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IMMUNOLOGY > IMMUNOLOGY- Immune Responses > Flashcards

IMMUNOLOGY- Immune Responses Flashcards

1
Q

Which are acute phase reactants?

A

Factors whose serum concetration change significantly in response to inflammation

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2
Q

When and where is produced the acute phase reaction?

A

Produced by the lieer in both acute and chronic inflammatory states

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3
Q

Who induces acute phase reactions?

A

IL-6, IL-1, TNF α and IFN γ

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4
Q

How are acute phase reactants classified?

A

Positive

Negative

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5
Q

Which is the upregulated and which is the downregulated in Acute phase phase reactants?

A

Positive (Upregulated)

Negative (Downregulated)

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6
Q

In Acute phase phase reactants which are positive regulators?

A 
Serum Amyloid A
C reactive protein 
Ferritin
Fibrinogen
Hepcidin
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7
Q

C reactive protein

A

Opsonin

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8
Q

Which is the function of Opsonin?

A

Fixes complement and facilitates complement

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9
Q

What is teh clinical meaning of C- reactive protein?

A

Sign of ongoing inflammation

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10
Q

Which is the relationship between ferritin and microbials?

A

ferritin binds ans sequesters iron to inhibit microbial iron scavenging

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11
Q

What is Fibrinogen?

A

Coagulation factor

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12
Q

What does Fibrinogen promotes?

A

Endothelial repair

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13
Q

Which lab correlates with Fibrinogen?

A

Erythrocyte sedimentation rate (ESR)

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14
Q

This is the function of Hepcidin

A

Prevents release of iron bound by ferritin

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15
Q

Which disease does Hepcidin prevents?

A

Anemia of chronic disease

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16
Q

These are Negative (Downregulators) or Acute phase reactants

A

Albumin

Transferrin

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17
Q

What is the effect of Albumin reduction?

A

Conserves amino acids for positive reactants

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18
Q

What is the effect of Transferrin?

A

Internalized by macrophages to sequester iron

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19
Q

What is the main purpose of the Complement?

A

System of interacting plasma proteins that play a role in innate immunity and inflamation

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20
Q

This is a mechanism of defense used in complement that uses the membrane?

A

Membrane Attack Complex (MAC)

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21
Q

From which bacterias does Membrane Atack complex (MAC) protects?

A

Against Gram negative bacteria

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22
Q

Which are the pathways to activate Complement?

A

Classic pathway
Alternative pathway
Lectine pathway

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23
Q

Who mediates classic pathway of complement?

A

IgG or IgM

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24
Q

Who stimulates the activation of alternative pathway of Complement?

A

Microbe surface molecules

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25
Q

Who stimulates Lectin pathway of complement?

A

Mannose or other sugars on microbe surface

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26
Q

What does C3b manages?

A

Opsonization

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27
Q

These complements carried anaphylaxis process

A

C3a, C4a and C5a

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28
Q

This complement manages Neutrophil chemotaxis

A

C5a

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29
Q

What is the purpose of C5b-9?

A

Cytolysis by membrane atack complex (MAC)

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30
Q

Which complement binds bacterias?

A

C3b

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31
Q

Who are the primary opsonins in bacterial defense?

A

C3b and IgG

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32
Q

Which other function does C3b has?

A

Helps clear immune complexes

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33
Q

Whoare inhibitors of Complement?

A

Decay accelerating factor and C1 esterase inhibitor help prevent complement activation on self cells (eg RBC)

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34
Q

Which are Decay accelerating factors?

A

DAF, aka CD55

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35
Q

These are complement disorders

A

C1 esterase inhibitor deficiency
C3 deficiency
C5- C9 deficiencies
DAF (GPI anchored enzyme) deficiency

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36
Q

What does C1 esterase inhibitor deficiency clinically cause?

A

Hereditary angioedema

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37
Q

Which medicines are contraindicated in C1 esterase inhibitor deficiency?

A

ACE inhibitors

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38
Q

Which diseases are increased in C3 deficiency?

A

Increase risk of Severe, recurrent pyogenic sinus and respiratory tract infections
Increases Susceptibility to type III hypersensitivity reactions

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39
Q

From which bacteria is increased the susceptibility in C5- C9 deficiencies?

A

recurrent Neisseria bacterimia

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40
Q

What does DAF (GPI anchored enzyme) deficiency cause?

A

Complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria

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41
Q

How is consider IL-1?

