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MS1 > Week 8 > Flashcards

Week 8 Flashcards

1
Q

Difference between B cell and T cells in terms of antigen presentation

A

B cells can recognize antigen in its native form as soluble protein, unlike T cells which require antigen to be degraded and presented on the surface of an antigen presenting cell in the context of MHC

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2
Q

How does primary antibody diversity occur in B cells? Where?

A

V(D)J rearrangement and junctional diversity - Bone marrow (variable region)

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3
Q

How does affinity maturation work in B cells? What type of mutations? Where?

A

Somatic hypermutations making certain antibodies better and selecting for them. Lymph node (Fc Region)

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4
Q

Describe Ig Isotype Switching? Where?

A

biological mechanism that changes a B cell’s production of antibody from one class to another; always starts IgM? Lymph node (Fc region)

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5
Q

How do B cells act as APCs?

A

bring in a soluble protein antigen by receptor-mediated endocytosis. and present it to activated or memory helper T cells

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6
Q

What are CDRs?

A

Complementarity-determining regions (CDRs) are part of the variable chains in immunoglobulins (antibodies) and T cell receptors, generated by B-cells and T-cells respectively, where these molecules bind to their specific antigen; Give B cell receptors their specificity

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7
Q

How is the antibody secreted from the B cell?

A

Through RNA splicing, which cuts off its membrane bound domain

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8
Q

Does light or heavy chain determine isotype?

A

Heavy

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9
Q

What does the Fc region bind to?

A

C3b and Fc receptor on phagocytic cells

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10
Q

How many variable and constant regions do the heavy and light chains have?

A

Heavy: 3 constant, 1 variable
Light: 1 constant, 1 variable

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11
Q

What do V L C D stand for in Ig Locus

A

V - variable
L- leader sequence
C- constant
D - diversity (only found in heavy chain locus)

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12
Q

Between the V and C exons there are what?

A

J- joining segments

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13
Q

What is changed in isotope switching/class recombination?

A

Only the germline code(variable region) but does not generate receptor diversity to bind antigen- alters Ig function

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14
Q

What is the first isotype to be expressed in B cells? What is the other isotype which is co-expressed in native B cells?

A

IgM, IgD

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15
Q

IgM has great ___? How?

A

Avidity; sum of affinities of all receptors that hold it together

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16
Q

What Ig isotype causes agglutination of incompatible blood types?

A

IgM

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17
Q

What is the most prevalent isotype in serum?

A

IgG

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18
Q

How many subclasses of IgG? Name them? Important 2?

A

IgG(1-4); 1 & 3 critical for opsonization and complement activation

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19
Q

Whats unique about IgG in terms of its size?

A

Small so it can cross placenta unlike IgM; can provide passive immunity

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20
Q

What is IgG important for?

A

Resistance against Viruses + Bacteria + Bacterial Toxins
- Think _G_Ps mainly deal with antibiotics and antivirals

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21
Q

What is IgE important for?

A

Allergies and Infections (attaches to basophils and mast cells (as do IgG)); Think EWWWWW0- allergies/anaphylaxiz/infections/helminths

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22
Q

Who is the poor useless Isotype?

A

IgD; this _D_um guy does nothing

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23
Q

What does IgA do? Subclasses?

A

Ascends to mucosal membranes/glandular secretions; its a dimer joined by J chain; IgA(1-2)

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24
Q

In bone marrow what are steps of B cell maturation

A

Pro B cell –> Pre-B cell –> Immature B cells (then goes through negative selection)–> Naive

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25
Q

When are BCRs expressed in the steps of B cell maturation?

A

Starting in preB cells (only one chain) by next step complete antigen receptor

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26
Q

What V/D/J genes do the heavy and light chains possess?

A

Heavy: V D J
Light: V J

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27
Q

What allows for the diversity of our antibodies?

A

Random recombination of limited set of inherited germinline DNA

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28
Q

How many possible B-cell clones from the limited genes in the Ig locus?

A

10^12

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29
Q

How many alleles for the heavy chain? How many for light chain? What are they?

A

1;2; k and lambda(only one of them expressed due to bi-allelic exclusion)

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30
Q

What nucleotides are added in DNA repair which contributes to junctional diversity?

A

P and N

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31
Q

Does affinity maturation occur in plasma cells or memory cell?

A

Memory

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32
Q

How does somatic hypermutation induce affinity maturation?

