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FMS > FMS Week 10 > Flashcards

FMS Week 10 Flashcards

Immunology

1
Q

What is graft-vs-leukemia effect?

A

T-cells from donated bone marrow have mild GVHD and kill residual cancer cells

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2
Q

How are PABs and MABs used in organ transplantation?

A

At the beginning, to suppress the immune system for a “clean start” or in crisis

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3
Q

Why does glucocorticoids cause increased WBC counts?

A

impaired neutrophil migration

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4
Q

What genes are important for MHCI matching?

A

HLA-A, HLA-B, HLA-C of chromosome 6

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5
Q

Features, symptoms, findings, and treatment of Leukocyte Adhesion Deficiency:

A

Defective neutrophil/lymphocyte migration

Type 1: defect in CD18 (LFA1) which is part of several integrins

Key findings: delayed umbilical separation, omphalitis (stump infection), recurrent bacterial infections, elevated WBC (especially neutrophilia)

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6
Q

What are TRECs?

A

Loops of DNA that are formed during recombination of TCR; presence indicates that SCID is unlikely in neonatal testing

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7
Q

What are the advantages of virus-like particle vaccines?

A

Very safe, do not need to grow pathogen, highly immunogenic, inside of particle can be modified with adjuvants

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8
Q

What is the primary target of HIV?

A

CD4 Th cells

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9
Q

What is the most common presentation of chronic rejection in the heart?

A

narrowing of coronary arteries

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10
Q

Where are H1 receptors most common?

A

Endothelial cells and sensory nerve endings

also GI/bronchial smooth muscle and brain

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11
Q

what is a xenograft?

A

transplant taken from another species

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12
Q

Why are steroids usually tapered down?

A

Can lead to adrenal insufficiency, steroid use suppresses HPA axis

Adrenal crisis: hypotension/shock, weakness, fever, confusion/coma, abdominal symptoms

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13
Q

What are the disadvantages of DNA vaccines?

A

effectiveness unclear (may be more effective in therapeutic vaccines), safety unclear, likely multiple doses/delivery platforms

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14
Q

What autoimmune diseases are associated with HLA-B27?

A

ankylosing spondylitis, psoriasis, IBD, Reiter syndrome

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15
Q

Who are most at risk of hyperacute rejection?

A

parrous women, people having received blood transfusions or previous transplants

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16
Q

Mechanisms, presentation, key findings and treatment of X-linked Agammaglobulinemia:

A

(Bruton Agammaglobulinemia) Defect in bruton tyrosine kinase gene (BTK); light chains of b-cells not produced

Symptoms begin around 6 months of age after loss of maternal antibodies

Recurrent respiratory bacterial infections (loss of opsonization): recurrent otitis media/sinusitis/pneumonia

GI pathogen infections (loss of IgA): enteroviruses &
giardia

Key findings: absence of mature peripheral B cells and antibodies, underdeveloped germinal centers of lymph nodes

Treatment: IVIG (intravenous immunoglobulin)

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17
Q

What is the most common organ transplant?

A

Kidney (you only need one)

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18
Q

What are the most important eicosanoids for protecting GI mucosa?

A

PGE2 and PGI2

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19
Q

what are the disadvantages of live attenuated vaccines?

A

can revert back to pathogenic form, requires system to grow virus, potential contamination, less safe

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20
Q

What is a syngenetic graft?

A

transplant taken from identical twin

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21
Q

What is the presentation of hyperacute rejection?

A

blood vessels spasm leading to intravascular coagulation and ischemia (white rejection)

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22
Q

What are the 3 main genes of HIV?

A

Gag (nucleocapsid)
Pol (polymerase)
Env (envelope proteins)

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23
Q

COX-1

A

constitutively expressed cyclooxygenase in all cells

important for GI mucosal function

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24
Q

Features, symptoms, findings, and treatment of ataxia telangiectasia:

A

Defective ATM gene on Chromosome 11 (dsDNA repair, nonhomologous end-joining)

Autosomal recessive; hypersensitivity of DNA to ionizing radiation

Symptoms: ataxia, spider veins, recurrent respiratory infections, high risk of cancer

Presents in childhood with progressive symptoms

Key findings: elevated AFP, low IgA

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25
Q

What is NF-KB

A

A key inflammatory transcription factor

Mediates response to TNF-alpha, controls synthesis of COX-2, PLA2, Lipoxygenase

Inactivated by glucocorticoids

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26
Q

Describe Avascular Necrosis:

A

Bone collapse, most commonly at the femoral head (probably from bone ischemia, thinning/demineralization, collapse)

Associated with long term steroid use; also with Lupus, sickle cell, alcoholism, trauma

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27
Q

What are the classes of anti-retroviral drugs?

