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POD 3 > Immuno/Path > Flashcards

Immuno/Path Flashcards

1
Q

What is central tolerance?

A

elimination of self reactive T and B cells during development in thymus or bone marrow

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2
Q

What is peripheral tolerance?

A

after the lymphocyte has left bone marrow or thymus and encounters self antigen

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3
Q

What are the mechanisms of T cell central tolerance?

A

if they react they will undergo apoptosis (negative selection) or become Treg cells

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4
Q

What is the significance of AIRE?

A

transcription factor that regulates expression of peripheral proteins in the thymus-allows T cells to see peripheral antigens within the thymus

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5
Q

What are the possible outcomes of central tolerance for a T cell?

A

positive selection-recognize MHC
negative selection-too much recognition
apoptosis-no recognition

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6
Q

What happens when AIRE is defective?

A

APS-T cells that interact escape into circulation

presents with musculocutaneous candidiasis, hypoparathyroidism, and adrenal insufficiency

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7
Q

What are Treg cells?

A

most are CD4 T cells

inhibit activation of CD4 and CD8 T cells by producing IL-10 and CTLA-4

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8
Q

What do Treg cells express?

A

CD25

transcription factor Foxp3

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9
Q

What results from mutations to Foxp3?

A

IPEX (immune dysregulation, polyendocrinopathy, enteropathy, X linked syndrome)

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10
Q

What can happen in peripheral T cell tolerance?

A

anergy-functional unresponsiveness
deletion through apoptosis
suppression by Treg cells

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11
Q

How does anergy happen?

A

lack of costimulation (problem in second signal of B7 and CD28)
inhibitory receptors-CTLA4

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12
Q

Where is CTLA4 expressed?

A

always on Treg cells

on cytotoxic T cells after activation-off switch

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13
Q

How can a self reactive T cell undergo apoptosis?

A

poor costimulation can cause leak of mitochondrial proteins-cytochrome c to activate caspases
Fas/FasL interaction

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14
Q

How do Treg cells inhibit activation of T cells?

A

Tregs grow in response to IL2

Tregs produce IL-10, TGF beta, express CTLA-4, and consume IL2 so it is unavailable for effector T cells

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15
Q

What can happen in B cell central tolerance?

A

edit receptors-efficient

apoptosis

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16
Q

How does B cell receptor editing occur?

A

reactivate RAG genes
resume light chain recombination, same heavy chain is expressed
strictly a B cell phenomenon

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17
Q

How do B cells become anergic in the peripheral tissues?

A

no interaction between CD40 and CD40L

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18
Q

How do we tolerate commensal microbes?

A

physical barrier
Treg cells
CD103+ DC promote Treg cells fr sampling
IL-10 secretion

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19
Q

How does a mother tolerate the fetus?

A

placental barrier
Treg cells
exclusion of inflammatory cells from uterus
poor antigen presentation in uterus

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20
Q

What HLA is associated with MS?

A

DR2

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21
Q

What HLA is associated with lupus?

A

DR2/DR3

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22
Q

What HLA is associated with T1DM?

A

DR3/DR4

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23
Q

What HLA is associated with rheumatoid arthritis?

A

DR4

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24
Q

What HLA is associated with anklosing spondylitis?

A

B27 (Reiters also-can’t pee, can’t see, can’t climb a tree)

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25
Q

What is NOD2 associated with?

A

Chrons

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26
Q

What are defects in C2, C4 associated with?

A

SLE

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27
Q

What are defects in FAS associated with?

A

ALPS

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28
Q

What are the environmental factors that can trigger autoimmune syndromes?

A 
infection
drugs
stress
chemicals
diet
hormones
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29
Q

How does infection promote autoimmunity?

A

molecular mimicry
release of sequestered antigens
bystander activation

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30
Q

What is molecular mimicry?

A

microbes may carry elements similar in structure to self antigens
activated B and T cells cross react to self

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31
Q

What is bystander activation?

A

infection causes nonspecific activation of surrounding lymphocytes (self reactive T cells that have not gone through peripheral tolerance are activated)

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32
Q

How does ankylosing spondylitis present?

A

young man with sacroiliac inflammation

axial spine-fusion of vertebra

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33
Q

How does SLE present?

A

usually in women
autoantibodies and immune complexes (type III hypersensitivity) deposit in tissues
ANA-antinuclear antibody (sensitive not specific)

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34
Q

How does rheumatoid arthritis present?

A

rheumatoid factor positive

DIPS are not swollen but PIPs and MCPs are

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35
Q

How does myasthenia gravis present?

A

autoantibody to acetylcholine receptor

eyelid drooping that gets worse with exertion

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36
Q

How does Graves disease present?

A

prominent eyes, hyperthyroidism

elevated T4, low TSH

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37
Q

How does scleroderma present?

A

heartburn and tight skin on face and hands
T cell stimulated collagen synthesis
CREST syndrome (calcinosis, raynauds, esophageal dysfunction, sclerodactylyl, telangiectasia)

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38
Q

How does MS present?

