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First aid Chs Part 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

what is the site of B cell localization and proliferation in the lymph node?

A

Follicle

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2
Q

Where are the follicles in a lymph node located?

A

Outer cortex

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3
Q

What do primary follicles look like in a lymph node?

A

Primary follicles are inactive and are dense and dormant

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4
Q

What do secondary follicles look like in a lymph node?

A

Secondary follicles have pale central germinal centers and are active

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5
Q

where are macrophages located in the lymph node?

A

medullary sinus

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6
Q

Where are plasma cells located in the lymph node?

A

Medullary cords

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7
Q

Where are T cells located in a the lymph node?

A

Paracortex

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8
Q

were do T and B cells enter the lymph node from the blood?

A

They enter via endothelial venules into the paracortex

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9
Q

What part of the lymph node enlarges in a cellular immune response?

A

Paracortex enlarges

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10
Q

where do lymph from the upper limb and lateral breast drain?

A

Axillary lymph node

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11
Q

where do lymph from the stomach drain?

A

Celiac lymph node

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12
Q

Where do lymph from the duodenum and jejunum drain?

A

Superior mesenteric lymph node

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13
Q

Where does lymph from the sigmoid colon drain?

A

Colic to inferior mesenteric lymph node

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14
Q

Where does lymph from the lower portion of the rectum of the anal canal above the pectinate line drain to?

A

Internal iliac

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15
Q

Where does lymph from the anal canal below the pectinate line drain to?

A

Supericial inguinal lymph node

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16
Q

Where does lymph from the testes drain to?

A

Superficial and deep plexuses to the para-aortic

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17
Q

Where does lymph from the scrotum drain?

A

Superficial inguinal lymph node

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18
Q

Where does lymph from the superficial thigh drain?

A

superficial inguinal lymph node

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19
Q

Where does lymph from the lateral side of the dorsum of the foot drain?

A

Popliteal lymph node

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20
Q

What drains the lymph of the right arm, right chest and right half of the head?

A

Right lymphatic duct

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21
Q

Where are T cells located in the spleen?

A

Periarterial lymphatic sheath (PALS) within the white pulp of the spleen

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22
Q

Were are B cells found in the spleen?

A

In follicles within the white pulp of the spleen

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23
Q

What do macrophages in the spleen do?

A

Remove damaged RBCs and remove encapsulated organisms

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24
Q

What do you see with splenic dysfunction?

A

Decreased IgM –> decreased complement activation –> decreased C3b opsonization –> increased susceptibility to encapsulated organisms

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25
Q

What are the encapsulated organisms you can have problems with in asplenia?

A

SHiNE SKS

  • Strep penumo
  • Haemophilus influenza type B
  • Neisseria meningitides
  • Salmonella
  • Klebsiella pneumoniae
  • group b Strep
  • E. coli
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26
Q

A patient presents with Howell jolly bodies (nuclear remnants), target cells and thrombocytosis - what don’t they have?

A

The patient doesn’t have a spleen

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27
Q

Name 3 situations where a patient would be missing a spleen

A

sickle cell patient with auto infarction
Trauma
Hereditary spherocytosis

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28
Q

What is the purpose of the thymus?

A

The thymus is the site of T cell differentiation and maturation

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29
Q

Is the thymus encapsulated?

A

Yes

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30
Q

What is the thymus derived from?

A

Epithelium of the 3rd bronchial pouches

note that lymphocytes are of mesenchymal origin

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31
Q

What type of cell is located in the cortex of the thymus?

A

The cortex is dense with immature T cells

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32
Q

What type of cell is located in the medulla of the thymus?

A

The thymus is pale with mature T cells and epithelial reticular cells containing Hassall’s corpuscles.

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33
Q

Where does positive and negative selection of T cells occur in the thymus?

A

Positive selection (MHC restriction) occurs in the cortex and negative selection (non-reactive to self) occurs in the medulla

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34
Q

What type of immunity consists of neutrophils, macrophages, dendritic cells, eosinophils, basophils, mast cells, natural killer cells (lymphoid origin), and complement

A

Innate immunity

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35
Q

What type of immunity has receptors that recognize pathogens that are germline encoded?