A

Activated B cells migrate into follices to form germinal centers where they proliferate producing a lot of antbodies resulting in decreasing levels of antigens so only B cells with high affinity to antigen can bind to low levels of antigen and survive;

B cells mutate their antibody genes in the dark zone of the germinal center; those with high affinity for antigen can captuare and process it on MHC II molecules for CD4+ cells’ B cells that can present antigents to Tfh cells will receive survival and cytogenic cytokine(IL-20( via CD40 and reenter dark zone to undergo additional mutations

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33
Q

What region of the heavy chain does isotype switching occur in?

A

Fc

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34
Q

What initiates somatic hypermutation?

A

Activation induced Cytidine Deaminase (AID)

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35
Q

Successful B cells which underwent somatic hypermutation express what to re-enter dark zone?

A

CXCR4

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36
Q

What important molecules/cytokines to TFH provide to allow for affinity maturation in B cells?

A

CD40 & IL-21

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37
Q

Immature B cells express what Igs ? Naive B cells express?

A

IgM; IgM & IgD

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38
Q

Describe steps of isotype switching?

A
  1. B cell is activated at periphery of primary follicle (takes in pathogen presents it on MHC II to CD4 helper T cell)
    2.Migrates into follicle and proliferates forming dark zone
  2. Helper T cells influnece cytokine switching through cytokines; cytokine switching causes isotype switching
  3. B cells leave into light zone
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39
Q

What cytokine release by Tfh stimulates isotype switching to IgE

A

IL-4

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40
Q

What cytokine release by Tfh stimulates isotype switching to IgA

A

Those released in mucosal tissues; TGF beta, BAFF, Il-5

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41
Q

How does isotype switching occur genetically speaking?

A

Depending on the transcription factor it binds to switcxh gergion of IgM and IgG chain and brings them together cutting out intervening DNA(looping it out_; based on what is looped out different isotypes)

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42
Q

What cytokine promotes change to IgG1 and IgG3

A

IL-21

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43
Q

Describe oponization, complement activation, neutralization by antibodies?

A

Neutralization- binds to antigen so it cannot affect cells

Opsonization- Fc tail of antibody sticks out so it can bind to phagocytes (such as NK cells which have Fc receptors)

Complement activation- can activate complement through Fc tail (through lysis, phagocytosis or inflammation)

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44
Q

What happens in Graves disease?

A

Antibody stimulates TSH receptor without hormones causing an overproduction of thyroid homrones

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45
Q

What causes myasthenia gravis?

A

Antibody inhibits binding of NT to receptor at NMJ causing muscle fatigue/weakeness

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46
Q

Function of IgG isotype?

A

▪ Neutralization of microbes and toxins
▪ Opnsonization of antigens for phagocytosis by macrophages and neutrophils
▪ Activation of the classical pathway of complement
▪ Antibody-dependent cellular cytotoxicity mediated by NK cells
▪ Neonatal immunity – transfer of maternal antibody across placenta and gut
▪ Feedback inhibition of B-cell activation

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47
Q

Function of IgM isotype?

A

Activation of the classical pathway of complement

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48
Q

Describe antibody dependent cellular cytotoxicity

A

IgG1 and IgG3 bind to antigens on the surface of infected cells, and their Fc regions are recognized by an Fcγ receptor on natural killer (NK) cells.

The NK cells are activated and kill the antibody-coated cells.
Involved in asthma

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49
Q

What Ig isotopes have an Fc region recognized by Fc-gamma receptor of NK cells

A

IgG1 and IgG3

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50
Q

What are the best antibodies at fixing complement

A

IgG ; they fix the C1 structure and allow for the cascade to begin

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51
Q

What produces IgA ?

A

Plasma cells in the lamina propia

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52
Q

Describe location of IgA and process of its release?

A

The dimeric IgA binds to a poly-Ig receptor in the lamina propria and is actively transported through epithelial cells through endocytosis and then secreted with a portion of the polyIg receptor

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53
Q

What happens when B cells are activated

A
  • Express proteins that promote survival
  • Present antigens to T cells
  • Increase expression of cytokine reeptors to make them more responsive to them
  • Increased expression of CCR7 allowing for migration from follicle to T-cell zone
  • Generate plasma cells for antibody secretion
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54
Q

What is expressed to allow activated B cells to go to T cell zone?

A

CCR7

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55
Q

What does genetic deficiency in CD40l cause?

A

Genetic deficiency of CD40 L greatly reduces class switching and causes abnormally high level of IgM, “hyper-IgM” syndrome 1
Patients are “immune” from developing allergies but get reccurrent sinopulmonary bacterial infections

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56
Q

T-dependent vs T-independent antibody responses? When?