A

urinary incontinence, sensory loss, blurry vision
MRI with multiple lesions
demyelination of brain and spinal cord

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39
Q

How does T1DM present?

A

increased thirst and urination

autoreactive CD8 cells destroy pancreatic Beta cells resulting in inability to produce insulin

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40
Q

What are the possible therapies for autoimmune diseases?

A

steroid-prednisone
antimetabolities-methotrexate
monoclonal antibodies-adalimumab (TNF inhibiting antibody)

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41
Q

What is the difference between fibrosis and repair/regneration?

A

Fibrosis occurs after persistent tissue damage

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42
Q

What occurs in labile tissue?

A

constant active self renewal

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43
Q

What occurs in stable tissue?

A

low level of renewal but has capacity to replace

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44
Q

What occurs in permanent tissue?

A

no capacity to replace cells

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45
Q

What role do macrophages play in repair?

A

secrete VEGF, FGF-2, PDGF for angiogenesis
chemotaxis for fibroblasts through PDGF, TGF beta, TNF, IL-1, KGF-7
deposition and remodeling of ECM through collagenase, MMPs, OPN, TNF, PDGF, TGF beta

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46
Q

What is the function of epidermal growth factor?

A

mitogenic for keratinocytes and fibroblasts; stimulates formation of granulation tissue

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47
Q

What is the function of TGF alpha?

A

stimulates proliferation of hepatocytes and other epithelial cells

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48
Q

What is the function of VEGF?

A

increases vascular permeability; stimulates endothelial cell proliferation

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49
Q

What is the function of PDGF?

A

chemotactic for neutrophils, macrophages, fibroblasts and smooth muscle cells; activates proliferation of fibroblasts, endothelial cells

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50
Q

What is the function of TGF-beta?

A

chemotactic for leukocytes and fibroblasts; suppresses acute inflammation

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51
Q

What are the steps in scar formation?

A

inflammation
formulation of granulation tissue
ECM deposition and remodeling

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52
Q

How does collagen differ in granulation tissue and a mature scar?

A

Type III in granulation

Type I in mature scar

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53
Q

How does first intention differ from second intention?

A

Minimal damage in first intention (edges of skin together vs gaping hole in second intention)

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54
Q

When does collagen deposition start?

A

3-5 days

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55
Q

What is responsible for wound contraction?

A

myofibroblasts

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56
Q

What systemic factors influence wound healing?

A

vitamin C deficiency
poor perfusion-atherosclerosis
glucocorticoids (inhibit TGF-beta)–>can be prescribed to decrease collagen deposition

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57
Q

What is the most important growth factor in fibrosis?

A

TGF beta

fibroblast migration and proliferation, angiogenesis and increased collagen and fibronectin production

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58
Q

What local factors can influence wound healing?

A

infections
mechanical factors-increased local pressure
size, location and type of wound

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59
Q

What causes a keloid?

A

excessive collagen formation

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60
Q

What is dehiscence?

A

inadequate granulation tissue

leads to ruptures of wound, common after abdominal surgery

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61
Q

What happens in excessive contraction?

A

contraction of skin

common in palms, soles, thorax in burn patients

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62
Q

What happens in exuberant granulation?

A

more granulation tissue than needed

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63
Q

What are desmoids?

A

fibrous overgrowths of dermal and subcutaenous connective tissue

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64
Q

What are immunodeficiencies impair maturation?

A

SCID
X linked agammaglobulinemia
DiGeorge

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65
Q

What immunodefieicines impair activation and function?

A

X linked hyper IgM syndrome
common varaible immunodeficiency
bare lymphocyte syndrome

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66
Q

What immunodeficiencies are defects in innate immunity?

A

chronic granulomatous disease
leukocyte adhesion deficiency
complement deficiencies
Chediak-Higashi syndrome

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67
Q

What are lymphocyte abnormalities associated with other diseases?

A

Wiskott Aldrich syndrome

Ataxia-telangiectawsia

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68
Q

Histologically where will T and B cell deficiencies be seen?

A

T-paracortex

B-germinal centers

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69
Q

What are characteristics of all immunodeficiencies?

A

increased susceptibility to newly acquired infections
reactivation of latent infections
increased incidence of cancers

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70
Q

What is the definition of SCID?

A

Decreased T cell

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71
Q

What is the mechanism of defect in X linked SCID?

A

mutation in gamma common chain; no IL-7 for maturation of T cells; no IL-15 for NK cells

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72
Q

What are some causes of autosomal recessive SCID?

A

IL-7R signaling, defect in RAG genes, missing JAK3

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73
Q

What does the common gamma chain act as a signal receptor for?

A

IL2, 4, 7, 9, 11, 15, 21

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74
Q

What is the most common AR SCID?

A

ADA deficiency

leads to accumulation of dATP

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75
Q

What accumulates in PNP deficiency?

A

dGTP

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76
Q

How can SCID be treated?