A

An endogenous pyrogen

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42
Q

This is another name for IL-1

A

Osteoclast activating factor

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43
Q

These are the clinical manifestations of IL-1

A

Causes fever

Acute inflamation

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44
Q

Which is the mechanism of action of IL-1?

A

Activates endothelium to express adhesion molecules; induces chemokine secretion to recruit leukocytes

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45
Q

How is classified IL-6?

A

An endogenous pyrogen

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46
Q

Who else can secrete IL-6?

A

Th2 cells and macrophages

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47
Q

What is the effect of IL-6?

A

Causes fever and stimulates production of acute phase proteins

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48
Q

Major chemotactic factor for neutrophils

A

IL-8

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49
Q

This IL Induces differentiation of T cells into Th1 Cells

A

IL-12

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50
Q

Which other effect does IL-12 has?

A

Activates NK cells

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51
Q

Who secretes IL-12?

A

B cells and macrophages

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52
Q

Which cytokines are secreted by macrophages?

A 
IL-1
IL-6
IL-8
IL-12
TNF α
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53
Q

Who mediates septic schock and activates endohtelium?

A

TNF α

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54
Q

What is the effect of TNF α?

A

Causes leukocyte recruitment, vascular leak

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55
Q

Which are the main effect of the first 6 IL?

A 
IL-1 FEVER
IL-2 stimulates T cells
IL-3 stimulates bone marrow
IL-4 stimulates IgE production
IL-5 stimulates IgA production
IL-6 stimulates acute phase protein production
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56
Q

These IL are secreted by all T cells

A

IL-2

IL-3

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57
Q

Which is the effect of IL-2

A

Stimulates growth of helper , cytotoxic and regulatory T cells

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58
Q

Supports the growth and differentiation of bone marrow stem cells

A

IL-3

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59
Q

Functions like GM-CSF

A

IL-3

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60
Q

Who secretes interferon γ?

A

Th1 cells

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61
Q

Which properties does Interferon γ has?

A

Antiviral and antitumoral properties

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62
Q

What cells are activated by Interferon γ?

A

NK to kill virus infected cells

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63
Q

Which other effect does Interferon γ has?

A

Increases MHC expression and antigen presentation in all cells

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64
Q

Which IL are produced by Th2 cells?

A

IL-4
IL-5
IL-6

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65
Q

What effect does IL-4 has on Th2 cells?

A

Induces differentiation into Th2 cells

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66
Q

Promotes growth of B cells. Enhances class switching to IgE and IgG

A

IL-4

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67
Q

Which are the effects of IL-5?

A

Promotes differentiation of B cells
Enhances class switching to IgA
Stimulates the growtlh and differentiation of eosonophils

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68
Q

This IL modulates inflamatory response

A

IL-10

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69
Q

What does IL-10 do?

A

Inhibits action of activated T cells and Th1

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70
Q

Who else secretes IL-1?

A

Th2 cells and regulatory T cells

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71
Q

Who else has similar actions as IL-10 by inhibiting inflamation?

A

TNF β

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72
Q

Which is the importance of Interferon α and β?

A

A part of innate host defence against both RNA and DNA viruses

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73
Q

What are the interferons?

A

Are glycoproteins synthesized by viral infected cekks that act locally on uninfected cells “priming them” from viral defense

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74
Q

Once the Virus infects primed cells, what does Viral dsRNA activates?

A

RNAase L

Protein kinase

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75
Q

Which is the effect of RNAase L?

A

Degradation of viral/ host mRNA

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76
Q

What does Protein kinase inhibits?

A

Inhibition of viral/host protein synthesis

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77
Q

What are the results of Interferon α and β?

A

Essentially results in apoptosis, thereby interrupting viral amplification

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78
Q

Which cells possess MHC I?

A

All cells except mature RBCs

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79
Q

Which are the cell surface proteins that T cells have?

A

TCR
CD3
CD28

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80
Q

This is the importance of TCR

A

Binds antigen -MHC complex

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81
Q

In which process is CD3 associated?

A

Associated with TCR fpr signal transduction

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82
Q

What is the effect of CD28?

A

Binds B7 to APC

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83
Q

These are the cell surface proteins on Helper T cells

A

CD4 and CD40 ligand

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84
Q

Which is the cell surface protein on Cytotoxic T cells?

A

CD8

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85
Q

Name all cell surface proteins for B cells

A

Ig (binds antigen)
CD19, CD20, CD21, CD40
MHC II, B7

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86
Q

This is the receptor for EBV

A

CD21

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87
Q

For Macrophages these are the cell surface proteins

A

CD14, CD40
MHC II, B7
Fc and C3b receptors

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88
Q

Cell surface proteins on NK cells

A

CD16

CD56

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89
Q

What is the effect of CD16?

