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Usmle Immuno-2 Flashcards

2
Q

What type of hypersensitivity reaction is seen in Erythroblastosis Fetalis?

A

Type II

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3
Q

What type of hypersensitivity reaction is seen in Rheumatic Fever?

A

Type II

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4
Q

What type of hypersensitivity reaction is seen in Goodpastures?

A

Type II

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5
Q

What type of hypersensitivity reaction is seen in Bullous pemphigoid?

A

Type II

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6
Q

What type of hypersensitivity reaction is seen in Pemphigus vulgaris?

A

Type II

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7
Q

What type of hypersensitivity reaction is seen in Grave’s disease?

A

Type II

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8
Q

What type of hypersensitivity reaction is seen in Myasthenia Gravis?

A

Type II

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9
Q

What type of hypersensitivity reaction is seen in SLE?

A

Type III

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10
Q

What type of hypersensitivity reaction is seen in RA?

A

Type III

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11
Q

What type of hypersensitivity reaction is seen in polyarteritis nodosum?

A

Type III

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12
Q

What type of hypersensitivity reaction is seen in Poststreptococcal GN?

A

Type III

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13
Q

What type of hypersensitivity reaction is seen in Serum Sickness?

A

Type III

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14
Q

What type of hypersensitivity reaction is seen in Arthus Reactions (swelling and inflammation following tetanus vaccine?)

A

Type III

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15
Q

What type of hypersensitivity reaction is seen in Hypersensitivity pneumonitis? (AKA farmer’s Lung)

A

Type III

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16
Q

What type of hypersensitivity reaction is seen in Type I DM?

A

Type IV

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17
Q

What type of hypersensitivity reaction is seen in MS?

A

Type IV

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18
Q

What type of hypersensitivity reaction is seen in Guillain-Barre?

A

Type IV

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19
Q

What type of hypersensitivity reaction is seen in Hashimoto’s Thyroiditis?

A

Type IV

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20
Q

What type of hypersensitivity reaction is seen in Graft-v-Host disease?

A

Type IV

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21
Q

What type of hypersensitivity reaction is seen in PPD reactions?

A

Type IV

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22
Q

What type of hypersensitivity reaction is seen in Contact dermatitis with poison ivy/nickel?

A

Type IV

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23
Q

What lymph nodes would drain the Upper limb or lateral breast?

A

Axillary

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24
Q

What lymph nodes would drain the Stomach?

A

Celiac

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25
Q

What lymph nodes would drain the duodenum and jejunum?

A

Superior mesenteric

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26
Q

What lymph nodes would drain the Sigmoid Colon?

A

Colic LNs to the inferior mesenteric

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27
Q

What lymph nodes would drain the Lower rectum and area above the pectinate line?

A

Internal iliac

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28
Q

What lymph nodes would drain the Anal canal below the pectinate line?

A

Superficial inguinal

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29
Q

What lymph nodes would drain the Testes?

A

Para-aortic AKA retroperitoneal

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30
Q

What lymph nodes would drain the Scrotum?

A

Superficial inguinal

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31
Q

What lymph nodes would drain the Superficial thigh?

A

Superficial inguinal

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32
Q

What lymph nodes would drain the lateral side of the dorsum of the foot?

A

Popliteal

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33
Q

What ultimately drains the right arm and right half of the head?

A

The right lymphatic duct

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34
Q

What drains the left side of the upper body and everything below the diaphragm?

A

The thoracic duct

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35
Q

What region of the LN contains the HEVs?

A

Paracortex

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36
Q

In what condition would you see an enlarged paracortex? Absent paracortex?

A

Enlarged–> viral or fungal infection

Absent–> DiGeorges

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37
Q

What part of the medulla of LNs is packed with plasma cells?

A

The medullary cords

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38
Q

What is the function of the medullary sinuses within LNs??

A

Communicate with efferent lymphatics…. They contain reticular cells and macrophages.

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39
Q

From what does the Thymus develop?

A

The third pharyngeal pouch

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40
Q

What is found within the medulla of the thymus?

A

Mature T-cells and epithelial reticular cells

HASSALLS corpuscles

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41
Q

Where within the thymus does MHC restriction (positive selection) and negative selection if autoreactive occur?

A

Positive selection occurs in the cortex…

Negative selection occurs in the medulla

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42
Q

What are three manifestations of a splenectomy on a peripheral blood smear?

A

Howell-Jolly bodies
Target Cells
Thrombocytosis

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43
Q

What can occur if there is a splenic dysfunction?

