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IPCS > Immunity Exam 2 > Flashcards

Immunity Exam 2 Flashcards

1
Q

During antigen recognition naive B cells are stimulated by antigen binding to cell surface IgM or IgD and _______________ of several B cell receptors

A

cross-linking

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2
Q

Expression of co-stimulatory molecules and cytokine receptors act as ____ in B cell activation

A

APC

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3
Q

Polysaccharides, lipids, nucleic acids are T independent. What does that mean

A

they are not seen by T cells

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4
Q

Multivalent antigen (repeated epitope) cross-links surface Ig on what kind of cells

A

B cells

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5
Q

Most proteins antigens are ___ ___________ antigens which mean they need T cell help for maximal response

A

T dependent

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6
Q

T independent antigens are most what kind of Ig response?

A

IgM sometimes IgG

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7
Q

How do T cells activate B cells

A

B cells present antigen and co-stimulators
activated T cells express CD40 and secrete cytokines
B cells are then activated

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8
Q

Do T cells and B cells bind the same epitope

A

no

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9
Q

What are haptens

A

a molecule that can be recognized by an antibody, but that cannot by itself induce antibody production (or T cell response)

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10
Q

Haptens are important in the generation of what

A

drug allergies

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11
Q

When attached to a carrier haptens become what

A

immunogenic, they can only be immunogenic when covalently coupled to a carrier

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12
Q

B cells need to __________ surface antibody

A

cross-link

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13
Q

Hapten on peptides can bind ______ and stimulate T cells

A

MHC
(A hapten on a carrier can stimulate T cell help by carrier-specific T cells. T cell recognizes foreign or modified peptides presented by the B cell.)

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14
Q

Poison Ivy reaction is a hapten-carrier reaction because urushiol is what

A

reactive

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15
Q

What happens in primary sensitization of poison ivy

A

sensitized T cells are produced and give rise to memory cells

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16
Q

What happens during second contact of poison ivy

A

T memory cells become activated; precipitate and inflammatory reaction and dermatitis

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17
Q

What happens during a sulfonamide-antibiotic allergy

A

reactive molecules can couple to proteins
antibodies recognize 5-membered ring
generate antibodies to the drug and T cells recognize it

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18
Q

T cells help induces what

A

more antibody production
heavy chain class switching
affinity maturation (antibody structure changes to have higher affinity for antigen)
memory B cell production

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19
Q

What do Ig B cells first secrete, how does this class swtich, and what happens in the decient individual

A

IgM first
-CD40L on T cell binds to CD40 on B cell
–CD40L deficiency have hyper-IgM

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20
Q

T cell cytokines determine new isotypes. What does IFN gamma cause, IL-4 cause, and TGF beta cause

A

IFNgamma -> IgG
IL-4 -> IgE (sometimes IgG)
TGFbeta -> mucosal tissues IgA

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21
Q

Isotype switching puts same ____ on a different Fc region. How does this activate the pathway

A

VH
Fc region recognized by Fc receptors and complement
Fc conformation changes when Ab binds to antigen

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22
Q

Fc conformation changes when Ab binds to antigen, so antigen-antibody complexes activate what

A

complement

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23
Q

What is the principle effector function of IgM

A

complement activation

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24
Q

What is the principle effector function of IgG

A

Fc receptor dependent phagocyte responses, complement activation, neonatal immunity

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25
Q

Principle effector functions of IgE

A

immunity against helminths
mast cell degranulation

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26
Q

Principle effector functions of IgA

A

mucosal immunity

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27
Q

What is the neonatal Fcgamma receptor

A

FcRn

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28
Q

What is FcRn responsible for

A

recycling IgG antibodies in the circulation
(controls half-life of antibodies and drugs)
(important in design of biologic drugs)

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29
Q

Once recycling of endosome occurs in the monocyte what happens when it reaches physiological pH in the blood

A

IgG dissociates

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30
Q

Dividing B cells accumulate point mutations in the what regions. What does this cause

A

Ig V, causes affinity of the Ab for Ag

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31
Q

During affinity maturation at low antigen levels, only high affinity what kind of cells bind and recieve the survival signals once a point mutation occurs

A

B cells

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32
Q

During the decline of humoral response the response subsides because what dies off

A

B cells dies off from lack of antigen stimulation

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33
Q

What kind of receptors are binded with low-affinity to Ag-Ab complexes on B cells. What does this further inhibit

A

Fc gamma RII
inhibit B cell receptor signaling causing no more production of antibodies

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34
Q

Too much antibody may reduce response to vaccine by enhanced clearance or what kind of inhibition

A

feedback

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35
Q

During memory B cells IgG or other isotypes can replace what two Igs on the cells surface

A

IgM and IgD

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36
Q

Why does IgG replace other isotypes on the surface during memory B cells

A

more antigen-specific cells present causing less time needed for production of high-affinity IgG

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37
Q

What is type 1 (Immediate hypersensitivity) caused by

A

IgE bound to mast cells
-allergic reaction, favored by TH2 cells

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38
Q

In types II and III hypersensitivity what is it caused by

A

antibody or immune complexes, often autoimmune
-damage by innate components interacting with adaptive components, often TH1

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39
Q

In delayed type hypersensitivity (Type IV) what is it caused by

A

cell mediated, usually CD4 cells

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40
Q

Why does hypersensitivity occur during adaptive memory for antigens

A

-Usually first contact with antigen produces memory, no damage
-Second contact causes damage

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41
Q

What is sensitization of immediate hypersensitivity (type 1)

A

-priming encounter causes no allergic symptoms, not inflammatory
-T cells are shifted to TH2 and IgE is produced

