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First Aid & Firecracker > First Aid: Immunology > Flashcards

First Aid: Immunology Flashcards

1
Q

What are the two parts of a lymph node’s medulla?

A

Medullary Sinuses: Connect with efferent lymph drainage and contain macrophages.
Medullary Cords: packed with lymphocytes and plasma cells.

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2
Q

Which type of cell is in the follicular center of a spleen sinusoid?

A

B Cell

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3
Q

Which type of cell is in the periarterial lymphatic sheath of a spleen sinusoid?

A

T Cell

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4
Q

Which type of cell is in the spleen red pulp?

A

RBCs

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5
Q

Which type of cells are in the marginal zone of a spleen?

A

Antigen Presenting Cells

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6
Q

Which infections are postsplenectomy patients more susceptible to?

A

SHiNE SKiS: Strep Pneumo, H. Influenza B, Neisseria meningitidis, E. Coli, Salmonella, Klebsiella, Strep Group B

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7
Q

What can be seen on a blood smear of a postsplenectomy patient?

A

Howell-Jolly Bodies (Nuclear remnants), Target Cell, Thrombocytosis

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8
Q

What is especial about the epithelial cells of the thymus?

A

Epithelial Reticular Cells in Hassall Corpuscles express AIRES which upregulates every plasma proteins for the negative selection of T Cells.

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9
Q

What are TLR and what do they do?

A

They are Toll Like Receptor of the innate immune system that recognize PAMPs.

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10
Q

Which type of antigen do MHC Class I present?

A

Endogenously expressed proteins (ie. viral) to cytotoxic CD8+ T Cells

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11
Q

Which type of antigen do MHC Class II present?

A

Exogenous protein to CD4+ T Helper Cells. MHC II are only in APC.

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12
Q

What is the quarteary structure of MHC I & II?

A

MHC I is a dimer with the alpha subunit doing the antigen presentation and beta2 microglobulin carrier the complex to the cell sruface. MHC II has an alpha and a beta subunit and the antigen presentation takes places in a groove between them.

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13
Q

Where does MHC II load its antigen?

A

In the RER after delivery by TAP.

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14
Q

Which HLA subtype is the most associated with disease? Which diseases?

A

HLA B27 is associated with Psoriasis, Ankylosing spondylitis, arthritis of Inflammatory bowel disease, Reactive arthritis (Reiter’s syndrome).

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15
Q

Which two diseases is HLA Subtype D4 associated with?

A

Rheumatoid Arthritis and DM Type I. (1 rheum has 4 walls.)

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16
Q

What are the three signals that induce Natural Killer Cell to kill?

A

Non-specific signals on cell surfaces. Lack of MHC I. Has an Fc receptor CD16 which allows it to kill cells with bound Ig.

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17
Q

Which cytokines enhance Natural Killer Cell activity?

A

IL-2 (Proliferation), IL-12, TNF (makes more IL-2 receptors), INF-alpha, INF-beta (both INF are non-specific “kill” signals.)

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18
Q

How does a Natural Killer Cell kill?

A

Using perforin to create a hole in the membrane followed by a release of Granzyme B.

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19
Q

What mechanism does a B Cell use to improve antigen affinity?

A

Somatic hypermutation

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20
Q

What role do activated CD4+ T Cells have?

A

Helper T Cells. They can only help. Seriously, they don’t do anything else.

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21
Q

What are the five different types of mature CD4+ T Cells?

A

Th1 (Macrophage activator), Th2 (Eosinophil, Mast cell and Plasma cell recruiter), Th17(Neutrophil recruiter), ThFC (B Cell activator, phenotypic switch), Treg (T Cell activation inhibitor)

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22
Q

What is the co-stimulatory signal required for T Cell activation?

A

B7 on APC surface binds CD28 on T Cell surface.

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23
Q

What is the co-stimulatory signal required for B Cell activation?

A

CD40 on the B Cell surface bind CD40L on the T helper surface.

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24
Q

What do Th1 cells do?

A

Secrete INF-gamma which activates macrophages and CTL.

