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USMLE Step 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

Primary lymphoid organs (2):

A

Thymus

Bone marrow

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2
Q

Site of B cell localization in a lymph node:

A

Follicle

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3
Q

Where the T cells in a lymph node are located:

A

Paracortex

This is right next to the follicle

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4
Q

Portion of a lymph node that becomes hugely enlarged in a robust cellular immune response:

A

Paracortex

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5
Q

Why do lymph nodes not enlarge in patients with DiGeorge?

A

They have no T cells. The paracortex, or T cell region, is what enlarges when a lymph node swells.

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6
Q

Where are the high endothelial venules of lymph nodes located?

A

Paracortex

T and B cells enter here

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7
Q

The primary lymph node drainage site for the upper limb and lateral breast:

A

Axillary

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8
Q

The primary lymph node drainage site for the stomach:

A

Celiac nodes

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9
Q

The primary lymph node drainage site for the duodenum and jejunum:

A

Superior mesenteric nodes

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10
Q

The primary lymph node drainage site for the sigmoid colon:

A

Colic nodes, which drain to inferior mesenteric nodes

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11
Q

The primary lymph node drainage site for the rectum above the pectinate line:

A

Internal iliac nodes

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12
Q

The primary lymph node drainage site for the anal canal below the pectinate line:

A

Superficial inguinal nodes

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13
Q

The primary lymph node drainage site for the testes:

A

Superficial and deep para-aortic plexes

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14
Q

The primary lymph node drainage site for the scrotum:

A

Superficial inguinal nodes

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15
Q

What does the right lymphatic duct drain? What happens if you obstruct this duct or it gets damaged?

A

The right arm, chest, and right half of the head.

Damage -> non-pitting edema of RUE.

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16
Q

Where does the thoracic duct empty?

A

Jx of L subclavian and IJ

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17
Q

Three ways you can become asplenic:

A

Sickle cell
Trauma
Surgery (eg for spherocytosis)

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18
Q

Where are T cells in the spleen?

A

They live in the peri-arteriolar lymphatic sheath (PALS).

Remember, P for Paracortex (LN) and PALS (spleen).

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19
Q

Where are B cells found in the spleen?

A

In the follicles in the white pulp.

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20
Q

T/F: T cells are found in the red pulp of the spleen.

A

F. PALS is where they live, this is in the white pulp.

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21
Q

Post-splenectomy, 3 buzzwords:

A

Howell-Jolly bodies
Target cells
Thrombocytosis

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22
Q

Asplenia renders someone vulnerable to what organisms? Which do we have vaccines for?

A 
Encapsulated ones.  Even Some Killers Have Pretty Nice Capsules:
E. coli
Strep pneumo *
Klebsiella
H. influenzae *
Pseudomonas
Neisseria (mening. and gonococcal *)
Cryptococcus
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23
Q

From what embryonic structure does the thymus come? What other structure develops from this origin?

A

The 3rd branchial pouch. Inferior parathyroids develop with the thymus.

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24
Q

In the thymus, where do mature T cells live? What kind of selection are they undergoing here?

A

Mature T cells live in the Medulla of the thymus, here they are undergoing (-) selection (learning not to kill the host cells).

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25
Q

In the thymus, where do immature T cells live? What kind of selection are they going through here?

A

Immature T cells live in the cortex.
Mature live in the Medulla.
They are undergoing (+) selection and learning to talk MHC.

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26
Q

The HLA subtypes associated with MHC I:

A

HLA-A
HLA-B
HLA-C

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27
Q

To what co-receptor does MHC I bind? MHC II?

A

CD8

CD4

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28
Q

Which cells express MHC I?

Which cells express MHC II?

A

MHC I is on the surface of all nucleated cells.

MHC II is only on APCs (macs, B cells, dendritic cells).

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29
Q

Which HLA subtypes are associated with MHC II?

A

Dr. is going to DQ to get a DrPepper.
HLA-DR
HLA-DQ
HLA-DP

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30
Q

Which MHC molecule needs to travel with b2 microglobulin to be displayed?

A

MHC I

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31
Q

HLA associated with hemochromatosis:

A

HLA-A3

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32
Q

HLA associated with the seronegative arthropathies:

Can you name 4 of these illnesses?