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42
Q

During immediate hypersensitivity (Type I) allergic response to second encounter what happens

A

no lag time due to IgE pre-bound to Fc epsilon RI on mast cells
immediate release of allergic mediators (histamine)

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43
Q

What is IgE’s half life in serum and how many days is it bound to mast cells in tissues

A

serum - 2 days
mast cells - 10 days

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44
Q

IgE production is dependent on what

A

TH2 CD4 cells stimulating B cells

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45
Q

What interleukins promote TH2 cells

A

IL-4, IL-5, IL-13

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46
Q

What inhibits production of IgE

A

TH1 CD4 production

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47
Q

What interleukins promote TH1 cells

A

IL-2, IL-12, INF gamma

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48
Q

What do histamine and serotonin do during Type 1 mediation

A

-loosen endothelial cell tight junctions increasing vascular permeability, tissue edema, drop BP
-constriction of smooth muscle cells; airway, GI

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49
Q

What does proteases do during Type 1 mediation

A

activation of complement
-increase vascular permeability, chemoattractant
activation of kinin cascade
-increase vascular permeability

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50
Q

What does proteoglycans do during type 1 mediation

A

heparin, chondroitin

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51
Q

What increases late phase symptoms that triggers smooth muscle contraction in the lungs

A

Leukotrienes

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52
Q

What are basophils attracted to and what attracts them

A

attracted to: IgE and mast cell inflammation
attracts them: D4 and E4

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53
Q

Basophils produce large quantities of what

A

leukotriene C4
(C4 converted to D4 and E4)

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54
Q

Are basophils present in the immediate phase of a type 1 reaction

A

no, they are involved with symptomology in late phase response

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55
Q

What are the chemotactins of eosinophils

A

leukotriene D4 and E4

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56
Q

Eosinophils are involved with ADCC which is triggered by what

A

IgG and IgA

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57
Q

What kind of cytokines do eosinophils produce

A

inflammatory
wound healing
-TGF-β, TGF-α, VEGF (vascular endothelial GF) and PDGF (platelet derived GF)

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58
Q

Antibodies may cause tissue injury and disease by what two things

A

binding directly to their target antigens on the surface of cells in extracellular matrix (type II hypersensitivity) or by form in immune complexes that deposit mainly in blood vessels (type III hypersensitivity)

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59
Q

What cells produce more complement-fixing isotypes (often autoimmune)

A

TH1 helper cells

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60
Q

Injury caused by antitissue antibody causes complement and Fc receptor mediated recruitment and activation of inflammatory cells which causes what

A

tissue injury
(effector mechanism of tissue injury caused by neutrophils and macrophages)

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61
Q

Type II hypersensitivity transfusion reactions are caused by what

A

mismatched blood types
-IgG destroys foreign RBC by complement mediated lysis
—produced fever, clots, lower back pain, Hgb in urine

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62
Q

What are the 2 fates of free Hgb during type II hypersensitivity

A

passes to the kidneys - hemoglobinuria
breaks down to bilirubin - can be toxic

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63
Q

During type III immune complex-mediated tissue injury, complement and Fc receptor-mediated recruitment and activation of inflammatory cells cause what

A

vasculitis

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64
Q

What are the 4 steps of type III hypersensitivity

A

-intermediate-sized immune complexes deposited in the tissue
-complement activation
-neutrophil chemotaxis
-neutrophil adherence and degranulation

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65
Q

What are the immune processes involved in type III hypersensitivity

A

classical complement pathway
phagocytic cells
takes hours to days to develop

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66
Q

High titers of what are required for type III hypersensitivity reactions

A

soluble antigen/IgG or IgM

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67
Q

What do type 1 reactions require the presence of

A

IgE (specific for the allergen’s antigenic determinant)

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68
Q

What are the newly formed mediators in Type 1 reactions

A

leukotrienes
Prostaglandins
Thromboxane
platelet-activating factor

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69
Q

What is the onset of reaction for type 1 sensitivity reactions

A

within 1 hour

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70
Q

What type 1 mediators are in bronchospasm

A

histamine
prostaglandins
leukotrienes
bradykinin
PAF

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71
Q

What type 1 mediators are in mucosal edema

A

histamine
prostaglandins
leukotrienes
bradykinin
PAF

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72
Q

What type 1 mediators are in mucus secretion

A

histamine
prostaglandins
leukotrienes

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73
Q

What type 1 mediators are in airway inflammation

A

PAF
ECF-A (eosinophil)
leukotrienes

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74
Q

What are types of allergic disease

A

food allergies
drug allergies

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75
Q

What are types of atopic disease

A

asthma
indoor/seasonal allergies
atopic dermatitis

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76
Q

What is a pseudoallergic reaction

A

immediate systemic reactions that mimic anaphylaxis but are NOT caused by IgE-mediated immune responses

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77
Q

What is the treatment for anaphylaxis

A

epi pen
inhaled beta agonist
antihistamine (second line, not monotherapy)
corticosteroid

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78
Q

What is the dose of an epi pen and what is the special counseling point for it

A

0.3 dose
always carry 2 pens

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79
Q

What is the treatment algorithm for allergic rhinitis

A

antihistamines
decogestants
intranasal steroids (only one to help with nasal congestion)
montelukast