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25
Q

What do Th2 cells do?

A

Secrete IL-4, IL-5, IL-6 and IL-13 to recruit eosinophils in induce IgE secretion.

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26
Q

Describe the feedback loop between macrophages and T cells.

A

Th1 cells secrete INF-gamma which stimulate macrophages. Macrophages release IL-12, which stimulate Th1 cells.

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27
Q

What are Th1 cells inhibited by?

A

IL-4 and IL-10 from Th2 cells.

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28
Q

What are Th2 cells inhibited by?

A

INF-gamma from Th1 cells.

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29
Q

What do Treg cells do?

A

When activated they secrete IL-10 and TGF-beta which are anti-inflammatory.

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30
Q

What are the 4 Cs of the Fc region?

A

C- terminal
Complement binding
Constant
Carbohydrate side chains

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31
Q

What is the function of IgG?

A

Serum antibody. Crosses placenta. Secondary to IgM. Monomer.

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32
Q

What is the function of IgM?

A

Serum antibody. Pentamer. Primary response before IgM.

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33
Q

What is the function of IgA?

A

Mucosa antibody. Does not bind compliement.

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34
Q

What is the function of IgE?

A

Type I Hypersensitivity. On the surface of mast cells and basophils. Monomer. Antihelmithic.

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35
Q

Which lymph nodes drain the foregut, midgut and hindgut?

A

Celiac, Superior Mesenteric and Inferior Mesenteric. Just like the arterial supply.

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36
Q

What are the two lymphatic drainage ducts and what do they drain?

A

Right Lymphatic Duct - Right side of the body above the diaphragm.
Thoracic Duct - Everything else and drains into the subclavian and jugular junction.

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37
Q

Which three proteins regulate serum iron during disease?

A

Ferritin increases as intracellular stores increase. Hepcidin increases and prevents ferritin from releasing iron. Transferrin is sequestered by macrophages to decrease iron transfer.

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38
Q

What happens to serum amyloid, albumin, C-reactive protein and fibrinogen when the immune system is activated?

A

They all increase except for albumin. C reactive promotes opsonization. Fibrinogen promotes endothelial repair.

39
Q

What does MAC defend against?

A

Gram Negatives

40
Q

Describe the three ways the complement cascade can be triggered?

A

Classical - IgG and IgM (GM makes classic cars.)
Lectin - Sugars on microbial surface
Alternative - Spontaneous and surfaces

41
Q

Which complements cause anaphylaxis?

A

3a, C4a, C5a

42
Q

Which complement causes neutrophil chemotaxis?

A

C5a

43
Q

Which complements make up the Membrane Attack Complex?

A

C5b through C9

44
Q

Which complement induces opsonization?

A

C3b

45
Q

What does C1 esterase inhibitor deficiency cause?

A

C1 esterase inhibitor inhibits activation of the Lectin and Alternative pathway. A deficiency leads to hereditary angioedema.

46
Q

What does a C3 deficiency cause?

A

Increased risk of purulent infection. Increased susceptibility to Type III hypersensitivity.

47
Q

What does deficiency in any of the complement from C5 through C9 cause?

A

Increased susceptibility to Neisseria infections.

48
Q

What do IL-1 through IL-6 stimulate?

A 
(Hot T-bone stEAKS)
1- Fever
2- T cells
3- Bone marrow
4- IgE
5- IgA
6- aKute-phase protein
49
Q

Which IL is the major chemotactant for neutrophils?

A

IL-8

50
Q

Which cytokine causes septic shock?

A

TNF-alpha

51
Q

Which cytokine has the most activity against viruses and tumors?

A

INF-gamma, It is secreted by Th1 cells and it activates NK cells.

52
Q

Which cell type is located in the follicle of a lymph node? Where are follicles located? What are their two states?

A

B-Cell localization and proliferation. Located in the outer cortex. They can be dormant (1o) or active (2o).

53
Q

Which cell type is located in the paracortex of a lymph node? What type of vessel do they contain?

A

T Cell. High Endothelial Venules, HEV. Note: Patient’s with DiGeorge’s syndrome have atrophied paracorteces.