A

HLA-B27

Ank. spondylitis, Reiters / reactive arthritis, IBD, psoriatic arthritis

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33
Q

HLA subtypes associated with celiac disease:

A

HLA-DQ2 / DQ8

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34
Q

HLA subtypes associated with MS, hay fever, SLE, and Goodpasture’s

A

HLA-DR2

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35
Q

HLA associated with type 1 diabetes (2):

A

HLA-DR3 / DR4

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36
Q

HLA associated with pernicious anemia:

A

HLA-DR5

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37
Q

Two surface markers for NK cells:

A

CD-16

CD-56

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38
Q

T/F: NK cells require T cell help to induce apoptosis of infected / cancerous cells:

A

F. They use perforin and granzymes on their own, respond to coded antigen and absence of MHC I.

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39
Q

Cytokines that enhance NK cell activity:

A

IL-2
IL-12
IFN-b
IFN-a

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40
Q

NK cells secrete this cytokine to activate macrophages:

A

IFN-g

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41
Q

What does CD-16 do and what cell types carry it?

A

Killers have it (macs, neut, monos, NK).

It binds the constant region of Ab and targets the Ab bearing cell for destruction.

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42
Q

Cell type that mediates hyperacute organ rejection:

A

B cells

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43
Q

TH1 cells secrete two main stimulatory cytokines. What do they do?

A

IFN-g calls out to macrophages
IFN-g also inhibits other T cells from going down the TH2 path
IL-2 stimulates T cells, NK cells

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44
Q

This cytokine is secreted by TH2 cells to inhibit TH1 cell development:

A

IL-10

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45
Q

These two cytokines are secreted by TH2 cells and stimulate B cells:

A

IL-4

IL-5

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46
Q

This interleukin drives TH1 development, where this interleukin drives TH2 development:

A

IL-12 drives TH1

IL-4 drives TH2

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47
Q

Which cell is the only cell that can activate a naive T cell?

A

Dendritic cell

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48
Q

Three APCs:

A

Dendritic cell
Macrophage
B cell

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49
Q

A naive T cell requires MHC + antigen + appropriate co-stimulation. What are these costimulatory molecules? A B cell requires a different pair of costimulatory moleucles, what are they?

A

CD28 on the T cell
CD80 = CD86 = B7 on the dendritic cell

CD40 on the B cell
CD40 ligand on the T cell

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50
Q

The macrophage activating cytokine:

A

IFN-g

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51
Q

Two cytokines that inhibit TH1 cells:

A

IL-4
IL-10
(both from TH2 cells)

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52
Q

Cytokine TH1 cells secrete that inhibits TH2 cells:

A

IFN-g

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53
Q

Four buzz-words for cytotoxic T cell killing mechanisms:

A

Perforin (enters cell)
Granzyme (serine protease)
Granulysin
FAS ligand (+ FAS receptor on host cells)

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54
Q

Three things expressed on the surface of regulatory T cells?

A

CD3
CD4
CD25

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55
Q

Where does complement bind an Ab?

A

The Fc, CH2 region (just below the hinge).

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56
Q

Gene products responsible for VDJ recombination. What do these proteins recognize?

A

RAG1 & RAG2

Recognize recombination signal sequences = RSSs

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57
Q

There are two light chains in human Ab:

What is the normal ratio in humans?

A

kappa
lambda
2K:1L

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58
Q

Most abundant Ab:

A

IgG

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59
Q

Crosses the placenta:

A

IgG

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60
Q

Life expectancy of a maternal Ab in a baby:

A

~21d

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61
Q

Ab that is a dimer when secreted:

A

IgA

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62
Q

Ab that is found in colostrum:

A

IgA

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63
Q

Ab that mediates type I hypersensitivity:

A

IgE

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64
Q

Ab that fixes complement (2):

A

IgG, IgM

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65
Q

This Ab prevents attachment of bacteria to mucous membranes:

T/F: It fixes complement.

A

IgA

F. No.

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66
Q

Two antibodies involved in the classic pathway of complement activation:

A

IgG

IgM

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67
Q

Triggers for each of the following complement pathways:

  1. Classic
  2. Lectin
  3. Alternative
A
  1. Classic = Ab mediated (IgG, IgM)
  2. Leptin = mannose binding protein made by the liver
  3. Alternative = molecules on the microbe
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68
Q

Complement protein for neutrophil chemotaxis:

Two other neutrophil chemotactic proteins:

A

C5a

IL-8, leukotriene B4

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69
Q

Complement proteins (2) responsible for anaphylaxis:

A

C3a, C5a for Anaphylaxis

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70
Q

Complement proteins involved in forming the membrane attack complex:

A

C5b-9

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71
Q

Two complement proteins that help prevent complement from activating on self cells:

A

Decay-accelarating factor (DAF)

C1 esterase inhibitor = C1 esterase = C1 inhibitor

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72
Q

What is C1 esterase?