A

entry inhibitors, RT inhibitors, Integrase inhibitors, protease inhibitors

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28
Q

Side effects of glucocorticoid use?

A

thin skin, easy bruising, Cushingoid appearance, osteporosis, Hyperglycemia, cataracts, myopathy, gastritis

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29
Q

What are the features of a good donor-recipient match?

A

same blood type, similar MHCs, negative cross-matching screen

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30
Q

What are MiHA?

A

minor histocompatibility antigens; polymorphic non-HLA proteins that are expressed by donated tissue that recipient T-cells have not been trained to tolerate

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31
Q

What autoimmune diseases are associated with HLA-A3?

A

hemochromatosis

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32
Q

What are the symptoms of graft vs host?

A

rash; GI:diarrhea, abdominal pain, inflammation; liver: elevated LFTs & Bilirubin

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33
Q

Features, symptoms, findings, testing, and treatment of SCID:

A

Loss of cell-mediated and humoral immunity (primarily T-CELL, secondary B-cell/antibody)

Most commonly X-linked (cytokine receptor gamma-c deficiency; especially IL-7 and IL-2); also caused by adenosine deaminase deficiency (decreased DNA synthesis)

Key findings: loss of T/B-Cell areas (thymic shadow & germinal centers)

Symptoms: Thrush, diaper rash, failure to thrive, other infections

Treatment: death w/o bone marrow transplant

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34
Q

Describe acute rejection:

A

Weeks/months after transplant; caused by infiltrating lymphocytes/monocytes; treatable with immunosuppresion

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35
Q

Features, symptoms, findings, and treatment of Thymic Aplasia:

A

DiGeorge (22q): failure of 3rd/4th pharyngeal pouches, usually de novo

Classic Triad: loss of thymus (T-cells, infections) loss of parathyroids (hypocalcemia, tetany), conotruncal heart defects (also palate defects)

Key findings: no thymus shadow on X-ray, low T-cell, underdeveloped T-cell structures

Treatment: thymic transplatation, hematopoietic cell transplantation

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36
Q

What are the advantages of DNA vaccines?

A

inexpensive, highly stable, quick development time

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37
Q

What type of allorecognition is involved in acute rejection?

A

direct (APCs from transplant activate recipient immune response)

38
Q

What is the difference between direct, indirect, and semi-direct allorecognition?

A

Direct involves donor APCs presenting to recipient T-cells

Indirect involves recipient APCs collecting and presenting donated antigens

Semi-direct involves recipient APCs taking on MHC molecules from donor cell membranes

39
Q

Features, symptoms, findings, and treatment of Chronic mucocutaneous candidiasis:

A

Defect in AIRE genes: Defective Dectin-1 (candida antigen response receptor), also endocrine autoimmunity (T-CELL)

Key findings: recurrent thrush, skin, and esophagus candida infections; hypoparathyroidism, adrenal failure; lack of candidemia (normal neutrophil defense)

40
Q

What are the odds of a sibling being a perfect HLA match?

A

25% (genes are transferred en block from father and mother to offspring)

41
Q

What are the 3 stages of HIV infection?

A

Acute, clinical latency, AIDS

42
Q

What are the disadvantages of subunit vaccines?

A

often poorly immunogenic without adjuvants, polysaccharide antigens elicit T-independent responses

43
Q

What are the advantages of inactivated vaccines?

A

no reversion, multiple antigens present

44
Q

What are the adverse effects of traditional NSAIDs?

A

decreased platelet aggregation, decreased renal blood flow, decreased GI mucosa, intersititial nephritis

45
Q

What are the advantages of live attenuated vaccines?

A

highly immunogenic (broad innate and adaptive response), multiple target antigens, single dose, inexpensive

46
Q

What are the most important HLA genes for solid organ transplants?

A

HLA-A, HLA-B, HLA-DR

47
Q

What are the key enzymes associated with HIV?