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80
Q

What is the important counseling point of taking medicine for allergic rhinitis

A

start a week before allergy season or exposure and continue throughout

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81
Q

What mediators do corticosteroids help with

A

decreases leukotrienes, prostaglandins, thromboxans

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82
Q

Adverse effects of oral antihistamines

A

sedation (1st gen)
dry mouth/eyes
dizziness
blurred vision
confusion
hypotension

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83
Q

Adverse effects of intranasal products

A

nasal irritation
throat irritation
headaches
nosebleed

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84
Q

What is atopic dermatitis

A

kind of eczema (dry skin, rash)
can be from weather or stress

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85
Q

How to treat atopic dermatitis

A

skin hydration
topical steroids
topical calcineurin inhibitors (tacrolimus, pimecrolimus)
monoclonal antibodies (dupilumab, tralokinumab)

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86
Q

What is the end goal of navigating drug allergies

A

de-label patients who are not truly allergic

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87
Q

What can be used to assess reactive risk to drugs

A

Skin testing followed by an optional oral challenge can be used to assess reactive risk to some drugs

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88
Q

A negative ____ result indicates that the risk of life-threatening immediate reactions is extremely low with the administration of penicillin or other β-lactams

A

PST (penicillin skin testing is only available commercial product IgE mediated)

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89
Q

When is drug desensitization used

A

when no other viable treatment options exist, and the patient has a type I hypersensitivity reaction to the medication needed

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90
Q

What is the MOA of desensitization, end goal, and how long does it take

A

process in which mast cells are rendered less responsive
goal to increase IgG antibodies by preventing binding of allergen to mast cell associated IgE
can be rapid or completed over hours (meds) or years (enviornmental allergies)

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91
Q

IgG4 can be produced in response to an allergen but does not do what

A

generate an allergic response

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92
Q

IL-10 is key to production of IgG4 versus what

A

IgE
(IgG4 and IgE are TH2 responses to allergens)

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93
Q

A rapid 12-step desensitization protocol has been described and tested in patients with both IgE and non IgE mediated reactions to what

A

antibiotics
platimum-containing chemotherapeutic agents
taxane chemotherapy agents
monoclonal antibodies

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94
Q

does successful desensitization remove the allergy long term

A

no, successful desensitization does not remove the allergy long-term from the medical record, but only allows for administration of the agent at that time.

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95
Q

During desensitization what happens if a dose is missed

A

therapy has to be started again
(Desensitization lasts only for as long as the patient is continuously exposed to the drug

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96
Q

Self reactive B and T cells can generate reactivity causing what diease

A

autoimmune

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97
Q

Where are self-reactive B and T cells deleted

A

bone marrow
thymus

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98
Q

Why are some self-reactive CD4 T cells not deleted in the thymus and what regulates them

A

they exit as regulatory T cells (Tregs) and then Tregs control anti-self responses in the peripheral immune organs

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99
Q

What are the 2 ways that self-reactive T cells are controlled

A

Tregs
Regulatory T cells by inhibiting effector T cell funciton

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100
Q

How do Tregs regulate

A

IL-10, TGF beta
Secrete adenosine which is inhibitory
Use IL-2
Induce APC inhibitory functions

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101
Q

Some T cells that see antigen w/out co-stimulators are made nonresponsive “anergy,” how can this be reversed

A

high IL-2 or inflammation
(this is why some autoimmune disease appear after viral infection)

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102
Q

Sometimes B or T cells escape tolerance and encounter the antigen in the body. What does this cause

A

tissue injury, inflammation
spread to other antigens
excess cytokines (IFN gamma, TNF)
complement activation

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103
Q

What could stimulate autoimmune disease

A

an infection may induce co-stimulatory molecules on a cell presenting self-antigen and overcome anergy

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104
Q

What is molecular mimicry

A

microbial peptide or proteins may be recognized by self-antigen reactive T or B cell

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105
Q

Autoreactive antibodies can cause tissue cytotoxicity. What kind of hypersensitivity reaction is that

A

Type II

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106
Q

Defects in what can cause autoimmune disease

A

MHC alleles that present peptides and dont delete anti-self T cells
regulatory cytokine defects
Complement C2 and C4 defects

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107
Q

Defects in complement C2 and C4 cause what

A

lupus-like disease
anti-DNA antibody (DNA complexes cause kidney damage)

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108
Q

What does a defect in HLA-DR4 cause

A

associated w/ increased risk of RA and insulin-dependent diabetes

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109
Q

Risk-Associated Genes for Systemic Lupus Erythematosus (SLE) is caused by defects in what

A

phagocytosis
complement and opsonization
too much IFN type 1
regulation of cytokines and cells

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110
Q

Antigens are often what molecules

A

dsDNA
small nuclear rebonucleoproteins
histones
phospholipids

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111
Q

Source of DNA for ANA (anti-nuclear antibodies) cause a defect in clearance of what

A

dying cells
antigen-antibody complexes

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112
Q

What is autoimmune psoriasis

A

inflammatory skin disease
uncontrolled growth of keratinocytes and dermal vascular endothelial cells
T cell, DC, neutrophil, and macrophage infiltration
genetics

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113
Q

How is triggering of auto-antigens caused

A

source unknown
could be minicry or microbiota

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114
Q

Inflammation recruits what 2 molecules

A

neutrophils
macrophages

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115
Q

What disease is caused by uncontrolled inflammatory cytokines leading to joint destruction, what is it mainly caused by

A

Autoimmune
-mainly TNF alpha and IL-1
-genetics

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116
Q

In RA antibodies created by autoantibody production cause the antibodies to go to what

A

citrullinated proteins

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117
Q

What are the cells involved with RA

A

TH1
TH17
B cells
innate cells
synovial cells
osteoclasts

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118
Q

What are the 3 stages of RA

A

induction
inflammation
destruction

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119
Q

Predominant genetic risk factors in MHC for RA

A

HLA-DR4
HLA-DR14
-inflammatory cytokine regulation
-B cell stimulation and antibody production
-T cell stimulation and regulation