A

An inhibitor of the complement cascade, prevents host cells from being attacked by complement.

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73
Q

What does C1 esterase deficiency cause?

A

Hereditary angioedema.

74
Q

You do not give this medicine to patients with C1 esterase deficiency. Why?

A

ACEi

C1 esterase def -> increased bradykinin, ACEi can also increase bradykinin

75
Q

What happens to people who have a C3 deficiency?

A

They cannot coat bacteria with C3. They end up with severe recurrent pyogenic sinus / resp tract infections.

76
Q

C3 deficiency, in addition to being associated with infection, is also associated with a hypersensitivity reaction:

A

Type III (glomerulonephritis)

77
Q

Deficiencies in C5-9 lead to susceptibility to infection with what kind of organisms?

A

Neisserii. We got both kinds.

78
Q

What is the complement defeciency associated with paroxysmal nocturnal hemoglobinuria?

A

Deficiency in decay accelerating factor, an inhibitory protein.

79
Q

DAF deficiency… what happens?

A 
RBCs lyse (complement-mediated)
You get paroxysmal nocturnal hemoglobinuria.
80
Q

These three acute phase reactants are secreted by macrophages:

A

IL-1
IL-6
TNF-a

81
Q

This is the major chemotactic factor for neutrophils:

A

IL-8

C5a, leukotriene B

82
Q

Two interleukins that act as pyrogens:

83
Q

The cytokine of septic shock:

84
Q

What does IL-3 do?

IL-4?

A

Hot T-Bone stEAk:
IL-3 stimulates Bone marrow stem cells
IL-4 drives IgE production

85
Q

Major T cell growth interleukin (all kinds of T cells):

86
Q

What is the function of IFN-g?

A

Activates NK, TH1, macrophages.
Suppresses TH2.
Antiviral / anti-tumor.

87
Q

What cell secretes these cytokines: IL-1, IL-6, IL-8, TNF-a:

A

Macrophages

88
Q

What is the function of a and b interferons?

g interferons?

A

a- and b- inhibit viral protein synthesis.

IFN-g upregulates MHC I and II and antigen presentation.

89
Q

Unique marker for T cells:

90
Q

Unique marker for helper T cells:

Cytotoxic T cells:

91
Q

Epsterin-Barr virus docks at this protein on the surface of B cells:

A

CD21

B at the Barr when you are 21.

92
Q

Protein carried by all APCs:

93
Q

What is special about CD56?

A

It is the unique marker for NK cells.

94
Q

This molecule binds the Fc of IgG:

95
Q

Four exposures you might want to consider passively immunizing someone for:

A

Tetanus
Botulism
HBV
Rabies

96
Q

If you want to confer passive immunity to someone, how often would you need to dose them?

A

Roughly monthly. t1/2 =~3w.

97
Q

These vaccines are live-attenuated:

A 
MMR
Oral polio = sabin
Varicella
Yellow fever
Intranasal flu
98
Q

These two vaccines are egg based, contraindicated in people with severe allergies:

A

Flu
Yellow fever
(MMR technically, though not a problem in administration)

99
Q

Which of the polio vaccines is live?

A

Oral is live (Sabin)

Injectable is inactivated (Salk)

100
Q

Live or killed? Cholera:

101
Q

Live or killed? Yellow fever:

102
Q

Live or killed? Sabin polio:

A

= Oral

Live

103
Q

Live or killed? Hep A vaccine:

104
Q

Live or killed? Rabies vaccine:

105
Q

Live or killed? MMR:

106
Q

The three hypersensitivity reactions that are mediated by antibodies?
The one mediated by cells?

A

I-III are Ab mediated

IV is cell-mediated

107
Q

Hypersensitivity associated with IgE:

108
Q

Hypersensitivity associated with IgM / IgG vs. cells:

109
Q

Hypersensitivity associated with delayed response:

110
Q

Hypersensitivity associated with immune complex formation and neutrophil activation:

111
Q

What causes the Arthus reaction? What kind of hypersensitivity is this?