A

Antibody responses to protein antigens require T cell help, and the antibodies produced typically show isotype switching and are of high affinity ; Nonprotein (e.g., polysaccharide) antigens are able to activate B cells without T cell help but require other signals (e.g. complement protein)

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57
Q

Whats produced in T-dependent vs T-independent antibody responses?

A

T-dependent- ,memory cells and long lived plasma cells
T-independent- mainly IgM, low affinity anitbodies, short lived plasma cells

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58
Q

How do TI-1 antigens work?

A

combination of the repeated structure cross-linking with the B-cell receptor with the PRR is enough to cause the B-cell to undergo proliferation and differentiation;

usually polysaccharides

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59
Q

Difference in high concentration vs low concentration TI-1 antigen response?

A

At high concentrations they elicit a polyclonal response.
At low concentrations these antigens can elicit a specific antibody response

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60
Q

How do TI-2 antigens work?

A

usually linear polymeric antigens that
have a repeating unit structure – such as polysaccharides. The repeating
structure allows simultaneous binding to, and cross-linking of, multiple
BCRs. This massive BCR cross-linking is thought to provide a sufficient
activation signal to over-ride the need for T cell help.

usually polymers

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61
Q

TI-2 cells can only activate ___ cells

A

mature

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62
Q

T/F ●Sometimes there is cytokine “help” and then the isotype can change to IgG for TI-2 antigens

A

T

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63
Q

4 types of hypersensitivies

A

1 - Allergies/Atophy/Anaphylaxis
2- Antibody recognizes target on cell and creates inflammatory reaction
3- Antiobody antigen immune complex formed and float in vasculature
4- Delayed; involves T cells

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64
Q

Type 1 hypersensitivity is mediated by what isotype

A

IgG

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65
Q

What are the 2 steps of Type 1 H

A

1- Sensitization - T cells picks up pathogen differentiates into Th2 which changes isotype from IgM to IgE; this attaches to Fc receptors on mast cells and sensitizes them

  1. 2nd exposure- Th2 cells see antigen again and activate B cells to release IgE which causes mast cell degrranulation
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66
Q

Type 2 H is antibody mediated/cytotoxic and is usually caused by what isotypes?

A

IgG , IgM

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67
Q

What usually causes Type 2 H

A

Drugs such as pencillin which fix to cell surfaces(causes death of platelets and RBCs); neutralized by anti drug IgG antibodies

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68
Q

What isotypes causes Type 3 H

A

IgA or IgG

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69
Q

T/F Large Ag/Ab immyune complex are hard to clear

A

F - Large complexes are cleared quickly; Small complexes are deposited on vessels 🡪 ligate FcR on leukocytes 🡪 tissue injury

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70
Q

Examples of Type 3 and Type 2 H

A

2- autoimmune blood disorders (hemolytic anemia, thrombocytopenia, transfusion reactions, autoimmune hemolytic anemia, fetal erythroblastosis)

3- Arthus skin reaction, serum sickness, farmer’s lung (hay-induced damage), rheumatoid arthritis, glomerulonephritis, SLE

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71
Q

What mediates Type 4 H

A

Effector T cells(Th1 cells which release cytokines and recruit phagocytes)

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72
Q

Examples of Type 4 H response

A

TB test; Poison ivy response, Patch testing for conatc dermatitis

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73
Q

Central vs Peripheral Tolerance

A

Central- Negative selection in BM/Thymus ; Peripheral- mechanism which limits activity of immune response

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74
Q

Give examples of peripheral tolerance

A

T reg cells; Clonal anergy/exhaustion; Clonal deletion

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75
Q

Where are autoantigens presented in the thymus

A

Medullary cells

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76
Q

By what are autoantigens expressed in thymus

A

Autoimmune regulatore gene (AIRE)

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77
Q

What happens when you are deficiency in AIRE

A

Can get APECED ; destruction of endocrine tissues islet cells(insulin production) and susceptible to fungal infections

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78
Q

T/F T reg cells have some affinity for self

A

True= they are self reactive in thymus but when they are activated they turn the immune response down

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79
Q

Does positive selection occur in B cells

A

Nope ; just T cells

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80
Q

What are immunoprivileged tissues

A

tissues that the immune system does not actively sample antigens from ex brain, testes, uterus

makes them resistant to inflammation however damage to this site can induce a dangerous autoimmune response

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81
Q

2 main functions of peripheral tolerance

A

o Control any self-reactive cells that “slipped through the cracks” of central tolerance
o Induce tolerance to important harmless antigens (i.e. foods) that are not present during thymic selection

**in peripheral lymphoid organs

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82
Q

Anergy

A

a state of hyporesponsiveness/inactivation of T cells because it doesn’t get co-stimulation

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83
Q

How does costimulation occur in T cells

A

involves T cell’s CD28 molecule binding to B7 (B7.1 and B7.2 or CD80/CD86) on the surface of the antigen presenting cell.