A

Decrease IgM leads to
Decreased compliment activation leads to
Decreased C3b opsonization leads to
Increased susceptibility to encapsulated bacteria

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44
Q

What is one of the main function of macrophages in the spleen?

A

Removal of encapsulated bacteria

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45
Q

What are the sinusoids of the spleen?

A

Vascular channels within the red pulp with a fenestrated basement membrane…Macrophages are found nearby

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46
Q

What are the main components of the innate immune system?

A 
Neutrophils
Macrophages
Dendritic Cells
NK cells
Complement--- fast, nonspecific and no memory
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47
Q

Thrombopoietin is used to treat?

A

Thrombocytopenia

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48
Q

Oprelvekin (IL-11) is used to treat?

A

Thrombocytopenia

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49
Q

Gamma interferon is used to treat?

A

Chronic Granulomatous Disease

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50
Q

Beta interferon is used to treat?

A

MS

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51
Q

Alpha interferon is used to treat?

A

Hep B and C
Kaposi sarcoma
Malignant melanoma

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52
Q

What is Sargramostim?

A

Granulocyte macrophage CSF

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53
Q

What is Filgrastim?

A

Granulocyte CSF

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54
Q

What is EPO used to treat?

A

Anemia, esp from renal failure

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55
Q

What is Aldesleukin ?

A

IL-2 analog

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56
Q

What is Aldesleukin used to treat?

A

RCC and Metastatic melanoma

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57
Q

What is Graft-v-Host disease?

A

When grafted immunocompetent T-cells proliferate in an immunocompromised host.

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58
Q

What are the major manifestation of G-v-Host disease?

A

Maculopapular rash
Jaundice
HS megaly
Diarrhea

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59
Q

What is responsible for the damage in Chronic transplant rejection?

A

T-cells and antibody mediated vascular damage—leads to obliterative vascular necrosis.

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60
Q

What is the time frame of Chronic Transplant rejection?

A

Months to years after transplant

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61
Q

What cells are responsible for the acute transplant rejection?

A

T-cells (cytotoxic t cells) reacting against foreign MHCs

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62
Q

What is the timeframe for Acute transplant rejection?

A

Weeks after transplantation.

63
Q

Is acute transplant rejection reversible?

A

Yes, with cyclosporine or OKT3

64
Q

What is the mechanism of damage in hyperacute transplant rejection?

A

Antibody mediated damage due to the presence of preformed antidonor antibodies….Occurs within minutes.

65
Q

What cell surface proteins are found on Macrophages?

A

MHC II
B7
CD 14
CD 40

66
Q

What is the major secretor of IL-1?

A

Macrophages

67
Q

What is the main function of IL-1?

A

Fever…causes acute inflammation
Induces chemokine production to recruit leukocytes
Activates endothelium to express adhesion molecules

68
Q

What is IL-2 secreted by?

69
Q

What is the function of IL-2?

A

Stimulates growth of T-cells, helper and cytotoxic

70
Q

What secretes IL-3?

A

Activated T-cells

71
Q

What is the main function of IL-3?

A

Supports growth and differentiation of BM stem cells

72
Q

What secretes IL-4?

73
Q

What is the function of IL-4?

A

Promotes growth of B-cells and enhances class switching to Ig E (and IgG)

74
Q

What secretes IL-5?

75
Q

What is the function of IL-5?

A

Promotes differentiation of B-cells
Promotes production and activation of Eosinophils
Enhances IgA class switching

76
Q

What secrete IL-6?

A

Th cells and macrophages

77
Q

What is the function of IL-6?

A

Stimulates production of acute phase reactants and immunoglobulins (pro-inflammatory)

78
Q

What is the function of IL-8?

A

The major chemotactic agent for neutrophils

79
Q

What secretes IL-10?

A

Regulatory T-cells

80
Q

What is the function of IL-10?

A

Inhibits actions of activated T-cells

81
Q

What secretes IL-12?

A

B cells and macrophages

82
Q

What is the function of IL-12?

A

Activates NK and Th1 cells

83
Q

What secretes IFN gamma?

84
Q

What is the function of IFN gamma?

A

Stimulate macrophages

85
Q

What secretes TNF?

A

Macrophages

86
Q

What are the functions of TNF?

A

Mediates septic shock

Causes leukocyte recruitment and vascular leak.

87
Q

How do you remember the important uses of ILs 1-5?

A 
HOT T-Bone stEAk
IL-1=HOT fever
IL-2= T-cells stimulation
IL-3= B-cell stimulation
IL-4= IgE production
Il-5= IgA production
88
Q

What are 4 things that lead to antibody diversity?