A

Binds Fc of IgG

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90
Q

Unique marker for NK

A

CD56

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91
Q

What is anergy?

A

Self reactive T cells become nonreactive without constimulatory molecule

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92
Q

Can B cells become anergic?

A

B cells also become anergic, but tolerance is less complete than in T cells

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93
Q

Who can produce Superantigens?

A

S. pyogenes

S. aureus

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94
Q

Which are the habilities of superantigen?

A

Cross link the β region of the T cell receptor to the MHC class II on APCs

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95
Q

What are the effects of superantigen on T cells?

A

Can activate any T cell, leading to massive release of cytokines

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96
Q

Who can produce Endotoxins/ lipopolysaccharide?

A

Gram negative bacteria

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97
Q

Which cells are stimulated by Endotoxins/ lipopolysaccharide?

A

Macrophages

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98
Q

How can Endotoxins/ lipopolysaccharide stimulate macrophages?

A

Directly stimulates macrophages by binding to endotoxin receptor CD14, Th cells are not involved

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99
Q

Which bacterias show Antigen variation?

A 
Salmonella (2 flagellar variants)
Borrelia (relapsing fever)
Neisseria gonorrhea (pilus protein)
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100
Q

Which is the classic virus that shows Antigen variation?

A

Influenza virus (major = shift, minor= drift)

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101
Q

This parasite has antigenic variation

A

Trypanosomes (programmed rearrangement)

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102
Q

How does passive acquisition of immunity happens?

A

Receiving preformed antibodies

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103
Q

How is the onset of acquiring passive immunity?

A

Rapid

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104
Q

How long does Passive immunity last?

A

Short span of antibodies (half life= 3 weeks)

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105
Q

Which are examples of Passive immunity?

A

IgA in breast milk
Maternal IgG crossing placenta
Antitoxin
Humanized monoclonal antibody

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106
Q

After which microorganism exposure are given preformed antibodies?

A

Tetanus toxin
Botulinum toxin
HBV
Rabies virus

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107
Q

How is active immunity acquired?

A

Exposure to foreign antigens

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108
Q

This is the onset of Active immunity

A

Slow

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109
Q

How long does Active immunity last?

A

Long lasting protection (memory)

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110
Q

Which are examples of Active immunity?

A

Natural infection
Vaccines
Toxoid

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111
Q

When is recommended the combined passive and active immunization?

A

For Hepatitis B or Rabies exposure

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112
Q

Which is the reason of vaccination?

A

Vaccines are used to induce an active immune response (humoral and/ or cellular) to specific pathogens

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113
Q

How are vaccines classified?

A

Live attenuated vaccine

Inactive or killed vaccine

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114
Q

What is a live attenuated vaccine?

A

Microorganism loses its pathogenicity but retains capacity for transient growth within inoculated host

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115
Q

Which kind of response does live attenuated vaccine induces?

A

Mainly induces a cellular response

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116
Q

Which is the advantage of administering live attenuated vaccines?

A

Induces strong, often lifelong immunity

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117
Q

Which disadvange do live attenuated vaccines have?

A

May revert to virulent form

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118
Q

When is contraindicated the use of live attenuated vaccines?

A

In pregnancy and immune deficiency

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119
Q

These are examples of live attenuated vaccines

A 
Measles
Mumps
Rubella
Polio (Sabin)
Influenza (intranasal)
Varicella
Yellow fever
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120
Q

Which are the characterisitics of Inactivated or killed vaccines?

A

Pathogen is inactivated by heat or chemicals; maintaining epitope structure on surface antigen is important for immune response

121
Q

Which immunity is induced with Inactivated or killed vaccines?

A

Humoral immunity induced

122
Q

This is an advantage of Inactivated or killed vaccines

A

Stable and safer than live vaccines

123
Q

This is a disadvantage of Inactivated or killed vaccines

A

Weaker immune response; booster shots usually required

124
Q

Which are examples of Inactivated or killed vaccines?

A 
Cholera
Heàtitis A
Polio (Salk)
Influenza (injection)
Rabies
125
Q

How many types of Hypersensitivity exist?

A

I, II, III, IV

126
Q

How else is Hypernsensitivity type I is known?

A

Anaphylactic and atopic

127
Q

Which is the mechanism of action of Hypernsensitivity type I?

