
Somatic Hypermutation following Ag stimulation (AID)
Addition of NTs to DNA during recombination by Terminal Deoxynucleotidyl Transferase

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58
Q

Mature B lymphocytes express what on their surface?

A

IgM and IgD

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59
Q

What mediates Isotype switching

A

Cytokines and CD40 ligand

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60
Q

IgG
Main Ab of what?
Abundance?
Function

A

Secondary Delayed Response
Most abundant type
Fixes complement, Crosses Placenta, Opsonizes bacteria, Neutralizes bacterial toxins and viruses

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61
Q 
IgA
Function 
Complement?
Single or group?
How does it cross epithelial cells 
Where is it found?
A

Prevents attachement of bacteria and viruses to mucous membrane
Doesn’t fix complement
Monomer in circulation, Dimer when secreted
Transcytosis where it picks up secretory component
Secretions (tears, saliva, mucus) and early breast milk (colostrum )

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62
Q 
IgM
When is it produced?
Function 
Placenta?
Single or group?
A

Primary immediate response to Ag
Fixes complement
Does not cross placenta
Monomer on B cells or Pentamer

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63
Q

IgD
Location
Function

A

Surface of B cells and in serum

Unclear function

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64
Q

IgE
Mediates what kind of Immunity?
Function
Abundance

A

Mediates immediate (type I) hypersensitivity through release of inflammatory mediators (histamine). Mediates immunity to worms by activating eosinophils
Binds mast cells and basophils. Cross links when exposed to allergen
Lowest concentration

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65
Q

Thymus Independent Antigens
What is it?
What do they stimulate
Memory?

A

Ags lacking peptide component and thus cannot be presented on MHC to T cells
Stimulate release of Ab
Do not result in memory

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66
Q

Thymus Dependent Antigens
What is it?
What do they stimulate
Memory?

A 
Ags containing protein component 
Stimulate class switching 
Memory results of direct contact of B cells w/ Th cells (CD40-CD40 Ligand interaction)
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67
Q

C3b

A

Opsonization

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68
Q

C3a and C5a

A

Anaphylaxis

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69
Q

C5a

A

Neutrophil Chemotaxis

70
Q

C5b-9

A

Cytolysis by MAC

71
Q

Complement Pathways

A

Classic: IgG and IgM
Alternative: Microbe Surface Molecule
Lectin: Mannose or other sugars on microbe surface

72
Q

Opsonins

A

IgG and C3b

73
Q

Inhibitors of Complement pathway

A

Decay-Accelerating Factor (DAF) and C1 esterase inhibitor

74
Q

Alternative Complement Pathway

A

Spontaneous and Microbal Surfaces turn C3 into C3b
B –> [D] –> Bb
C3 –> [C3bBb (C3 Convertase)] –> C3a + C3b

75
Q

Classic Complement Pathway

A

Ab –> C1
C2 –> [C1] –> C2a and C2b
C4 –> [C1] –> C4a and C4b
C3 –> [C4bC2a (C3 convertase)] –> C3a + C3b

76
Q

Lectin Complement Pathway

A

Mannose Binding Lectin –> [MASP] –> C1-like Complex
C4 –> [C1LC] –> C4a + C4b
C3 –> [C4b2a] –> C3a + C3b

77
Q

Common Complement Pathway

A

C3bBb3b (C5 convertase)
C4b2a3b (C5 convertase)
C5 –> [C5 convertase] –> C5a + C5b
C5b + C6 through C9) = MAC

78
Q

C1 Esterase Inhibitor Deficiency
Presentation
Contraindications

A

Hereditary Angioedema

ACE inhibitors Contraindicated

79
Q

C3 Deficiency Presentation

A

Severe, recurrent pyogenic sinus and respiratory tract infections
Susceptibility to Type III hypersensitivity reactions

80
Q

C5-C9 Deficiency

A

Recurrent Neisseria Bacteremia

81
Q

DAF (GPI anchored enzyme) deficiency

A

Complement mediated lysis of RBCs and Paroxysmal Nocturnal Hemoglobinuria

82
Q

IL1
Secreted by what cell?
Function

A

Macrophages
Endogenous pyrogen. Causes fever, acute inflammation, activates endothelium to express adhesion molecules, Induces chemokine secretion to recruit leukocytes

