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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
What do Th2 cells do?
Secrete IL-4, IL-5, IL-6 and IL-13 to recruit eosinophils in induce IgE secretion.
26
Describe the feedback loop between macrophages and T cells.
Th1 cells secrete INF-gamma which stimulate macrophages. Macrophages release IL-12, which stimulate Th1 cells.
27
What are Th1 cells inhibited by?
IL-4 and IL-10 from Th2 cells.
28
What are Th2 cells inhibited by?
INF-gamma from Th1 cells.
29
What do Treg cells do?
When activated they secrete IL-10 and TGF-beta which are anti-inflammatory.
30
What are the 4 Cs of the Fc region?
C- terminal Complement binding Constant Carbohydrate side chains
31
What is the function of IgG?
Serum antibody. Crosses placenta. Secondary to IgM. Monomer.
32
What is the function of IgM?
Serum antibody. Pentamer. Primary response before IgM.
33
What is the function of IgA?
Mucosa antibody. Does not bind compliement.
34
What is the function of IgE?
Type I Hypersensitivity. On the surface of mast cells and basophils. Monomer. Antihelmithic.
35
Which lymph nodes drain the foregut, midgut and hindgut?
Celiac, Superior Mesenteric and Inferior Mesenteric. Just like the arterial supply.
36
What are the two lymphatic drainage ducts and what do they drain?
Right Lymphatic Duct - Right side of the body above the diaphragm. Thoracic Duct - Everything else and drains into the subclavian and jugular junction.
37
Which three proteins regulate serum iron during disease?
Ferritin increases as intracellular stores increase. Hepcidin increases and prevents ferritin from releasing iron. Transferrin is sequestered by macrophages to decrease iron transfer.
38
What happens to serum amyloid, albumin, C-reactive protein and fibrinogen when the immune system is activated?
They all increase except for albumin. C reactive promotes opsonization. Fibrinogen promotes endothelial repair.
39
What does MAC defend against?
Gram Negatives
40
Describe the three ways the complement cascade can be triggered?
Classical - IgG and IgM (GM makes classic cars.) Lectin - Sugars on microbial surface Alternative - Spontaneous and surfaces
41
Which complements cause anaphylaxis?
3a, C4a, C5a
42
Which complement causes neutrophil chemotaxis?
C5a
43
Which complements make up the Membrane Attack Complex?
C5b through C9
44
Which complement induces opsonization?
C3b
45
What does C1 esterase inhibitor deficiency cause?
C1 esterase inhibitor inhibits activation of the Lectin and Alternative pathway. A deficiency leads to hereditary angioedema.
46
What does a C3 deficiency cause?
Increased risk of purulent infection. Increased susceptibility to Type III hypersensitivity.
47
What does deficiency in any of the complement from C5 through C9 cause?
Increased susceptibility to Neisseria infections.
48
What do IL-1 through IL-6 stimulate?
``` (Hot T-bone stEAKS) 1- Fever 2- T cells 3- Bone marrow 4- IgE 5- IgA 6- aKute-phase protein ```
49
Which IL is the major chemotactant for neutrophils?
IL-8
50
Which cytokine causes septic shock?
TNF-alpha
51
Which cytokine has the most activity against viruses and tumors?
INF-gamma, It is secreted by Th1 cells and it activates NK cells.
52
Which cell type is located in the follicle of a lymph node? Where are follicles located? What are their two states?
B-Cell localization and proliferation. Located in the outer cortex. They can be dormant (1o) or active (2o).
53
Which cell type is located in the paracortex of a lymph node? What type of vessel do they contain?
T Cell. High Endothelial Venules, HEV. Note: Patient's with DiGeorge's syndrome have atrophied paracorteces.
54
To which lymph nodes does the skin above the umbilicus drain?
Axillary. Just like the breast.
55
What does deficiency in Decay Accelerating Factor (DAF) cause?
DAF inhibits complement cascade and it is one of the GPI anchored proteins. It can cause paroxysmal nocturnal hemoglobinuria.
56
Which ones are the anti-inflammatry cytokines?
IL-10 and TGF-beta. Inhibit T cell action. Secreted by Tregs.
57
What triggers the release of Interferons?
Cells infected by viruses release it to prime surrounding cells against viruses.
58
How do cell primed by interferons respond to viral infection?
Viral dsRNA activates RNAase L and protein kinase. Translation is inhibited.
59
What is ti called when a T cell becomes nonreactive?
Anergy
60
What is the B Cel surface marker?
CD20 and CD21 (EBV receptor)
61
What is the T cell surface marker?
CD3 (TCR helper) and CD28 (binds B7)
62
What is the Macrophage surface marker?