A

Innate immunity

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36
Q

Which form of immunity has no memory

A

innate immunity

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37
Q

Which form of immunity has receptors that recognize pathogens by undergoing VDJ recombination during lymphocyte development?

A

Adaptive immunity

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38
Q

What form of immunity has a slow response on first exposure but the memory response is faster and more robust?

A

Adaptive immunity

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39
Q

Which type of immunity consists of T cells, B cells and circulating antibodies?

A

adaptive immunity

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40
Q

What is the purpose of MHC?

A

They present antigen fragments to T cells and bind TCR

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41
Q

what do MHC-I bind?

A

TCR and CD8

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42
Q

What cells express MHC-I?

A

Expressed on all nucleated cells, not expressed on RBCs

cells use MHC-I to show CD8 cells that they are normal healthy cells

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43
Q

Which MHC mediates viral immunity?

A

MHC-1

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44
Q

Which MHC pairs with Beta2-microglobulin to get to the cell surface?

A

MHC-I

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45
Q

What do MHC-II bind?

A

TCR and CD4

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46
Q

What cells express MHC-II?

A

Antigen presenting cells

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47
Q

Which MHC loads the antigen following release of invariant chain in an acidified endosome?

A

MHC-II

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48
Q

What disorder is HLA-A3 associated with?

A

Hemochromatosis

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49
Q

What disorders is HLA-B27 associated with?

A

Psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reiter’s syndrome
(PAIR)

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50
Q

What disorder is HLA-DQ2/DQ8 associated with?

A

Celiac disease

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51
Q

What disorders is HLA-DR2 associated with?

A

Multiple sclerosis, hay fever, SLE, Goodpasture’s

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52
Q

What disorders is HLA-DR3 associated with?

A

DM type 1, Grave’s disease

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53
Q

What disorders if HLA-DR4 associated with?

A

Rheumatoid arthritis, DM type 1

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54
Q

What disorders are HLA-DR5 associated with?

A

Pernicious anemia (B12 deficiency), Hashimoto’s thyroiditis

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55
Q

what is the only lymphocyte that is a member of the innate immune system?

A

NK cells

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56
Q

what CD markers are found on an NK cell?

A

CD16 and CD56

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57
Q

what do NK cells secrete to activate macrophages?

A

IFN-gamma

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58
Q

What’s so great about CD16?

A

Helps cells to recognize and kill Ig-coated cells via antibody dependent cell mediated cytotoxicity

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59
Q

Which cytokines are known to increased the activity of NK cells?

A

IL-2, IL-12, IFN-Beta, IFN- alpha

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60
Q

when are NK cells induced to kill another cell?

A

When exposed to a non-specific activation signal on a target cell and/or to an absence of class I MHC on target cell surface

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61
Q

What do B cells secrete to neutralize viruses?

A

IgG

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62
Q

what do CD4 T-cells do?

A

Help B cells make antibody and produce cytokines to activate other cells of the immune system

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63
Q

What do CD8 T-cells do?

A

Kill virus-infected cells directly

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64
Q

In what part of T cell selection occurs in the thymic cortex and involves T cells expressing TCRS that are capable of binding surface self MHC molecules will survive?

A

Positive selection

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65
Q

In what part of T cell selection occurs in the thymic medulla and involves TCRs with high affinity for self antigens undergoing apoptosis?

A

negative selection

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66
Q

What are the two necessary signals for naïve T cell activation?

A

Signal 1 - foreign antigen is presented on MHC II and recognized by TCR on Th cells. Antigen is presented on MHC-I to Tc cells

Signal 2 - “costimulatory signal” is given by interaction of B7 and CD28

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67
Q

What are the two necessary signals for B cell activation and class switching?

A

Signal 1 - b cell receptor mediated endocytosis; foreign antigen is presented on MHC II and recognized by TCR of Th cells

Signal 2 - CD40 receptor on B cell binds CD40 ligandon TH cell

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68
Q

what cytokine(s) does Th1 cells secrete?