A

Free antigen cross links IgE on presensitized mast cells and basophilsm triggering immediate release of vasoactive aminesthat act at postcapillary venules (eg. histamine)

128
Q

Why does the reaction develops rapidly in Hypernsensitivity type I?

A

Because of preformed antibody

129
Q

Whho manages the delayed reaction in Hypernsensitivity type I?

A

Due to production of arachidonic acid metabolites (leukotrienes)

130
Q

Which Hypernsensitivity types are mediated by antibodies?

A

Types I, II, III

131
Q

Which test helps in Hypernsensitivity type I?

A

Skin test for specific IgE

132
Q

This is the alternative name for Hypernsensitivity type II

A

Cytotoxic (antibody mediated)

133
Q

How does Hypernsensitivity type II works?

A

IgM, IgG bind to fixed antigen on enemy cell, leading to cellular destruction

134
Q

Which the three mechanism of Hypernsensitivity type II?

A

Opsonization leading to phagocytosis or complement activation
Complement mediated lysis
Antibody dependent cell mediated citotoxicity, ussually due to NK cells or macrophages

135
Q

In Hypernsensitivity type II, who lead to Membrane attack complex?

A

Antibody and complement

136
Q

Which lab test helps for Hypernsensitivity type II?

A

Direct and Indirect Coombs

137
Q

What does Direct Coombs detects?

A

Detects antibodies thathave adhered to patients RBCs

138
Q

Which is an example of Direct Coombs?

A

Test an Rh + infant of an Rh - mother

139
Q

This is what indirect coombs detects

A

Detects antibodies that can adhere to other RBCs

140
Q

Give an example of Indirect coombs

A

Test an Rh - woman for Rh + antibodies

141
Q

This Immunity type is also known as Immune complex

A

Hypernsensitivity type III

142
Q

What happens in Immune complex immunity?

A

Antigen- antibody (IgG) complex activate complement, which attracts neutrophils; neutrophils release lysosomal enzymes

143
Q

Which diseases are Immune complex immunity related?

A

Serum sickness

Arthus reaction

144
Q

What happens in Serum sickness?

A

An immune complex disease in which antibodies to the foreign proteins are produced

145
Q

How much times does it takes for antibodies to be produced in Serum sickness?

A

5 days

146
Q

How is damage produced in Serum sickness?

A

Immune complexes form and are deposited in membranes, where they fixed complement (leading to tissue damage)

147
Q

Who is more common Serum sickness or Arthus reaction?

A

Serum sickness

148
Q

What is Arthus reaction?

A

A local subacute antibody mediated hypersensitivity (type III) reaction

149
Q

This an example of how to cause Arthus reaction

A

Intradermal onjection of antigen induces antibodies, which form antigen-antibody complexes in the skin

150
Q

Which are the clinical manifestations of Arthus reaction?

A

Edema, necrosism and activation of complement

151
Q

What causes most cases of Serum sickness?

A

By drugs acting as haptens

152
Q

When do you suspect Serum sickness?

A

Fever, urticaria, arhtralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure

153
Q

What causes Arthus reaction?

A

Antigen- antibody complexes

154
Q

Which test can be used for Arthus reaction?

A

Immunofluorescent staining

155
Q

Delayed type of Immunity

A

Hypersensitivity Type IV

156
Q

Who mediates delayed type of immunity?

A

T cell mediated

157
Q

How does Hypersensitivity Type IV works?

A

Sensitized T lymphocytes encounter antigen and then release lymphokines

158
Q

Which is the final result of Hypersensitivity Type IV?

A

Macrophage activation; no antibody involved

159
Q

Can Hypersensitivity Type IV be transferable by serum?

A

Cell mediated; therefore it is not transferable by serum

160
Q

Which test are used for Delayed immunity?

A

Patch test, PPD

161
Q

Which is the mnemonic for Hypersensitivity types?

A 
ACID
Anaphylactic and Atopic (Type I)
Cytotoxic (Type II)
Immune complex (Type III)
Delayed (cell mediated, Type IV)
162
Q

Which are examples Hypersensitivity type I disorders?

A

Anaphylaxis

Allergic and Atopic disorders

163
Q

Bee sting, some food/drug allergies, are examples of this Hypersensitivity disorder

A

Hypersensitivity type I- anphylaxis

164
Q

These are allergic and atopic disorders

A 
Rhinitis
Hay fever
Rczema
Hives
Asthma
165
Q

Which are the presentation of Hypersensitivity type I disorders?

