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IHO > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What are the 3 main inflammatory cytokines?

A

-TNFalpha
-IL-1
IFNgamma

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2
Q

What are the 2 names of direct anti-microbial molecules tissue cells can make?

A
  • defensins

- cathelicidins

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3
Q

Where are dendritic cells found?

A
  • skin, lymph nodes, spleen, within/underneath mucosal epithelia
  • also in thymus (present self-antigens to developing T cells)
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4
Q

How many types of receptors do lymphocytes have? macrophages? neutrophils?

A
  • lymphocytes- 1 kind of receptor (all identical)

- Macrophages and neutrophils have many different receptors on cell surface

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5
Q

How many days does it take to induce the adaptive immune system?

A
  • 7-10 days
  • rare B and T lymphocytes with identical antigen recognition sequences must find each other to proliferate
  • another 1-5 days to develop memory
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6
Q

What parts of the body/ job do B cells protect? T cells?

A
  • B cells: protect extracellular spaces (tissue fluids, blood, secretions) by releasing antobodies = humoral immunity
  • T cells: survey surfaces of cells looking for mutations= cell-mediated immunity
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7
Q

What CD molecule is expressed on all T cells?

A

CD3 (part of the T cell receptor)

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8
Q

What CD molecules are found on all B cells?

A
  • CD79a and CD79b

- both part of B cell receptor complex

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9
Q

Do MHC class 1 and 2 present to T cells, B cells, or both?

A
  • only to T cells (MHC 1 to CD8 and MHC 2 to CD4)

- B cell receptors see antigen and secrete antibodies

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10
Q

What 2 Ig molecules can activate complement?

A

2 IgGs or 1 IgM molecule

GM makes “classic” cars - classic complement pathway

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11
Q

Which is the only antibody that can cross the placenta?

A

IgG

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12
Q

Which Ig is the B cell antigen receptor?

A

IgD

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13
Q

Which Ig is mostly in secretions and has a chain called the “Secretory Component”. What does it do?

A
  • IgA

- Secretory component makes it resistant to digestive enzymes

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14
Q

Which Ig attaches to mast cells and controls mediators of inflammation?
-also role in parasite resistance

A
  • IgE
  • causes mast cells to make prostaglandins, leukotrienes, and cytokines
  • mast cells degranulate releasing histamine
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15
Q

What would cause increased reticulocytes?

A

-blood loss or hemolytic processes
(normal reticulocyte count if immune system destroys red cell precursors)
-should correspond with hematocrit (low hematocrit should increase reticulocytes)

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16
Q

What causes macrocytic cells? (MCV>100)

A
  • B12, folic acid deficiency

- drugs that impair DNA synthesis

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17
Q

What causes microcytic cells? (MCV<80)

A
  • iron deficiency
  • Thalassemia trait
  • Anemia of chronic disease
  • Sideroblastic anemias
18
Q

With low serum B12, what can be detected as elevated in serum?

A

-elevated serum methylmalonic acid levels

19
Q

What are common lab findings with iron deficiency?

A
  • decreased Hgb
  • microcytic MCV
  • decreased serum iron
  • increased or normal TIBC
  • decreased iron saturation
20
Q

Which is more severe: Thalassemia alpha or beta?

A

-alpha

21
Q

What’s the pathogenesis of Anemia of Chronic Disease?

A
  • cytokine production causes:
  • decreased EPO production
  • suppression of erythroid progenitors
  • blocking transferrin iron release
  • normal/increased ferritin
22
Q

What is the order of complement activation in Classical Pathway?

A

C1, C4, C2, C3, C5, C6, C7, C8, C9

23
Q

What defective parts of the complement pathway result in meningococcal infections?

A
  • Membrane attack complex (C5-C9)

- Alternative pathway (Factor B and D, properdin)

24
Q

What type of enzyme does the proteolytic steps of Classical complement pathway?

A

-serine esterases

25
Q

What parts of complement are covalently attached to surface by thioester bonds?

A

C4b and C3b

26
Q

What results from absence or mutation in C1 inhibitor of complement classic pathway?

A

hereditary angioedema

-Tx: anabolic steroids to increase C1 INH synthesis

27
Q

C4b interacts with which complement receptors on white cells?

A

CR1

28
Q

What is the classical pathway C3 convertase called?

A

C4b2a

29
Q

What are the 2 ways to form C4b2a?

A
  • Classic: C1q interaction with C1r and C1s

- MBL: MASP-1 and MASP-2

30
Q

What is the name of the alternative pathway C3 convertase?

-What stabilizes it?

A

C3bBb

-Stabilized by Properdin

31
Q

What are the 2 C5 convertases?

A
  • C4b2aC3b

- C3bBbC3b

32
Q

Binding of C5b-7 to what prevents membrane insertion of MAC?

A

S protein

33
Q

What does Vitronectin (CD59/ Protectin) do and where is it located?

A

-on self membranes to inhibit binding of C9 and its polymerization (saves it from MAC)

34
Q

What is an example of a fluid phase inhibitor of C3 Convertase?

A

Factor H

  • if it sees C3bBb floating around, it binds and dissociates Bb to inactivate it
  • “Decay acceleration of the convertase”
  • Factor H also can be cofactor for cleavage by Factor I (if by sialic acid residue= on host cell)
35
Q

What can result from deficiency in DAF (CD55) and CD59?

A
  • complement mediated intravascular hemolysis in paroxysmal nocturnal hemoglobinuria (PNH)
  • increased RBC MAC-mediated lysis
36
Q

What parts of complement pathway are inflammatory mediators?

A

C3a and C5a

  • bind anaphylatoxin receptors
  • CD88 = C5a receptor
37
Q

What receptor is for clearing immune complexes?

Which for augmentation of humoral immunity?

A

-CR1 for clearing ICs
-CR2 (CD21) for augmentation of humoral immunity (C3 fragments interact with complement receptors)
-CR1 (CD35) on RBCs
CR2 (CD21) on B cells

38
Q

What should you always do if you see nucleated RBCs?

A

-bone marrow biopsy

39
Q

What do you add to H antigen to make A antigen? B?

A

A: N-acetylgalactosamine
B: galactose

40
Q

What causes Febrile Transfusion Reactions?

A

-recipient antibodies against donor WBC

41
Q

What happens in Graft vs. Host disease?

A
  • donor lymphocytes attack host
  • usually fatal
  • prevent by irradiating products

IHO (7 decks)

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