84
Q

What happens to costimulation as the immune response is about to end

A

Decrease in costimulation as T reg cells decrease amount of B7 expressed in APCs and CD4 T cells express CTLA-4/CD152 which inhibit CD8 cells

CTLA-4 binds 20 times as strong as CD28

85
Q

What cells is CTLA-4 expressed in

A

Activated CD4+ cells and T reg cells

86
Q

Progress of CD28 and CTLA-4 expression on T cells

A

When first activated lots of CD28 on on surgace but overtime more CTLA-4 causing inhibition and inactivation

CTLA4 may also inhibit CD80/86 making them tolerogenic(slowing down reaction with APCs)

87
Q

Where are T reg cells found

A

Peripheral tissues and blood

88
Q

2 types of T reg cells

A

Natural T regs and Inducible/Peripheral T regs

89
Q

What are nTregs

A

self-reactive T cells matured during thymic selection and sent into circulation to suppress any other self-reactive cells that slipped through the system; supress reactive T cells through cell to cell contact

90
Q

What suppressive cytokines do nTregs release to suppress self reactive cells

A

Il-10 and TGF-Beta

91
Q

What are iTregs/pTregs

A

T regulatory cells of any specificity that mature via cytokine signals in the periphery with a regulatory/suppressive phenotype

92
Q

Cytokines from DCs or other Tregs such as : ….. induce iTRegs

A

IL-10, TGF-beta, retinoic acid (RA), indoleamine 2,3-deoxygenase (IDO)
-mainly in gut

93
Q

What are 2 subpopulations of T regs and what cytokine do they mainly produce

A

Tr1- Il-10

Th2- TFG beta

94
Q

Allergies is a failure of what type of tolerance

A

Peripheral

95
Q

What allows for successful induction of Tregs for foods

A

o Timing of exposure (e.g. 6 months vs. 12 months of age)
o Route/site of exposure (e.g. skin vs. gut)
o Dosage of antigen
o PAMP(MAPM)/PRR signals to local APCs

96
Q

How does Il-10 regulate the immune response

A
  • Decrease Il-2 and TNF alpha produced by T cells reducing killing ability
  • preventing DC maturation
  • decreasing expression of MHC and co-stimulatory molecules on APCS preventing antigen presentation
97
Q

T/F Il-10 also helps B cell survical and maturation and increases cytotoxic T cell activity

A

True; but immunosuppressive effect much larger

knocking it out cause autoimmune diseases**

98
Q

Treg suppressive roles in HSV, P.carnii fungus(in HIV), HCV/HIV , L.major infection

A

HSV- decreases inflammation preventing severe disease
P.carnii- restrains pulmonary inflammation
HCV/HIV- supress antiviral CD8+ T cell response
L/major- impair effector T cells ability to eliminate pathogens in dermis

99
Q

T/F All reg. cells produce Il-10

A

True

100
Q

What do B-reg cells produce

A

Il-10, Il-35, TGF- beta

101
Q

What do alternatively activated macrophages produce

A

Il-10

102
Q

What do tolerogenic DCs produce

A

Il-10, TGF-beta, IDO, RA

103
Q

What do CD8+ supressor cells produce

A

IL-10

104
Q

Allergic rxn vs Side effect vs Intolerance to drugs

A

Allergic Reaction: an adverse reaction to a drug in which an immunological mechanism is present or suspected (e.g. urticaria, erythema multiforme).

Side Effect: a pharmacologic effect of the drug that is usually undesirable but unavoidable in standard therapeutic doses (e.g. epinephrine given for an allergic reaction often also causes increased heart rate and muscle tremor because it is a stimulant).

Intolerance: an individual susceptibility to a drug where the normal effects of the drug occur at a lower than usual therapeutic dose; that is, there is a lowered threshold

105
Q

When do allergic rxns in response to drugs begin

A

During drug therapy or at max a few days after stopping

106
Q

What do immediate/accelerated IgE mediated reaction suggect vs delayed IgE reaction?

A

Immediate and accelerated IgE-mediated reactions imply prior exposure and sensitization with rapid response on re-exposure.

More delayed IgE-mediated reactions beginning more than a week after starting therapy may represent the lag phase between exposure and sensitization during first exposure to the drug.