83
Q

IL6
Secreted by what cell?
Function

A

Macrophages and TH2

Endogenous pyrogen. Fever and Production of acute phase proteins

84
Q

IL8
Secreted by what cell?
Function

A

Macrophages

Neutrophil chemotactic

85
Q

IL12
Secreted by what cell?
Function

A

Macrophages and B cells
Induces differentiation of Th1 cells
Activate NK cells

86
Q

TNFα
Secreted by what cell?
What does it mediate?
Function

A

Macrophages
Mediates septic shock
Activates endothelium, Leukocyte recruitment, Vascular leak

87
Q

Interleukin Mnemonic

A 
"Hot T-Bone stEAk"
IL1: Hot (fever)
2: stimulate T cells 
3: Stimulates Bone marrow
4: IgE
5: IgA
88
Q

Cytokines secreted by all T cells w/ function

A

IL2: Stimulates growth of Th, Tc, and Treg cells
IL3: Supports growth and differentiation of bone marrow stem cells (like GM CSF)

89
Q

Interferon-γ
What kind of cells secrete it?
Function

A

Th1 cells
Activate Macrophages and Th1 cells
Suppresses Th2 cells
Antiviral and antitumor properties (upregulates MHCI and MHCII and Ag presentation in all cells)

90
Q

Cytokines secreted by Macrophages

A

1, 6, 8, 12, TNFα

91
Q

Cytokines secreted by Th2 cells

A

4, 5, 6, 10

92
Q

IL4
What kind of cells secrete it?
Function

A

Th2
Induces differentiation into Th2 cells
Promotes growth of B cells
Enhances class switching to IgE and IgG

93
Q

IL5
What kind of cells secrete it?
Function

A

Th2
Promotes differentiation of B cells
Enhances class switching to IgA
Stimulates Eosinophils

94
Q

IL10
What kind of cells secrete it?
Function
Like what other molecule

A

Th2 and Treg
Modulates immune response
Inhibits actions of activated T cells and Th1
Similar to TGFβ in that it inhibits inflammation

95
Q

Interferon
Kinds
Function

A

α, β, γ
Place uninfected cells in an antiviral state
Induce production of ribonuclease that inhibits viral protein synthesis by degrading viral mRNA
Activate NK cells

96
Q

IFNα and IFNβ function

A

Inhibit viral protein synthesis

97
Q

T cell surface markers
Th
Tc

A

T: TCR, CD3 (associated with TCR), CD28 (binds B7 on APC)
Th: CD4, CD40 lingand
Tc: CD8

98
Q

B cell surface markers

A

“Drink Beer at the Bar when you’re 21”

Ig, CD19, CD20, CD21 (EBV receptor), CD40, MHCII, B7

99
Q

Macrophage surface markers

A

CD14, CD40, MHCII, B7, Fc receptor, C3b receptor

100
Q

NK cell surface markers

A

CD16 (binds Fc of IgG), CD56

101
Q

Anergy
What is it?
B vs T

A

Self-reactive T cells become non reactive without costimulatory molecule
B cells also become anergic but tolerance is less complete than in T cells

102
Q

Superantigen
Produced by what?
Mechanism

A

S Pyogenes and S aureus

Cross link β region of T cell receptor to MHCII on APC activating T cell and producing massive release of cytokines

103
Q 
Endotoxin
AKA
Made by what?
Receptor?
Other cells involved?
A

Lipopolysaccharide
Gram neg
Directly stimulate Macrophages by binding to CD14
Th not involved

104
Q

Classic Antigen Variation in Bacteria

A

Salmonella (2 flagellar variants), Borrelia (relapsing fever), Neisseria gonorrhoeae (pilus protein)

105
Q

Classic Antigen Variation in Viruses

A

Influenza
Major = Shift
Minor = Drift

106
Q

Classic Antigen Variation in Parasites

A

Trypanosomes (programmed rearrangement)

107
Q 
Passive Immunity 
Means of acquisition
Onset
Duration 
Examples
A

Receiving preformed Abs
Rapid
Short (Ab half life is 3 weeks)
IgA in breast milk, Antitoxin, Humanized monoclonal Abs

108
Q

Diseases in which patients are given preformed Abs as treatment?