A

Reverse transcriptase, Aspartate protease (cleaves proteins), Integrase (integrates DNA into host cell)

48
Q

What is the reason for kidney damage by NSAIDs?

A

Decreased renal vasodilation due to decreased PGE2

49
Q

what are the disadvantages of virus-like particle vaccines?

A

may require multiple doses, limited immune response (only surface antigens), can be expensive

50
Q

What type of allorecognition is associated with chronic rejection?

A

indirect (antigens from transplant are being taken up by recipient APCs)

51
Q

Describe function of glucocorticoids:

A

diffuse across cell membranes (steroids), bind to glucocorticoid receptor, GR-steroid complex moves to nucleus where it alters gene expression

one mechanism is through inactivation of NF-KB

52
Q

Features, symptoms, findings, and treatment of Hyper-IgM syndrome:

A

Class-switching disorder (only IgM): Usually defective CD40L on T-Cells (Type 1) also CD40 (type 3), both x-linked; also from defective AID (activation-induced deaminase, type 2, autosomal)

Symptoms: recurrent bacterial infections (encapsulated; no IgG opsonization)

Treatment: CD40 defects by HC transplant and AID with IVIG & antibiotic prophylaxis

53
Q

what is an allograft?

A

a transplant taken from the same species

54
Q

What are the 3 basic categories of immunosuppressive drugs?

A

Anti-inflammatory, T-cell activation signalling inhibition, cytotoxic (DNA replication interference)

55
Q

Where are H4 receptors most common?

A

eosinophils, neutrophils, CD4 T Cells

56
Q

What is the most common presentation of chronic rejection in kidneys?

A

fibrosis of capillaries and glomeruli

57
Q

What are the regulatory genes of HIV?

A

Tat (transcription activator)

Rev (mRNA transport to cytoplasm)

58
Q

Describe the capsid of HIV

A

multiple copies of p24 protein (non variable, not neutralized by antibodies)

59
Q

What is graft versus host disease?

A

opposite of rejection; donor T-cells attack recipient cells; typically in bone marrow transplants

60
Q

what are the disadvantages of inactivated vaccines?

A

risk of incomplete inactivation, system to grow virus, requires handling of virulent pathogen, expensive, requires boosting

61
Q

Describe the envelope of HIV

A

phospholipid membrane from human cells; contains env protein

Important glycoproteins:
gp120 (attachment to T-cells)
gp41 (fusion and entry)
Both are cleaved from gp160

62
Q

What is an autograft?

A

donor and recipient of transplant are the same person

63
Q

What are the advantages of conjugated vaccines?

A

T-dependent response, most effective in children (strong IgG memory response)

64
Q

What is Cushingoid appearance?

A

truncal obesity, buffalo hump, moon face, thin skin

due to excessive use to glucocorticoids

65
Q

Describe hyperacute rejection:

A

within minutes of transplant; caused by preexisting antibodies in recipient to ABO or HLA antigens; treatable with cross-matching screening

66
Q

What type of primary immunodeficiency is most common?

A

antibody/B cell deficiencies (65%)

67
Q

COX-2

A

Inducible cyclooxygenase

mostly in inflammatory cells

68
Q

What is the most common presentation of chronic rejection in lungs?

A

bronchiolitis obliterans

69
Q

What are the tropes of HIV?

A

Receptors used to enter cells

CCR5 (early after infection, Tmemory/macrophages)

CXCR4 (occurs later, in T-cells)

70
Q

What is the significance of C4d in transplant rejection?

A

C4d is a product of compliment activation, which suggests antibody response to transplanted tissue

71
Q

What are the advantages of subunit vaccines?

A

specific immune responses against molecules involved in virulence/pathogenesis

72
Q

What is the typical mechanism of vaccines against extracellular bacteria?

A

anti body production (neutralization and/or lysis)

73
Q

Features, symptoms, findings, and treatment of chronic granulomatous disease:

A

Loss of function of NADPH Oxidase (cannot generate H202 for respiratory burst)

Cannot breakdown catalase positive bacteria and fungi: leads to recurrent infections of staph aureus, pseudomonas, serratia, nocardia, aspergillus (chronic T-cell stimulation and granulomas)

Testing: negative Nitroblue tetazolium test (stains NADPH oxidase in neutrophils blue)

Treatment: Lifelong antibiotic prophylaxis, early diagnosis, aggressive management (40yo prognosis)

74
Q

What are alloantigens?