A

stem cell transplant

gene therapy-most successful against ADA deficiency

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77
Q

What virus is now used as a viral vector for gene therapy? What are the dangers?

A

lentivirus

fear of inserting near oncogene and activating cancer

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78
Q

What happens in Bruton’s agammaglobulinemia?

A 
mutation in Bruton tyrosine kinase
inability of preB cells to develop into mature B cells
usually diagnosed at 6 months
absence of Ig classes
treated with gamma globulin injections
no CD19 B cells in peripheral blood
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79
Q

What causes DiGeorge syndrome?

A

dysmorphogenesis of third and fourth pharyngeal pouches
aplasia of thymus and parathyroid, facial and heart abnormalities
present with neonatal tetany
22q11 deletion
associated with schizophrenia and bipolar disorder

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80
Q

What happens in X-linked hyper IgM syndrome?

A

mutation in CD40L
absence of CD40L on T cells-no class switching
high levels of IgM

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81
Q

What happens in IgA deficiency?

A

most common
no IgA secreting plasma cells-low IgA
can be asymptomatic or have recurrent infections and diarrhea

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82
Q

What happens in common variable immunodeficiency?

A

failure of B cells to mature into plasma cells
low serum IgA and IgG, normal IgM
respiratory and GI infections with pyogenic bacteria

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83
Q

What is the triad associated with Wiskott Aldrich syndrome?

A

thromocytopenia
eczema
recurrent bacterial infections

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84
Q

How does ataxia telangiectasia present?

A

neuro-staggering
abnormal dilation of vaculature
defects for T and B cells
low IgA and IgG

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85
Q

What happens in leukocyte adhesion deficiency?

A

defect in adhesion (selectin ligand or beta chain of integrin)
poor recruitment
infections without pus formation

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86
Q

What happens in Chediak-Higashi syndrome?

A

giant cytoplasmic granules (defect in cytoskeleton so lysosomes and phagosomes cannot fuse)
cannot kill bacteria

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87
Q

What happens in chronic granulomatous disease?

A

defective production of ROI

test with nitroblue tetrazolium test

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88
Q

What does the nitroblue tetrazolium test demonstrate?

A

respiratory burst

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89
Q

What do complement deficiencies present with?

A

C1/C3-infections with encapsulated organisms
C2/C4-SLE
C5-C9-Neisseria

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90
Q

What is hereditary angioedema?

A

deficiency in C1 inhibitor

results in excessive C4 and C2 activation and localized edema

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91
Q

What is paroxysmal nocturnal hemoglobulinemia?

A

Deficiency in DAF
host cells not protected from complement activation
intravascular hemolysis-occurs at night as pH drops

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92
Q

What can cause secondary immunodeficiencies besides AIDS?

A

protein calorie malnutrition
cancer-bone marrow tumors
measles-infect lymphocytes
herpes can secrete proteins like IL10
Trypanosoma cruzi-reduced IL2 receptors
absence of spleen-increased susceptibility to encapsulated bacteria
drugs-immunosupprssive, anti-inflammatory

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93
Q

What is physiologic hypogammaglobulinema?

A

neonate protection from IgG because development of Th1 and CD8 T cell responses are delayed

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94
Q

What is transient hypogammaglobulinemia of infancy?

A

prolongation of physiologic hypogammaglobulinemia
may take 2-4 years
2 standard deviations below IgG

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95
Q

What is immunosenescence?

A

impaired ability to respond to new antigens in the elderly
unsustained memory response
results-increased infection, cancer, autoimmune diseases

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96
Q

What are the possible laboratory tests for diagnosing immunodeficiencies?

A 
lymphocyte counts and morphology
flow cytometry
serum protein electrophoresis
Ig levels
antibody response to immunization
DTH skin testing
T cell proliferation assays
cytokine assays
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97
Q

What are some examples of tumor antigens?

A

products of mutated oncogenes or tumor suppressor genes
mutated forms of cellular genes
normal proteins over expressed in tumor cells
products of oncogenic viruses
oncofetal antigens-fetal development proteins
glycolipids and glycoproteins

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98
Q

What are examples of mutated forms of cellular genes?

A

BCR/ABL
RAS
mutated p53

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99
Q

What are examples of cellular proteins that undergo abnormal expression?

A

proteins expressed in gametes and trophoblasts

Her2/Neu

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100
Q

What are examples of antigens expressed from oncogenic viruses?

A

E6 and E7 of HPV in cervical carcinomas

EBNA-1 of EBV

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101
Q

What are examples of oncofetal antigens?

A

CEA-carcinoembryonic antigen

alpha-fetoprotein

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102
Q

What are some altered glycoproteins?

A

gangliosides expressed in high levels in neuroblastomas, melanomas, and sarcomas

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103
Q

What are some tissue specific antigens?

A

PSA-prostate specific antigen

CD20 on B cell lymphomas

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104
Q

What is the innate anti-tumor immunity?

A

NK cells-kill tumors that decrease expression of MHC I if activated by NK cells
Macrophages-M1 kill tumor cells (IFN gamma necessary)
M2 may contribute to tumor progression

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105
Q

What is the adaptive anti-tumor immunity?