A

“To Be Healed Rapidly”

Tetanus toxin, Botulinum toxin, HBV, Rabies virus

109
Q 
Active Immunity 
Means of acquisition
Onset
Duration 
Examples
A

Exposure to foreign Ag
Slow
Long lasting
Natural infection, vaccines, toxoid

110
Q

Combined passive and active immunization can be given in the case of…

A

HBV or Rabies

111
Q

Live Attenuated Vaccine
What kind of response does it generate?
Examples

A

Cellular response

Measles, Mumps, Rubella, Varicella, Yellow Fever, Polio (Sabin)

112
Q

Inactivated or Killed Vaccine
What kind of response does it generate?
Examples

A

Humoral Immunity

Cholera, HAV, Rabies, Polio (Salk)

113
Q

Hypersensitivity Reactions that are Ab mediated?

A

I, II, and III

114
Q 
Type I Hypersensitivity Reaction
Description 
Process
Onset 
Test
A

Anaphylactic and Atopic
Free Ag cross-links IgE on presensitized mast cells and basophils triggering release of vasoactive amines that act at post-capillary venules (histamine)
Rapid because of preformed Ab
Skin test for specific IgE

115
Q 
Type II Hypersensitivity Reaction
Description 
Process
Mechanisms 
Test
A

Cytotoxic. Ab mediated
IgM, IgG bind to fixed Ag on “enemy” cell leading to cellular destruction
Opsonization, Complement activation, Ab-Dependent Cell-Mediated cytotoxicity (ADCC) due to NK cells
Direct and Indirect Coombs’ Test

116
Q

Type III Hypersensitivity Reaction
Description
Process

A

Immune Complex

Ag-Ab (IgG) complex activates complement which attracts Neutrophils which release lysosomal enzymes

117
Q 
Serum Sickness 
What is it?
PathoPhys
Timeframe 
Frequency 
What causes it?
Presentation
A

Immune Complex Disease
ICs are deposited in membranes where they fix complement leading to tissue damage
5-10 days after exposure
More common than Arthus
Drugs acting as haptens
Fever, Urticaria, Arthralgias, Proteinuria, Lymphadenopathy

118
Q 
Arthus Reaction 
What is it?
PathoPhys
Presentation 
Test 
Frequency
A

Local Subacute Ab mediated hypersensitivity type III reaction
Intradermal injection of Ag induces Abs which form Ag-Ab complexes in the skin which activate complement
Edema, Necrosis
Immunofluorescent staining
Less common than serum sickness

119
Q 
Type IV Hypersensitivity Reaction
Description 
Process
Transferable?
Mnemonic 
Test
A

Delayed T cell mediated reaction
Sensitized T lymphocytes encounter Ag and release lymphokines leading to macrophage activation. No Ab involvement
Not transferable in serum
“4Ts: Tcells, Transplant rejection, TB skin test, Touching (contact dermatitis)”
Patch test, PPD

120
Q

Hypersensitivity Reactions

A 
"ACID"
I: Anaphylactic and Atopic
II: Cytotoxic
III: Immune Complex 
IV: Delayed (cell mediated)
121
Q

Examples of Type I Hypersensitivity Reactions

A

Anaphylaxis (allergy)

Allergic and Atopic disorders (Rhinitis, Hay Fever, Eczema, Hives, Asthma)

122
Q

Examples of Type II Hypersensitivity Reactions

A 
"Go PIE TRAP"
Goodpasture's Syndrome
Pernicious Anemia
Idiopathic Thrombocytopenic Purpura
Erythroblastosis Fetalis
Acute Hemolytic Transfusion Reaction
Rheumatic Fever
Autoimmune Hemolytic Anemia
Bullous Pemphigoid, Pemphigus Vulgaris
123
Q