54
Q

To which lymph nodes does the skin above the umbilicus drain?

A

Axillary. Just like the breast.

55
Q

What does deficiency in Decay Accelerating Factor (DAF) cause?

A

DAF inhibits complement cascade and it is one of the GPI anchored proteins. It can cause paroxysmal nocturnal hemoglobinuria.

56
Q

Which ones are the anti-inflammatry cytokines?

A

IL-10 and TGF-beta. Inhibit T cell action. Secreted by Tregs.

57
Q

What triggers the release of Interferons?

A

Cells infected by viruses release it to prime surrounding cells against viruses.

58
Q

How do cell primed by interferons respond to viral infection?

A

Viral dsRNA activates RNAase L and protein kinase. Translation is inhibited.

59
Q

What is ti called when a T cell becomes nonreactive?

A

Anergy

60
Q

What is the B Cel surface marker?

A

CD20 and CD21 (EBV receptor)

61
Q

What is the T cell surface marker?

A

CD3 (TCR helper) and CD28 (binds B7)

62
Q

What is the Macrophage surface marker?

A

CD14 (TLR coreceptor) and CD40

63
Q

What is the NKC surface marker?

A

CD56

64
Q

What can directly activate macrophages?

A

LPS can activate TLR receptors, CD14, and cause systemic effects.

65
Q

Name three bacteria which undergo antigenic variation?

A

Salmonella has two flagella, Borrelia can undergo recombination, Neisseria gonorrhoeae can change their pili.

66
Q

What is the difference between passive versus active immunity?

A

Passive is the acquisition of preformed antibodies. Active requires exposure to an antigen and creation of the antibody.

67
Q

After which 4 exposures are Igs administered?

A

Tetanus, Botulinum, HBV and Rabies. (To Be Healed Rapidly)

68
Q

Which vaccines are generally live vaccines?

A

Smallpox, yellow fever, chicken pox, polio, MMR and influenza (Live! Small yellow chickens with Sabin, MMR and the flu.)

69
Q

Live versus killed vaccine. Pros and cons.

A

Live elicits a cellular response and last longer, but may reactivated. Killed is safer but has weaker and shorter immunity.

70
Q

Mechanism of action of type I hypersensitivity.

A

Antigen+IgE/FcR complex aggregation causes the release of histamines from mast cells or basophils. Post-capillary venules are dilated by histamine. Leads to anaphylaxis.

71
Q

Mechanism of action of type II hypersensitivity.

A

IgM or IgG bind to the antigen that is itself stuck on a self cell. Causes cytotoxicity via MAC, NKC or Macrophages. Tested using Coomb’s test.

72
Q

Mechanism of action of type III hypersensitivity.

A

IgG-Antigen complex causes complement activation which leads to neutrophil recruitment, etc. Serum sickness; fervor, urticaria, arthralgias, LAD, 5 days after exposure. Also Arthus reaction and complex deposition (ie. Post-Strep, SLE).

73
Q

Mechanism of action of type IV hypersensitivity.

A 
T Cell mediated. Four Ts.
T cells
Transplant Rejection
TB skin test
Touching (contact dermatitis)
74
Q

What type of hypersensitivity causes the complications of ABO mismatch in transfusion?

A

Type II. It is called acute hemolytic transfusion reaction. Febrile non-hemolytic transfusion reaction is also type II but the antigen are leukocytes only.

75
Q

Which infections are more likely in a deficiency of granulocytes?

A

Staph, Burkholderia cepacia, Serratia, Nocardia (Bacteria) Candida, & Aspergillus (Fungi)

76
Q

Which infections are more likely in a deficiency of complement?

A

Neisseria

77
Q

Which infections are more likely in a deficiency of B cells?

A

Bacteria are the same as asplenic patients (SHiNE SKiS) Strep pneumo, H Flu, Neisseria, E Coli, Salmonella, Klebsiella, GBS. Plus enteroviruses and Giardia.

78
Q

What are the three B Cell disorders? Give a quick synopsis of the etiology.