CD14 (TLR coreceptor) and CD40
63
What is the NKC surface marker?
CD56
64
What can directly activate macrophages?
LPS can activate TLR receptors, CD14, and cause systemic effects.
65
Name three bacteria which undergo antigenic variation?
Salmonella has two flagella, Borrelia can undergo recombination, Neisseria gonorrhoeae can change their pili.
66
What is the difference between passive versus active immunity?
Passive is the acquisition of preformed antibodies. Active requires exposure to an antigen and creation of the antibody.
67
After which 4 exposures are Igs administered?
Tetanus, Botulinum, HBV and Rabies. (To Be Healed Rapidly)
68
Which vaccines are generally live vaccines?
Smallpox, yellow fever, chicken pox, polio, MMR and influenza (Live! Small yellow chickens with Sabin, MMR and the flu.)
69
Live versus killed vaccine. Pros and cons.
Live elicits a cellular response and last longer, but may reactivated. Killed is safer but has weaker and shorter immunity.
70
Mechanism of action of type I hypersensitivity.
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
Mechanism of action of type II hypersensitivity.
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
Mechanism of action of type III hypersensitivity.
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
Mechanism of action of type IV hypersensitivity.
``` T Cell mediated. Four Ts. T cells Transplant Rejection TB skin test Touching (contact dermatitis) ```
74
What type of hypersensitivity causes the complications of ABO mismatch in transfusion?
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
Which infections are more likely in a deficiency of granulocytes?
Staph, Burkholderia cepacia, Serratia, Nocardia (Bacteria) Candida, & Aspergillus (Fungi)
76
Which infections are more likely in a deficiency of complement?
Neisseria
77
Which infections are more likely in a deficiency of B cells?
Bacteria are the same as asplenic patients (SHiNE SKiS) Strep pneumo, H Flu, Neisseria, E Coli, Salmonella, Klebsiella, GBS. Plus enteroviruses and Giardia.
78
What are the three B Cell disorders? Give a quick synopsis of the etiology.
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
What are the four T Cell disorders? Give a quick synopsis of the etiology. (AIDS is not one)
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
Along with histamine, which other molecule is released by mast cells in degranulation?
Tryptase
81
What are the four combined B Cell & T Cell disorders? Give a quick synopsis of the etiology.
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
What are the three phagocyte disorders? Give a quick synopsis of the etiology.
1. Leukocyte Adhesion Def I (Def in LFA-1 integrin) 2. Chediak-Higashi (Microtubule Dysfunction) 3. Chronic Granulomatous Disease (Def NADPH Oxidase)
83
What is the pathophysiology of hyperacute rejection? Timeline?
Type II with pre-formed Ab. Thrombosis in vessels leads to ischemia. Minutes.
84
What is the pathophysiology of acute rejection? Timeline?
Either cellular (CTL against MHC) or Humoral (Abs form after Trx) leads to vasculitis & lymph infiltrate. Weeks to months.
85
What is the pathophysiology of chronic rejection? Timeline?
T cells detect antigens presented on Trx's MHC. (Not MHC itself) Months to Years.
86
What is the pathophysiology of Graft-versus-Host?
Marrow Trx T Cells rejects the host. Maculopapular rash, hepatosplenomegaly, jaundice.
87
What are the two Calcineurin inhibitors and what is their main side effect?
Cyclosporine (binds cyclophilin) & Tracolimus (binds FKBP) they PREVENT IL-2 TRANSCRIPTION and thus T Cell activation. Nephrotoxicity, HTN, Hyperlipidemia
88
What are the mechanism, use and toxicity of Sirolimus/Rapamycin?
mTOR inhibitor through FKBP. Used for renal Trnx. Anemia, Thrombocytopenia, Leukopenia, insulin resistance.
89
What are the mechanism, use and toxicity of Basiliximab?
IL-12R blocker. Renal trnx. Edema, HTM & tremor.
90
What are the mechanism, use and toxicity of Azathioprine?
Inhibit purine synthesis. General trnxs, rheumatoid, Crohn, & glomerulonephritis. Can cause anemia, leukopenia & thrombocytopenia.
91
What are the mechanism, use and toxicity of Glucocorticoids? (In immunosupression)
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
What are the mechanism and use of Infliximad and Adalimumab?
MAB against TNF-a used for RA, IBD, ankylosing spondylitis, and psoriasis.(Inlfix pain in da lims)
93
What are the mechanism and use of Natalizumab?
Anti alpha4-integrin (leukocyte adhesion) used in MS and Crohn.
94
What are the mechanism and use of Infliximad and Omalizumab?
Anti IgE used in asthma.

First Aid & Firecracker (7 decks)

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