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Step 1 > Immunology > Flashcards

Immunology Flashcards

0
Q

Hilar Lymph node

A

lungs

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1
Q

Cervical lymph node

A

Head and neck

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2
Q

Mediastinal lymph node

A

trachea and esophagus

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3
Q

Axillary lymph node

A

upper limb, breast, skin above umbilicus

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4
Q

Celiac lymph node

A

liver, stomach, spleen, pancreas, upper duodenum

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5
Q

Superior Mesenteric lymph node

A

lower duodenum, jejunum, ileum, colon to splenic flexure

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6
Q

inferior mesenteric lymph node

A

colon from splenic flexure to upper rectum

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7
Q

Internal iliac lymph node

A

lower rectum to anal canal (above pectinate line), bladder, vaginal (middle third), prostate

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8
Q

Para-aortic lymph node

A

testes, ovaries, kidneys, uterus

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9
Q

Superficial Inguinal

A

Anal canal (below pectinate line), skin below umbilicus (except popliteal area)

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10
Q

Popliteal lymph node

A

Dorsolateral foot, posterior calf

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11
Q

Right lymphatic duct

A

drains right side of body above diaphragm

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12
Q

Thoarcic lymphatic duct

A

drains everything else into junction of left subclavian and internal jugular veins

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13
Q

What structures are in the lymph node cortex?

A

Follicles- contain B cells

  • Primary follicles: more dense and dormant
  • Secondary follicles: lighter and active
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14
Q

What structures are in the lymph node medulla?

A

Medullary cords- tightly packed lymphocytes and plasma cells
Medullary sinuses- contain reticular cells and macrophages–> communicate with efferent lymphatics

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15
Q

What is the paracortex of the lymph node?

A

Region between the follicles and the medulla; contains T cells and high endothelial venules through which T-cells and B-cells enter from blood
** Paracortex enlarges in an extreme cellular immune response (viral infection)**

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16
Q

What are the sinusoids of the spleen? Where are they found?

A

long, vascular channels in the red pulp with fenestrated barrel-hoop basement membranes. Cells mechanically are filtered and damaged cells get devoured by surrounding macrophages

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17
Q

What is in the splenic red pulp?

A

RBCs and sinusoids

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18
Q

Explain the structure of the white pulp.

A

White pulp- really is blue = contain lymphocytes

  • Contains central arteriole surrounded by periarteriolar lymphatic sheath (T cells)
  • Mostly comprised of lymphatic nodules (B cells) –> can mature to germinal center @ marginal zone once antigen presented
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19
Q

What is the marginal zone of the spleen?

A

The marginal zone is the area between the red pulp and the white pulp; it contains APCs and B cells

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20
Q

Where do T cells mature?

A

Thymus

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21
Q

Describe the structure of the thymus.

A

Encapsulated and lobulated

  • Cortex is dense with immature T cells = site of positive selection
  • Medulla is pale with mature T cells= site of negative selection
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22
Q

What are Hassall corpuscles?

A

located in the thymus; whorl-shaped clusters of epithelial reticular cells; eosinophilic staining
- reticular epithelial cells function to form a structural network for the thymus

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23
Q

Positive selection

A

Process in the maturation of T cells. T cells that express a TCR that binds self MHC (I or II) survives. Occurs in the thymus cortex.

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24
Q

Negative selection

A

Process in T cell maturation. T cells that TCR binds self MHC too tightly undergo apoptosis. Occurs in the thymus medulla.

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25
Q

What cell surface markers to immature T cells express?

A

TCR that binds self MHC, double positive= CD4+ & CD8+

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26
Q

CD8+

A

Cytotoxic T cells; kills virus infected, neoplastic, and donor graft cells
-CD8 binds MHC I on virus infected cells

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27
Q

CD4+

A

Helper T cells; Differentiate into Th1, Th2, Th17 & Treg cells
-CD4 binds MHC II on APCs

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28
Q

Th1 cells

A

:Helper T cell CD4+, activates macrophages and CTLs

  • Macrophages release of IL-12 stimulates Cd4+ T cells to differentiate into Th1 cells
  • CELL MEDIATED IMMUNITY
  • secretes IFN-gamma to stimulate macrophages, and IL-2 which has autocrine effect of TH1 cell proliferation
  • inhibited by IL-4 and IL-10 from Th2 cells
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29
Q