A

IFN-Gamma

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69
Q

what cytokine(s) does Th2 cells secrete?

A

IL-4, IL-5, IL-10, IL-13

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70
Q

What do Th1 cells do?

A

activate macrophages

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71
Q

What do Th2 cells do?

A

recruits eosinophils for parasite defense and promotes IgE production by B cells

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72
Q

What inhibits TH1 cells?

A

IL4 and IL10

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73
Q

What inhibits TH2 cells?

A

IFN-gamma

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74
Q

what is the macrophage-lymphocyte interaction?

A

Activated lymphocytes released IFN gamma and macrophages release IL1 and TNF alpha which they each stimulate each other

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75
Q

what cells kill virus infected, neoplastic and donor graft cells by inducing apoptosis?

A

Cytotoxic T cells

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76
Q

what makes cytotoxic T cells so toxic?

A

They release cytotoxic granules containing preformed proteins like perforin which helps to deliver the content of granules into the target cell and granzyme which is a serine protease, activates apoptosis inside the target cell
granulysin is antimicrobial and also induces apoptosis

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77
Q

which T cells express CD3, CD and CD25?

A

Regulatory T cells

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78
Q

What T cells suppress CD8 and CD4 cells?

A

Regulatory T cells

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79
Q

what cytokines to activates regulatory T cells secrete?

A

anti-inflammatory cytokines like IL10 and TGF-Beta

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80
Q

what portion of IgM and IgG fix complement?

A

The Fc portion (CH2 part of Fc)

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81
Q

how many antigenic specificities are expressed per B cell?

A

one

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82
Q

What occurs following antigen stimulation that allows for antibiotic diversity?

A

Somatic hypermutation

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83
Q

what is the only immunoglobulin that can directly opsonize?

A

IgG

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84
Q

What is the only immunoglobulin that can cross the placenta?

A

IgG

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85
Q

What is the only immunoglobulin that participates in Antibody dependent cellular cytotoxic ?

A

IgG

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86
Q

What immunoglobulins are on the surface of mature naïve B cells?

A

IgM and IgD

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87
Q

Which cytokines cause class switching to IgA?

A

IL5 and TGF Beta

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88
Q

What is the valence of a secreted IgM?

A

IgM is a pentamer which gives a valence of 10 - can bind a total of 10 antigens

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89
Q

What immunoglobulin is at the lowest concentration in the serum?

A

IgE

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90
Q

What cytokines cause class switching to IgE?

A

IL4 and IL 13

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91
Q

what is a thymus independent antigen?

A

Lacks a peptide component so it can’t be presented by MHC to T cells - stimulates release of antibodies but does not result in immunologic memory

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92
Q

What is a thymus dependent antigen?

A

Contains a protein compound which causes class switching and immunologic memory as a result of direct contact of B cells with Th cells via the CD40/CD40L interaction

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93
Q

A patient presents with an anaphylactic response to a bee sting - what’s the first antibody made in this response?

A

IgM

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94
Q

What is the function of C3b?

A

Opsonization

C3b also helps to clear immune complexes

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95
Q

What is the function of C3a and C5 a?

A

anaphylaxis

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96
Q

What is the function of C5a?

A

Neutrophil chemotaxis

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97
Q

What is the function of C5b-9?

A

MAC

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98
Q

how does activation of the alternative pathway of complement occur?

A

by microbe surface molecules or it can also occur spontaneously

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99
Q

What two inhibitors help prevent complement activation on self cells?

A

C1 esterase inhibitor and DAF (decay-accelerating factor)

100
Q

which two cytokines inhibit complement C9 binding?

A

CD55 (DAF) and CD59

101
Q

A patient presents with hereditary angioedema - what is the disorder?

A

C1 esterase inhibitor deficiency

102
Q

What drug is contraindicated in patients with C1 esterase inhibitor deficiency and why?