A
  1. X-linked Bruton agammaglobulinemia - defect in BTK
  2. Selective IgA deficiency - Unknown and relatively asymptomatic
  3. Common variable immunodeficiency - Many causes and can be acquired in 20s or 30s. Recurrent infections and lymphoma.
79
Q

What are the four T Cell disorders? Give a quick synopsis of the etiology. (AIDS is not one)

A
  1. DiGeorge - Thymic aplasia
  2. IL-12 receptor Deficiency - No Th1 response
  3. Autosomal Dominant hyper-IgE Syndrome (Job syndrome) - Th17 def from STAT3 mutation
  4. Chronic Mucocutaneous Candidiasis - General T cell dysfunction
80
Q

Along with histamine, which other molecule is released by mast cells in degranulation?

A

Tryptase

81
Q

What are the four combined B Cell & T Cell disorders? Give a quick synopsis of the etiology.

A
  1. SCID (Def in IL-2R or Adenosine Deaminase)
  2. Ataxia Talangiectasia (dsDNA breaks)
  3. Hyper-IgM Syndrome (def CD40L)
  4. Wiskott-Aldrich Syndrome (WATER, Throm Purp, Eczema, Recur Infx)
82
Q

What are the three phagocyte disorders? Give a quick synopsis of the etiology.

A
  1. Leukocyte Adhesion Def I (Def in LFA-1 integrin)
  2. Chediak-Higashi (Microtubule Dysfunction)
  3. Chronic Granulomatous Disease (Def NADPH Oxidase)
83
Q

What is the pathophysiology of hyperacute rejection? Timeline?

A

Type II with pre-formed Ab. Thrombosis in vessels leads to ischemia. Minutes.

84
Q

What is the pathophysiology of acute rejection? Timeline?

A

Either cellular (CTL against MHC) or Humoral (Abs form after Trx) leads to vasculitis & lymph infiltrate. Weeks to months.

85
Q

What is the pathophysiology of chronic rejection? Timeline?

A

T cells detect antigens presented on Trx’s MHC. (Not MHC itself) Months to Years.

86
Q

What is the pathophysiology of Graft-versus-Host?

A

Marrow Trx T Cells rejects the host. Maculopapular rash, hepatosplenomegaly, jaundice.

87
Q

What are the two Calcineurin inhibitors and what is their main side effect?

A

Cyclosporine (binds cyclophilin) & Tracolimus (binds FKBP) they PREVENT IL-2 TRANSCRIPTION and thus T Cell activation. Nephrotoxicity, HTN, Hyperlipidemia

88
Q

What are the mechanism, use and toxicity of Sirolimus/Rapamycin?

A

mTOR inhibitor through FKBP. Used for renal Trnx. Anemia, Thrombocytopenia, Leukopenia, insulin resistance.

89
Q

What are the mechanism, use and toxicity of Basiliximab?

A

IL-12R blocker. Renal trnx. Edema, HTM & tremor.

90
Q

What are the mechanism, use and toxicity of Azathioprine?

A

Inhibit purine synthesis. General trnxs, rheumatoid, Crohn, & glomerulonephritis. Can cause anemia, leukopenia & thrombocytopenia.

91
Q

What are the mechanism, use and toxicity of Glucocorticoids? (In immunosupression)

A

NF-kB inhibitors, inhibit both T cell and B cell activation. General immunosupression. Can cause hyperglycemia, osteoporosis, central obesity, muscle breakdown, psychosis, acne, hypertension, cataracs, peptic ulcers (Cushinoid +)

92
Q

What are the mechanism and use of Infliximad and Adalimumab?

A

MAB against TNF-a used for RA, IBD, ankylosing spondylitis, and psoriasis.(Inlfix pain in da lims)

93
Q

What are the mechanism and use of Natalizumab?

A

Anti alpha4-integrin (leukocyte adhesion) used in MS and Crohn.

94
Q

What are the mechanism and use of Infliximad and Omalizumab?

A

Anti IgE used in asthma.

First Aid & Firecracker (7 decks)

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