A

Antigen-Ab complexes in the skin get attacked by neutrophils. This is Type III hypersensitivity.

112
Q

What is serum sickness?

A

Give someone foreign proteins.
Ab vs foreign proteins are made by host.
These Ab form complexes that deposit on membranes, inflammation causes damage.
This is Type III hypersensitivity.

113
Q

The 3 things stuck together in type III hypersensitivity:

A

Antigen
Ab
Complement

114
Q

PSGN is an example of this kind of hypersensitivity:

A

Type III (Ab vs. antigen depositing in tissues)

115
Q

Rheumatic fever is an example of this kind of hypersensitivity:

A

Type II (Ab vs. self)

116
Q

Allergic and atopic disorders fall into the category of this kind of hypersensitivity:

117
Q

Multiple sclerosis is an example of this kind of hypersensitivity:

118
Q

The PPD test for TB is an example of this kind of hypersensitivity:

119
Q

Pernicious anemia is an example of this kind of hypersensitivity:

A

Type II (Ab vs host protein)

120
Q

Goodpasture syndrome is an example of this kind of hypersensitivity:

A

Type II (anti-GBM Ab, NOT immune complex deposition)

121
Q

SLE and RA are both an example of this kind of hypersensitivity:

A

Type III, oddly.

122
Q

Acute hemolytic transfusion reaction… what type of hypersensitivity am I?

A

Type II.

Can be intravascular (ABO incompatible) or extravascular (host Ab vs. foreign antigen on donor cell).

123
Q

What kinds of infections would someone who had no granulocytes be vulnerable to (4)?

A

Staph
Brukholderia cepacia
Serratia
Nocardia

124
Q

Someone with no B cells would be particularly vulnerable to this viral infection:

A

Enteroviral encephalitis

125
Q

Anti-dsDNA is most commonly seen in this autoimmune disorder:

A

SLE (more specific for renal involvement)

126
Q

Anti-Smith Ab are seen in:

127
Q

Anti-histone Ab are most commonly seen in this autoimmune disorder:

128
Q

You measure a positive RF for someone you suspect has RA. What is your confirmatory test?

A

Anti-CCP Ab

129
Q

Ab associated with sceroderma:

A

Anti-centromere (CREST)

Anti-Scl-70 (diffuse)

130
Q

Antimitochondrial Ab are found in this disease:

A

Primary biliary cirrhosis

131
Q

Anti-endomysial Ab:

A

Celiac disease

132
Q

Ab for Goodpasture syndrome:

133
Q

Ab for Hashimoto (2):

A

Anti-thyroglobulin

Anti-microsomal

134
Q

Anti-desmoglein Ab are most commonly seen in this autoimmune disorder:

A

Pemphigus vulgaris

135
Q

You suspect Sjogren syndrome. Order these two Ab titers especially:

A

Anti-Ro (SSA)

Anti-La (SSB)

136
Q

Anti-smooth muscle Ab are seen with this disease:

A

Autoimmune hepatitis

137
Q

c-ANCA Ab are seen in this illness:

A

Granulomatosis with polyangiitis (Wegener’s granulomatosis)

138
Q

p-ANCA Ab are seen in these disorders (2):

A

Microscopic polyangiitis

Churg-Strauss syndrome

139
Q

These two Ab may mark Type 1 DM:

A

Anti-islet cell Ab

Anti-glutamate decarboxylase Ab

140
Q

You suspect autoimmune hepatitis. What Ab titer do you order?

A

Anti-smooth muscle Ab

141
Q

A deficiency of this cell type would leave someone particularly prone to GI giardiasis. Why?

A

B cells

There is no IgA to guard the gut

142
Q

The three main X-linked immunodeficiencies you deemed it prudent to study:

A

Wiskott-Aldrich
Bruton’s agammaglobulinemia
CGD
Hyper-IgM

143
Q

Immunodeficiency linked with a defective tyrosine kinase:

A

Bruton’s X-linked agammaglobulinemia

144
Q

Clinical presentation of a patient with Bruton’s X-linked agammaglobulinemia:

A

6 months into life, child with recurrent bacterial infections. Low B cell count, low Ig of all types.

145
Q

Disorder in which there is no B cell maturation:

Disorder in which B cell maturation becomes defective:

A

Bruton’s X-linked agammaglobulinemia

Common variable immunodeficiency

146
Q

Most common primary immunodeficiency:

A

Selective IgA deficiency

147
Q

What happens if you give IgA containing blood products to someone with selective IgA deficiency?