107
Q

Characteristics of Non-IgE mediated reactions

A

Rarely immediate and less frequently accelerated

Discontinuation of the drug usually results in complete resolution of skin manifestations in days as the drug is eliminated, although type III and IV hypersensitivity may take weeks to resolve without treatment.; other organ systems take longer to recover

108
Q

T/F Urticaria lasting weeks or months after cessation of drug therapy implies that the drug was not the causative agent.

A

True

109
Q

T/F Allergic rxn to drug taken for months/yrs are common

A

False

110
Q

What illness can be associated with utricarial or other rashes

A

Viral, Steptococcal, Mycoplasmal pneumonia

111
Q

2 most common causes of allergic reactions to drugs

A

Pencillins and Sulfonamides

Rare: local anesthetics, `acetaminophen, and macrolide antibodics

112
Q

3 examples of classic non-allergic drug reactions

A

ACE inhibitors- cough or angioedema
ASA/beta blocker- bronchospasm
Opiate/NSAODS/RCM/Niacin- Flushing or Urticaria

113
Q

3 examples of classic allergic reactions

A

Cefaclor- Serum sickness
Sulfoamides- erthyema multiforme or Stevens- Johnson syndrome
Amoxicilin- Ampicilin rash

114
Q

T/F Allergy testing is widely available for drugs

A

False

115
Q

What is difficulty of doing allergy testing on drugs

A

is that the complete metabolic pathways of the drug must be known and the reactive metabolites identified, isolated, and polymerized for use as a test reagent.

116
Q

Only low molecular weight drug testing is avaialble for

A

Penicillin

117
Q

Allergy skin testing can easily be done on ___ molecular weight peptide drugs where allergen is drug itself

A

High

118
Q

Limited testing can be performed with other drugs such as ____ and ____, where a positive test with the native drug in non-irritant concentrations implies greater risk of allergy but a negative test does not exclude an allergy for the reasons stated above.

A

vancomycin & cephalosporins

119
Q

What do we do if complete allergy testing is no avaialble? What conditions?

A

Oral challenge; used to rule out drug allergy when there is low probability of it based on history or if allergy tests are negative

120
Q

What do you do if there is no suitable alternatives for the drug and the person is highly at risk to being allergic? Through what route(s)

A

Drug desensitizatoin; can be performed by parenteral (not through the gastrointestinal or oral tract) or oral route, although the oral route is safer and preferred.

do not use if previous reactions caused life threatening disorders, exfoliative dermatitis or immune cytopenias

121
Q

Is desensitization long or short term

A

The desensitization induced in this fashion is very short term, resulting in temporary immune unresponsiveness to the drug for only as long as it is being given in therapeutic doses.

122
Q

Risk factors for drug allergics

A

Genetics (HLA phenotype), Nature of drug(high MW higher odds at stimulating IgE antibody formation), duration/dose (longer/more increased risk), route of exposure(topical is most sensitizing then parenteral), prior drug rxns (allergies to other drugs increase risk to be allergic to pencillin)

123
Q

Non-risk factors

A

Family history, Age , Beta blocker therapy

124
Q

What is urticaria?

A

hives/welts; is an erythematous, raised eruption occurring suddenly and evolving in minutes or hours.

125
Q

How long does urticaria last?

A

Usually minutes to few hours; max 1 day ; reoccurs in other days over days or weeks

126
Q

How does urticaria look like?

A

urticaria is a wheal (flat topped, pale, tense area) surrounded by a flare (area of erythema). look at pic

127
Q

Erthema multiforme vs utricaria

A

EM are fixed and last few days and do not blach under pressure (more dusky)

128
Q

Utricaria usually results from what hypersensitivity?

A

Type 1; due to release of Histamine from mast cells(hence treatment is antihistamines) or complement activation

129
Q

What does biopsy show in utricaria

A

Capillary and venule dilation in superficial dermis and widening of dermis papillae (top layer)

130
Q

___ occurs in half of patients with utricaria

A

Angioedema(usually in the face); legions originate in deep dermis and subcutaneous tissue

131
Q

T/F Angioedema is more associated with pain or burning compared to urtricaria

A

True

132
Q

Is it common to see angioedema without utricaria?

A

No; if you see it usually hereditary angioneurmtic edema, idiosyncratic rxn, or ACE inhibitor therapy

133
Q

Vasculitis is caused by what hypersensitivity

A

Type 3

134
Q

How does vasculitis present

A

Urticarial, purpuric, or erythematous skin lesions that are fixed and last several days — unlike classical transient urticaria — with residual post-inflammatory hyperpigmentation and systemic symptoms (e.g., low grade fever, malaise)

135
Q

T/F You see systemic inflammation in vasculitis?