A

CD8 cells-surveillance, require cross priming by DC

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106
Q

What is cross priming?

A

Activation of naive CD8 T cells by APCs that acquire antigens from another cell

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107
Q

How do tumors evade the immune system?

A

intrinsic mechanisms
extrinsic mechanisms
myeloid-derived suppressor cells

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108
Q

What are the extrinsic methods to suppress the immune system?

A

TAM=promote tumor growth
M2 impair T cell activation
Treg may suppress T cell responses to tumors

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109
Q

What are the intrinsic methods to evade the immune system?

A

tumors lose expression of immunogenic antigens
inaccessible to immune system-expressing glycocalyx to mask immune epitopes
TGF beta and PDL1 inhibit immune system
FasL to stimulate WBC apoptosis

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110
Q

How do myeloid derived cells suppress the immune system?

A

Immature cells leave bone marrow and induce development of Tregs, skew T helper towards Th2, and dampen chronic inflammation

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111
Q

What are the different types of tumor vaccines?

A 
killed tumor vaccine
purified tumor antigens
dendritic cell vaccines
cytokine and costimulator enhanced vaccines
DNA vaccines
viral vectors
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112
Q

How are dendritic cell vaccines made?

A

pulsed with Ag and then transfect DC with Ag genes

113
Q

What is adoptive cellular therapy?

A

reinfuse IL-2 activated host PBMCs

114
Q

What are lymphokine-activated killer cells?

A

NK cells that are expanded and gain enhanced tumor killing activity by in vitro culture with IL2

115
Q

What are tumor infiltrating lymphocytes?

A

lymphocytes expanded in vitro culture with tumor cells and IL-2 enriched

116
Q

What are some monoclonal antibodies?

A

Anti-Her2Neu

Anti-CD20

117
Q

How does the immune system contribute to tumor growth?

A

chronic inflammation-risk factor for tumors

TAMs (tumor associated macrophages) can produce VEGF, MMP, and growth factors to help tumors grow

118
Q

Why do we vaccinate?

A

protection
stronger and faster immune response through memory immune response
decrease the number of susceptible hosts-herd immunity

119
Q

What are properties of a good candidate for vaccine development?

A

organism causes significant illness
only one serotype
antibody blocks infection or systemic spread
organism does not have strong oncogenic potential
vaccine is heat stable

120
Q

What is passive immunization?

A

transferred to naive individual from another individual already immune to an infection

  • transplacental transfer of maternal IgG to fetus
  • IgA in breast milk
121
Q

What are the advantages of passive immunization?

A

prevent disease after known exposure
ameliorate symptoms of ongoing disease
protect immunodeficient individuals
block bacterial toxins and prevent the disease they cause

122
Q

What are the different types of globulin?

A

human serum-pooled plasma
hyperimmune globulins-high titers of antibody
available for HBIG, CMVIG, VZIG, RSVIG

123
Q

What is active immunization?

A

immune response is stimulated due to challenge (natural immunization or vaccines)

124
Q

How does the immune system respond to protein antigens?

A

B cells making immunoglobulin

longer lived in germinal centers

125
Q

How does the immune system respond to polysaccharide antigens?

A

do not activate germinal cells

Ig for just a little bit

126
Q

What is the advantage of T dependent response?

A

isotype switching
high affinity antibodies
long-lived plasma cells

127
Q

How do the primary and secondary responses differ?

A

primary-IgM>IgG; lower affinity

secondary-IgG; higher affinity

128
Q

What are the different types of vaccines?

A

inactivated-toxoid, subunit, conjugate vaccines
live, attenuated vaccines
DNA vaccines
recombinant vector vaccines

129
Q

What are the advantages of inactivated vaccines?

A

antibody response without risk of infection

induce immunity but may cause recurrent infection or have oncogenic potential

130
Q

How are inactivated vaccines produced?

A

heat or chemical inactivation of bacteria, bacterial toxins, or viruses
can be produced by purification or synthesis of the components or subunits of the infectious agents

131
Q

What are adjuvants?

A

administered with inactivated vaccines
boost immunogenicity by enhancing uptake by or stimulating dendritic cells and macrophages
some stimulate TLR to activate APC

132
Q

What is the most common adjuvant?

A

alum

others-MF59, MPL, emulsions, liposomes, molecular cages for antigen, polymeric surfactants

133
Q

What are the major types of inactivated bacterial vaccines?

A

toxoid
inactivated (killed) bacteria
capsule or protein subunits of bacteria-includes polysaccharide capsule subunits

134
Q

What are examples of inactivated viral vaccines?

A

polio, Hep A, influenza, rabies

Salk poli-prepared with formaldehyde inactivation

135
Q

What do subunit vaccines consist of?

A

bacterial or viral components
surface structures of bacteria and viral attachment proteins
T cell antigens may also be included

136
Q

How are toxoid vaccines made?

