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Immuno > FA > Flashcards

FA Flashcards

0
Q

What are the primary opsonins?

Which are involved in anaphylaxis? Which helps neutrophil chemotaxis? Which causes cytolysis by MAC?

A

Primary opsonins: C3b (also clears immune complexes) and IgG
Anaphylaxis: C3a, C4a, C5a
Chemotaxis: C5a
MAC cytolysis: C5b-9

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1
Q

What are the activators for the various complement cascades?

A

Classic-IgG or IgM
Alternative-microbe surface mcs
Lectin- mannose on microbe surface

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2
Q

What are the complement inhibitors? What disorders occur when they are absent?

A

C1 esterase inhibitor and DAF

  • hereditary angioedema (avoid ACEi)
  • complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria
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3
Q

What cytokines do macrophages release?

A 
IL1: Causes fever and acute inflammation
IL6: production of acute phase proteins
IL8: chemotaxis for neutrophils
IL12: Th1 differentiation
TNF-alpha: septic shock, cachexia in malignancy
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4
Q

What do IL2 and 3 do? What secretes them?

A

All T cells, 2: stimulates growth of T cells and Nk cells

3: stimulates bone marrow, like GM-CSF

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5
Q

What cytokines do helper T cells release?

A 
IL 4: class switching to IgE and IgG, Th2 differentiation
IL 5: class switching to IgA, B cell differentiation
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6
Q

What secretes interferon-gamma? What does it do?

A

Th1; Stimulates macrophages after stimulation from macrophages’ IL-12

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7
Q

Which cytokines are anti-inflammatory?

A

TGF-beta and IL-10

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9
Q

What defect do patients with CGD have? How do they present?

A

NADPH oxidase, cant make own reactive oxygen species to kill bacteria.
Granulomas, severe bacterial and fungal infections
-Present with catalase positive organisms: Listeria, Aspergillus, Candida, E coli, S aureus, and Serratia

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9
Q

What are the lab findings in CGD?

A

Abnormal dihydrohodamine test and negative nitroblue tetrazolium dye reduction

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10
Q

How does C3 and C5-9 deficiencies present?

A

C3: severe recurrent pyogenic sinus and respiratory tract infections, inc susceptibility to type III reactions
C5-9: terminal complement def, inc susceptibility to Neisseria bacteremia

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11
Q

What surface proteins do T cells have?

A

All: TCR, CD28, CD3-signal transduction
Helper: CD4, CD40L
Cytotoxic: CD8
Regulatory: CD25, CD4

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12
Q

What proteins do b cells uniquely have?

A

CD19-21

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13
Q

How do superantigens like Strep pyogenes and Staph aureus cause cytokine release?

A

Cross link the beta region of TCR to MHC II

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14
Q

How do endotoxins cause problems?

A

Gram neg bacteria: Stimulate macrophages directly by binding to TLR4/CD14

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15
Q

Which diseases are prevented with passive immunity after exposure?

A

Tetanus, botulism, HBV, Varicella, Rabies

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16
Q

What is releases immediately in type 1 hypersensitivity? Where does it work? What is released later on?

A

Histamine- postcapillary venules

Arachidonic acid metabolites: leukotrienes

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17
Q

What are the three mechanisms of type II hypersensitivity?

A

Opsonization, complement and Fc receptor inflammation, antibody mediated cell destruction leading to MAC

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18
Q

How is type 3 hypersensitivity started?

A

Antigen-antibody complexes activate complement, causing neutrophils to release lysosomal enzymes

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19
Q

What causes serum sickness? How does it present?

A

Drugs

-Fever, urticaria, arthralgia, proteinuria, lymphadenopathy 5-10 days after exposure

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20
Q

Which disorders are associated with type 1?

A

Atopic and anaphylaxis

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21
Q

Type 2 disorders?

A

Acute hemolytic transfusion, GBS, ITP

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22
Q

Type 3 disorders?

A

Arthus reaction, vasculitis: SLE, Polyarteritis nodosa, PSGN

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23
Q

Type 4 disorders?

A

Contact dermatitis, GVHD, MS, PPD

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24
Q

Which population is at risk for anaphylaxis reaction?