A

Anaphylaxis

148
Q

Immunodeficiency assoc. with 22q11:

149
Q

IL-12 receptor deficiency leads to a decrease in this type of cell response:

150
Q

Immunodeficiency associated with tetany:

151
Q

Suspect this deficiency in a child with disseminated mycobacterial infections:

A

IL-12 deficiency –> absence of TH1 response

152
Q

T cell disorder in which primary teeth are retained:

A

Job’s syndrome (hyper-IgE)

153
Q

What cytokine is deficient in Job’s syndrome?

154
Q

High IgE, eosinophilia, and a failure of neutrophils to deal with business:

A

Job’s syndrome (hyper-IgE)

155
Q

Cold staph abscesses and eczema:

A

Job’s syndrome

156
Q

Defective NADPH oxidase:

157
Q

Treatment for CGD:

A

IFN-g

TMP-SMX prophylaxis

158
Q

Truncal eczema is associated with this immune deficiency disease:

A

Wiskott-Aldrich.

159
Q

Immunodeficiency with high IgA, low IgM, high IgE:

A

Wiskott-Aldrich

160
Q

This immune deficiency results from a defective adenosine deaminase enzyme:

161
Q

Absence of thymic shadow, T cells, and germinal centers is associated with which immune deficiency? What are the two most common causal genetic defects?

A

SCID
IL-2 receptor malformed
Adenosine deaminase deficiency

162
Q

Tyrosine kinase defect is associated with which immune deficiency disorder?

A

Bruton’s agammaglobulinemia

163
Q

Severe pyogenic infections early in life in the presence of both B and T cells are associated with which immune deficiency?

164
Q

Immune deficiency with elevated AFP:

A

Ataxia-telangiectasia.

165
Q

Immune deficiency in which the only intact part of the immune system is NK cells:

166
Q

Mode of inheritence for CGD:

167
Q

Immune deficiency disease where you would see neutrophils filled with giant granules:

A

Chediak-Higashi

168
Q

Cerebellar defects and immune deficiency, what disease am I? What would you see on labs?

A

Ataxia-telangiectasia. See high AFP, low IgA and T lymphs.

169
Q

Albinism and problems with infections, what disease am I?

A

Chediak-Higashi

170
Q

I am a child with recurrent staph and strep infections and peripheral neuropathy. What is my gene defect? Mode of inheritence for my disorder?

A

LYST = problem with phagosome / lysosome fusion. Autosomal recessive. This is Chediak-Higashi.

171
Q

Immune deficiency in which you would be susceptible to infection by S. aureus, E. coli, Aspergillus, Klebsiella, and Candida:

A

CGD.

You have no respiratory burst, can still make H2O2, but can’t kill catalase (+) organisms.

172
Q

Immune disease associated with the triad of thrombocytopenia, eczema, and infections:
What’s the other one where you are likely to see eczema?

A

Wiskott-Aldrich
WAITER mnemonic
Job’s, Hyper IgE

173
Q

You see spider angiomas in a 5-year-old child with poor visual smooth pursuit. Before you put them in front of an X-ray film, stop! Suspect this immunodeficiency:

A

Ataxia telangiectasia.

174
Q

I am an immunodeficiency associated with neutrophilia. What protein is defective?

A

Leukocyte adhesion deficiency.

CD18 = LFA-1 integrin defect.

175
Q

In a child with delayed separation of the umbilical cord, suspect:

A

Leukocyte adhesion deficiency

176
Q

Langerhans cell histiocytosis – dendritic cell would have this characteristic inclusion:

A

Birbeck granule, shaped like a tennis racket

177
Q

What molecules are on the surface of a dendritic cell that is prepared to present antigen?

A

MHC I / II
CD80 / 86
CD40 (expressed by all APC)

178
Q

Which cytokines inhibit T cells?

A

IFN-g inhibits TH2 cells

IL-10 inhibits TH1 cells

179
Q

Macrophages produce three important acute-phase cytokines:

A

IL-1
IL-6
TNF-a

180
Q

What is a degmacyte?

A

A bite cell, an RBC a macrophage has chomped to get at something inside it (ex denatured Hb).

181
Q

Why are people with asplenia prone to thrombocytosis?

A

Spleen sequesters platelets.

Platelets with no home are in the circulation -> thrombocytosis.

USMLE Step 1 (18 decks)

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