A

Immediate
Anaphylctic
Atopic

166
Q

Name examples of Hypersensitivity type II disorders

A 
Autoimmune hemolytic anemia
Pernicious anemia
Idiopathic thrombocytopenic purpura
Erytroblastosis Fetalis
Acute hemolytic transfussion reactions
Rheumatic fever
Goodpasture syndrome
Bullous pemphigoid
Pemphigus vulgaris
167
Q

Which are the characteristics of Hypersensitivity type II disorders?

A

Disease tends to be specific to tissue or site where antigen is found

168
Q

Give examples of Hypersensitivity type III disorders

A 
SLE
Polyartheritis nodosa
Poststreptococcal glomerulonephritis
Serum sickness
Arthus reaction (swelling and inflammation following tetanus vaccine)
169
Q

Which possible presentations can Hypersensitivity type III disorders have?

A

Can be associated with vasculitis and systemic manifestations

170
Q

These are Hypersensitivity type IV disorders

A 
Multiple sclerosis
Guillian Barre syndrome
Graft versus host disease
PPD (test for M. tuberculosis)
Contact dermatitis (poison ivy, nockel allergy)
171
Q

What is a characteristic of Hypersensitivity type IV disorders?

A

Response is delayed and does not involve antibodies

172
Q

Which are the possible blood transfusion reaction?

A

Allergic reaction
Anaphylactic reaction
Febrile nonhemolytic transfusion reaction
Acute hemolytic transfusion reaction

173
Q

Which is the pathogenisis of Allergic reaction to Blood transfusion?

A

Type I hypersensitivity reaction against plasma proteins in transfused blood

174
Q

In case of allergic reaction to blood transfusion which could be the clinical presentations?

A

Urticaria, pruritusm wheezing, fever

175
Q

How do you treat Allergic reaction to Blood transfusion?

A

With antihistamines

176
Q

What is anaphylactic reaction to blood transfusion?

A

Severe allergic reaction

177
Q

What happens in anaphylactic reaction to blood transfusion? and what is the solution?

A

IgA deficient individuals must receive blood products that lack IgA

178
Q

Which is the clinical presentation of anaphylactic reaction to blood transfusion?

A

Dyspnea, bronchospasm, hypotensionm respiratory arrestm shock

179
Q

Which kind of Hypersensitivity disorder is Febrile nonhemolytic transfussion reaction?

A

Type II hypersensitivity reaction

180
Q

What happens in Febrile nonhemolytic transfussion reaction?

A

Host antibodies against donor HLA antigens and leucocytes

181
Q

These are the manifestations Febrile nonhemolytic transfussion reaction

A

Fever, headachesm chills, flushing

182
Q

Which kind of Hypersensitivity disorder is Acute hemolytic transfussion reaction?

A

Type II hypersensitivity reaction

183
Q

How is Acute hemolytic transfussion reaction classify?

A

Intravascular hemolysis

Extravascular hemolysis

184
Q

What happens in Intravascular hemolysis in Acute hemolytic transfussion reaction?

A

ABO blood group incompatibility

185
Q

This is what happens in Extravascular hemolysis in Acute hemolytic transfussion reaction

A

Host antibody reaction against foreign antigen in donor RBCs

186
Q

Clinical presentation of Acute hemolytic transfussion reaction

A

Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinemia (intravascular), jaundice (extravascular hemolysis)

187
Q

Which could be the complication caused by bacterias in case of No T cells?

A

Sepsis

188
Q

In case of No B cells which bacterias can caused disease?

A 
Encapsulated (SHiNE SKiS)
S. pneumoniae
H. influenzae type B
Neisseria meningitidis
Escherichia coli
Salmonella
Klebsiella pneumoniae
Strep group B
189
Q

We are at risk of these bacterias infection in case of no granulocyte

A

Staphylococcus
Burkholderia cepacia
Serratia
Nocardia

190
Q

Which bacteria is the principal that affects in case of no complement?

A

Neisseria (No membrane attack complex)

191
Q

These viruses increased the risk of infection if No T cells

A

CMV, EBV, JCV, VZV

Chronic infection with respiratory/ GI viruses

192
Q

Which vaccines are contraindicated in patients with no B cells?

A

Live vaccines

193
Q

Which viruses infect in patients without B cells?

A

Enteroviral encephalitis

Polivirus

194
Q

For patients with no T cells, are at higher risk for these Fungi infections

A

Candida

Pneumocystis Pneumoniae

195
Q

For patients without IgA this is the most common parasite infection

A

GI giardiasis

196
Q

No granulocyte patients are at higher risk of these fungi infection

A

Candida, Aspergillus

197
Q

Patients with no B cells are at higher risk of recurrent infection by…

A

Bacterias

198
Q

For patients with no T cells these microorganism are the most probable cause of infection

A

Fungal and Viral infection

199
Q

Which are B cell disorders?

