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TT BL and DD Exam1 > BL 2 > Flashcards

BL 2 Flashcards

1
Q

Define reticulocyte count + absolute reticulocyte count

A
  • Reticulocyte count: % of reticulocytes when 1000 RBCs are counted
    • Absolute reticulocyte: %of reticulocyte x RBC count
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2
Q

What anemias are going to be associated w/ decrease in exercise tolerance?

A

Any of them, but mainly Iron deficiency, Anemia due to renal dysfunction

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3
Q

How is hepcidin regulated, and what does it do?

A

Hecidin is released from hepatic cells during high iron intake or infection/inflammation –> increased accumulation of ferritin –> lower plasma iron

(save it for a rainy day or keep away from bad guys)

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4
Q

Where does absorption of Iron from diet take place? What form of Fe is it in?

A

duodenum

Ferric iron arrives at duodenum -> converted to Ferrous iron (via surface reductase) -> gets absorbed as Ferrous ion (via DMT1 transport) then

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5
Q

Which anemia is associated with sore tongue?

A

B12 and folate deficiency

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6
Q

Erythropoietin (EPO) made by what in response to what?

A

Made by kidney cells in response to hypoxia and promotes erythropoiesis

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7
Q

Granulopoiesis makes what 3 types of granulocytes? Via what growth factor?

A

Neutrophils, Eosinophils, Basophils

via G-CSF or GM-CSF

*GM = Granulocyte-monocyte

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8
Q

IL-5 Promotes production of which granulocytes?

A

eosinophils

*count fingers

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9
Q

IL-3 Promotes production of which granulocytes?

A

basophils

*count fingers

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10
Q

order of progression of the different precursor and mature cell types in erythroid maturation

A

HSC -> CFU-GEMM (pluripotent stem cell) -> BFU-E (progenitor) -> CFU- E (progenitor) -> Pronormoblast -> basophilic normoblast -> polychromatophilic normoblast -> orthochromatic normoblast -> reticulocyte -> erythrocyte

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11
Q

order of progression of the different precursor and mature cell types in granulocytic maturation

A

HSC > CFU-GEMM > CFU-GM/G > myeloblast > promyelocyte > myelocyte > metamyelocyte > band > granulocyte (basophil, neutrophil, or eosinophil)

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12
Q

order of progression of the different precursor and mature cell types in monocytic maturation

A

HSC > CFU-GEMM > CFU-GM/M > Monoblast > Promonocyte > Monocyte > Macrophage

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13
Q

order of progression of the different precursor and mature cell types in megakaryocytic maturation.

A

HSC > CFU-GEMM > CFU-Meg > Megakaryoblast > Promegakaryocyte > megakaryocyte > platelet

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14
Q

When looking at a bone marrow biopsy, what is the normal myeloid:erythroid ratio around?

A

2:1 - 4:1

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15
Q

Does BM hyperplasia indicate increased destruction or decreased production?

A

increased destruction

  • Growth factors should signal marrow to make more of what is being destroyed
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16
Q

What would CML and leukemoid rxns indicate in peripheral blood smears?

A

increased blood neutrophils indicating hyperplasia

17
Q

Would MCV be high or low in B12/Folate deficiency anemias?

A

High

deficiency -> impaired DNA synth > cell cannot progress from G2 to M stage. So cell continues to grow w/o division

18
Q

examples of PMN cells

A

Neutrophils, basophils, eosinophils

(granulocytes) - cell whos nucleus is lobulated due to granules

19
Q

What is the opposite of an immunogen?

A

Toleragen

delivered antigen that does not = immune response AND furthermore prevents immune response to subsequnt exposure to immunogen.

20
Q

How must the antigenic determinant of an antigen fit the lymphocyte receptor (at hypervariable region) to be activated? (3 things must happen)

A
  1. Fit must be specific
  2. Nearby receptors simultaneously bound by antigen
  3. Other cell surface molecules costimulated
21
Q

humoral vs cell mediated immunity

A

a. Humoral: this is the antibody mediated response,
i. Occurs extracellularly where all the bacteria etc. live.
ii. B lymphocytes are the main cells involved.
iii. B cells transform into plasma cells which secrete antibodies. Cytokines are also released.
iv. Can be transferred by serum.

b. Cell mediated immunity:
i. T lymphocytes become activated → activate macrophages, NK cells, and cytotoxic T lymphocytes.
ii. Cytokines are released when the T cells become activated. Not transferred by serum.