A 
Random recombination of VJD and VJ genes
Random combination of Heavy and Light chians
Addition of nucleotides to DNA via Tdt
Somatic Hypermutation (following Antigen stimulation)
89
Q

What is the benefit of opsonization?

A

The antibody promotes phagocytosis after it has bound antigen

90
Q

What is the benefit of Neutralization?

A

So many Antibodies have bound a bacteria that it cannot adhere to cell surfaces.

91
Q

What is the benefit of antibodies WRT complement?

A

IgG activates complement cascade, leading to enhanced opsonization and lysis.

92
Q

What are 4 important things to remember about the Fc portion of an Antibody?

A 
It is 
Constant
Carboxy terminal of the antibody
Carbohydrate side chains are present
Complement binding occurs here (IgG and IgM)
Determines Isotype
93
Q

What are two things important to remember about the Fab region of an antibody?

A

Determines Idiotype
and
It is the Antigen Binding fragment.

94
Q

What is the function of the variable region of the light and heavy chains?

A

Recognizes antigens

95
Q

What is the importance of the Fc portion of IgG and IgM?

A

Fixes complement

96
Q

What two signals are required for B-cell class switching?

A

1: IL-4, IL-5 or Il-6 signal from Th2 cell
2: CD40 receptor activation by binding CD40L on Th cell

97
Q

What signals are required for Cytotoxic T-cell activation?

A

1: Endogenously synthesized protein presented on MHC1 recognized by T-cell Receptor on Tc cell
2: IL-2 from Th cell activates Tc cell to kill virus infected cell.

98
Q

What two signals are required for T-helper cell activation?

A

1: Foreign body must be phagocytosed by APC and the antigen has to be presented to the Th cells TCR via MHC II interaction.
2: Costimulatory signal of B7 on APC interacting with CD 28 on the Th cell—leads to secretion of cytokines by Th cell.

99
Q

What results if you degrade an Ig molecule with Pepsin?

A

1 divalent Fab molecule that is still able to bind and bridge antigens and it can agglutinate antigens. Gives you a ‘cup’ that you can hold Pepsi in. Pepsi, Pepsin.

100
Q

What do you get it you degrade an Ig molecule with papain?

A

3 fragments– 2 monovalent Fab fragments that cannot agglutinate Ab
and
1 Fc portion

101
Q

What is they underlying structure of an IgM molecule?

A

It is a pentamer…each section can bind 2 molecules to it has a valence of 10.

102
Q

GM is classic….

A

IgG and IgM activate classic complement

103
Q

What is the FIRST antigen made to any response?

A

IgM.. even if it an allergic reaction mediated by IgE, IgM always had to be activated first before the class switch could occur.

104
Q

What is avidity WRT Ig molecules?

A

It corresponds to the number of antigen binding sites! IgM has the highest avidity, of 10 since it is a pentamer. IgA has the next highest, of 4 since it is bivalent.

105
Q

What is affinity WRT Ig molecules?

A

The attractiveness between an antigen and the antigen binding site on an Ig molecule… IgG has the highest affinity.

106
Q

Where within the body does class switching between Ig molecules occur?

A

In the germinal center of secondary lymphoid tissues during an immune response.

107
Q

The secondary immune response to an antigen (the same antigen) is primarily mediated by…

108
Q

What is somatic hypermutation?

A

Point mutations in an already rearranged VDJ regions, esp during immune response, as the DNA polymerase does not have time to fix errors.

109
Q

What is the result of somatic hypermutation?

A

Increased affinity of an Ig for its antigen…Those with point mutations that decreased the affinity cannot bind the antigen and die off anyway.

110
Q

What is the only Ig that can cross the placenta?

111
Q

What is the Ig with the highest concentration in breast milk and colostrum?

112
Q

Where is IgA synthesized?

A

In the submucosa

113
Q

What are two cytokines needed to switch to IgA?

A

TGF-Beta

IL-5

114
Q

What is the major benefit of the secretory component of IgA?

A

It binds the dimer, holding it together and protecting it from degradative enzymes in the mucosa.

115
Q

How does IgA get into the mucosa?

A

It binds via its J-chain holding the dimer together to the Poly Ig receptor in the mucosa. This PolyIG receptor becomes the secretory component later on.

116
Q

What are the two cytokines that are used to class switch to IgE?

A

IL-4

Il-13

117
Q

Which Ig causes mast cell degranulation?

118
Q

What are the two major Complement anaphalatoxins?

A

C3a and C5a—they can both bind mast cells and cause degranulation without involving IgE

119
Q

What is the major constituent of complement that allows for removal of immune complexes?

120
Q

What is the major difference between the alternative and classical complement pathway?