A

X-linked agammaglobulinemia

200
Q

This is an alternative name for X-linked agammaglobulinemia

A

Bruton agammaglobulinemia

201
Q

Which inheritance mode does Bruton agammaglobulinemia has? who are affected?

A

X linked recessive

Increase in boys

202
Q

What is defective in X-linked agammaglobulinemia?

A

Defect in BTK, atyrosine kinase gene→ No B cell maturation

203
Q

Which is the clinical presentation of X-linked agammaglobulinemia?

A

Recurrent bacterial and enteroviral infections after 6 months (Decreased maternal IgG)

204
Q

These could beclinical findings in X-linked agammaglobulinemia

A

Absent/ scanty lymph nodesand tonsils

205
Q

Which are the findings in Bruton agammaglobulinemia?

A

Normal CD19+ B cell count

↓ Pro B, ↓ Ig of all classes

206
Q

Which is the most common immunodeficiency?

A

Selective IgA deficiency

207
Q

Which is the defect in selective IgA deficiciency?

A

Unknown

208
Q

Which is the clinical presentation of selective IgA deficiciency?

A

Majority Asymptomatic
Can see:
Airway and GI infection. Autoimmune disease, Atopy, anaphylaxia to IgA containing products

209
Q

These are the lab results in selective IgA deficiciency

A

IgA <7 mg/ dL with normal IgG, IgM levels

210
Q

What is wrong in Common variable immunodeficiency?

A

Defect in B cell differentiation

Many causes

211
Q

When can Common variable immunodeficiency be acquired?

A

In 20-30s

212
Q

These could be findings in patients with Common variable immunodeficiency

A

Increase risk of autoimmune disease

Bronchiectasis, lymphoma, sinopulmonary infections

213
Q

Which labs are affected in Common variable immunodeficiency?

A

Decreased plasma cells

Decreased Immunoglobulins

214
Q

These are T cell disorders

A

Thymic aplasia
IL-12 receptor deficiency
Autosomal dominant hyper IgE syndrome
Chronic mucocutaneous candidiasis

215
Q

Thymic aplasia is also known as…

A

DiGeorge Syndrome

216
Q

What is affected in DiGeorge syndrome?

A

22q11 deletion; failure to develop 3rd and 4th pharyngeal pounches→ Absent thymus and parathyroids

217
Q

Which are the clinical manifestations of DiGeorge syndrome?

A

Tetany (hypocalcemia)
Recurrent Viral/Fungal infections (T cell deficiency)
Conotruncal abnormalities

218
Q

Name Conotruncal abnormalities

A

Tetralogy of Fallot

Truncus arteriosus

219
Q

Which are the findigs in Thymic aplasia?

A

↓ T cells, ↓ PTH, ↓ Ca2+
Absent Thymic shadow on CXR
22q11 deletion defected by FISH

220
Q

What is wrong in IL-12 receptor deficiency?

A

↓ Th1 response

221
Q

Which is the inheritance mode of IL-12 receptor deficiency?

A

Autosomal recessive

222
Q

When can IL-12 receptor deficiency be presented?

A

After administration of BCG vaccine

223
Q

This is how IL-12 receptor deficiency can manifest

A

Disseminated mycobacterial and fungal infections

224
Q

What is decreased in IL-12 recetor deficiency?

A

↓ IFN γ

225
Q

Also known as Job syndrome

A

Autosomal dominant hyper IgE syndrome

226
Q

What is the defect in Autosomal dominant hyper IgE syndrome?

A

Deficiency of Th17 cells due to STAT3 mutation→ Impaired recruitment of neutrophilstp sites of infection

227
Q

These are the clinical findings in Job syndrome

A

FATED

coarse Facies, cold (noninflamed) sthapylococcal Absceses, retained primary Teeth, ↑ IgE, Dermatologic problems (eczema)

228
Q

We see this lab alteration in Autosomal dominant hyper IgE syndrome

A

↑ IgE, ↓ IFN γ

229
Q

What is altered in Chronic mucocutaneous candidiasis?

A

T cell dysfunction. Many causes

230
Q

This is the presentation of Chronic mucocutaneous candidiasis

A

Noninvasive Candida Albicans infections of skin and mucous membranes

231
Q

What can be found in Chronic mucocutaneous candidiasis?