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120
Q

What are citrullinated peptides

A

lose postive charge
unfold protein
recognized by B cells as foreign

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121
Q

When does citrullinated peptides happen

A

defective clearance of apoptosis and inflammation
B cells recognize them and create anti-citrullinated (CPP) peptide antibodies (aka ACPA)

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122
Q

Inflammation alters what kind of glycosylation

A

Fc
(Ab galactosylation is reduced w/ proinflammatory activity, galactosylation and sialylation results in anti-inflammation)

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123
Q

What type of Ig molecule is RA

A

mainly IgM but could be any isotype

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124
Q

Defective glycosylation of IgG can lead to Fc regions that are recognized by what

A

anti-Fc antibodies

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125
Q

Where can the generation of self-reactive B cells and T cells occur

A

happen in the lymph nodes or peripheral lymphoid organs (immune complexes can enter the joints or be formed there)

126
Q

Inflammatory innate cytokines lead to infiltration of leukocytes into the ________. What cytokine is important in this process

A

synovium
TNF

127
Q

What cells favor production of inflammatory cytokines and favor complement-activating IgG Anti-CCP antibodies and rheumatoid factor (RF)

A

TH1

128
Q

What 2 cells favor osteoclast development and bone degradation

A

TH1 and TH17

129
Q

What cells activate synoviocytes

A

TH17

130
Q

Defective shutdown of the T cell response is caused by what

A

CTLA4

131
Q

What is pannus

A

abnormal tissue growth, thickening of the synovium

132
Q

T cells activate chondrocytes to degrade ________

A

cartilage

133
Q

T cells promote osteoclasts to degrade ____

A

bone

134
Q

______ from macrophages and other cells continues inflammation in destructive RA

A

TNF alpha

135
Q

Epidemiology of Lupus

A

women (15-45)
more severe in men and children
non-whites

136
Q

Etiology of Lupus

A

genetics
enviornment (smoking, UV, air pollution)
Hormones (estrogen and progesterone)

137
Q

What are the drugs associated with drug induced lupus

A

Methyldopa
Hydralazine
Anti-TNF agents

138
Q

What organs are affected with lupus

A

almost any organ

139
Q

What are the clinical criteria for lupus

A

rash
ulcers
alopecia
arthritis
serositis
renal
neurologic symptoms
hemolyic anemia
leukopenia
thrombocytopenia

140
Q

What are the immunologic criteria for lupus

A

ANA
anti-dsDNA
anti-SM
antiphospholipid
low complement (C3, C4, CH50)
Coombs test

141
Q

What is the criteria for lupus

A

4 criteria w/ at least one from each category; or biopsy proven nephritis w/ ANA or Anti-dsDNA

142
Q

What are the cutaneous signs of lupus

A

Malar rash (butterfly rash)
Discoid rash
Other rashes: maculopapular, urticarial, bullous
Photosensitivity
Oral ulcers
Alopecia

143
Q

What are the systemic signs of lupus

A

Fatigue
Malaise
Fever
Nausea
Anorexia
Weight loss

144
Q

What are the musculoskeletal signs of lupus

A

Arthralgias/myalgias
Nonerosive polyarthritis
Hand deformities
Myopathy
Ischemic necrosis of the bone

145
Q

What are the renal signs of lupus

A

Proteinuria (> 500 mg/24 hours)
Cellular casts
Nephrotic syndrome
Renal failure

146
Q

What are the cardio signs of lupus

A

Pericarditis
Myocarditis
Endocarditis

147
Q

What are the hematologic signs of lupus

A

Anemia of chronic disease
Hemolytic anemia
Leukopenia
Thrombocytopenia
Lupus anticoagulant
Splenomegaly

148
Q

What are the neurologic signs of lupus

A

Cognitive dysfunction
Headaches
Psychosis
Seizures
Depression and anxiety associated with being chronically ill

149
Q

What are the ocular signs of lupus

A

Retinal vasculitis
Conjunctivitis
Sicca syndrome (aka Sjogren Syndrome)

150
Q

Nonpharm therapy for lupus

A

aerobic exercise
photosensitivity
smoking cessation

151
Q

What is the general approach to therapy of lupus

A

NSAIDs (for mild symptoms)
Antimalarials
Corticosteroids

152
Q

If therapy for lupus is ineffective or major organs are involved what kind of drugs are added

A

immunosuppressive or immunomodulatory

153
Q

FDA approved agents for lupus

A

aspirin
prednisone
hydroxycloroquine
belimumab
anifrolumab
voclosporin

154
Q

Off label use of meds for lupus

A

NSAIDs
cyclophosphamide
MMF (mycophenolate mofetil)
azathioprine
methotrexate
rituximab

155
Q

Use of NSAIDs in lupus

A

Used as first-line treatment for arthritis, musculoskeletal complaints, fever, and serositis
Patients with mild disease likely to benefit
Dose used should be adequate to provide anti-inflammatory effects
Non-disease modifying; used for symptom relief

156
Q

What are the problems with NSAIDs in lupus

A

GI
renal
-hepatotoxicity

157
Q

Hydroxychloroquine use for lupus

A

Anti-inflammatory, immunomodulatory, anti-thrombotic
response time is 3-6 months

158
Q

Hydroxychloroquine high quality evidence

A

decrease disease activity and improves survival

159
Q

Hydroxychloroquine moderate quality evidence

A

increase bone mineral density and protects against thrombosis and irreversible organ damage

160
Q

Hydroxychloroquine low quality evidence

A

reduce severe flares, enhance response of other agents in patients w/ nephritis, benefit for lipids, protect against cancer

