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Rapid Rev USMLE 1 > immunology > Flashcards

immunology Flashcards

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USMLE® Step 1 flashcards
1
Q

Interleukin-1 (IL-1)

A

Function: Causes fever, acute inflammation. Activates endothelium to express adhesion molecules. Induces chemokine secretion to recruit WBCs. Also called osteoclast-activating factor.
Mnemonic: Hot T-bone stEAK (IL-1: fever [hot])

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2
Q

What is the function of Interleukin-1 (IL-1)?

A

Causes fever, acute inflammation. Activates endothelium to express adhesion molecules. Induces chemokine secretion to recruit WBCs. Also called osteoclast-activating factor.

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3
Q

What is the mnemonic for Interleukin-1 (IL-1)?

A

Hot T-bone stEAK (IL-1: fever [hot])

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4
Q

What is the function of Interleukin-2 (IL-2)?

A

Stimulates growth of helper, cytotoxic, and regulatory T cells, and NK cells.

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5
Q

What is the mnemonic for Interleukin-2 (IL-2)?

A

T-bone stEAK (IL-2: stimulates T cells)

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6
Q

What is the function of Interleukin-3 (IL-3)?

A

Supports growth and differentiation of bone marrow stem cells. Functions like GM-CSF.

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7
Q

What is the mnemonic for Interleukin-3 (IL-3)?

A

T-bone stEAK (IL-3: stimulates bone marrow)

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8
Q

What is the function of Interleukin-4 (IL-4)?

A

Induces differentiation of T cells into Th2 cells. Promotes growth of B cells. Enhances class switching to IgE and IgG.

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9
Q

What is the mnemonic for Interleukin-4 (IL-4)?

A

Ain’t too proud 2 BEG 4 help (IL-4)

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10
Q

What is the function of Interleukin-5 (IL-5)?

A

Promotes growth and differentiation of B cells. Enhances class switching to IgA. Stimulates growth and differentiation of eosinophils.

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11
Q

What is the mnemonic for Interleukin-5 (IL-5)?

A

I have 5 BAEs

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12
Q

What is the function of Interleukin-6 (IL-6)?

A

Causes fever and stimulates production of acute-phase proteins.

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13
Q

What is the mnemonic for Interleukin-6 (IL-6)?

A

T-bone stEAK (IL-6: stimulates aKute-phase protein production)

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14
Q

What is the function of Tumor Necrosis Factor-α (TNF-α)?

A

Activates endothelium. Causes WBC recruitment, vascular leak. Causes cachexia in malignancy. Maintains granulomas in TB. Can mediate fever and sepsis.

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15
Q

What is the function of Interleukin-8 (IL-8)?

A

Major chemotactic factor for neutrophils.

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16
Q

What is the mnemonic for Interleukin-8 (IL-8)?

A

Clean up on aisle 8

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17
Q

What is the function of Interleukin-12 (IL-12)?

A

Induces differentiation of T cells into Th1 cells. Activates NK cells. Facilitates granuloma formation in TB.

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18
Q

What is the function of Interferon-γ (IFN-γ)?

A

Secreted by NK cells and T cells in response to antigen or IL-12 from macrophages. Stimulates macrophages to kill phagocytosed pathogens. Inhibits differentiation of Th2 cells. Induces IgG isotype switching in B cells. Increases MHC expression and antigen presentation by all cells. Activates macrophages to induce granuloma formation.

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19
Q

What is the function of Interleukin-10 (IL-10)?

A

Attenuates inflammatory response. Decreases expression of MHC class II and Th1 cytokines. Inhibits activated macrophages and dendritic cells. Also secreted by regulatory T cells.

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20
Q

What is the function of Interleukin-13 (IL-13)?

A

Promotes IgE production by B cells. Induces alternative macrophage activation.

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21
Q

What is the mnemonic for Interleukin-13 (IL-13)?