Examples of Type III Hypersensitivity Reactions

A 
"LAPPS"
SLE
Arthus
Polyarteritis nodosa
PSGN
Serum Sickness
124
Q

Examples of Type IV Hypersensitivity Reactions

A 
"Ms PuGG's CD"
MS
PPD test for TB
Gullian Barre
Graft vs Host
Contact Dermatitis (Poison Ivy, Nickel allergy)
125
Q

Allergic Reaction to blood transfusion
Type
Presentation
Treatment

A

Type I
Urticaria, Pruritus, Wheezing, Fever
Antihistamines

126
Q

Anaphylactic Reaction to blood transfusion
Severity
Precaution
Presentation

A

Severe
IgA deficient individuals must receive blood that lacks IgA
Dyspnea, Bronchoconstriction, Hypotension, Respiratory Arrest, Shock

127
Q

Febrile NonHemolytic Transfusion Reaction (FNHTR)
Type
Mechanism
Presentation

A

II
Host Ab against donor HLA Ags and leukocytes
Fever, Headaches, Chills, Flushing

128
Q

Acute Hemolytic Transfusion Reaction (AHTR)
Type
Mechanism
Presentation

A 
II
Intravascular hemolysis (ABO blood group incompatibility) or Extravascular hemolysis (host Ab reaction against foreign Ag or donor RBC)
Fever, Hypotension, Tachycardia, Flank Pain, Hemoglobinemia (intravascular), Jaundice (extravascular)
129
Q 
ANA
Anti dsDNA, Anti Smith
Anti-Histone
RF, CCP
Anti centromere 
Anti Scl70 (topoisomerase)
A 
SLE, nonspecific 
SLE
Drug induced SLE
RA
CREST
Scleroderma (diffuse)
130
Q

Anti-Mitochondiral
IgA anti endomysial, IgA anti Tissue Transglutaminase
Anti BM
Anit Desmoglein

A

Primary Biliary Cirrhosis
Celiac Disease
Goodpasture’s Syndrome
Pemphigus vulgaris

131
Q

Anti-Microsomal, Anti-Thyroglobulin
Anti Jo1, Anti SRP, Anti Mi2
Anti SSA, Anti SSB
Anti U1 RNP

A

Hashimoto’s Thyroiditis
Polymyositis, Dermatomyositis
Sjogren’s
Mixed connective tissue disease

132
Q

Anti Smooth Muscle
Anti Glutamate Decarboxylase
cANCA
pANCA

A

Autoimmune hepatitis
DM1
Wegeners
Microscopic polyangiitis, Churg Strauss syndrome

133
Q

No T cells
Bacteria
Virus
Fungi/Parasites

A

Sepsis
CMV, EBV, VZV, Chronic Respiratory and GI viruses
Candida, PCP

134
Q

No B cells
Bacteria
Virus
Fungi/Parasites

A

Encapsulated bacteria “SHiN SKiS”
Enteroviral Encephalitis, Poliovirus
GI Giardiasis (no IgA)

135
Q

No Granulocytes
Bacteria
Virus
Fungi/Parasites

A

Staph, Burkholderia cepacia, Serratia, Nocardia
N/A
Candida, Aspergillus

136
Q

No Complement
Bacteria
Virus
Fungi/Parasites

A

Neisseria
N/A
N/A

137
Q 
X linked (Burton's) Agammaglobinemia 
PathoPhys
Inheritance
Presentation 
Findings
A

Defect in BTK (a tyrosine kinase gene) –> no B cell maturation
Recurrent bacterial infections (bacteria, enterovirus, Giardia- get these 3 whenever defect in immunoglobulins) after 6 months of age
Norma pro-B cells, ↓ # of B cells, ↓ Immunoglobulins of all classes

138
Q

Selective IgA Deficiency
Frequency
Presentation
Labs

A

Most common primary immunodeficiency
Majority Asymptomatic. Sino-Pulmonary Infections, GI infections, Autoimmune disease, Anaphylaxis to IgA containing blood products
Low IgA with normal IgM and IgG. False positive βhCG test due to heterophile Ab

139
Q 
Common Variable Immunodeficiency (CVID)
PathoPhys
Epidemiology 
Risks 
Labs
A

Defect in B cell maturation by many causes
Acquired in 20s-30s
Infections with bacteria, enterovirus, Giardia- get these 3 whenever defect in immunoglobulins
Autoimmune disease, Lymphoma, Sinopulmonary infections
Normal # of B cells with ↓ Plasma cells and Immunoglobulin