Th2 cells

A

: helper T cell CD4+; Initiates Ab response, promotes class switching, recruits eosinophils for parasite defense

  • HUMORAL IMMUNITY
  • Secretes IL-4, IL-5, IL-10, IL-13
  • inhibited by IFN-gamma from Th1 cells
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30
Q

CTLs

A

Kills virus infected, neoplastic, and donor graft cells by inducing apoptosis. Releases cytotoxic granules containing performed proteins

  • perforin: delivers content of granules to target cell
  • granulysin: antimicrobial, induces apoptosis
  • granzyme B: a serine protease, activates apoptosis inside cell
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31
Q

Regulatory T cells

A

Suppress CD4 and CD8 T cell effector functions

  • produce anti-inflammatory cytokines; IL-10 and TGF-B
  • identified by expression cell surface markers: CD3, CD4, CD25 and transcription factor FOXP3
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32
Q

Toll-like receptors

A

cell surface receptors on macrophages, dendritic cells, NK cells that recognize pathogen associated molecular patterns (PAMPs)

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33
Q

MHC I

A
  • encoded by: HLA-A, HLA-B, HLA-C
  • expressed on all nucleated cells; none on RBCs
  • presents endogenously synthesized antigens to CD8 cells
  • antigens loaded onto MHC in RER after delivery via TAP peptide transporter
  • B2- microglobulin transports to cell surface
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34
Q

MHC II

A
  • encoded by HLA-DR, HLA-DP, HLA-DQ
  • expressed on APCs only
  • presents exogenously synthesized antigen
  • antigen loaded following release on invariant chain in an acidified endosome
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35
Q

Natural Killer cells

A

:use perforin and granzymes to induce apoptosis of virally infected cells

  • only lymphocyte member of the innate immunity
  • induced to kill when exposed to activation signal on target cell or absence of MHC class I
  • kills via Ab-dependent cell mediated cytotoxicity (CD16 binds to Fc portion of bound Ig = activates NK cell
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36
Q

What is the significance of costimulatory signaling?

A

Naive T cell activation

  • APCs( Dendritic cells, macrophages, B cells) present antigen via MHCII or host cells present antigen via MHC I to CD4 helper T cells or CTLs respectively [signal 1]
  • Costimulatory signal: B7 on APC binds to CD28 on T cell
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37
Q

How do T cells activate B cells?

A
  • CD4 helper cells are activated via APCs
  • B cells present antigen via MHC II to TCR on CD4 cell [signal 1]
  • B cell is activated when CD40 ligand on T cell interacts with CD40 on B cell surface [signal 2]
  • Cytokines secreted by T cell promotes class switching, affinity maturation and antibody production
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38
Q

Antibody structure

A

2 heavy chains + 2 light chains, 2 Ab binding sites per molecule
-Ab binding site made up of variable region of each chain

39
Q

Fc portion of Ab

A

: consists of Constant region of heavy chain, Carboxy terminal, Carbohydrate side chains, Complement binding
-determines isotype (IgG, IgM, etc)

40
Q

Fab portion of Ab

A

: Consists of heavy and light chain

- Determines idiotype: specific antigen binding pocket

41
Q

How is antibody diversity generated?

A
  1. Random recombination of VJ (light chain) and VDJ (heavy chain)
  2. Insertion of DNA nucleotides during recombination by terminal deoxynucleotidyl transferase
  3. Random combination of heavy and light chains
  4. Somatic hypermutation following antigen stimulation
42
Q

IgG

A

: fixes complement, crosses placenta (passive immunity), opsonizes bacteria, neutralizes bacterial toxins and viruses
-Most abundant isotype in serum; main antibody in secondary (delayed) response to antigen

43
Q

IgA

A

: prevents attachment of bacteria to mucus membranes; released into secretions (saliva, tears, colostrum, mucus)

  • monomer in circulation but dimer when secreted
  • Most produced antibody overall
  • crosses epithelial cells via trancytosis and picks up a secretory component before secretion
44
Q

IgM

A

: antigen receptor on the surface of mature B cells

  • produced in primary (immediate) response to antigen
  • monomer on B cell but pentamer when secreted
45
Q

IgD

A

: unclear function, found on surface of mature B cells

46
Q

IgE

A

:binds mast cells and basophils; activates eosinophils (worm immunity)