A

Absent in vitro T cell proliferation in response to Cnadida Antigens
Absent cutaneous reaction to Candida antigens

232
Q

Which are B and T cell disorders?

A

Severe combined immunodeficiency (SCID)
Ataxia Telangiectasia
Hyper IgM syndrome
Wiskott Aldrich syndrome

233
Q

How can we classified the defects in SCID?

A

Defective IL-2R gamma chain (most common, X linkes)

Adenosine Deaminase Deficiency (Autosomal recessive)

234
Q

This is how SCID can be presented

A

Failure to thrive, chronic diarrhea, thrush

Recurrent viral, bacterial, fungal and protozoal infections

235
Q

Which is the treatment for SCID?

A

Bone marrow transplant

236
Q

Is it possible to have a Bone marrow transplant rejection in SCID?

A

No concern for rejection

237
Q

These are the findings in SCID

A 
↓T cell receptor excision circles (TRECs)
Absence of thymic shadow (CXR)
Germinal centers (lymph node biopsy) and T cells (flow cytometry)
238
Q

Which is the problem in Ataxia Telangiectasia?

A

Defects in ATM gene → DNA double strand breaks → cell cycle arrest

239
Q

Which is the triad for Ataxia Telangiectasia?

A 
Cerebellar Defects (Ataxia)
Spider Angiomas (telangiectasia)
IgA deficiency
240
Q

These are the findings in Ataxia Telangiectasia

A

↑ AFP
↓ IgA, IgG and IgE
Lymphopenia, cerebellar athrophy

241
Q

What is the defect in Hyper IgM syndrome?

A

Most commonly due to defective CD40L on Th cells= class swithcing defect

242
Q

How is Hyper IgM syndrome genetically classify?

A

X linked recessive

243
Q

Which are the infection that can occur in Hyper IgM syndrome?

A

Severe pyogenic infections early in life

Oportunistic infection with Pneumocystis, Cryptosporidium, CMV

244
Q

In Labs what is altered in Hyper IgM syndrome?

A

↑ IgM

↓↓ IgG, IgA, IgE

245
Q

Which is the mutation in Wiskott- Aldrich syndrome?

A

Mutation in WAS gene

246
Q

Which is the inheritance mode of Wiskott- Aldrich syndrome?

A

X linked recessive

247
Q

What is the problem with T cells in Wiskott- Aldrich syndrome?

A

T cells unable to reorganize actin cytoskeleton

248
Q

These is the mnemonic for Wiskott- Aldrich syndrome

A 
WATER
Wiskott- Aldrich syndrome
Thrombocytopenic purpura
Eczema
Recurrent infections
249
Q

Which risk are higher in Wiskott- Aldrich syndrome?

A

Increased risk of Autoimmune disease and malignancy

250
Q

These are the lab alterations in Wiskott- Aldrich syndrome

A

↑ IgE, IgA
↓ to normal IgG, IgM
Fewer and smaller platelets

251
Q

These diseases are classified as Phagocyte dysfunction

A

Leukocyte adhesion deficiency (type 1)
Chédiak- Higashu syndrome
Chronic granulomatous disease

252
Q

Which is the defect in Leukocyte adhesion deficiency (type 1)?

A

Defect in LFA-1 integrin (CD18) protein on phagocytes;

253
Q

What happens if there is a defect in LFA-1 integrin (CD18) protein on phagocytes?

A

Impaired migration and chemotaxis

254
Q

Inheritance mode of Leukocyte adhesion deficiency (type 1)?

A

Autosomal recessive

255
Q

These are characteristics of clinical presentation of Leukocyte adhesion deficiency (type 1)

A

Recurrent bacterial skin and mucosal infections, absent pus formation, impaired wound healing, delayed separation of umbilical cord (>30 days)

256
Q

What is increased in Leukocyte adhesion deficiency (type 1) ?

A

Neutrophils

257
Q

Although Neutrophils are increased in Leukocyte adhesion deficiency (type 1) what is the problem with them?

A

Absence of neutrophils at infection sites

258
Q

In this phagocyte dysfunction there is a defect in lysosomal trafficking regultator gene (LYST)

A

Chediak Higashi syndrome

259
Q

Which is other problem in Chédiak Higashi syndrome?

A

Microtubule dysfunction in phagosome lysosome fusion

260
Q

Which is the inheritance pattern for Chédiak Higashi syndrome?

A

Autosomal recessive

261
Q

Who are the main bugs who cause recurent pyogenic infections in Chédiak Higashi syndrome?