A

IgA deficiency

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25
Q

What type of reactionis febrile nonhemolytic transfusion reaction? How does it present?

A

Type II; fever, headaches, chills, flushing

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27
Q

How does acute hemolytic transfusion reaction present?

A

Fever, hypotension, tachycardia, flank pain, either hemoglobinuria (intravascular hemolysis) or jaundice (extravascular)

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28
Q

Which immunodeficiency presents with recurrent bacterial and enteroviral, Giardia infections after 6 months, typically a boy?

A

X-linked, Bruton agammamglobinemia, BTK defect, no B cell maturation.

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29
Q

What are the findings of Bruton agammaglobinemia?

A

Absent B cells in peripheral blood, low Ig, absent/scant LN

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30
Q

What are the findings of selective IgA deficiency? Are the majority sick?

A

Low IgA, normal IgG, M. Most asymptomatic. Can see airway and GI infections

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31
Q

How does common variable immunodeficiency present?

A

Acquired in 20s-30s, defect in B cell differentiation, low plasma cells and immunoglobulins, inc risk of autoimmune disease

32
Q

How does DiGeorge present immunologically?

A

Dysmorphic facies, Tetany (hypoCa2+), recurrent viral/fungal infections, Cardiac: ToF, TA

33
Q

What is the deletion in DiGeorge? What embryologically fails to develop?

A

22q11, 3rd and 4th pharyngeal pouch -> absent thymus and parathyroids

34
Q

How does IL12 receptor deficiency present? What’s the cause?

A

Disseminated mycobacterial and fungal infections; dec Th1 response causing low IFN gamma

35
Q

What disease presents with coarse facies, cold staph abscesses, retained primary teeth, high IgE and derm problems (eczema)

A

Autosomal dominant hyper IgE syndrome

36
Q

What is the defect in hyper IgE ? Labs?

A

Def of Th17 due to STAT3 mutation; high IgE and low IFN-gamma

37
Q

What does an absent cutaneous response to Candida represent?

A

T cell dysfunction

38
Q

What immunodeficiency presents with FTT, chronic diarrhea, mucocutaneous Candida, recurrent viral, fungal, protozoal infections? How is it treated?

A

Severe combined immunodeficieny; bone marrow transplant

39
Q

What are the possible defects in SCID? What are the findings?

A

IL-2R gamma chain or adenosine deaminase deficiency; absence of thymic shadow and germinal shadows

40
Q

What immunodeficiency presents with cerebellar defects, spider angioma, and IgA def

A

Ataxia-telangiectasia

41
Q

What is the defect and findings of Ataxia-telangiectasia?

A

ATM (failure to repair double strand breaks); high AFP, low IgA, G, and E

42
Q

How does Hyper IgM syndrome present?

A

severe pyogenic infections early in life, opportunistic infections (Pneumocystis, Crypto, CMV)

43
Q

What is the defect in Hyper IgM? Findings?

A

CD40L, class switching defect. Low IgG, IgA, IgE

44
Q

What disease presents with thrombocytopenic purpura, eczema, recurrent infections? Defect?

A

Wiskott-Aldrich; mutation in WAS gene (T cell cant reorganize actin cytoskeleton)

45
Q

Which immunodeficiency presents with absent pus formation, delayed umbilical cord separation, recurrent bacterial skin infections

A

Leukocyte adhesion def integrin (CD18), impaired migration

46
Q

What disease presents with recurrent staph and strep pyogenic infections, oculocutaneous albinism, peripheral neuropathy? Defect?

A

Chediak-Higashi syndrome

47
Q

What is the defect in Chediak-Higashi syndrome? Findings?

A

Lysosomal trafficking regulator gene (LYST), microtubule dysfunction; Giant granules in granulocytes; pancytopenia

48
Q

What type of transplant rejection presents with widespread thrombosis of graft vessels? How is it treated?

A

Hyperacute (within minutes); Caused by pre-existing antibodies (type II)

49
Q

What type presents with graft vessel vasculitis with dense interstitial lymphocytic infiltrate? Treatment?