161
Q

Problems w/ Hydroxychloroquine

A

ocular
-baseline eval and appointments every 6-12 months

162
Q

Corticosteroid use in Lupus

A

Control flares and maintain low disease activity
doses should be kept as low as possible

163
Q

corticosteroid therapy dose for lupus

A

1-2 mg/kg/d
low dose <10
medium 10-20
high >20

164
Q

Cushing disease

A

develop when the adrenal gland produces too much cortisol, or if exogenous steroids are taken in doses higher than the normal amount of endogenous cortisol

165
Q

Addisons disease

A

Addison’s disease can be thought of as the opposite
The adrenal gland is not making enough cortisol
If exogenous steroids are stopped suddenly, it can cause an Addisonian Crisis
Hallmark signs & symptoms: volume depletion hypotension

166
Q

Cyclophosphamide dosing and ADR

A

1-3 mg/kg/d
-carcinogenic, nausea, alopecia, anemia, infection

167
Q

Azathioprine dose and ADR

A

1-3 mg/kg/d
can be “steroid-sparing” therapy
leukopenia, infection, nausea, rash, alopeica, arthralgia

168
Q

Belimumab dose and ADRs

A

for pts with autoantibody postitive, receiving standard therapy
10 mg/kf at 2 wk intervals for first 3 doses and 4 wk intervals after
bradycardia, mylagia, rash, anaphylaxis, nausea, pyrexia, insomnia, pain

169
Q

Rituximab dose and ADRs

A

iv 1,000 mg twice 2 wks apart
methylprenisiolone 100 given 30 min prior
antihistame and APAP adr

170
Q

Hydroxychloroquine dose

A

400 po d or bid

171
Q

Monitoring for NSAIDs/salicylates

A

CBC
platelets
creatinine
AST/ALT
bp

172
Q

Monitoring for glucoccorticoids

A

bp
serum glucose
lipids
bone density
ophthalmic exams

173
Q

Monitoring for hydroxychloroquine

A

fundoscopic and visual field exam
CBC
AST/ALT
albumin

174
Q

Monitoring for belimumab

A

infection
depression
mood change
suicidal thoughts
hypersensitivity

175
Q

Monitoring for cyclophosphamide

A

CBC
platelets
creatine
AST/ALT
urinalysis
urine cytology
PAP

176
Q

Monitoring for mycophenolate mofetil

A

CBC
platelets
creatine
AST/ALT
BMP
chest x ray

177
Q

Monitoring for azathioprine

A

CBC
platelets
creatine
AST/ALT
BMP
albumin
PAP

178
Q

Monitoring for methotrexate

A

CBC
platelets
creatine
AST/ALT
BMP
bilirubin
alkaline phosphate

179
Q

Monitoring for rituximab

A

CBC
platelets
creatine
vital signs
human antichimeric Ab

180
Q

Pregnancy risk for mothers with lupus

A

maternal mortality
cesarean delivery
preterm labor
lupus nephritis flares
gestational diabetes
preeclampsia
Hemolysis with Elevated Liver tests and Low Platelets (HELLP)
thrombotic, infectious, and hematologic complications are increased

181
Q

Fetal risk for mothers with lupus

A

include fetal loss
preterm birth
preterm premature rupture of membranes
intrauterine growth restriction

182
Q

What is RA

A

common, chronic, progressive autoimmune condition that primarily affects the joint and synovium (soft-tissue membrane that lines the joints)

183
Q

epidemiology for RA

A

women
north america and northern europe

184
Q

Joint involvement for RA

A

bilaterally
warmth and swelling w or w/out pain

185
Q

Extra articular involvement for RA

A

rheumatoid nodules
vasculitis
pulmonary
ocular
cardiac
felty’s syndrome
renal

186
Q

ACR/EULAR Rheumatoid Arthritis Classification Criteria

A

patients who have at least 1 joint w/ clinical synovitis and with the synovitis not better explained by another disease
(joint, ACPA +, abnormal CRP/ESR, over 6 wk)

187
Q

Osteoarthritis

A

wear and tear
degradation of cartilage, decreased chondrocytes
risk factors: heredity, obesity, injury, overuse
pain, asymmetrical, stiffness, crepitus, radiology

188
Q

Conventional DMARDs in RA

A

methotrexate
hydroxychloroquine
sulfasalazine
leflunomide

189
Q

Biologic DMARDs in RA

A

anti TNF
-etanercept, infliximab, adalimumab
non TNF
-anakinra, abatacept, rituximab

190
Q

Approach to therapy for RA

A

double or triple DMARD
Tofacitnib in combo w/ DMARD
low dose glucocorticoid for short duraiton if disease stays high

191
Q

Methotrexate dose for RA

A

7.5-15 mg once weekly
combine with folic acid

192
Q

ADRs of methotrexate

A

gi
pulmonary
hepatic
alcohol consumption

193
Q

monitoring in methotrexate

A

AST
ALT
alkaline phosphate
albumin
bilirubin
hepatitis B and C
CBC w/ platelets
Scr

194
Q

Leflunomide dose for RA

A

100 mg po for 3 days
maintenance of 20 mg po daily

195
Q

ADR leflunomide

A

liver toxic
bone marrow toxic
teratogenic
GI
alopecia

196
Q

Sulfasalazine dose for RA

A

500 mg po bid
increase to 1 g po bid

197
Q

ADRs Sulfasalazine

A

nausea, diarrhea, rash, leukopenia, alopecia, discolor of skin

198
Q

Hydroxychloroquine dose for RA

A

200-300 mg bid
after 1-2 months decrease to 200 bid or d

199
Q

Recommended safety monitoring for Hydroxychloroquine, Sulfasalazine, Methotrexate, Leflunomide

