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TT BL and DD Exam1 > Friday Review > Flashcards

Friday Review Flashcards

1
Q

In neutropenia, what are two ways that can cause decreased bone marrow production?

A
  1. acquired

2. congenital

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2
Q

3 congenital disorders that can lead to neutropenia?

A
  1. Kostmann syndrome
  2. Shwachmann-Diamond
  3. Cyclic neutropenia
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3
Q

Kostmann syndrome

A
  • most severe congenital neutropenia
  • dont make precursors
  • G-CSF mutation
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4
Q

Shwachmann-Diamond syndrome

A 
fat malabsoprtion
pancreatic insufficiency
bony abnormality
growth delay
autosomal recessive
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5
Q

Cyclic neutropenia

A

linked to apoptosis in marrow

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6
Q

In neutropenia, what are two ways that can cause increased turn over rate?

A
  1. Immune

2. Non immune

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7
Q

3 examples of syndromes that cause autoimmune neutropenia (increased turnover rate)

A

SLE, Evan’s syndrome, Felty’s syndrome

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8
Q

What does G-CSF do?

How?

A

Treat neutropenia

§ Give G-CSF at 3-5 μg/kg daily or every other day (stimulating factor -tell BM to make more neutrophil)

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9
Q

What does “left shift” indicate?

A

increase in segs and bands (Neutrophils)

*think shifting left towards the start - the first responders

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10
Q

Basophilia cause by?

A

primarily food or drug hypersensitivity

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11
Q

Eosinophilia cause by?

A

allergic disorders, parasitic infections, and drug reactions

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12
Q

Monocytosis caused by?

A
  • Hematologic disorders, lymphomas
  • Collagen Vascular Disease
  • Granulomatous Disease
  • Infection
  • Malignancy
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13
Q

Chediak Higashi syndrome

  • what type of disorder is it?
  • molecular defect
  • functional defect
  • clinical presentation
  • does it cause neutropenia or neutrophilia?
A

Granule defect disorder

-molecular defect: alteration in membrane fusion -> giant leaky granules
-functional defect: neutropenia, large leaky granules that dont work
-clinical presentation: hepatosplenomegaly:
Oculocutaneous albinism, nystagmus photophobia. Recurrent infections of skin, ect.

causes neutropenia (only one of the neutrophil disorders that do)

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14
Q

Myeloperoxidase deficiency

  • what type of disorder is it?
  • molecular defect
  • functional defect
  • clinical presentation
A
  • what is it? granule defect disorder
  • functional defect: deficiency myeloperoxidase (killing bacteria power)
  • clinical presentation: overall healthy, increased fungal infection, associated with diabetes

“myelo, my little toe has gangrene”

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15
Q

Leukocyte adhesion deficiency I

  • what type of disorder is it?
  • molecular defect
  • functional defect
  • clinical presentation
A

adherence disorder “the -itis”

-functional defect:
Neutrophilia.
Decreased adherence to endothelial surface leading to a defect in movement of neutrophils to infected tissue sites.
(especially bad after surgery)

-clinical presentation:
Recurrent soft tissue infections (skin, mucous membranes), gingivitis, mucositis, peridontitis, cellulitis, abscesses.
Delayed separation of umbilical cord/omphalitis.
Poor wound healing.

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16
Q

IFN gamma is made by which helper t cell

A

Th1

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17
Q

IL-2 is made by which helper t cell

A

Th1

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18
Q

2 ways that CTL can give “kissof death”

A
  1. CTL’s fas ligand (CD95L) binds “death receptor” Fas (CD95) on target→ linkage activates apoptosis pathway
  2. Secrete lytic granules (containing granzyme proteases) → Secrete perforins to allow granzymes to penetrate → proteases trigger apoptosis
19
Q

Useful markers on B cells:

A

CD20

20
Q

Useful markers on T cells:

A

○ CD3 → found on all T cells
§ It’s the transducer of the antigen-binding signal to inside the cell.
○ CD4 → found on all T helpers
○ CD8 → found on CTL

21
Q

Chemokine function

A 
cause inflammation
(small short mediators)
22
Q

Cytokine function

A

affect behavior of same or another cell

23
Q

Main lymphokines made by Th1, Th2, Th17 and Treg cells, and their biological functions.

A
  1. Th1 → interferon gamma IFNγ and IL-2 →Pro-inflammatory→ Attracts/activates M1 macrophages
  2. Th2 → Interleukin 4 (IL-4) →Pro-inflammatory →attracts/activates M2 macrophages
  3. Th17 → Interleukin 17 (IL-17) → Attracts/activates M1 macrophages
  4. Treg → TGFβ →FoxP3 → (IL-10) → Anti-inflammatory cytokine
24
Q

2 types of mitogens

-what do they do?

A

2 plant lectins: PHA, PWM

-cause t cell mitosis:
Essentially they ‘fool’ every T cell they contact into thinking they’re being bound by antigen.

25
Q

Diff between mitogen and antigen?

A

mitogen doesnt actually bind to site on T cell (only binds CD3 domain that controls signal tranduction from antigen binding chains)

26
Q

CTL recognize what class?

Helper T cells?

A

CTL: class I think that there is only one type of killer T vs 5 helper

Helper T cells: Class II

27
Q

Which class of MHC is intrinsic pathway? Extrinsic?

A

Class I MHC “intrinsic pathway”

  • Allows cells to say, “look what I’ve been making” (not endocytosed)
  • All cells have Class I
  • Class I is regulated by CTL
  • CTL have CD8

Class II MHC “extrinsic pathway”

  • “look what I’ve been eating”
  • Professional APC (ie: dendritic cell)
  • Helper T cells are activated by Class II
28
Q

Which immunoglobins responds most to T independent antigens?

A

IgM

-makes sense bc IgM is the first Ig.

29
Q

Which HLA make up class I MHC?

A

HLA-A

HLA-B

30
Q

Which HLA make up class II MHC?

A

HLA D

31
Q 
Which class of MHC do APCs have? 
Who recognizes it?
A

Class II MHC

-recognized by T-helper cells

32
Q

Which types of cells have Class I MHC?

Who recognizes it?

A

all nucleated cells

-recognized by CTLs

33
Q

If you are a helper cell, which part of you recognizes MHC type II?

A

CD4

34
Q

HLA-D are all part of the Class __?__ MHCs

A

Class II MHCs

35
Q

Which HLA is mainly involved in transplant?

A

HLA-DR

36
Q

Which HLA is mainly involved in autoimmune diseases?

A

HLA-DP and DQ

*but not always….. or hardly ever on his table

37
Q

Which HLA leads to type I diabetes?

A

HLA DQ

38
Q

If Th1 is activated, and CTLs are not during a transplant, what happens?

A

Rej

39
Q

Which is the most important to match for transplant? MHC class I or II?

A

It would be preferential to match MHC Class II (HLA-D match)

40
Q

If HLA-D match but HLA-A and B do not:

A
  • preferential
    ○ No MLR (mixed leukocyte rxn)
    ○ No Th1 activation and therefore no IL-2 produced
    ○ Few CTLs activated (bc needs IL-2)

MOST IMPORTANT TO MATCH for transplant

41
Q

If HLA-A and B match but HLA-D do not:

A

○ Activate Th1 cells
○ No direct CTLs activated
○ Rejection still occurs, but more slowly

42
Q

in T cell selection, how many points of recognition are there? Where?

A

6 CDRs total

  • 4 bind to MHC
  • 2 bind to peptide
43
Q

Which HLA is involved w/ Ankylosing spondylitis?

A

HLA-B27

-90% greater chance of getting AS if you have the gene

TT BL and DD Exam1 (23 decks)

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