A

Acute rejection (weeks to months), CD8 T cells against donor MHCs and antibodies. Treat with immunosuppresion

50
Q

What type presents with proliferation of vascular smooth muscle proliferation and parenchymal fibrosis, arteriosclerosis

A

Chronic (months to years): Recipient T cells present donor peptides to CD4 T cells

51
Q

How does Graft v Host present?

A

Maculopapular rash, jaundice, diarrhea, HSM

52
Q

What is the cause of GVHD?

A

Immunocompetent T cells against host. Can be helpful in leukemia

53
Q

Which drugs are calcineurin inhibitors? What do they bind to?

A

Cyclosporine (cyclophilin) and Tacrolimus (FKBP)

54
Q

What is the effect of cyclosporine and tacrolimus? What’s toxicity?

A

Block T cell activation and preventing IL 2 transcription; Nephrotoxicity

55
Q

What does Sirolimus do? Toxicity?

A

mTOR inhibitor, binds FKBP; prevents IL2 response from T cell activation
-not nephrotoxic, anemia, thrombocytopenia, leukopenia

56
Q

What does daclizumab, basiliximab block?

A

IL2R

57
Q

What is azathioprine?

A

Antimetabolite precursor of 6 mercaptopurine, blocks nucleotide syntheis

58
Q

Toxicity? What med increases risk

A

Leukopenia, anemia, thrombocytopenia, increased by allopurinol since 6MP is degraded by xanthine oxidase

59
Q

What do glucocorticoids inhibit?

A

NF kappa B, suppresses B and T cell function

60
Q

What disease does an AIRE mutation cause? How does it present?

A

Autoimmune polyendocrine syndrome. hypoparathyroidism, adrenal failure, chronic candida

61
Q

What causes Autoimmune lymphoproliferative syndrome?

A

Defect in Fas (most common), FASL, or caspases leading to loss of peripheral tolerance. PResents as cytopenias, HSM, and LAD

62
Q

Regulatory T cells have which 3 receptors?

A

CD4, CD25 (IL-2R) and FoxP3

63
Q

What diseases are associated with CD25 polymorphism?

A

MS and T1DM

64
Q

What disease does FOXP3 mutation cause?

A

Immune dysregulation, polyendocrinopathy (thyroiditis or DM), enteropathy (diarrhea), X-linked (IPEX syndrome) in infants

65
Q

How is Libman-Sacks endocarditis differentiated from other forms?

A

Vegitations are present on both sides

66
Q

What type of hypersensitivity is SLE in general? which one is involved in anemia, thrombocytopenia, or leukopenia?

A

Type III (immune complexes); type II (direct antibodies)

67
Q

What labs are falsely abnormal in the presence of antiphospholipids?

A

VDRL and RPR (must test FTAB to determine its not syphillis) and elevated PTT

68
Q

Which drugs cause drug-induced lupus?

A

Isoniazid, hydralyzine, procainamide

69
Q

What type of hypersensitivity reaction is Sjogren’s?

A

Lymphocyte mediated, type IV

70
Q

What risk factors are associated with the presence of Anti SSA and SSB?

A

Extraglandular manifestations, AntiSSA crossing the placenta causing neonatal lupus and heart block

71
Q

Sjoren’s increases the risk of which malignancy? Presentation?

A

B cell (marginal) lymphoma, unilateral parotid enlargement

72
Q

The following markers correlate with which autoimmune diseases: anti-Histone, Anti-centromere, anti-topoisomerase I, anti U1 RNP

A

anti histone= drug induced lupus, anti-centromere=CREST, antitopoisomerase/Scl 70: diffuse Scleroderma, anti U1 RNP= mixed connective tissue disease

73
Q

What is the marker for hematopoetic stem cells?

A

CD34

74
Q

Which mineral is essential for collagen scar formation?

A

Zinc

75
Q

What does FGF do?

A

Its important for angiogenesis and skeletal development

76
Q

Which deficiencies cause delayed wound healing and why?

A

Zinc co-factor for collagenase, vit C (co-factor for hydroxylation of proline and lysine), copper: co-factor for lysyl oxidase which cross links lysine and hydroxylysine

Immuno (3 decks)

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