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USMLE Step 1 > Immunology 1 > Flashcards

Immunology 1 Flashcards

0
Q

Adaptive immunity

A

Slower on first exposure, specific. Cell mediated (T) and humoral (B).

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1
Q

Innate immunity

A

Rapid, nonspecific. E.g. physical barriers, cells (neutrophils, macrophages, dendritic cells), complement.

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2
Q

Passive immunity

A

Type adaptive immunity. Preformed Abs from source outside body. E.g. milk, antitoxins, Abs (HBV, rabies)

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3
Q

Active immunity

A

Type of adaptive immunity.
Body’s intrinsic mechanism to fight infection.
Lymphocytes, lymphoid organs

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4
Q

Primary lymphoid organs

A

Bone marrow, thymus.

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5
Q

Secondary lymphoid organs

A

Spleen, LNs.

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6
Q

Site of positive and negative selection of T cells

A

Starts in corticomedullary junction in thymus, continues until reaches medulla.

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7
Q

Embryology of thymus

A

3rd branchial pouch

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8
Q

Parenchyma of spleen

A

Red pulp and white pulp

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9
Q

White pulp (spleen)

A

Immune cell interaction. Central arteriole surrounded by PeriArterial Lymphatic Sheath

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10
Q

Red pulp (spleen)

A

RBC storage and turnover. Rich vasculature with splenic cords and fenestrated capillaries.

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11
Q

Marginal zone (spleen)

A

Separates red and white pulp.

Contains APCs.

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12
Q

Primary lymph nodes

A

Inactive follicles.

Stored lymphos awaiting antigen presentation

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13
Q

Secondary lymph nodes

A

Active follicles.

Pale germinal centers within cluster lymphos. B cells proliferate here and produce Abs.

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14
Q

Lymph drainage-stomach

A

Celiac

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15
Q

Lymph drainage-upper arm, lat breast

A

Axillary

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16
Q

Lymph drainage-duodenum, jejunum

A

Superior mesenteric

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17
Q

Lymph drainage-sigmoid colon

A

Colic -> inf. mesenteric

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18
Q

Lymph drainage-lower rectum and anal canal above pectinate

A

Internal iliac

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19
Q

Lymph drainage-anal canal below pectinate

A

Superficial inguinal

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20
Q

Lymph drainage-testes

A

Para-aortic

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21
Q

Lymph drainage-scrotum

A

Superficial inguinal

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22
Q

Lymph drainage-superficial thigh

A

Superficial inguinal

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23
Q

Lymph drainage-lat side dorsum foot

A

Popliteal

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24
Q

Cells of innate immunity

A

Phagocytic cells, APCs, NK cells

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25
Q

Phagocytes

A

Neutrophils
Macrophages
Dendritic cells

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26
Q

Antigen Presenting Cells (APCs)

A

Dendritic cells
Macrophages
B cells

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27
Q

NK cells

A

Contain lytic granules that attack and kill virus infected or tumor cells via antibody-dependent cellular cytotoxicity

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28
Q

Activation of classic pathway (complement)

A

C1 recognizes and binds constant fragment of IgG or IgM

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29
Q

Activation of alternative pathway (complement)

A

Activated C3 recognizes certain nonspecific antigens

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30
Q

Activation of lectin pathway (complement)

A

Mannose-binding lectin recognizes carbohydrate antigens on surfaces of microorganisms

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31
Q

C1 esterase inhibitor

A

Breaks apart C1.

Deficiency leads to hereditary angioedema, due to uncontrolled activation classic pathway

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32
Q

Decay Accelerating Factor (DAF)

A

Disrupts formation C3 convertase, thus halts complement.
If protein that associates DAF with RBC abnormal, can result in Paroxysmal Nocturnal Hemoglobinuria, as RBCs are more susceptible to complement-induced hemolysis.

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33
Q

C5b-C9 deficiency

A

Recurrent Neisseria infections

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34
Q

Deficiency in C3a, C3b

A

Recurrent pyogenic infections (respiratory tract)

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35
Q

Tc cells

A

CD8. Kills cells infected with viruses or intracellular bacteria

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36
Q

Main function of B cells

A

Recognize extracellular pathogens and differentiate into plasma cells that produce Abs

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37
Q

Functions of Abs

A

Opsonization
Neutralization
Complement activation
Antibody-dependent cellular cytotoxicity

38
Q

MHCs

A

Encoded by HLA genes.