A

Yes’ (elevated erythrocyte sedimentation rate, decreased complement, and elevated liver enzyme)

136
Q

Serum sickness is caused by what hypersensitivity

A

Type 3

137
Q

When do symptoms begin for for serum sickness

A

7-10 days; rexposure takes 2-5 days

138
Q

What symptoms do you see in serum sickness

A

Vasculitis, urticaria, fever , lymphadenopathy, splenomegaly, join pain/swelling(arthalgias)

139
Q

Erythema multiforme/SJ syndrome caused by what hypersensitivies

A

Type 3 and 4

140
Q

What drugs induce EM/SJ syndrome

A

Sulfonamides, pencillin, barbituates, saicylates(ex. ASA), viral infections

141
Q

How does EM/SJ syndrome legions present?

A

Round/oval erythemous lesions are fixed, raised, last days or weeks, and have central necrosis presenting as central dusky blue target or iris lesions. ; change morphological feautures over several days

142
Q

What is prodrome?

A

symptoms observed before onset of disease

143
Q

Prodrome of EM/SJ syndrome

A

headache/fever/sore throat/cough,

rhinorrhea, lymphadenopathy, malaise

144
Q

What is EM major / SJ

A

is a more severe form of reaction that is potentially life-threatening.

There is mucous membrane involvement, especially of the eyes and oral mucosa, with bullous (large blister) and hemorrhagic crusts and high fever.

145
Q

Ampicillin rash is seen with what 2 drugs

A

Amoxicillin and Ampicillin

146
Q

Signs of ampicillin rash

A

Maculopapular, slightly pruritic, discrete pink lesions starting on trunk and spreading outwards; may include palms and soles.

147
Q

Onset and duration of ampicillin rash

A

7 days; 1-7 days (2.8 median)

148
Q

T/F Ampicillin rash is IgE mediated

A

False

149
Q

Ampicillin rash is common with concomitant viral infections such as EBV and Infectious mononucleosis which do what

A

Activate B cell proliferation

150
Q

Alternative to Penicllin treatment

A

cephalosporin

151
Q

What would you see in Cx of someone with SCID

A

Hyperinflation, Ateclasia(absence of gas in lung), absence of thymic tissue, bone abnormalities in ribs

152
Q

Why is B cell development defects less critical vs T cell development defect in first few months of life

A

Due to the maternal IgG, which crosses the placental barrier, they are often protected from serious infection until later in infancy.

153
Q

What causes combined immunodeficiency

A

The absence of T-cells cripples the immune system, leaving the patient with little ability to mount a specific immune response against a given pathogen.

Very rare; usually caused by mutation in gene involved in T cell development

154
Q

Most common form of SCID

A

X-linked; mutation in Il-2 receptor g chain

155
Q

What other interleukins affected by mutation in Il-2 g chain

A

2,4,7,9,15 (Without Il 7 and 15 differentiation of T and NK cells can not happen)

156
Q

What are 2 autosomal recessive mutations that can lead to SCID

A

Mutation in Il-7 receptor -a chain (B cells less affected here compared to Il-2 mutation in X linked)

Mutation in kinase JAK3 (required for IL-7 signal trandsuction)

157
Q

What nucleic deficiencies cause SCID

A

Adenosine deaminase(ADA) and Purine nucleotide Phosphorylase(PNP); prevent purine metabolism causing accumulation of toxic products which poison T cells(not as much but B cells as well)

158
Q

What is bare lymphocyte syndrome type 2

A

Patients suffering from bare lymphocyte syndrome, type II lack expression of MHC class II molecules on antigen presenting cells and on thymic epithelial cells.

Thus, positive selection of developing CD4+ T-lymphocytes in the thymus cannot occur and thus few CD4+ lymphocytes develop.

Usually mutations in its transcription rather than the gene itself

159
Q

What is bare lymphocyte syndrome type 1

A

Patients suffering from bare lymphocyte syndrome, type I lack expression of MHC class I molecules.

Overall, this syndrome is less severe than bare lymphocyte syndrome, type II, but patients suffer of chronic respiratory bacterial infections, skin ulcerations and vasculitis

160
Q

Mutation in what gene leads to bare lymphocyte syndrome

A

TAP gene (required for proper transport of antigen peptides)

161
Q

Omen’s syndrome

A

syndrome describes patients with mutations in either the RAG-1 or RAG-2 gene.; The most common genetic mutations are found in the RAG-1 and RAG-2 genes, which are required for V(D)J recombination of the antibody chains and TCR chains

162
Q

With this mutation there is a failure in V(D)J recombination leading to few mature T and B-cells.