A

ACE inhibitors

it’s thought that the deficiency is due to increased bradykinin and ACE inhibitors also increase this

103
Q

A patient presents with severe, recurret pyogenic sinus and respiratory tract infections and increased susceptibility to type III HS reactions (especially in glomerulonephritis) - what is the disorder?

A

C3 deficiency

104
Q

A patient presents with recurrent Neisseria bacteremia - what is the disorder?

A

C5-9 deficiency

105
Q

A patient presents with complement-mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria - what is the disorder?

A

DAF (GPI anchored enzyme) deficiency

DAF=CD55

106
Q

This cytokine is an endogenous pyrogen - causing fever and inflammation. It also activates endothelium to express adhesion molecules; induces chemokine secretion to recruit leukocytes.

107
Q

What is the mnemonic for cytokines?

A

“Hot T-Bone stEAk”

IL-1: fever (hot)
IL-2: stimulates T cells
IL-3: stimulates Bone marrow
IL-4: stimulates IgE production
IL-5: stimulates IgA production
108
Q

This cytokine is an endogenous pyrogen that is also secreted by TH2 cells - causes fever and stimulates production of acute phase proteins

109
Q

This cytokine is a major chemotactic factor for neutrophils

110
Q

This cytokine induces differentiation of T cells into TH1 cells, activates NK cells and is also secreted by B cells

111
Q

This cytokine mediates Septic shock - activates endothelium causing leukocyte recruitment and a leaky vasculature

112
Q

What cytokines are secreted by TH1 cells?

A

IL2, 3, IFN-G

113
Q

What cytokines are secreted by TH2 cells?

A

IL2, 3, 4, 5, 10

114
Q

This cytokine stimulates growth of helper, cytotoxic and regulatory T cells

115
Q

This cytokine supports the growth and differentiation of bone marrow stem cells - functions like GM-CSF

116
Q

This cytokine activates macrophages and TH1 cells. It also suppresses TH2 cell and has antiviral and antitumor properties

117
Q

This cytokine induces differentiation into TH2 cells, promotes growth of B cells and enhances class switching to IgE and IgM

118
Q

This cytokine promotes differentiation of B cells, enhances class switching to IgA, and stimulates growth and differentiation of eosinophils

119
Q

This cytokine modulates the inflammatory response. It also inhibits actions of activated T cells and TH1, also secreted by regulatory cells.

120
Q

Which two cytokines are involved with shutting down the immune response?

A

IL10 and TGF beta

121
Q

What is the function of interferons?

A

They place uninfected cells into an antiviral state and they also activate NK cells to kill virus-infected cells

122
Q

What do interferon alpha and beta do?

A

They inhibit viral protein synthesis (by degrading viral mRNA) to help neighboring cells avoid viral infection

123
Q

What does Interferon gamma do?

A

Increases MHCI and II expression and antigen presentation in all cells

124
Q

What CD marker binds to B7 on APCs?

125
Q

What CD markers are found on TH cells?

A

TCR, CD3, CD28, CD4, CD40L

126
Q

What CD markers are found on TC cells?

A

TCR, CD3, CD28, CD8

127
Q

what cell surface proteins are found on B cells?

A

Ig
CD19, CD20, CD21
MHC-II, B7

128
Q

what cell surface proteins are found on macrophages?

A

CD14, CD40
MHC-II, B7
Fc and C3b

129
Q

What cell surface proteins aer found on NK cells?

A

CD16 (binds Fc portion of IgG for ADCC) and CD56

130
Q

what is anergy?

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

131
Q

how do superactigens cause problems?

A

Superactigens cross link the Beta region of the T cell receptor to the MHC class II on APCs. They can activate any T cell, leading to massive release of cytokines.

132
Q

How do endotoxins/lipopolysaccharides from gram neg cells cause an effect?

A

they directly stimulate macrophages by binding to endotoxin receptor CD 14, TH cells are not involved

133
Q

what is the duration of passive immunity?

A

Short span of antibodies - half life of 3 weeks

134
Q

What are some examples of passive immunity?

A

IgA in breast milk, antitoxin, humanized monoclonal antibody, Palivizumab TX for RSV

135
Q

what are some exposures that a patient can have that may make you give them passive immunity via pre-formed antibodies?