A

inactivated with formalin
cannot cause disease and no possibility of reversion to virulence or spread
stable

137
Q

What are conjugate vaccines?

A

used when polysaccharide of capsule is linked to a protein carrier (typically diptheria, neisseria)

138
Q

What are the disadvantages of inactivated vaccines?

A 
immunity is not lifelong
immunity may only be humoral
no local IgA response
booster required
larger dose necessary
139
Q

How are live vaccines prepared?

A

avirulent or attenuated
especially useful for protection against infections caused by enveloped viruses that require T-cell immune responses for resolution of the infection

140
Q

How are live viral vaccines prepared?

A

attenuated by growth in embryonated eggs at nonphysiologic temperatures and away from selective pressures of the host immune response
mutants that grow poorly at human temp, cannot escape immune control, may replicate at benign site but not disseminate

141
Q

What are the disadvantages of live vaccines?

A

may be dangerous to immunosuppressed people or pregnant women
may revert to virulent viral form
viability of vaccine must be maintained

142
Q

What are DNA and recombinant vector vaccines?

A

DNA attempted vaccine against West Nile Virus
recombinant-similar to DNA but use attenuated virus to introduce microbial DNA to cells in body (vector refers to virus or bacterium as carrier)

143
Q

Why are steroids slow acting?

A

act on transcription factors

144
Q

When is cortisol highest? When is aldosterone highest?

A

cortisol-morning

aldo-constant throughout the day

145
Q

What are the properties of glucocorticoids?

A

metabolism of fats and glucose
negative calcium balance
hypertension and polycythemia
bone resportion

146
Q

What makes glucocorticoids anti-inflammatory?

A

increase lipocortin levels which inhibits phospholipase A2

reduces NF kappa B levels (reduces proteolytic enzymes, reduces vasoactive cytokines, reduces COX2 and NOS)

147
Q

What modulates mineralocorticoid release and what does it do?

A

release modulated by renin angiotensin system

regulate sodium, water and potassium (promotes K excretion, enhances sodium and water reabsorption)

148
Q

What is the MOA of aminoglutethimide?

A 
inhibits CYP11A1 (reduces all corticosteroids)
need fludrocortisones to replace mineralocorticoids
149
Q

What are the drug interactions for aminoglutethimide?

A

increased metabolism of warfarin, theophyline, and digitoxin

150
Q

What is the MOA of ketoconazole?

A

inhibit CYP17 (inhibit glucocorticoid and androgen) and CYP11A1 (all steroidogenesis)

151
Q

What are the drug interactions for ketoconazole?

A

increase P-gp substrates

cardiac arrhythmias from ergot derivatives, cisapride, or triazolam

152
Q

What is the MOA of metyrapone?

A

selective inhibitor of CYP11B1 (mores selective for cortisol)

153
Q

What are the side effects of metyrapone?

A

hirsuitism from increased androgens

154
Q

What is the MOA for etomidate?

A

anesthetic drug that blocks 11-beta-hydroxylation

155
Q

What is the MOA of mitotane?

A

inhibits CYP11B1 and CYP11A1

pharmacological ablation

156
Q

What is the MOA of mifepristone?

A

block glucocorticoid receptors from being released from chaperone proteins
also abortion pill

157
Q

What are the side effects of mifepristone?

A

vaginal bleeding, abdominal pain

158
Q

What is the common defect in CAH? What is the clinical manifestation?

A

CYP21 most common

pseudohermaphroditism in females and precocious puberty in males

159
Q

Why are glucocorticoids given every other day when in remission?

A

reduces suppression of HPA axis

160
Q

What can occur from treatment of asthma with glucocorticoids?

A

oral candidiasis

161
Q

What is fludrocotrisone used for?

A

aldo replacement only

162
Q

When are betamethasone and dexamethasone used?

A

immature lungs

most potent

163
Q

How are the drugs transported?

A

bound to protein (CBG and albumin)

164
Q

What is the difference in the distribution of HSD?

A

HSD1 activates in gluco tissues

HSD2 inactivates in mineralocorticoid tissues

165
Q

How are corticoids eliminated?

A

conjugation with glucoronides (first pass varies)

renal excretion

166
Q

What are the withdrawal effects?

A

looks like Addisons

HPA suppression

167
Q

What are the side effects?

A

looks like Cushings

dose and time dependent

168
Q

What are the contraindications?

A

children
immunosuppression
mask viral infections-cannot give live vaccines
be careful with CHF, HTN, osteoprosis, diabetic, psychotic

169
Q

What are the drug interactions?

A 
estrogen increases (induces CYP3A4)
barbituates, carbamazepine, phenytoin promote corticosteroid metabolism
170
Q

What are the products of dihomo-gamma-linolenic acid?

A

PGE1, PGI1, TXA1

171
Q

What is the main pathway for arachidonic acid byproducts?

A

liver from linoleic acid
main-phospholipase A2
secondary-PLC

172
Q

What are the products of eicosapentaneoic acid?