  • cross-links when exposed to antigen = immediate type I hypersensitivity
  • lowest concentration in serum
47
Q

Acute Phase Reactants

A

: produced in acute and chronic inflammation from the liver, induced by IL-6, IL-1, TNF-a, IFN-gamma

  • amyloid A, CRP, ferritin, fibrinogen, hepcidin, albumin, transferrin
  • amyloid A, CRP, ferritin, fibrinogen, hepcidin concentration increase
  • albumin, transferrin concentration decrease
48
Q

IL-1

A

aka “osteoclast activating factor”
:causes fever, acute inflammation, activates endothelium to express adhesion molecules, induces chemokine secretion to recruit leukocytes

49
Q

Hot T-Bone stEAK

A 
IL-1: hot 
IL-2: stimulates T cells 
IL-3: stimulates Bone marrow 
IL-4: stimulates IgE production 
IL-5: stimulates IgA production 
IL-6: stimulates aKute phase reactants
50
Q

IL-6

A

:causes fever, secreted by Th2 cells, stimulates production of acute phase reactants

51
Q

IL-8

A

major chemotactic factor for neutrophils

52
Q

IL-12

A

:induces differentiation of T cells into Th1 cells, activates NK cells, secreted by B cells

53
Q

TNF-a

A

:mediates septic shock, activates endothelium, causes leukocyte recruitment and vascular leak

54
Q

IL-2

A

stimulates growth of helper, cytotoxic and regulatory T cells

55
Q

IL-3

A

supports growth and differentiation of bone marrow stem cells; functions like GM-CSF

56
Q

IFN-gamma

A

: antiviral and antitumor properties, activates NK cells to kill virus infected cells, increases MHC expression and antigen presentation of in cells

57
Q

IL-4

A

:induces differentiation into Th2 cells, promotes growth of B cells, enhances class switching to IgE and IgG

58
Q

IL-5

A

:promotes B cell maturation to plasma cells, enhances class switching to IgA, stimulates growth and activation of eosinophils

59
Q

IL-10

A

:inhibits actions of activated T cells; secreted by Treg

-TNF-B has similar actions

60
Q

IFN-a & IFN-B

A

:interferes with viruses; part of innate response

  • IFNs are secreted by virally infected cells and prime nearby uninfected cells = priming
  • when virus infects a primed cell, viral nucleic acids activate RNAase L (degrades viral/host mRNA & protein kinase (inhibition of viral/host protein synthesis)
  • essentially causes apoptosis –>interrupting viral amplification
61
Q

Complement functions (4)

A
  1. Opsonization: C3b + IgG are key opsonins –> Macrophages have complement and Fc receptors for phagocytosis
  2. C3b clears immune complexes
  3. MAC: C5b +C6-C9; important in killing gram negative bacteria
  4. Anaphylaxis: C3a, C4a, C5a–> binds mast cells and basophils and mediates non-IgE degranulation (histamine)
  5. Neutrophil chemotaxis: C5a
62
Q

Hereditary angioedema

A

Caused by C1 esterase inhibitor deficiency; ACE inhibitors contraindicated
- basically complement system cannot be turned off until all proteins exhausted

63
Q

C5-C9 deficiency

A

Increased susceptibility to recurrent Neisseria bacteremia

  • Recall: MAC complex plays and important role in eliminating gram negative bacteria
  • Gram negative bacteria cannot be displayed by MHC because LPS lacks peptide component
64
Q

C3 deficiency

A

Increased risk of severe, recurrent pyogenic sinus and respiratory tract infections; increased susceptibility to type III hypersensitivity reactions

65
Q

DAF Deficiency

A

DAF = Decay accelerating factor;
:causes complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria
-Recall: PNH caused by deficiency in enzyme necessary to make GPI anchor; DAF is anchored to cell membrane via GPI

66
Q

Anergy

A

: mechanism of tolerance where cells are functionally inactive following an encounter with antigen

  • T cells become anergic without costimulatory molecule
  • B cells also become anergic but to a lesser degree than T cells
67
Q

Live Attenuated Vaccines

A

: organism loses it pathogenicity but retains transient growth; induces CELLULAR immunity
- life-long immunity but unsafe in pregnancy or immunodeficiency

68
Q

Inactivated/Killed vaccines

A

: pathogen inactivated but cell surface epitope structure important for immune response; HUMORAL immunity response
- safer than live vaccines but often require booster shots