A

HLA mismatches

75
Q

Adverse effects of COX-2 Inhibitors

A

Increase risk of MI and stroke; sulfa drugs

76
Q

What are the types of NSAIDs?

A

Traditional: ibuprofen, naproxen, indomethacin, ketorolac, diclofenac

COX2 inh: celecoxib

Irreversible: Aspirin (anti-platelet)

77
Q

Features, symptoms, findings, and treatment of Chediak-Higashi Syndrome:

A

Falure of lysosomes to fuse with phagosomes (microtubule dysfunction from CHS1/LYST gene)

Symptoms: recurrent bacterial infections (staph and strep), severe neuro impairment

Key findings: oculocutaneous albinism, coagulation defects

Treatment: HC transplant, prophylactic antibiotics

Prognosis: 7y life w/o transplant; but usually debilitating neuro deficits by 20yo

78
Q

What are RAG1 and RAG2?

A

Proteins associated in VDJ recombination

79
Q

Benefits of COX-2 inhibitors

A

Less risk of GI ulcers/bleeding

80
Q

Features, symptoms, findings, and treatment of Wiskott-Aldrich Syndrome:

A

X-linked disorder of WAS gene: dysfunctional T-Cell cytoskeleton/immunologic synapse (cannot react to APCs)

Worsens with age, appears at 6mo

Key findings: immune dysfunction, low platelets, eczema, elevated IgE/IgA

Treatment: Bone marrow transplant, prophylactic antibiotics, platelet transfusions

81
Q

Features, symptoms, findings, and treatment of Hyper-IgE syndrome:

A

AKA Job Syndrome, rare, immune symptoms with skin/bone findings

Defective Th17 (consequently no IL-17); loss of attraction of otherwise normal neutrophils; defects in STAT3 signalling pathway

Key findings: elevated IgE, low IFN-gamma

rash/eczema in first few weeks of life, “cold” abscesses of face/scalp

otitis, sinusitis, facial deformities, retained primary teeth

82
Q

Why is it difficult to create antibodies to gp120?

A

it is highly variable and mutates rapidly

83
Q

Features, symptoms, findings, and treatment of CVID:

A

common variable immunodeficiency: defective B-cell maturation, loss of plasma cells and antibodies; varying genetic causes

Findings: normal B cell count; absence of IgG (sometimes IgA/IgM)

Symptoms similar to X-linked Agammaglobulinemia: respiratory bacterial infections, enteroviruses/giardiasis
DIFFERENCES: Not X-linked, later onset (20-45yo)

Common along w/ RA, pernicious anemia, lymphoma

Treatment: IVIG to replace low Ig

84
Q

Features, symptoms, findings, and treatment of Selective IgA Deficiency:

A

very common (1 in 600); defective IgA B-Cells; mostly asymptomatic

Symptoms: recurrent otitis media/sinusitus/PNA, giardiasis

Blood transfusions may lead to anaphylaxis due to anti-IgA antibodies; Commonly along with lupus and rheumatoid arthritis; may have false positive beta-HCG pregnancy test

Key findings: serum IgA <7mg/dl; normal IgG/IgM

Treatment: prophylactic antibiotics, IVIG (compensates w/ extra IgG/IgM)

85
Q

Describe Acute Interstitial Nephritis:

A

unknown type of hypersensitivity reaction; usually triggered by drugs (NSAIDs)

not a disease of the nephron itself; classic finding is urine eosinophils

days to weeks after exposure: fever, rash, oliguria, +BUN/Cr

86
Q

Why do MHCII molecules also need to match in transplants?

A

some donor APCs may be carried in tissue; also vascular endothelial cells may express MHCII

87
Q

What is the typical mechanism of vaccines against intracellular bacteria?

A

cytotoxic lymphocytes; though there are not really effective vaccines of this type that are approved

88
Q

Describe chronic rejection:

A

months/years after transplant; occurs in most transplants; inflammation and fibrosis, especially of vessels; involves cell-mediated and humoral immunity

89
Q

What genes are important for MHCII matching?

A

HLA-DM, HLA-DO, HLA-DP, HLA-DQ, HLA-DR of chromosome 6

90
Q

What are the primary markers for HIV infection?

A

Low CD4 T-cell count, viral load (amt of HIV RNA)

FMS (10 decks)

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