A

PGE3, PGI3, TXA3

173
Q

What are the steps of the cyclo-oxygenase pathway?

A

hydration

oxidation of 15-hydroxyl to ketone by 15-OH dehydrogenase

174
Q

Where is COX1 found?

A

endothelial cells, stomach, kidney

constitutive form

175
Q

Where is COX2 found?

A

elevated by inflammation

constitutive in brain and kidney

176
Q

What are the actions of prostacyclin PGI2?

A 
vasodilator
inhibit platelet aggregation
bronchodilator
inhibits gastric acid secretion
increase GFR, stimulates renin
relax uterine muscles
induces pain
177
Q

What are the actions of prostaglandin PGE2?

A 
vasodilator
inhibit platelet aggregation (high levels)
increase GFR, stimulates renin
relax uterine at high 
induces pain
induces fever
178
Q

What are the actions of thromboxane TXA2?

A 
synthesized by platelets, lung, and kidney
vasoconstrictor
platelet aggregation
constrict airway
intrarenal constriction 
uterine contraction
179
Q

What are the actions of PGFalpha2?

A

vasoconstrictor
contracts airway
contracts uterine muscle
eyes-decrease intraocular pressure

180
Q

What is misoprostol?

A

PGE1 analog
given for NSAID therapy to reduce ulcers
can induce labor in pregnant women

181
Q

What is latnoprost?

A

PGF2 alpha analog

opthalmic-decrease intraocular pressure

182
Q

What is alprostadil?

A

PGE1 analog

temporarily maintains PDA in newborns

183
Q

What are 5HPETE and LTB4?

A

chemotactic agents for PMN leukocytes, eosinophils, monocytes

184
Q

What is zafirlukast?

A

LTD4 receptor antagonist
inhibits bronchoconstriction
prophylaxis
more side effects (inhibits 3A4, food decreases bioavailability, older kids)

185
Q

What is montelukast?

A

LTD4 receptor antagonist
inhibits bronchoconstriction
side effect-headache
can be used for anyone over 1

186
Q

What is Zileuton?

A

inhibitor of 5-lipoxygenase (decrease all LT synthesis)
must monitor liver
drug interactions-theophylline, warfarin, propanolol
contraindicated in liver disease, ergot alkaloids

187
Q

What are the side effects of NSAIDs?

A

increased GI ulcer
increased bleeding risk
fluid retention
cross sensitivity with aspirin

188
Q

What is the MOA of aspirin?

A

irreversible inhibitor of cyclo-oxygenase

acetylates ser530 in cox1 and ser516 in cox2

189
Q

What are the uses of aspirin?

A

analgesic local and brain but does not interact with opioid receptor
therapeutic limits for arthritis

190
Q

What is salicyclism?

A

intoxication characterized by tinnitis

191
Q

What are the propionic acid derivatives? What are the drug interactions?

A

ibuprofen and naproxen (better anti-inflammatory)

ACE inhibitors and antacids

192
Q

What is the heteroarylacetic acid prep? What is it used for?

A

ketorolac

used for cataract surgery-good for those with morphine habits

193
Q

What is the phenylacetic acid prep? What is it used for?

A

diclofenac
opthalmic post cataract surgery
not during pregnancy

194
Q

What is the indole derivative?

A

indomethacin
can treat gouty arthritis
and close PDA

195
Q

What are the side effects and contraindications for indomethacin?

A

displaces bilirubin from albumin and decreases urine output

do not give during hyperbilirubinemia and renal failure

196
Q

What are the coxibs?

A

COX2 inhibitors
low GI pain
for RA and ankylosing spondylitis
monitor fluco

197
Q

What is true of NSAIDs and pregnancy?

A

inhibit uterine motility-PGE, PGF
induce bleeding in last trimester
premature closing of ductus arteriosus

198
Q

What NSAID has the highest risk of acute renal failure?

A

indomethacin

199
Q

What are the net effects of NSAIDs on the kidney?

A

hyperkalemia

fluid retention

200
Q

What are the advantages of acetaminophen?

A 
for people sensitive to aspiring
weak anti-inflammatory
less GI upset
drug interaction with alcohol
hepatic toxicity and renal toxicity
201
Q

What is the MOA for gold salts?

A

inhibition of function and maturation of T cells
decreased levels of rheumatoid factor
inhibits phagocytosis in macrophages

202
Q

What are the side effects?

A

chrysiasis (gray skin) and mucosal lesion
anemia and thrombocytopenia
anaphylactic reaction to injection

203
Q

What are the contraindications for gold salts?

A

renal disease
lupus
eczema

204
Q

What is the mechanism of type I reaction?

A

release of mediators from IgE sensitized mast cells

205
Q

What happens in sensitization?

A

antigen activation of Th2 cells and stimulation of IgE class switching in B cells (IL4 mediated), IgE to mast cells

206
Q

What causes the immediate hypersensitivity?

A

vasoactive amines

207
Q

What causes the late phase reaction?