A

Exposure to: tetanus toxin, botulinum toxin, HBV, or Rabies

“To Be Healed Rapidly”

136
Q

What are some examples of active immunity?

A

Natural infection, vaccines, toxoid

137
Q

what type of vaccination produces a mainly cellular response with memory T cells?

A

Live attenuated vaccine

138
Q

What type of vaccination produces a humoral immunity with the production of antibodies?

A

Inactivated or killed vaccine

139
Q

what are examples of live attenuated vaccines?

A

Measles, mumps, polio (sabin), rubella, varicella, yellow fever

140
Q

What type of hypersensitivity: Reaction develops rapidly after antigen exposure because of preformed antibodies

A

Type I hypersensitivity

141
Q

What type of hypersensitivity: Anaphylactic and atopic

142
Q

What type of hypersensitivity: Free antigen crosslinks IgE on presensitized mast cells and basophils, triggering release of vasoactive amines that act at postcapillary venules

143
Q

What type of hypersensitivity: Cytotoxic (Ab mediated)

144
Q

What type of hypersensitivity: IgM, IgG bind to fixed antigen on a cell leading to cellular destruction

145
Q

What type of hypersensitivity: Antibody and complement lead to membrane attack complex

146
Q

what are the 3 mechanisms of Type 2 HS?

A
  1. opsonization leading to phagocytosis or complement activation
  2. complement-mediated lysis
  3. antibody-dependent cell mediated cytotoxicity (ADCC) usually due to NK cells
147
Q

What type of hypersensitivity: Immune complexes

148
Q

What type of hypersensitivity: Antigen-antibody (IgG) complexes activate complement, which attracts neutrophils and the neutrophils release lysosomal enzymes

149
Q

What type of hypersensitivity: An immune complex disease in which antibodies to foreign proteins are produced (takes 5 days) - immune complexes are formed and deposit in membranes where they fix complement leading to tissue damage

A

Type 3 HS - serum sicknes

150
Q

What type of hypersensitivity: A local subacute antibody mediated HS reaction with intradermal injection of antigen inducing antibodies which form antigen-antibody complexes in the skin - characterized by edema, necrosis and activation of complement

A

Type 3 HS - arthus reaction

151
Q

What type of hypersensitivity: Antigen + antibody + complement

152
Q

What type of hypersensitivity: Delayed (T-cell mediated)

153
Q

What type of hypersensitivity: Sensitized T lymphocytes encountered antigen and then release lymphokines leading to macrophage activation, no antibody involvement

154
Q

What type of hypersensitivity: Delayed, cell mediated, is not transferable by serum

155
Q

What type of hypersensitivity: rhinitis, hay fever, bee sting, allergies, eczema

156
Q

What type of hypersensitivity: Autoimmune hemolytic anemia

A

Type II HS

157
Q

What type of hypersensitivity: Pernicious anemia

A

Type II HS

158
Q

What type of hypersensitivity: Idiopathic thrombocytopenic purpura, erythroblastosis fetalis, acute hemolytic transfusion reaction

A

Type II HS

159
Q

What type of hypersensitivity: Rheumatic fever, Goodpastures syndrome

A

Type II HS

160
Q

What type of hypersensitivity: Bullous pemphigoid, Pemphigus vulgaris

A

Type II HS

161
Q

What type of hypersensitivity: SLE

A

Type III HS

162
Q

What type of hypersensitivity: Polyarteritis nodosa

A

Type III HS

163
Q

What type of hypersensitivity: Serum sickness, arthus reaction

A

Type II HS

164
Q

What type of hypersensitivity: Poststreptococcal glomerulonephritis

A

Type III HS

165
Q

What type of hypersensitivity: Multiple sclerosis

A

Type IV HS

166
Q

What type of hypersensitivity: Guillain barre

A

Type IV HS

167
Q

What type of hypersensitivity: Graft versus Host disease

A

Type IV HS

168
Q

What type of hypersensitivity: PPD

A

Type IV HS

169
Q

What type of hypersensitivity: Contact dermatitis, poison ivy, nickel allergy

A

Type IV HS

170
Q

This is a type of blood transfusion that is severe, example being that patients that are IgA deficient have to receive blood products that lack IgA