69
Q

Helper T cell surface markers

A

TCR, CD3 (signal transduction), CD28 (binds B7 of APC), CD40 ligand, CD4

70
Q

CTL cell surface markers

A

TCR, CD3 (signal transduction), CD28 (binds B7 of APC), CD8

71
Q

B cell surface markers

A

Ig (binds antigen), CD19/20/21 (signal transduction + EBV receptor), CD40, MHCII, B7

72
Q

Macrophage cell surface markers

A

CD14 (TLR that recognizes LPS of gram neg), CD40, B7, MHC II, Fc & complement receptors

73
Q

NK cell surface markers

A

CD16 (binds Fc of IgG), CD56 (unique NK marker)

74
Q

Type I hypersensitivity

A
  • Immediate hypersensitivity; Th2 cells involved in sensitization and Ige class switching
  • Re-exposure causes IgE mediated mast cell and basophil degranulation (histamine)
  • Delayed response is the result of phospholipid breakdown and synthesis of arachidonic acid derivatives leukotrienes –> vasoconstriction, bronchoconstriction, increased vascular permeability + recruitment of eosinophils w/degranulation
75
Q

Type II hypersensitivity

A

Ab mediated cytotoxicity (IgG or IgM); requires prior sensitization
-Antibodies activate complement system, mediate opsonization and subsequent phagocytosis by macrophages, and cause Ab-dependent cell mediated cytotoxicity (NK cells)

76
Q

Type III hypersensitivity

A 
Immune complex (IgG) mediated destruction
-immune complexes activate complement which attracts neutrophils; neutrophils release lysosomal contents
77
Q

Serum Sickness

A

Type III hypersensitivity; antiserum or drugs causes formation of immune complexes (IgG) –> complement, neutrophils
- develops 5 days after exposure; characterized by fever, urticaria, arthralgias, proteinuria, lymphadenopathy

78
Q

Arthus Reaction

A

Type III hypersensitivity; local intradermal injection of antigen causes formation of immune complexes
- local reaction; edema, necrosis, and activation of complement

79
Q

Type IV hypersensitivity

A

Delayed type- Cell mediated; sensitized T cells encounter antigen and then release lymphokines (leads to macrophage activation—> spill out endosomal contents into ECF = damage)
“4 T’s”: T lymphocytes, TB, Touch (contact dermatitis), Transplant rejections
-Candida extract skin test

80
Q

Blood transfusion reaction: Patient - urticaria, pruritis, wheezing, fever.

A

Type I hypersensitivity- reaction to plasma proteins in transfused blood
Treat with antihistamines

81
Q

Blood transfusion reaction: Patient- dyspnea, bronchospasm, hypotension, respiratory arrest, shock.

A

Anaphylactic reaction. IgA deficient individuals must receive blood products that lack IgA

82
Q

Blood transfusion rxn: Patient- fever, headaches, chills, flushing

A

Febrile non-hemolytic transfusion reaction; Type II hypersensitivity rxn. Host antibodies against donor HLA antigens and leukocytes

83
Q

Blood transfusion rxn: Patient- fever, hypotension, tachypnea, tachycardia, flank pain, hemogoblinemia/jaundice

A

acute hemolytic transfusion rxn; type II hypersensitivity.

  • Intravascular hemolysis (ABO blood group incompatibility) =hemoglobinemia
  • extravascular hemolysis (host Ab reaction against foreign antigen on donor RBCs) = jaundice
84
Q

Patient-Increased susceptibility to catalase positive organisms. What do they have? What test do your run? Results?

A

Catalase positive organisms PLACESS: Psuedomonas, Listeria, Aspergillus, Candida, E.coli, S. aureus, Serratia
: Chronic granulomatous disease; defect in NADPH oxidase = decreases ROS and absent respiratory burst in neutrophils; X-linked recessive
-Dihydrorhodamine flow cytometry test- expect abnormal result; neutrophils cannot oxidize DHR d/t absent respiratory burst
-Nitroblue tetrazolium dye- expect negative result; NADPH reduces nitroblue to a blue compound; the greater the blue the greater functionality the neutrophil has

85
Q

Patient- recurrent infections with staph and strep, partial albinism, peripheral neuropathy, progressive neurodegeneration, neutropenia. What do they have? What findings do you expect?