A

Alternative is Completely innate and does not require antibody mediation to become activated

121
Q

What are two ways a cytotoxic T cell can kill a target cell?

A

Either through Fas-Fas ligand interactions which releases TNF. When this binds the TNF receptor on the target cell it triggers Apoptosis
OR
CD8 and MHC1 interaction leads to the release of granules with perforin and toxic substances that degrade the cell.

122
Q

NK cells cannot specifically bind antigen, so how to they know which cells to target??

A

They look for cells that do not have MHC I expressed (happens in virally infected cells due to masking or downregulation to evade Tc cells)

123
Q

What is the main Ig that facilitate ADCC, antibody dependent cellular cytotoxicity?

A

IgG—can bind cells that express foreign cell surface proteins and then bind via Fc portion to receptors on NK cells

124
Q

What is the one time IgG is not the Ig mediating Antibody dependent cellular cytotoxicity?

A

IgE can do it IN A PARASITIC infection

125
Q

Look at the last 5 minutes of the cell mediated effector mechanisms chapter in Kap….

A

And vaccines at 6 minutes into the immunocompromised section …Good flow diagram

126
Q

What is an example of natural passive immunity?

A

Placental IgG transport or colostrum transport of IgA leading to immunity

127
Q

What is an example of Natural active immunity?

A

The hard way…getting an infection and having your body mount an immune response.

128
Q

What are examples of active artificial immunity?

A

All vaccinations…Hep B
Polio..
MMR…

129
Q

What types of immunity do live attenuated vaccines bestow?

A

Humoral and cellular BUT they can revert to virulent strains

130
Q

What types of immunity do Killed vaccines bestow?

A

Only Humoral, but they are stable and cannot revert

131
Q

Who should NOT be administered a live attenuated vaccine?

A

Immunocompromised, their close contacts
or
Pregnant women

132
Q

Which vaccines have been killed?

A 
RIP Always
Rabies
Influenza
Polio (SalK)--K=Killed
Hep A
133
Q

What are two examples of recombinant vaccines?

A

HBV—The antigen is recombinant HbsAg
and
HPV types 6, 11, 16 and 18

134
Q

What are the live attenuated vaccines?

A 
MMR
Sabin Polio
VZV
Smallpox
Yellow Fever
135
Q

What is the underlying mechanism behind interferon use?

A

It puts uninfected cells in an antiviral state…They induce production of ribonuclease that inhibits viral protein synthesis by degrading viral mRNA.

136
Q

Main function of interferon Alpha and Beta?

A

Inhibit viral protein synthesis

137
Q

Main function of interferon Gamma?

A

Increases MHC I and MHC II expression and antigen presentation in cells

138
Q

What is the effect of interferons on NK cells?

A

Activates them to kill virus-infected cells

139
Q

Main function of the MAC?

A

Cytolysis by punching holes in cell membranes.

140
Q

What does deficiency of C1 esterase inhibitor lead to?

A

Hereditary angioedema due to inability to turn of complement….leads to massive inflammation at mucosal surfaces

141
Q

What does C3 deficiency lead to?

A

Severe recurrent pyogenic infections esp in sinus and URT.

Increases the susceptibility to type III hypersensitivity reactions as C3b is not around to clear immune complexes

142
Q

What does deficiency of the MAC or any component of it lead to?

A

Increased Neisseria infections.

143
Q

What does the deficiency of DAF (decay accelerating factor) lead to? (DAF being absent due to a defect in a GPI linkage)

A

Complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria

144
Q

What is the general function of C1 esterase inhibitor and DAF?

A

Prevention of complement activation on self cells

145
Q

Number 1 vaccine not given to pregnant women?

A

MMR (Or VZV)

146
Q

What are three vaccines not given to ppl with egg allergies?

A

MMR
Yellow Fever
Influenza

147
Q

What is the only Ig useful in diagnosing infections in infants?

A

IgM….IgG and IgA could have come from the placenta or breast milk

148
Q

Name two component vaccines

A

HPV and Hep B (surface antigen)

149
Q

What is the purpose of giving an adjuvant along with a vaccine?

A

Allows for a longer persistence of the Antigen in the body, so it can make Abs to it instead of just clearing it.

150
Q

What is the only thing the USMLE could give you on a question that would lead you to think Myeloperoxidase deficiency is the answer?

A

Inability to make hypochlorite…otherwise, no symptoms

151
Q

Rx for Selective IgA deficiency?

A

Antibiotics, but do NOT give Igs, as they might cross react and cause anaphylaxis.

Usmle Immunology (3 decks)

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