140
Q 
Thymic Aplasia 
Name
PathoPhys
Genetics 
Presentation 
Labs
XR
A

DiGeorge Syndrome
Failure to develop 3rd and 4th Pharyngeal Pouches
22q11 deletion
Tetany (hypocalcemia), Recurrent viral/fungal infections (T cell deficiency), Congenital Heart and Great Vessel Defect
↓ T cells, ↓ PTH, ↓ Ca
Absent Thymic Shadow on CXR

141
Q

IL12 Receptor Deficiency
PathoPhys
Presentation
Labs

A

↓ Th1 response
Disseminated Mycobacterial Infections
↓ IFNγ

142
Q 
Hyper IgE Syndrome 
Name
PathoPhys
Presentation 
Labs
A

Job’s Syndrome
Th1 cells fail to produce IFNγ leading to inability to attract neutrophils
“FATED”
course Facies, cold (non inflamed) staphylococcal, Abscesses, retained primary Teeth, ↑IgE, Dermatologic problems (eczema)
↑IgE

143
Q

Chronic Mucocutaneous Candidiasis
PathoPhys
Presentation

A

T cell dysfunction –> Candida albicans infection of skin and mucous membrane

144
Q 
Severe Combined Immunodeficiency 
Kind of disorder 
PathoPhys
Presentation 
XR
Histo
Blood
Treatment
A

Combined B and T cell disorder
Defective IL2 receptor (most common, X linked) or Adenosine Deaminase deficiency
Failure to thrive, Chronic Diarrhea, Thrush. Recurrent viral, bacterial, fungal, and protozoal infections
No Thymic shadow
No Germinal centers on lymph node biopsy, ↓ T cell recombinant Excision Circles (TREC)
No B or T cells in peripheral blood
Bone Marrow Transplant

145
Q

Ataxia Telangiectasia
PathoPhys
Presentation
Labs

A

Defect in ATM gene coding for DNA repair enzyme
Cerebellar defects (ataxia), Spider angiomas (Telangiectasia), IgA deficiency
↑AFP

146
Q

Hyper IgM Syndrome
PathoPhys
Presentation
Antibodies

A

Defective CD40L on Th cells = inability to class switch
Severe pyogenic infections in early life
↑IgM, ↓ IgG, IgA, and IgE

147
Q 
Wiskott-Aldrich Syndrom 
Inheritance 
PathoPhys
Presentation 
Labs
A

XL
WASP gene mutation = T cells unable to reorganize actin cytoskeleton
“TIE”
Thrombocytopenic Purpura, Infections, Eczema
↑IgE, ↑IgA, ↓IgM, Thrombocytopenia

148
Q 
Leukocyte Adhesion Deficiency Type 1
Dysfunction of what?
PathoPhys
Presentation 
Findings
A

Phagocyte Dysfunction
Defect in LFA1 integrin (CD18) protein on phagocytes
Recurrent bacterial infections, absent pus formation, Delayed separation of umbilical cord
Neutrophilia

149
Q 
Chediak Higashi Syndrome 
Dysfunction of what?
Inheritance 
PathoPhys
Presentations 
Histo
A

Phagocyte dysfunction
AR
Defect in lysosomal trafficking regulator gene –> MT dysfunction in phagosome-lysosome fusion
Recurrent pyogenic infections by Staph and Strep, Partial Albinism, Peripheral Neuropathy
Giant Granules in Neutrophils

150
Q 
Chronic Granulomatous Disease 
Dysfunction of what?
PathoPhys
Presentation 
Diagnostic test
A

Phagocyte dysfunction
Lack of NADPH oxidase –> ↓ ROS and absent respiratory burst in neutrophils
Susceptibility to catalase + organisms (S aureus, E coli, Aspergillus)
Abnormal dihydrorhodamine (DHR) flow cytometry test
Nitroblue Tetrazolium due reduction test no longer preferred

151
Q

Synteneic Graft

A

Graft from Identical Twin or Clone

152
Q

Hyperacute Transplant rejection
Onset after transplantation
PathoPhys
Presentation