A

CBC
liver transaminases
serum creatinine

200
Q

Infliximab (Remicade) ADRs

A

infusion reactions
fever, chills, pruritus, rash
APAP, benadryl, corticosteroids
lupus-like symtoms
mylagia, arthralgia
fatigue
pericarditis, pleuritis

201
Q

Adalimumab (Humira) ADRs

A

tuberculosis
other infection risk

202
Q

Etanercept (Enbrel) ADRs

A

tuberculosis
other infection risk

203
Q

Rituximab (Rituxin) ADRs

A

infection risk
antihistamine, APAP can help with infection risk along with methylprednisolone 30 minutes prior to infusion

204
Q

Tofacitinib (Xeljanz) ADRs

A

infection
malignancy GI perforations
upper respiratory tract infections
headache, diarrhea
nasopharyngitis

205
Q

What do Abs bind to that interfere with binding to host cells and infection

A

free microbes

206
Q

What are neutralizing antibodies

A

antibodies that not only bind but also prevent infection

207
Q

Abs bind to toxins and prevent them from killing what

A

host cells

208
Q

What are the steps of opsonization of phagocytosis

A

opsonization of microbe by IgG
binding of opsonized microbes to phagocyte Fc receptors
Fc receptor signals activate phagocyte
phagocytosis of microbe
killing of ingested microbe

209
Q

Where is IgA antibody produced

A

mucosal tissues
-high levels of TGF beta
-T independent B1 cells also make IgA

210
Q

What moves IgA across the mucosal epithelium

A

a special transport molecule, this prevents colonization by microbes and blocks their entry to the body

211
Q

Why do we need a different flu vaccine each year

A

different strains
change hemagglutinin and neuraminidase molecule each year
microbes can change their surface molecules to evade antibody production

212
Q

What is antigenic drift

A

one or several mutations change a few epitopes

213
Q

What is antigenic shift

A

a change in complement or gene leading to changes in many epitopes

214
Q

What determines Type A or B

A

Type of M proteins of virus envelope and nucleoprotein

215
Q

Type A has 15 antigenic forms in what? Type A has 9 antigenic forms in what?

A

15 - H = hemagglutinin
9 - N = neuraminidase

216
Q

Type A both drift and shift while type B only does what

A

drift only
(annual changes are difts)

217
Q

What are killed or subunit vaccines

A

less effective
cannot replicate host
multiple boosters
produce antibody response (not CD8 mediated)

218
Q

What are live vaccines (natural, mild infection, attenuated)

A

replicate host for short time
long term protection
produce Ab and CD8 cell mediated protection
produce mucosal immunity
cause disease in immunocompromised host

219
Q

What are adjuvants

A

substances that trigger the innate response to enhance adaptive immunity

220
Q

What are freunds adjuvant’s for incomplete and complete

A

incomplete: mainly mineral oil
complete: mineral oil plus killed mycobacteria

221
Q

What are alum adjuvants (mainly used in humans)

A

aluminum compound precipitate allows slow release
mainly TH2

222
Q

What are synthetic cell components adjuvants

A

muramyl dipeptide - stimulate macrophage

223
Q

What are toll-like receptor ligands adjuvant

A

want TH1 stimulating compounds

224
Q

What are bacterial components adjuvant

A

pertussis toxin

225
Q

What is AS01 Adjuvant

A

controls properties of liposome
activated inflammasome
(IFN pathway creating pro-inflammatory cytokines by attracting granulocytes and monocytes)
TLR ligand

226
Q

What is the Lymph Node Response to AS01- Vaccine

A

antigen and AS01 drain from the injection site w/in 30 minutes
house later migratory DCs and monocytes follow

227
Q

What are the different vaccine strategies

A

whole organism
DNA/mRNA
subunit

228
Q

What are the whole organism vaccines

A

-natural
-live attenuated
-killed
-recombinant

229
Q

What are the subunit vaccines

A

-viral or bacterial
-conjugate

230
Q

What are the response expected for “Live” vaccines

A

intracellular and extracellular
CD8 and CD4, B cells (antibody)

231
Q

What are the live vaccines

A

natural/attenuated virus
recombinant virus
DNA/RNA

232
Q

What are the response expected for “dead” vaccines

A

extracellular only
CD4, B cells (antibody)

233
Q

What are the dead vaccines

A

killed bacteria/virus
subunit - protein or carb
toxin
conjugate

234
Q

What vaccines are natural virus vaccines

A

vaccinia
smallpox

235
Q

What vaccines are live attenuated vaccines

A

viral
-sabin oral polio vaccine
-MMR: measles, mumps, rubella
FluMist
Varicella (chicken pox)

236
Q

What vaccines are killed virus vaccines

A

Salk polio vaccine
Influenza vaccine
Hepatitis A

237
Q

What are recombinant viral vectors

A

can generate live vaccine with a nonpathogenic virus
-vaccinia virus (attenuated virus)
-adenovirus (cold virus, SARS cov-2)

238
Q

What is the Johnson & Johnson/ Janssen SARS-Cov-2 vaccine

A

gives antibodies and CD4 and CD8 T cells because people do not have antibodies to Ad26

239
Q

What are DNA/RNA vaccines

A

DNA or stabilized mRNA ingested by host antigen-presenting cells
Intracellulat antigen generation produces cell-mediated response

240
Q

What is the Pfizer-BioN Tech and Moderna SARS-CoV-2 Vaccines

A

stabilized mRNA
cell surface and cytoplasmic spike protein
generate antibodies CD4 and CD8 T cells