Most important molecules in transplantation

39
Q

MHC I

A

On all nucleated cells
Present intracellular peptides
Binds TCR, CD8+ coreceptor

40
Q

MHC II

A

On APCs
Present extracellular peptides (engulfed antigens)
Binds to TCR, CD4+ coreceptor

41
Q

Hyperacute rejection

A

Preformed antidonor Abs. Minutes.

42
Q

Acute rejection

A

Tc reaction with foreign MHCs. Reversible with immunosuppression, Weeks.

43
Q

Chronic rejection

A

Ab mediated damage of vasculature. Irreversible. Months-years.

44
Q

Graft v host disease

A

Irradiated immunocompromised host. Grafted T cells recognize body as foreign.
Rash, jaundice, diarrhea

45
Q

CD3

A

Mature T cells. Assoc with TCR

46
Q

CD4

A

Th. Coreceptor fo MHC II on APCs.

Coreceptor for HIV

47
Q

CD8

A

Tc. Coreceptor for MHC I.

48
Q

CD40

A

Isotype switching

49
Q

CD28

A

T cell activation

50
Q

CD19, CD20

A

B lymphocytes

51
Q

CD21

A

Complement pathway, EBV receptor

52
Q

IFN-alpha, IFN-beta

A

Signal cell to produce protein to decrease viral mRNA

53
Q

IFN-gamma

A

Increases expression MHC I and II; stimulates phagocytosis by macrophages.

54
Q

T cell activation

A

TCR binds antigen on MHC of APC, then costimulatory molecule required.

55
Q

Isotype switching

A

Naive B cells express IgM but do not secrete Ab until activation and isotype switching occurs.
When IgM binds antigen, antigen peptides loaded onto MHC II. When that MHC II binds to TCR, CD4 + CD40, T cell produces cytokines which induce isotype switching

56
Q

T cell anergy/tolerance-mechanisms

A 
Positive selection (thymic cortex)
Negative selection (thymic medulla)
Peripheral tolerance by clonal deletion, anergy, active suppression, ignorance.
57
Q

Positive selection

A

Ensures T cells that do not recognize self do not survive in periphery

58
Q

Negative selection

A

T cells that react to self antigen deleted

59
Q

Clonal deletion

A

T cell that binds repeatedly (e.g. high concentration of self antigen) leads to apoptosis

60
Q

Anergy

A

Recognize self antigen but remains inactive due to lack costimulatory molecules required for its activation

61
Q

Active suppression

A

Kept nonfunctional if self antigen at low levels-these differentiate into regulatory cells-secrete cytokines to prevent other cells from reacting to that antigens

62
Q

Ignorance

A

If self reactive T cell never encounters its antigen–dies from lack of stimulation

63
Q

B cell Anergy and Tolerance

A

Clonal deletion, Anergy, Clonal ignorance

64
Q

Type I hypersensitivity-definition

A

IgE mediated. Immediate. Anaphylactic or atopic.

65
Q

Type I hypersensitivity-examples

A

Urticaria, Allergic rhinitis, asthma, anaphylaxis

66
Q

Urticaria

A

=Hives. Mildest form atopy. Histamine release leads to vasodilation and visible wheal and flare.

67
Q

Type II hypersensitivity-definition

A

Antibody mediated. Activates complement.

68
Q

Type II hypersensitivity-examples

A

Blood transfusions
Erythroblastosis fetalis
Goodpasture syndrome

69
Q

Erythroblastosis fetalis

A

Rh- mother (sensitized) with Rh+ fetus. Mother’s antigens attack fetus, can cause brain damage.
Treated with anti-Rh IgG (RhoGAM)

70
Q

Goodpasture

A

anti-GBM, which bind to type IV collagen. Ab complexes in kidney (leading to GN) and lung (leading to pulmonary hemorrhage).