A

Minutes
Type II: Preformed antidonor Ab
Occludes graft vessels causing ischemia and necrosis

153
Q 
Acute Transplant rejection 
Onset after transplantation 
PathoPhys
Reversible? 
Histo
A

Weeks
Cell mediated reaction: CTLs react against foreign MHC
Reversible with immunosuppression
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate

154
Q 
Chronic Transplant rejection 
Onset after transplantation 
PathoPhys
Reversible?
Histo
A

Months to years
Non-self MHCI recognized as self and presents non-self Ag
Irreversible
T cell and Ab mediated vascular damage (obliterative vascular fibrosis), Fibrosis of graft tissue and blood vessels

155
Q 
Graft Vs Host Disease 
Onset after transplantation 
PathoPhys
Presentation 
What kind of transplants  
When can it be potentially beneficial?
A

Varies
Grafted T cells attack host
Maculopapular rash, Jaundice, HSM, Diarrhea
Usually in Bone Marrow and Liver Transplants
Potentialy beneficial in Bone Marrow Transplant

156
Q

Cyclosporine
MoA
Use
Tox

A

Binds Cyclophilins. Complex blocks differentiation and activatino of T cells by inhibiting Calcineurin thereby preventing production of IL2 and its receptor
Suppress organ rejection. Autoimmune disorders
Nephrotoxicity, HTN, Hyperlipidemia, Hyperglycemia, Tremor, Gingival Hyperplasia, Hirsutism

157
Q 
Tacrolimus
AKA
MoA
Use
Tox
A

FK506
Binds FK binding protein thereby inhibiting calcineurin and secretion of IL2 and other cytokines
Organ transplant
Nephrotoxicity, HTN, Hyperlipidemia, Hyperglycemia, Tremor

158
Q 
Sirolimus 
AKA
MoA
Use
Tox
A

Rapamycin
Inhibits mTOR thereby inhibiting T cell proliferation in response to IL2
Kidney transplant w/ cyclosporine and corticosteroids. Drug Eluting Stents
Hyperlipidemia, Thrombocytopenia, Leukopenia

159
Q

Azathioprine
MoA
Use
Tox

A

Antimetabolite precursor to 6MP that interferes with the metabolism and synthesis of nucleic acids. Toxic to proliferating lymphocytes
Kidney transplantation, Autoimmune disorders (including glomerulonephritis and hemolytic anemia)
Bone Marrow Suppression

160
Q 
Muromonab CD3 
AKA
MoA
Use
Tox
A

OKT3
Ab that binds CD3 on T cell surface. Blocks cellular interaction with CD3 protein responsible for T cell signal transduction
Kidney Transplant
Cytokine release syndrome, Hypersensitivity Reaction

161
Q

Recombinant IL2
Name
Use

A

Aldesleukin

Renal Cell Carcinoma, Metastatic Melanoma

162
Q

Recombinant EPO
Name
Use

A

Epoetic Alfa

Anemias (especially renal failure)

163
Q

Recombinant Granulocyte CSF
Name
Use

A

Filgrastim

Recovery of bone marrow

164
Q

Recombinant Granulocyte Macrophage CSF
Name
Use

A

Sargramostim

Recovery of Bone Marrow

165
Q

Recombinant IFNα Use

A

HBV, HCV, Kaposi Sarcoma, Leukemias, Malignant Melanoma

166
Q

Recombinant IFNβ Use

A

MS

167
Q

Recombinant IFNγ Use

A

Chronic Granulomatous Disease

168
Q

Recombinant IL11
Name
Use

A

Oprelvekin

Thrombocytopenia

169
Q

Recombinant Thrombopoietin Use

A

Thrombocytopenia

170
Q

Omalizumab

A

anti IgE Ab used in asthma

171
Q

Rituximab

A

Anti CD20 Ab used in B cell Non-Hodgkin’s Lymphoma

172
Q

Abciximab

A

Anti GP IIb/IIIa Ab used to prevent cardiac ischemia in unstable angina and in pts treated with percutaneous coronary intervention

USMLE STEP 1 (25 decks)

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