A

DNA-PK enzyme

163
Q

Bloom syndrome

A

mutation in DNA helicase which can lead to lower levels of T cells

164
Q

In Di George what changes is seen in thymus and what does this cause

A

Absence of Thymus; SCID

165
Q

What are potential treatments for SCID

A

Avoidance of crowds and sick people.
Prophylactic antibiotics and anti-mycotics to control/reduce infections
IVIG – patients are infused with an intravenous solution of antibodies from a donor.
Enzyme therapy for ADA deficiency – 90% effective for patients suffering from an ADA deficiency causing their SCID.
Bone marrow or cord blood transplantation – this is the only known cure for SCID.
Gene therapy – for SCID patients who do not respond well to conventional treatment, clinical trials testing the efficacy of gene therapies for SCID are underway.

165
Q

What are potential treatments for SCID

A

Avoidance of crowds and sick people.
Prophylactic antibiotics and anti-mycotics to control/reduce infections
IVIG – patients are infused with an intravenous solution of antibodies from a donor.
Enzyme therapy for ADA deficiency – 90% effective for patients suffering from an ADA deficiency causing their SCID.
Bone marrow or cord blood transplantation – this is the only known cure for SCID.
Gene therapy – for SCID patients who do not respond well to conventional treatment, clinical trials testing the efficacy of gene therapies for SCID are underway.

166
Q

How often to IVIG have to be injected for those with SCID

A

3-4 weeks

167
Q

T/F Anaphylaxis is a sudden (minutes to hour) rxn

A

True

168
Q

Death caused by what in analphylaxis

A

Closure of airways or cardiovascular event

169
Q

3 criterion for high likelihood of Anaphylaxis

A
  1. Acute onset with mucosal membrane involvement (utricaria, pruritic, flushing swollen lips, uvula)
  2. Respiratory compromise (wheeze, stridor, low PEF, hypoexima)
  3. Reduced BP or signs of end organ dysfunction(collapse, syncope, incontinence)
170
Q

What causes coloring of hives?

A

Raised central white or red wheals
o The wheal is due to edema around the blood vessel due to vasodilation and extravasation of fluid into surrounding tissue.

Surrounding erythema or flare, with itch or burning
o The flare is an axonal (nerve-mediated) reflex triggered by histamine causing reflex vasodilation of surrounding blood vessels causing erythema

171
Q

What is difference between angioedema and hives in terms of position in skin?

A

Angioedema occurs in deeper subcutaneous tissues (+ not itchy or painful)

172
Q

What causes respiratory compromise?

A

Histamine causes the smooth muscle that lines the bronchi and gastrointestinal tract to contract, making those passageways narrow and tougher for air and food to get through.

173
Q

Difference between anaphylaxis and a simple allergic rxn?

A

In a simple allergic reaction, pro-inflam molecules would cause some localized damage, like swelling.; In anaphylaxis, these molecules leak into the bloodstream and reach multiple organ systems.

174
Q

What causes decrease in BP and edemas in anaphylaxis?

A

,Histamine causes blood vessel dilation and increased permeability, meaning that while blood vessel diameter and blood flow to the affected area increase, fluid is also allowed to more easily leak out the blood vessel wall and get into the interstitium.

That causes the pressure in the vessels to fall, and causes swelling or edema, as well as urticaria or hives

175
Q

____ is released by mast cells and it is a protease which casues tissue injury

A

Tryptase

176
Q

In certain scenarios what do mast cells and basophils release in allergic reactions

A

Cytokines
IL-4, IL-13, (cause B cells to release more IgE antibodies and TNF-a

Leukotrienes
B4 and C4 (attract immune cells)

177
Q

What are the preformed chemical mediators of anaphylazxis? What are the newly formed?

A

Preformed: histamine, ECF-A, NCF, Heparin, Tryptase
Newly formed: leukotrienes B-E4, PGD2, PAF

178
Q

What are the effects of leukotrienes and PAF

A

Leukotrienes; bronchoconstriction, mucous production, and increased vascular permeability
PAF- bronchospasm and platelet activation

179
Q

T/F Children tend to have more cardiac symptoms in anaphylaxis

A

F; Adults tend to have more cardiac symptoms – perhaps with age and some degree of coronary disease or arterial thickening, they are less resilient to cardiac insult than children