71
Q

Type III hypersensitivity-definition

A

Antigen-antibody complexes form when antigen is abundant. Immune complex deposits in tissues.
Clearance of infections creates antigen-Ab complexes
Some smaller complexes deposit in BV walls-they accumulate in endothelium (vasculitis) and synovium (arthritis)

72
Q

Type III hypersensitivity-examples

A

SLE
Serum sickness
Arthus reaction

73
Q

Serum sickness

A

When serum/Abs, e.g. horse antivenom, administered. +1 week–Abs to foreign proteins, leading to lymphadenopathy, fever, arthralgia, urticarial plaques.

74
Q

Arthus reaction

A

Local swelling at site injection of antigen to which pt immunized. E.g. desensitization allergy shots

75
Q

Type IV hypersensitivity-definition

A 
Cell mediated (delayed).
Initial exposure leads to memory cells.  On repeated exposure, effector T cells drawn to site, proliferate, and activate macrophages.
76
Q

Type IV hypersensitivity-examples

A

Tuberculin skin test

Contact dermatitis

77
Q

B cell immunodeficiencies

A

Transient hypogammaglobulinemia of infancy
Bruton Aggamaglobulinemia
Dysgammaglobulinemia

78
Q

T cell immunodeficiencies

A

Thymic aplasia (DiGeorge)
Chronic mucocutaneous candidiasis
AIDS

79
Q

Combined immunodeficiencies

A

SCID
Wiskott-Aldrich syndrome
Hyper-IgM syndrome
Ataxia Telangiectasia

80
Q

Transient hypogammaglobulinemia (of infancy)

A

Maternal IgG disappearing but infant’s B cells not producing sufficient quantities of Abs

81
Q

Bruton agammaglobulinemia

A

X linked.
Defect in Bruton tyrosine kinase (B cell differentiation, maturation, signaling).
Low amts all Igs.
Recurrent extracellular pyogenic and enterovirus infections.
Tx: IVIG

82
Q

Dysgammaglobulinemia

A 
Defective B cell class switching.
Most common type is low IgA, thus chronic lung infections (give Abx)
83
Q

Thymic Aplasia (DiGeorge)

A

Hypocalcemia, tetany, no T cells
Defective formation 3rd, 4th pharyngeal pouches
Assoc with 22q11 microdeletions
Tx: thymic transplantation

84
Q

Chronic mucocutaneous candidiasis

A

Lack of T cell reactivity (not number) to candida species

85
Q

AIDS

A

Loss cell mediated (Th) immunity.

General wasting, constitutional sxs, opportunistic infections

86
Q

SCID

A 
Malfunctioning B and T cells.  
Deficiency in adenosine deaminase or purine nucleotide phosphorylase.
X linked version most comm.
Failure to thrive, chronic infections.
Death within 1 year birth if untreated
87
Q

Wiskott-Aldrich

A

X linked defect in WASP-defects in actin cytoskeleton.
Affects all hematopoietic cells, esp platelets, T cells.
Pyogenic infections, bleeding diathesis, eczema.
Increased risk AI disorders, lymphoma
Decreased IgM, normal IgA, IgG
Small platelets

88
Q

Ataxia Telangiectasia

A

AR defect in ATM-insufficient response to DNA damage
Lymphocytes targeted due to high rate proliferation
IgA deficiency and malignancy
Cerebellar ataxia and telangiectasias
Most die mid 20s

89
Q

Phagocyte Deficiencies

A

Leukocyte Adhesion defficiency
Chronic Granulomatous Disease
Chediak Higashi syndrome

90
Q

Leukocyte adhesion deficiency

A

AR defect in integrin receptor, which helps phagocytes bind endothelium.
Bacterial infections WITHOUT pus

91
Q

Chronic granulomatous disease

A

Defective NADPH oxidase, involved in ROS killing
Accumulation of immune cells in granulomas.
Infections with catalase positive bacteria or fungal infections.
Test: nitroblue tetrazolium dye.

92
Q

Chediak Higashi sydrome

A

AR. Failure of vesicle fusion in neutrophils, platelets, melanocytes
Recurrent infections, esp strep and staph.
Increased bleeding, peripheral neuropathy

USMLE Step 1 (15 decks)

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