241
Q

What are subunit vaccines

A

Portions of a bacteria or virus, usually an isolated protein or carbohydrate
-usually recombinant proteins
-often need adjuvant to get strong response

242
Q

What are the viral subunit vaccines

A

Hepatitis B vaccine
Shingrix
AREXVY
Inflluenza

243
Q

What are the bacterial subunit vaccines

A

Inactivated bacterial toxins
-Cholera, diphtheria, tetanus
-DTaP vaccine for children

244
Q

What are the conjugate vaccines

A

Haemophilus influenzae type B
Streptococcus pneumoniae

245
Q

What is the Pneumococcal conjugate vaccine (PCV)Prevnar

A

Pneumococcal polysaccharide vaccine (PPV) conjugated to inactive diphtheria toxin
Polysaccharides from multiple (13) strains in one vaccine protect against most strains

246
Q

What is direct allorecognition

A

Recipient’s T cells recognize donor’s antigen presenting cells or tissue cells with foreign MHC and foreign peptides
Strong reaction
CD4 and CD8 T cells, B cells can be helped

247
Q

What is indirect allorecognition

A

Recipient APC pick up donor peptides from graft and stimulate recipient T cells in lymph node
Recipient T cells move to graft and stimulated by recipient APC that have been picked up donor peptides
Usually CD4 T cells

248
Q

T cells require what to proliferate making them a good target for inhibiting T cells

A

IL-2

249
Q

How does cyclosporine A, CsA (Sandimmune) immunosuppress Drugs Targeting IL-2

A

CsA through formation of a complex with cyclophilin inhibits the phosphatase activity of CALCINEURIN, which REGULATES NUCLEAR TRANSLOCATION and subsequent activation of NFAT TRANSCRIPTION FACTORS. Also inhibits other signaling pathways in T cell activation.

250
Q

What is cyclosporine A, CsA (Sandimmune)

A

Fungal cyclic, lipophilic polypeptide
Inhibits activation needed for IL-2 production

251
Q

How does FK506 (Tacrolimus) immunosuppress IL-2

A

Fungal macrolide antibiotic
receptor of immunophilin (FK-binding protein, FKBP-12) inhibits calcineurin
Inhibits activation needed for IL-2 production

252
Q

How does Sirolimus (Rapamune) immunosuppress IL-2R

A

The cellular target of sirolimus is FKBP12
binds to and inhibits mTOR
Sirolimus inhibits cell activation
-response to IL-2, cytokines, cell growth, metabolism, cytokine production

253
Q

How does Anti-IL-2Rα (CD25) antibody (Basiliximab) immunosuppress IL-2

A

IL-2Rα expression upregulated on activated T cells
Prevents IL-2 binding/eliminates activated T cells
Does not block binding to intermediate or low affinity IL-2 receptors
Chimeric antibody

254
Q

How does Alemtuzumab Target CD52 on T and B Cells

A

Innate cells express low or no CD52
CD52 expressed on mature T cells, B cells, monocytes, and some dendritic cells
eliminates most mature T cells, fewer B cells and monocytes

255
Q

How is Mycophenolate Mofetil (CellCept) an Immunosuppressant

A

Prodrug form of mycophenolic acid
Inhibitor of de novo purine biosynthesis (GMP)
-T and B cell proliferation, apoptosis of T cells
Inhibits adhesion molecule function
-Inhibits NO biosynthesis

256
Q

____ needed for nucleic acid biosynthesis, glycosylation of cell surface proteins, and cofactors used to make NO

A

GMP
(starts with Ribose-5-Phosphate and turns into nucleic acid synthesis)

257
Q

What drugs are used in induction therapy

A

Basiliximab
Alemtuzumab
High dose steroids

258
Q

What drugs are used in Maintenance immunosupporession

A

Tacrolimus
Sirolimus
Mycophenolate mofoetil

259
Q

Roles of a pharmacist in transplant

A

patient counseling
increase adherence
recognizing and preventing potential drug interactions
be a resource for patients and providers

260
Q

What is the role of CMS in transplant

A

individuals with the appropriate qualifications, training, and experience in the relevant areas of pharmacology

261
Q

What is the role of OPTN (UNOS) in transplant

A

-at least one clinical transplant pharmacist on staff
-provision of pharmacological expertise to transplant r-recipients, families, and members of transplant team
-licensed pharmacist with experience in transplant pharmacotherapy

262
Q

Pre transplant: CMS/OPTN

A

OPTN

263
Q

Pre donation: CMS/OPTN

A

CMS

264
Q

Peri transplant: CMS/OPTN

A

CMS and OPTN

265
Q

Peri donation: CMS/OPTN

A

CMS

266
Q

Post transplant: CMS/OPTN

A

OPTN

267
Q

Post donation: CMS/OPTN

A

none

268
Q

Induction: corticosteroids

A

methylprenisolone

269
Q

Induction: IL-2 antagonist

A

basiliximab

270
Q

Induction: Anti-CD52

A

alemtuzumab

271
Q

Induction: polyclonal t-cell depleting agents

A

ATGAM
thymoglobulin

272
Q

Corticosteroids adverse effects

A

hyperglycemia
fluid retention
HTN
mental changes

273
Q

T cell sparing drug

A

basiliximab (simulect)

274
Q

T cell depleting drug

A

thymoglobulin
atgam
alemtuzumab (campath)