A

Anaphylactic reaction

171
Q

Type II HS reaction where host antibodies act against HLA antigens and leukocytes

A

Febrile nonhemolytic transfusion reaction

172
Q

Type II HS reaction where intravascular hemolysis (ABO blood group incompatibility) or extravascular hemolysis (host antibody reaction against foreign antigen on donor RBCs) occurs

A

Acute hemolytic transfusion reaction

173
Q

A patient presents with recurrent bacterial infections after 6 months of birth and has normal pro-B, decreased maturation, decreased number of B cells and decreased immunoglobulins of all classes - what is this?

A

X linked Bruton’s agammaglobulinemia

Problem occurs after 6 months due to a decrease in maternal IgG - opsonization defect resulting in recurrent bacterial infections

174
Q

What is the deficiency associated with a defect in BTK, a tyrosine kinase gene which results in no B cell maturation?

A

X linked Bruton’s agammaglobulinemia

175
Q

A patient presents mostly asymptomatic but they sometimes have sinopulmonary infections, GI infections, autoimmune diseases and anaphylaxis to IgA containing blood products - what is the deficiency?

A

Selective IgA deficiency

176
Q

A patient has <7mg/dl of IgA, with normal IgG, IgM and IgG vaccine titers.

A

Selective IgA deficiency

Patient may have false positive beta-hCG tests due to the presence of heterophile antibody

177
Q

A patient presents with tetany, recurrent viral/fungal infections, and congenital heart and great vessel defects - what is the deficiency?

A

Thymic aplasia - DiGeorge syndrome

178
Q

What is the defect in DiGeorge syndrome?

A

22q11 deletion, failure to develop 3rd and 4th pharyngeal pouches

The thymus and parathyroids fail to develop leading to decreased T cells, decreased PTH, decreased calcium, and absent thymic shadow on chest X ray

179
Q

A patient presents with disseminated mycobacterial infections and decreased IFN-gamma - what is the defect and what is the deficiency?

A

IL-12 receptor deficiency - the defect is a decrease in Th1 response

180
Q

A patient presents with FATED: coarse Facies, cold (noninflamed) staphylococcal Abscesses, retained primary Teeth, increased igE, Dermatologic problems (Eczema) - what is the disorder?

A

Hyper-IgE syndrome (Job’s syndrome)

181
Q

What is the defect seen in hyper-IgE syndrome?

A

Th1 cells fail to produce IFN-gamma and therefore there’s an inability of neutrophils to respond to chemotactic stimuli

182
Q

a patient presents with a T cell dysfunction with constant candida albicans infections of the skin and mucous membranes - what is the disorder ?

A

Chronic mucocutaneous candidiasis

183
Q

What are some of the possible defects that can cause SCID?

A

IL2 receptor defect (most common, X linked)

adenosine deaminase deficiency

184
Q

A patient presents with decreased T cell recombinant excision circles, an absent thymic shadow, absent germinal centers on LN biopsy and absent T cells on flow cytometry - what is the disorder?

185
Q

A patient presents with failure to thrive, chronic diarrhea, thrush, recurrent viral, bacterial, fungal and protozoal infections. What is the disorder?

186
Q

How do you treat SCID?

A

Bone marrow transplant (no allograft rejection)

187
Q

A patient presents with cerebellar defects leading to ataxia, spider angiomas and IgA deficiency - what is the disorder?

A

Ataxia-telangiectasia

188
Q

A patient presents with a AR defect in the ATM gene, which codes for DNA repair enzymes and they have increased AFP - what is the disorder?

A

Ataxia-telangiectasia

189
Q

A patient presents with severe pyrogenic infections early in life and as a CD40L defect on helper T cells - what is the disorder and what immunoglobulin findings would they have?