A

Il-5 from mast cells and Th2 recruit and activate eosinophils
eosinophils release additional mediators

208
Q

What are the clinical examples of type I hypersensitivity?

A

hay fever
food allergies
bronchial asthma
anaphylaxis-food or bee sting

209
Q

What is a common sign of possible progression to allergies?

A

atopic dermatitis

210
Q

How can type I hypersensitivity be tested?

A

skin tests-observe wheal and flare
allergen specific IgE levels-plate with allergen and labeled anti-E added (for young and dermatographia)
total IgE levels-immunodeficient

211
Q

What is immunotherapy?

A

inject subcutaneously

rise in serum IgG leading to suppression of IgE (changing relative ratio between the two)

212
Q

What are the characteristics of type II hypersensitivity?

A

involves IgM or IgG antibodies

involves antigen on surface of cell in circulation or in tissue

213
Q

What is antibody dependent cellular cytotoxicity?

A

IgG antibodies serve as bridge to link target cells to effector cells

214
Q

What are examples of type II hypersensitivity?

A 
transfusion reaction
hemolytic disease of newborn
Goodpastures-antiBM
autoimmune hemolytic anemia-antiRBC
pemphigus vulgaris-antiEcadherin
rheumatic fever-antiM
pernicious anemia-antiIF (decreased B12 absorption
myasthenia-antiAchR
graves-antiTSHR
215
Q

What is hemolytic disease of newborns?

A

second pregnancy of RhD- woman and RhD+ baby

treat with rhogam

216
Q

How is Goodpasture’s disease treated?

A

plasmapheresis and immunosuppressant drugs

217
Q

What is the staining pattern for type II hypersensitivity?

A

linear

218
Q

What are the tests for type II hypersensitivity?

A

direct-antibodies on surface of RBC (hemolytic disease of newborn, autoimmune hemolytic anemia, transfusion reaction)
indirect-measure anti RBC abs in serum

219
Q

What are the characteristics for type III hypersensitivity?

A

immune complexes deposit in tissue
IgM or IgG that react with soluble antigens
complement activated-leading to tissue damage
microthrombus

220
Q

Where are the favored sites for type III hypersensitivity?

A 
kidneys
joints
small vessels
heart
skin
mostly small IC in ab excess
221
Q

What are the examples of type III hypersensitivity?

A 
serum sickness
rheumatoid arthritis (IgM on Fc to IgG)
systemic lupus
post-streptococcal GN
polyarteritis nodosum-hepB antigen
drug interactions-penicillins
222
Q

What is the staining characteristic of type III hypersensitivity?

A

lumpy bump

223
Q

What are the pathologic lesions for type III hypersensitivity?

A

vessels-vasculitis
kidney-glomerulonephritis
joints-arthritis

224
Q

What is the arthus reaction?

A

skin test for type III
antigen intradermally in presence of preformed ab
skin reaction-peaks at 4-10 hours, necrosis around

225
Q

How can type III be diagnosed?

A

measure complement
decrease with active deposition of immune complexes
direct-tissue biopsy

226
Q

What are the characteristics of type IV hypersensitivity?

A

cell mediated-initiated by antigen specific Th1 cells
delay in time for reaction to develop
recruitment of macrophages and extensive damage
cytokines-IFN gamma and TNF alpha

227
Q

What are teh clinical examples of type IV sensitivity?

A

contact dermatitis
haptens-nickel or chromate
tuberculosis
multiple sclerosis and T1DM-autoimmune

228
Q

What is the DTH skin test?

A

assess immunologic memory of specific antigens
injected intradermally-peaks at 48-72 hrs
positive when sensitized
PPD, candida, tetanus diptheria

229
Q

What is the patch test?

A

assess reactivity to contact antigens

sensitizing on skin and covered with dressing

230
Q

What are the advantages to the TB from blood test?

A

interferon gamma release assays

single visit and prior BCG does not cause false positive

231
Q

What is granulomatous hypersensitivity?

A 
form of DTH
epithelioid cells and multineuclated giant cells
IL-12/APC drive Th1
TGF beta to increase fibrosis
central zone of necorsis
232
Q

What is anergy?

A

inability to react to a battery of common skin tests

associated with AIDS, RA, Hodgkin lymphoma, CLL, sarcoidosis, influenza, mumps, measles, TB, leprosy

233
Q

What is allograft?

A

different member of same species

234
Q

What is autograft?

A

one part of body to another

235
Q

What is isograft?

A

genetically identical individuals

236
Q

What is xenograft?

A

member of different species

237
Q

What genes contribute to rejection?

A

MHC and HLA

238
Q

What is the direct graft response?

A

T cells recognize allogenic MHC molecules on graft

displayed by donor dendritic cells in graft, processed and presented by host dendritic cells to activate T cells

239
Q

What is the indirect graft response?

A

graft cells are ingested by recipient dendritic cells, donor allogens are presented by self MHC molecules on recipient APCs

240
Q

What happens in hyperacute rejection?