180
Q

4 outcomes of anaphylaxos

A
  1. Resolution
  2. Death
  3. Biphasic (2-31%)
    4.Protracted
181
Q

What are Biphasic and protracted outcomes of anaphylaxis

A

Biphasic- a recurrence of symptoms that develops following the apparent resolution of the initial anaphylactic episode with no additional exposure to the causative agent (avg 10 hours but can be up to 38 hours)

Protracted- anaphylactic reaction that lasts over 24 hours

182
Q

What is done if a biphasic reaction is observed

A

Consider observing patients for 4 to 6 hours post anaphylactic reaction

Consider prolonged observation times or hospital admission for patients with severe or refractory symptoms

183
Q

Another name for insects

A

hymonptera

184
Q

Food allergies are __x more prevalent in children than in adults

A

4x ; 2 vs 8%

185
Q

What 2 allergies are usually lifelong

A

Peanut and tree nuts

186
Q

What is the highest risk factor for developing anaphylaxis

A

Asthma

187
Q

What is the usual onset and duration of food allergies

A

Within 30 min(max 4 hours); duration 4-6 hours

188
Q

T/F Excercise can aggravate allergic rxns

A

True

189
Q

What body parts if stung can have fatal outcomes

A

Head/Neck

190
Q

What can hymenoptera Venom Allergy be cured with?

A

Immunotherapy

191
Q

What can cause direct mass degranulation?

A

radiocontrast material, tubocurarine, dextran, opiates

192
Q

What can cause anaphylaxis through complement activation?

A

incompatible blood transfusion (type II hypersensitivity), tissue plasminogen activator, possibly some insect stings

193
Q

Anaphylaxtoxins

A

C3a C4a C5a. (Mast cells have receptors to C3a and C5a)

194
Q

What drugs induce COX-1 inhibition? How does it lead to anaphylaxis?

A

ASA & NSAIDs ; shunts arachidonic acid metabolism from COX pathway to lipo-oxygenase pathway resulting in over-generation of inflammatory metabolites

195
Q

With anaphylaxis plasma histamine levels peak at ____ minutes and are undetectable by an ___

A

5-10 minutes; 60 minutes

196
Q

Serum tryptase is another lab marker for anaphylaxis which is elevated at ____ and in what type of reactions

A

1-2 hr; insect stings (not often in food related rxns)

197
Q

___tryptase is more specific mast cell activation marker than total tryptase

A

Beta

198
Q

First line of treatment for Anaphylaxis?Where?

A

Epinephrine (preferably given in IM at thigh - higher levels reach blood)

199
Q

After epinephrine what are other treatments for anaphylaxis?

A

Bronchodilaters and Antihistamine (should not delay time to get to hospital to give these)

200
Q

What are effects of Epinephrine

A

Increase BP/cardiac contractibility (alpha-adrenergic activity)
Reduce urticaria and angioedema (alpha-adrenergic activity)
Bronchodilation (beta 2 adrenergic acticity)
Prevent mast cell degranulation

201
Q

When do you give epinephrine

A

For anaphylatic food allergy when you see allergic rxn
Significant exposure to allergen which in past has caused life threatning anaphylaxis (even before symptoms)

202
Q

Precautions for epinephrine

A
  1. Do not inject into hands or feet
  2. Pre-existing cardiac problems, untreated hypertension or hyperthroidism
203
Q

Precautions for epinephrine

A
  1. Do not inject into hands or feet
  2. Pre-existing cardiac problems, untreated hypertension or hyperthroidism
  3. No contraindications for life threatening allergic rxn
  4. Concurrent treatment MOAIS(mono amine oxidase inhibitors) or tricyclic antidepressants (block effects of epinephrine)
  5. Pregnancy (Can cause premature uterine contraction)
  6. Use of beta blockers (also block effect of epinephrine)- even eye drops
204
Q

Precautions for epinephrine

A
  1. Do not inject into hands or feet
  2. Pre-existing cardiac problems, untreated hypertension or hyperthroidism
  3. No contraindications for life threatening allergic rxn
  4. Concurrent treatment MOAIS(mono amine oxidase inhibitors) or tricyclic antidepressants (block effects of epinephrine)
  5. Pregnancy (Can cause premature uterine contraction)
  6. Use of beta blockers (also block effect of epinephrine)- even eye drops
205
Q

How many doses if over 30 minutes from medical help

A

2-3 doses

206
Q

What to do if someone is in anaphylactic shock?

A

● Check epinephrine expiry dates but use outdated epinephrine if no choice
● After epinephrine use, keep patient supine (lying down) unless vomiting or too dyspneic – ‘empty heart syndrome’
● Do not go off alone during a reaction
● Go to hospital after epinephrine use

MS1 (2 decks)

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