A

Interleukin thirtEEn promotes IgE

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22
Q

What is the defect in X-linked (Bruton) Agammaglobulinemia?

A

Defect in BTK, a tyrosine kinase gene → no B-cell maturation; X-linked recessive (↑ in Boys)

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23
Q

What is the presentation of X-linked (Bruton) Agammaglobulinemia?

A

Recurrent bacterial and enteroviral infections after 6 months (↓ maternal IgG)

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24
Q

What are the findings in X-linked (Bruton) Agammaglobulinemia?

A

Absent B cells in peripheral blood, ↓ Ig of all classes, absent/scanty lymph nodes and tonsils (1° follicles and germinal centers absent)

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25
Q

What is the defect in Selective IgA Deficiency?

A

Unknown

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26
Q

What is the presentation of Selective IgA Deficiency?

A

Majority Asymptomatic; can see airway and GI infections, autoimmune disease, atopy, anaphylaxis to IgA in blood products

27
Q

What are the findings in Selective IgA Deficiency?”

A

↓ IgA with normal IgG, IgM levels; ↑ susceptibility to giardiasis

28
Q

What is the defect in Common Variable Immunodeficiency?

A

Defect in B-cell differentiation. Cause unknown in most cases

29
Q

What is the presentation of Common Variable Immunodeficiency?

A

May present in childhood but usually diagnosed after puberty. ↑ risk of autoimmune disease, bronchiectasis, lymphoma, sinopulmonary infections

30
Q

What are the findings in Common Variable Immunodeficiency?

A

↓ plasma cells, ↓ immunoglobulins

31
Q

What is the defect in Thymic Aplasia (DiGeorge Syndrome)?

A

22q11 microdeletion; failure to develop 3rd and 4th pharyngeal pouches → absent thymus and parathyroids

32
Q

What is the presentation of Thymic Aplasia (DiGeorge Syndrome)?

A

CATCH-22: Cardiac defects, Abnormal facies, Thymic hypoplasia, Cleft palate, Hypocalcemia

33
Q

What are the findings in Thymic Aplasia (DiGeorge Syndrome)?

A

↓ T cells, ↓ PTH, ↓ Ca2+, thymic shadow absent on CXR

34
Q

What is the defect in IL-12 Receptor Deficiency?

A

↓ Th1 response; autosomal recessive

35
Q

What is the presentation of IL-12 Receptor Deficiency?

A

Disseminated mycobacterial and fungal infections; may present after administration of BCG vaccine

36
Q

What are the findings in IL-12 Receptor Deficiency?”

A

↓ IFN-γ

37
Q

What is the defect in Hyper-IgE Syndrome (Job Syndrome)?

A

Deficiency of Th17 cells due to STAT3 mutation → impaired recruitment of neutrophils to sites of infection

38
Q

What is the presentation of Hyper-IgE Syndrome (Job Syndrome)?

A

Cold staphylococcal abscesses, retained baby teeth, coarse facies, eczema, ↑ IgE, bone fractures from minor trauma

39
Q

What are the findings in Hyper-IgE Syndrome (Job Syndrome)?”

A

↑ IgE, ↑ eosinophils

40
Q

What is the defect in Chronic Mucocutaneous Candidiasis?

A

T-cell dysfunction; impaired cell-mediated immunity against Candida sp.

41
Q

What is the presentation of Chronic Mucocutaneous Candidiasis?

A

Persistent noninvasive Candida albicans infections of skin and mucous membranes

42
Q

What are the findings in Chronic Mucocutaneous Candidiasis?”

A

Absent in vitro T-cell proliferation in response to Candida antigens, absent cutaneous reaction to Candida antigens

43
Q

What is the defect in Severe Combined Immunodeficiency (SCID)?

A

Several types including defective IL-2R gamma chain (most common, X-linked recessive); adenosine deaminase deficiency (autosomal recessive); RAG mutation → VDJ recombination defect

44
Q

What is the presentation of Severe Combined Immunodeficiency (SCID)?