22
Q

How can malignancies/sepsis result in anemia?

which cytokines are involved?

A

-Malignancy/sepsis > TNF > ↓ iron store availability > ↓ production of EPO > ↓ Erythropoiesis

–Malignancy/sepsis > INF-β ↓ erythropoiesis

23
Q

How can chronic infection/inflammation result in anemia?

which cytokines are involved?

A
  • IL-1 ↓ iron mobilization -> ↓ production of EPO
  • IL-6 > high hepcidin
  • INF-γ -> ↓ erythropoiesis
24
Q

How can renal insufficiency result in anemia?

A

↓ EPO made in juxtaglomerular region of kidneys -> ↓RBC production = anemia

25
Q

Can you get vit B12 from plants? What about folate?

A

No - B12 (cobalamin) not from plants - meat, eggs, milk

Yes - Folate can be from plants - meat, milk, bread, fruits, vegies, fish

26
Q

Mechanism how B12 is absorbed for use

A

Food releases B12 in stomach acid → gastic parietal cells secret intrinsic factor IF and binds to B12 → B12 absorbed in terminal ileum → released from IF, binds to transcobalamin binding protein II (TcII) → B12 + TcII are transported to liver for storage or BM for use

27
Q

Mechanism how folate is absorbed for use

A

Food w/ folate → absorbed in jejunum → altered (hydrolyzed, reduced, and methylated) → distributed to liver for storage (as methyltetrahydrofolate) + tissue for use → liver undergoes “turnover”

28
Q

Would you have high or low retic count for B12 and folate deficiency? why?

A

Low due to impaired erythropoiesis

29
Q

Would you have high or low retic count for hemolytic anemias?? why?

A

High

Lytic -> so you must compensate. (nothing is stopping you)

30
Q

Hereditary spherocytosis and thalassemias are considered hemolytic anemias, T or F?

A

True

microcytic, hemolytic

31
Q

Mneumonic to remember basic shape of hemoglobin O2 dissociation curve:

A

○ “30-60, 60-90, 40-75”
partial pressure - % saturation

At partial pressure of 30 mmHg, % saturation = ~60%
At partial pressure of 60 mmHg, % saturation = ~90%
At partial pressure of 40 mmHg, % saturation = ~75%

32
Q

What is P50 indicating?

A

partial pressure of O2 at which O2 carrying protein (Hb) is 50% saturated

33
Q

at high O2 [ ], does myoglobin have a high or low affinity for O2?

A

low affinity

*notices a lot of O2, not worried about having some

34
Q

at low O2 [ ], does myoglobin have a high or low affinity for O2?

A

High affinity

  • think of chart low affinity = left shift = higher affinity
  • senses O2 is low and starts getting greedy
35
Q

At birth what is the % of HbF vs HbA?

A

65-95% HbF and 20% HbA

36
Q

How does HbF bind O2 different than HbA?

A

Binds 2,3-BPG poorly
↑er Bohr effect

→ favor O2 transfer from maternal→ fetal circulation

37
Q

Ferrous or Ferric iron in Hb binds to oxygen? What happens if it is ferric?

A

Ferrous

Ferric iron → methemoglobin → decreased O2 binding

38
Q

Describe humoral immunity:

  • occur intracellulary or extracellularly?
  • Which lymphocyte is mainly involved?
  • Are cytokines released?
  • Can it be transferred by serum?
A

Humoral: this is the antibody mediated response,

i. Occurs extracellularly where all the bacteria etc. live. 
ii. B lymphocytes are the main cells involved. 
iii. B cells transform into plasma cells which secrete antibodies. Cytokines are also released. 
iv. Can be transferred by serum.
39
Q

Describe Cell mediated immunity:

  • occur intracellulary or extracellularly?
  • Which lymphocyte is mainly involved?
  • Are cytokines released?
  • Can it be transferred by serum?
A

Cell mediated immunity:

i. Intracellular
   ii. T lymphocytes become activated → activate macrophages, NK cells, and cytotoxic T lymphocytes. 
iii. Cytokines are released when the T cells become activated. 
    iv. Not transferred by serum.

TT BL and DD Exam1 (23 decks)

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