275
Q

Basiliximab (simulect) mechanism and side effects

A

IL-2 receptor antagonist
chills, fever, injection site reaction, anaphylaxis

276
Q

Alemtuzumab (campath) mechanism and side effects

A

Anti-CD52 monoclonal antibody
rigor, fever, anemia, neutropenia

277
Q

anti-lymphocyte antibodies ATGAM, thymoglobulin mechanism and side effects

A

T cell clearance from circulation
inhibition of proliferative response of T-cells
infusion site reaction, flu, cytokine release syndrome, hypersensitivity, bone marrow suppression

278
Q

Maintenance Immunosuppression drugs

A

calcineurin inhibitor (tacrolimus)
antimetabolite (mycophenolate)
corticosteroid (prednisone)
combo of two or more agents w/ different mechanisms

279
Q

Calcineurin inhibitors drugs MOA

A

tacrolimus (FK)
cyclosporine
block production of IL-2 and other cytokines by T-helper cells

280
Q

Dose conversion astagraf XL

A

100% IR dose given daily

281
Q

Dose conversion envarsus XR

A

70-80% IR dose given daily

282
Q

Tacrolimus side effects

A

seizure, headache, tremor
alopecia
QT prolongation
diabetes
nephrotoxicity, hypomagnesemia, hyperkalemia

283
Q

Cyclosporine side effects

A

gingival hyperplasia
HTN, HLD
hephrtoxicity
hirutism

284
Q

Antimetabolite drugs

A

MMF (mycophenolate mofetil)
MPA (mycophenolic acid)
AZA (azathioprine)

285
Q

mycophenolate MOA

A

IMPDH
inhibit de novo guanosine nucleotide synthesis
block DNA synthesis and inhibit leukocyte recruitment to sites of inflammation

285
Q

mycophenolate side effects

A

GI***
leukopenia, thrombocytopenia
teratogenicity

286
Q

MMF IV formulation dose change

A

1:1 conversion

287
Q

MPA IV formulation dose change

A

1000 mg IV MMF = 720 mg oral MPA

288
Q

Azathioprine Mechanism

A

azathiprine
6-MP
6-thioguanine nucleotide
inhibit DNA synthesis

289
Q

Azathioprine side effects

A

alopecia
skin cancer
n/v
leukemia

290
Q

mTOR drugs

A

sirolimus (rapamune)
everolimus (zortress)

291
Q

mTOR side effects

A

mouth ulcers
elevated cholesterol and triglycerides
(lipid panel and urinalysis)*****

292
Q

Belatacept (nulojix) MOA

A

bind to CD80-86 receptors on antigen presenting cells thereby preventing costimulation of the T cell, cytokine production and cell proliferation

293
Q

Belatacept (nulojix) side effects

A

PTLD
increase CNS disease risk
EBV
PML
tuberculosis

294
Q

Tacrolimus/Cyclosporine Interactions

A

Pgp bioavailability
Cyp 3A4
nephrotoxic meds (avoid NSAIDs)

295
Q

mTOR inhibitor interactions

A

Pgp
CYP3A4

296
Q

CNI and mTOR CYP3A4 interactions increase

A

protease inhibitor
azole antifungal
macrolides
verapamil, dilt
amiodarone
letermovir
grapefruit juice

297
Q

CNI and mTOR CYP3A4 interactions decrease

A

CYP3A54 inducers
rifampin
anti-convulsants
st john wart

298
Q

cyclosporine interactions increase

A

digoxin
colchine
statins***
sirolimus

299
Q

Azathioprine interactions

A

xanthine oxidase inhibitor (allopurinol/febuxostat) not recommended****
cause bone marrow suppression

300
Q

Mycophenolate interactions

A

antacids (2 hours after)
PPI (MMF only)
cyclosporine
antimicrobials affecting gut flora
sevelamer
BAS
hormonal contraception

301
Q

Acute cellular rejection severity: banff IA, banff IB, banff IIA/IIB, banff III

A

banff IA least
banff IB
banff IIA/IIB
banff III most

302
Q

Corticosteroids side effects

A

blood glucose
fluid retention
blood pressure
mental changes

303
Q

acute cellular rejection meds to give during banff IA, banff IB, banff IIA/IIB, banff III

A

banff IA (no thymoglobin)
banff IB
banff IIA/IIB
banff III
treatment resistant

all methyprednislone 500 mg IV for 3 doses****
thymglobin

304
Q

Plasmaphersis (PP)/ plasma exchange (PE) MOA and monitoring

A

filtering of plasma to target removal of a specific toxin or substance
hypocalcemia, hypotension, coagulopathy

305
Q

IVIG MOA and side effects

A

autoantibody neutralization, block Fc, cytokine modulation, immune cell/complement regulation, passive immunity
infusion reaction, thromboemolism, hemolysis, fluid overload, aseptic meningitis, acute kidney injury, liver function, hypersensitivity, IgA related anaphylaxis

306
Q

Bortezomib (velcase) MOA and side effects

A

proteasome inhibitor resulting in plasma cell apoptosis
bone marrow suppression, cardio, hepatoxicity, herpes reactivation, neuropathic pain, GI, glycemia, hypotension

307
Q

Rituximab MOA and side effects

A

inhibit CD20 antigen on the surface of B cells
bone marrow suppression, Hep B reactivation, bowel perforation, infusion reaction

308
Q

Eculizimab (soliris) MOA, side effects

A

humanized monoclonal IgG antibody that binds to complement protein C5, preventing cleavage into C5a and C5b
infusion reaction, bone marrow suppression, HTN, REMS

309
Q

Acute antibody mediated rejection order of meds

A

IVIG + PP
IVIG + PP + bortezomib +/- rituximab
IVIF + PP
IVIG + PP + eculizimab

IPCS (9 decks)

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