A

This is Hyper-IgM syndrome

They would have increased IgM, decreased IgG, IgA, and IgE

The defect in CD40L keeps them from being able to class switch

190
Q

A patient presents with thrombocytopenic purpura, infections and eczema - what is the disorder?

A

Wiskott Aldrich syndrome

191
Q

What is the defect seen in Wiskott Aldrich syndrome?

A

X linked, in WAS gene on X chromosomes so T cells are unable to reorganize actin cytoskeleton

192
Q

WHat are the findings seen in Wiskott Aldrich syndrome?

A

Increased IgE and IgA and decreased IgM, and thrombocytopenia

193
Q

A patient presents with recurrent bacterial infections, absent pus formation, and delayed separation of the umbilical cord. They also have neutrophilia. What is the dysfunction and what is the defect?

A

Dysfunction: leukocyte adhesion deficiency type 1

defect: Defect in LDA-1 integrin (CD18) on phagocytes

194
Q

A patient presents with recurrent pyogenic infections by staph and strep, partial albinism and peripheral neuropathy and they also have giant granules in their neutrophils - what is the dysfunction and the defect?

A

This is Chediak-Higashi syndrome which is an AR defect in lysosomal trafficking regulator gene. Microtubule dysfunction in phagosome-lysosome fusions

195
Q

A patient presents with increased susceptibility to catalase positive organisms and abnormal dihydrohodamine flow cytometry test. Their nitroblue tetrazolium dye reduction test is negative - it doesn’t change from yellow to blue/black. what is the dysfunction and what is the defect?

A

Chronic granulomatous disease

Lack of NADPH oxidase leading to decreased reactive oxygen species and absent respiratory burst in neutrophils

196
Q

What is an autograft?

197
Q

What is a syngeneic graft?

A

From identical twin or clone

198
Q

What is a allograft?

A

From nonidentical individual of the same species

199
Q

What is a xenograft?

A

From different species

200
Q

When is the onset of rejection after transplantation with a hyperacute rejection?

A

Within minutes

201
Q

When is the onset of rejection after transplantation with a acute rejection?

A

Weeks later

202
Q

When is the onset of rejection after transplantation with a Chronic rejection?

A

months to years

203
Q

When is the onset of rejection after transplantation with a Graft versus host?

204
Q

A patient has occluded graft vessels causing ischemia and necrosis - what is the type of rejection that occurred?

A

Hyperacute rejection

205
Q

A patient has vasculitis of graft vessels with dense interstitial lymphocytic infiltrate - what is the type of rejection that occurred?

A

Acute rejection

206
Q

A patient has irreversible damage with T cell and antibody mediated vascular damage that has caused obliterative vascular fibrosis - there is fibrosis of the graft tissue and blood vessels - what is the type of rejection that occurred?

A

Chronic rejection

207
Q

A patient presents with a maculopapular rash, jaundice, hepatosplenomegaly and diarrhea. what is the type of rejection that occurred? When is this seen and in what cases can it be beneficial?

A

This is a graft versus host transplant rejection

Usually occurs in bone marrow and liver transplant (organs rich in lymphocytes)

This can potentially be beneficial in bone marrow transplant

208
Q

What is the pathogenesis of hyperacute transplant rejection?

A

Antibody mediated (Type II) because of the presence of preformed anti-donor antibodies in the transplant recipient

209
Q

What is the pathogenesis of acute transplant rejection?

A

Cell-mediated due to Cytotoxic T cells reacting against foreign MHCs. Reversible with immunosuppressants

210
Q

What is the pathogenesis of chronic transplant rejection?

A

Irreversible! class I-MHC non-self is perceived by cytotoxic t cells as class I-MHC self that is presenting a non-self antigen

211
Q

What is the pathogenesis of graft-versus-host transplant rejection?

A

Grafted immunocompetent T cells proliferate in the irradiated immunocompromised disease host and reject cells with “foreign” proteins, resulting in severe organ dysfunction

212
Q

What drug binds to cyclophilins and the complex blocks the differentiation and activation of T cells by inhibiting calcineurin - thus preventing the production of IL-2 and its receptor

A

Cyclosporine

213
Q

What drug has the following toxicity: nephrotoxicity, hypertension, hyperlipidemia, hyperglycemia, tremor, gingival hyperplasia, hirsutism?