A 
happens within minutes
antibody-antigen reaction
target Ags on endothelium
thrombotic occlusion of capillaries
fibrinoid occlusion of arterial walls, kidney cortex get infarction with necrosis
241
Q

What happens in acute rejection?

A

humoral and cellular mechanisms

242
Q

What happens in humoral acute rejection?

A

mediated by antidonor antibodies, intima thickening if proliferative, necrosis and polyps if necrotizing vasculitis

243
Q

What happens in cellular acute rejection?

A

extensive mononuclear infiltrate

CD8 cells invade and damage vascular endothelium

244
Q

What happens in chronic rejection?

A

slow rise in creatinine
intimal fibosis and interstitial fibrosis
glomerular-duplication of basement membrane

245
Q

Where and when does GVHD happen?

A

bone marrow transplant

target organs are skin, liver, and intestine

246
Q

What happens in GVHD?

A

effector donor T cells enter tissues and cause destruction after being activate in 2nd lymph organs

247
Q

How can rejection be minimized?

A

ABO blood typing

HLA typing

248
Q

What are the limitations to immunopharmacology therapy?

A

increased risk of infection

increased risk of lymphomas and related cancer

249
Q

What is the MOA of cylcosporine?

A

calcineurin inhibitor by binding to cyclophilin (NFAT remains phosphorylated, decrease in IL2 synthesis)

250
Q

What are the toxicities of cyclosporine?

A

nephrotoxicity
hypertension
hepatotoxicity

251
Q

What is the MOA for tacrolimus?

A

calcineurin inhibitor by binding to FK506

more potent than cyclosporine

252
Q

What are the toxicities of tacrolimus?

A

nephrotoxicity

neurotoxicity

253
Q

What is the MOA for sirolimus and everolimus?

A

binds FKBP and inhibits mTOR

blocks T cell at G1 to S transition

254
Q

What are the toxicities associated with sirolimus and everolimus?

A

hyperlipidemia

delayed wound healing

255
Q

What is the MOA for azathioprine?

A

converted to 6MP and blocks de novo synthesis of purines (selective for lymphocytes due to lack of salvage pathway)

256
Q

What are the toxicities and drug interactions for azathioprine?

A

bone marrow suppression

allopurinol inhibits xanthine oxidase

257
Q

What is the MOA for mycophenolate mofetil?

A

inhibitor of IMPDH (inosine monophosphate dehydrogenase)

inhibits guanine synthesis

258
Q

What are the toxicities and drug interactions for mycophenolate mofetil?

A

GI effects

antacids decrease absorption

259
Q

What is antithymocyte globulin?

A

ATGAM-polyclonal antibody to T lymphocytes

260
Q

What are the toxicities for ATGAM?

A

serum sickness, nephritis, chills, fever and rashes

261
Q

What is basiliximab?

A

chimeric anti CD25 antibody that binds alpha subunit of IL2 on T cells
given prior to surgery to prevent rejection

262
Q

What is alemtuzumab?

A

humanized anti-CD52 antibody

induces cytolysis upon binding lymphocytes, monocytes, macrophages and NK cells

263
Q

What is tocilizumab?

A

humanized anti-IL6

264
Q

What is the MOA for efalizumab?

A

binds CDIIa on LFA1 (withdrawn)

265
Q

What is rituximab?

A

chimeric anti CD20 antibody against B lymphocytes to cause apoptosis

266
Q

What is etanercept?

A

decoy TNF alpha receptor

267
Q

What are the anti TNF drugs?

A

infliximab
certolizumab
adalimumab
golimumab

268
Q

What are abatacept and belatecept?

A

CTLA4Ig

binds CD80 and CD86 (B7) on APC to prevent binding to CD28 (inhibits costim)

269
Q

What are immunostimulants?

A

treat immunodeficiency through cellular or humoral immunity

270
Q

What can natural adjuvant be used for?

A

immune globulin to prevent measles, hep A, and tetanus

271
Q

What is the BCG vaccine?

A

mycobacterium bovis with muramyl dipeptide to stimulate NK and T cells
treat bladder cancer
can cause hypersensitivity and shock

272
Q

What is levamisole?

A

antihelminic agent that inhibits T suppressor cells

273
Q

What is isoprinosine?

A

NK cell cytotoxicity increases and activity of T cells

274
Q

What is thalidomide?

A

for ENL, multiple myeloma
reduces TNF levels in ENL
contraindicated in women who are pregnant

275
Q

What is IFN alpha used for?

A

macrophages, T lymph, NK cell activation
treat cancers, hep B and hep C
can cuase flu like symptoms

276
Q

What is IL-2 used for?

A

activates cellular immunity
indicated for metastatic melanoma, renal carcinoma, aids
can lead to hypotension and cardiovascular toxicity

277
Q

What is GCSF?

A

increases number of granulocytes and monocytes

used to reduce neutropenia

278
Q

What is the MOA of muromonab?

A

internalization of T cell receptor

adverse-cytokine release syndrome, CNS toxicity, anaphylactic reactions

POD 3 (4 decks)

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