A

: Chediak-Higashi syndrome; defect in lysosomal trafficking regulator gene (LYST), autosomal recessive. Microtubule dysfunction results in phagosome-lysosome fusion & dysfunctional cellular trafficking
Findings: giant granules in neutrophils and platelets, pancytopenia, mild coagulation defects
pg 13 in pathoma

86
Q

Patient- recurrent bacterial skin and mucosal infections with absent pus formation, impaired wound healing, delayed separation of umbilical cord (>30 days). What do they have? What findings to you expect?

A

:Leukocyte adhesion deficiency type 1. Defect in LFA-1 integrin (CD18 subunit) on phagocytes, autosomal recessive; impaired migration and chemotaxis.
-Findings: increased neutrophils but absence of neutrophils at infection site
Recall: marginal pool of neutrophils adhere to lung epithelium via integrins awaiting infection–> impaired adhesion = more PMNs in blood

87
Q

Patient- failure to thrive, chronic diarrhea, thrush. Recurrent viral, bacterial, fungal, protozoal infections, opportunistic infections. What do they have? Findings? Treatment?

A

: Severe combined immunodeficiency (SCID). Several types including defective IL-2R gamma chain (most common, X-linked), Adenosine deaminase deficiency (autosomal recessive)

  • Findings:Absent CD3+ T cells, decreased T cell receptor excision circles (TRECs), absence of thymic shadow (CXR), decreased Ig of all classes
  • Treatment: bone marrow transplant ( no concern for rejection)
88
Q

Patient- Cerebellar defects, spider angiomas (telegiectasia), recurrent sinopulmonary infections. What do they have? Findings?

A

: Ataxia-telengiectasia. Defects in ATM gene–> DNA double strand breaks–> cell cycle arrest.

  • Findings: Increases AFP (alpha fetoprotein); decreased IgA, IgG and IgE. lymphopenia, cerebellar atrophy.
  • Have increased risk of malignancy= impaired DNA repair
89
Q

Patient- severe pyogenic infections early in life, opportunistic infection with pneumocystis, cryptosporium, CMV. What do they have? Findings?

A 
\:Hyper-IgM syndrome. Commonly d/t defective CD40L on Th cells = class switching defect;X-linked recessive. 
-Findings: Increased IgM, decreased IgG, IgA, IgE
90
Q

Patient- Thrombocytopenic purpura, eczema, recurrent infections. What do they have? Findings?

A

: Winskott-Aldrich syndrome; triad of symptoms. Mutation in WAS gene (X-linked recessive); T cells unable to reorganize actin cytoskeleton

  • Findings: decreased to normal IgG, IgM, increased IgE, IgA, fewer and smaller platelets
  • have increased risk of autoimmune disease and malignancy
91
Q

Patient-recurrent bacterial infections and enteroviral infections, and Giardia after 6 months. What do they have? Findings?

A

: X-linked (Burton) agammaglobulinemia; maternal IgG decreases after 6 months. Defect in BTK, a tyrosine kinase gene–> naive B cells cannot mature to plasma cells. X-linked recessive.
-Findings: decreased Ig of all classes, absent/scant lymph nodes and tonsils

92
Q

Selective IgA deficiency

A

:unknown cause; most common immunodeficiency!
Most ASYMPTOMATIC. May see respiratory and GI infections, autoimmune disease, atopy, anaphylaxis to IgA containing products (blood transfusion).
Findings: IgA < 7mg/dL with normal IgG and IgM levels
- commonly associated with celiac disease

93
Q

Patient- tetany, recurrent viral/fungal infections, conotruncal cardiac abnormalities, craniofacial abnormalities. What do they have? Findings?

A

:Thymic aplasia or DiGeorge Syndrome. 22q11 deletion; failure to develop 3 and 4 pharynegeal pouches–> absent thymus (T cell deficiency) and parathyroids (tetany from hypocalcemia), conotruncal abnormalities (tetrology of fallot, truncus arteriosis)
-Findings: Decreased T cells, PTH, Ca2+; absent thymic shadow (CXR), 22q11 deletion on FISH

94
Q

Patient- disseminated mycobacterial and fungal infections after BCG administration. What do they have? Findings?

A

:IL-12 receptor deficiency, autosomal recessive. Decreased Th1 response.
Findings: decrease IFN-gamma

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