A

Cyclosporine

214
Q

What drug binds to FK-binding protein, inhibiting calcineurin and secretion of IL2 and other cytokines?

A

Tacrolimus

215
Q

What drug has the following toxicity: nephrotoxicity, hypertension, hyperlipidemia, hyperglycemia and tremor?

A

Tacrolimus

216
Q

What drug inhibits mTOR and inhibits T cell proliferation in response to IL2?

217
Q

What drug is used for immunosuppression after kidney transplantation in combo with cyclosporine and corticosteroids, also used to drug eluting stents?

218
Q

What drug has the following toxicity: Hyperlipidemis, thrombocytopenia, leukopenia?

219
Q

What drug is an antimetabolite precursor of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acids making it toxic to proliferating lymphocytes?

A

Azathioprine

220
Q

What drug is used in kidney transplants and autoimmune disorders like glomerulonephritis and hemolytic anemia?

A

Azathioprine

221
Q

What drug has the following toxicity: bone marrow suppression, active metabolite mercaptopurine is metabolized by xanthine oxidase so there can be toxic effects increased with use of allopurinol

A

Azathioprine

222
Q

What drug is a monoclonal antibody that binds to CD3 on the surface of T cells and blocks cellular interaction with CD3 protein responsible for T cell signal transduction?

223
Q

What is the toxicity seen with muromonab-CD3?

A

Cytokine release syndrome, hypersensitivity reaction

224
Q

what drug binds to CD25 and blocks IL2 signaling?

A

Daclizumab

225
Q

What drug inhibits IMP-dehydrogenase thereby preventing synthesis of guanine resulting in decreased cell replication?

A

Mycophenolate

226
Q

When can you use mycophenolate?

A

Transplants and lupus nephritis

There’s increased risk of lymphoma though and it’s teratogenic (not used in pregnancy)

227
Q

What recombinant cytokine can you use to treat renal cell carcinoma or metastatic melanoma?

A

Aldesleukin (IL2)

228
Q

What recombinant cytokine can you use to treat Anemias (especially in renal failure)?

A

Epoetin alfa (Epo)

229
Q

What recombinant cytokine can you use to treat Recovery of bone marrow?

A 
Filgastrim (G-CSF)
or Sargramostim (granulocyte macrophage colony stimulating factor)
230
Q

What recombinant cytokine can you use to treat Hepatitis B and C, Kaposi sarcoma, leukemia, or malignant melanoma?

A

Alpha interferon

231
Q

What recombinant cytokine can you use to treat Multiple sclerosis?

A

Beta interferon

232
Q

What recombinant cytokine can you use to treat thrombocytopenia?

A

Oprelvekin (IL-11) or Thrombopoietin

233
Q

What drug is not a monoclonal antibody but rather is a decoy receptor that’s anti-TNF alpha so it binds up all of the TNF-alpha?

A

Etanercept

234
Q

What is the target for infliximab?

235
Q

What is the target for Adalimumab?

236
Q

What is the target for Abciximab?

A

Glycoprotein IIb/IIIa

237
Q

What is the target for Trastuzumab (Herceptin)?

238
Q

What is the target for Rituximab?

239
Q

What is the target for Omalizumab?

240
Q

What is infliximab used to treat?

A

Crohn’s disease, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis

241
Q

What is Adalimumab used to treat?

A

Crohn’s disease, RA, psoriatic arthritis

242
Q

What is Abciximab used to treat?

A

Prevents cardiac ischemia in unstable angina and in patients treated with percutaneous coronary intervention

243
Q

What is Trastuzumab used to treat?

A

HER-2 overexpressing breast cancer

244
Q

What is Rituximab used to treat?

A

B cell non-Hodgkin lymphoma

245
Q

What is Omalizumab used to treat?

A

Additional line of treatment for severe asthma

First aid Chs Part 1 (8 decks)

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