A

Staphylococci and streptococce

262
Q

These are the clinical manifestations of Chédiak Higashi syndrome

A 
Recurrent pyogenic infections
Partial albinism
Peripheral neurophaty
Progressive neurodegeneration
Infiltrative lymphohistiocytosis
263
Q

These lab result are altered in Chédiak Higashi syndrome

A

Giant granules in neutrophils and platelets
Pancytopenia
Mild coagulation defects

264
Q

What is the defect in Chronicgranulomatous disease?

A

Defect in NADPH oxidase→ ↓ reactive oxygen species (superoxide) and absent respiratory burst in neutrophils

265
Q

This is the inheritance mode in Chronic granulomatous disease

A

X linked recessive

266
Q

From which microorganisms are patients suceptible in Chronic granulomatpus disease?

A 
↑ Suceptibility to catalase + organisms (PLACESS)
Pseudomona
Listeria
Aspergillus 
Candida
E. Coli
S. aureus
Serratia
267
Q

Which lab test help in the diagnosis of Chronic Granulomatous?

A 
Abnormal dihydrorhodamine (flow cytometry) test
Nitrobuline tetrazolinum test is - (test out of favor)
268
Q

Name all types of Graft

A

Autograft
Syngeneic graft
Allograft
Xenograft

269
Q

What is a autograft?

A

From self

270
Q

This kind of graft comes form identical twn or clone

A

Syngeneic graft

271
Q

What is a Allograft?

A

From nonidentical individual of same species

272
Q

This type of Graft comes from different species

A

Xenograft

273
Q

These are all the Transplant rejection types

A

Hyperacute
Acute
Chronic
Graft versus host disease

274
Q

How long does it take for rejection to be categorized as Hyperacute?

A

Within minutes

275
Q

Which is the pathogenesis in Hyperacute rejection?

A

Pre-existing recipient antibodies react to donor antigen (Type II reaction)

276
Q

What is activated in Hyperacute reaction?

A

Activates complement

277
Q

These are the results of Hyperacute reaction

A

Widespread thrombosis of graft vessels → Ischemic/necrosis

278
Q

Which are the alternatives if treatment in Hyperacute transplant reaction?

A

Graft must be removed

279
Q

In this kind of Trasnplant rejection it takes weeks to months for the onset

A

Acute rejection

280
Q

Which are the types of Acute transplant rejection?

A

Cellular

Humoral

281
Q

What happens in the cellular Acute Rejection?

A

Cytotoxic T lymphocites activated against donor MHCs

282
Q

Which is the difference between Hyperacute and Acute Humoral rejection?

A

Humoral is similar to Hyperacute, except antibodies develop after transplant

283
Q

Which is the pathogenisis in Acute Transplant rejection?

A

Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate

284
Q

How do you manage Acute transplant rejection?

A

Prevent/ reverse with immunosupressants

285
Q

How long does it takes for Chronic transplant rejection to onset?

A

Months to years

286
Q

Recipient T cells perceive donor MHC as recipient MHC and react against donor antigens presented

A

Chronic Transplant rejection

287
Q

Does Chronic Transplant rejection has cellular or Humoral components?

A

Both

288
Q

How do you manage chronic transplant rejection?

A

Irreversible. T-cell and antibody mediated damage

289
Q

Which organs could be the main affected by Chronic Transplant rejection

A

Heart
Lungs
Liver
Kidney

290
Q

This is the main damage in chronic transplant rejection to the heart

A

Atherosclerosis

291
Q

How is manifested the chornic transplant rejecetion in Lungs?

A

Bronchiolitis obliterans

292
Q

What is the effect of Chronic transplant rejection in Liver=

A

Vanishing bile ducts

293
Q

Which are the main features in Kidneys during chronic transplant rejection?

A

Vascular fibrosis

Glomerulopathy

294
Q

How much times does Graft versus host disease takes to onset?

A

Varies

295
Q

What happens in Graft versus host disease?

A

Grafted immunocompetent T cells proliferate in the immunocpromised host and reject host cells with foreign proteins

296
Q

Which is the result of Graft versus host disease?

A

Severe organ dysfunction

297
Q

Which are the clinical features of Graft versus host disease?

A

Macupapular rash
Jaundice
Diarrhea
Hepatosplenomegaly

298
Q

In which kind of transplants is more common to see Graft versus host disease?

A

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

299
Q

When is beneficial Graft versus host disease?

A

Potentially beneficial in bone marrow transplant for leukemia (Graft versus tumor effect)

IMMUNOLOGY (5 decks)

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