A

Failure to thrive, chronic diarrhea, thrush, recurrent infections

45
Q

What are the findings in Severe Combined Immunodeficiency (SCID)?”

A

↓ T-cell receptor excision circles (TRECs), absence of thymic shadow, germinal centers, and T cells

46
Q

What is the defect in Ataxia-Telangiectasia?

A

Defects in ATM gene → failure to detect DNA damage → failure to halt cell cycle progression → mutations accumulate; autosomal recessive

47
Q

What is the presentation of Ataxia-Telangiectasia?

A

Triad: cerebellar defects (Ataxia), spider Angiomas (telangiectasia), IgA deficiency

48
Q

What are the findings in Ataxia-Telangiectasia?”

A

↑ AFP, ↓ IgA, IgG, and IgE, lymphopenia, cerebellar atrophy

49
Q

What is the defect in Hyper-IgM Syndrome?

A

Most commonly due to defective CD40L on Th cells → class switching defect; X-linked recessive

50
Q

What is the presentation of Hyper-IgM Syndrome?

A

Severe pyogenic infections early in life; opportunistic infection with Pneumocystis, Cryptosporidium, CMV

51
Q

What are the findings in Hyper-IgM Syndrome?”

A

Normal or ↑ IgM, ↓ IgG, IgA, IgE, failure to make germinal centers

52
Q

What is the defect in Wiskott-Aldrich Syndrome?

A

Mutation in WAS gene; leukocytes and platelets unable to reorganize actin cytoskeleton → defective antigen presentation; X-linked recessive

53
Q

What is the presentation of Wiskott-Aldrich Syndrome?

A

WATER: Wiskott-Aldrich: Thrombocytopenia, Eczema, Recurrent infections; ↑ risk of autoimmune disease and malignancy

54
Q

What are the findings in Wiskott-Aldrich Syndrome?”

A

↓ to normal IgG, IgM; ↑ IgE, IgA; fewer and smaller platelets

55
Q

What is the defect in Leukocyte Adhesion Deficiency (Type 1)?

A

Autosomal recessive defect in LFA-1 integrin (CD18) protein on phagocytes leads to impaired migration and chemotaxis by C5a, IL-8, and leukotriene B4

56
Q

What is the presentation of Leukocyte Adhesion Deficiency (Type 1)?

A

Late separation (>30 days) of umbilical cord, absent pus, dysfunctional neutrophils → recurrent skin and mucosal bacterial infections

57
Q

What are the findings in Leukocyte Adhesion Deficiency (Type 1)?”

A

↑ neutrophils in blood, absence of neutrophils at infection sites

58
Q

What is the defect in Chédiak-Higashi Syndrome?

A

Defect in lysosomal trafficking regulator gene (LYST); microtubule dysfunction in phagosome-lysosome fusion; autosomal recessive

59
Q

What is the presentation of Chédiak-Higashi Syndrome?

A

PLAIN: Progressive neurodegeneration, Lymphohistiocytosis, Albinism (partial), recurrent pyogenic Infections, peripheral Neuropathy

60
Q

What are the findings in Chédiak-Higashi Syndrome?”

A

Giant granules in granulocytes and platelets, pancytopenia, mild coagulation defects

61
Q

What is the defect in Chronic Granulomatous Disease?

A

Defect of NADPH oxidase → ↓ reactive oxygen species (e.g., superoxide) and ↓ respiratory burst in neutrophils; X-linked form most common

62
Q

What is the presentation of Chronic Granulomatous Disease?

A

↑ susceptibility to catalase-positive organisms, recurrent infections, and granulomas

63
Q

What are the findings in Chronic Granulomatous Disease?”

A

Abnormal dihydrorhodamine (flow cytometry) test (↓ green fluorescence), nitroblue tetrazolium dye reduction test fails to turn blue

Rapid Rev USMLE 1 (12 decks)

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