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Strom - Hematology > 3.17.14* Hematopoiesis > Flashcards

3.17.14* Hematopoiesis Flashcards

Prestudy PPT* Lecture Notes* Powerpoint

1
Q

Bands are counted by hematology analyzer as

A

bands and other immature granulocytes are counted as neutrophils

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2
Q

What stimulates erythropoesis?

A

hypoxia. In a PBS you will see more of the precursor.

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3
Q

what is the most direct representation of iron stores in the body?

A

ferritin.

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4
Q

Q. Low iron stores will show:

a. reduced serum iron, reduced soluble transferrin receptor
b. increased TIBC, reduced ferritin
c. increased serum iron, increased soluble transferrin receptor
d. macrocytosis
e. reduced TIBC, reduced transferrin

A

b. reduced ferritin, increased TIBC

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5
Q

What is seen in a patients bone marrow in a patient with excess GM-CSF

A

myeloid hyperplasia

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6
Q

another name for pluripotent stem cell

A

blasts

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7
Q

precursors to RBCs

A

common myeloid progenitor

burst forming unit (BFU)

colony forming unit (CFU)

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8
Q

What molecule regulates granulocyte growth (granulopoiesis)?

A

GM-CSF

G-CSF (mostly neutrophils)

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9
Q

What stimulates erythropoeitin (Epo) production in the renal peritubular cells?

A

hypoxia (thus renal failure usually results in anemia).

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10
Q

What cell type makes platelets?

A

megakaryocytes

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11
Q

What molecule regulates platelet production? Where is it produced?

A

thrombopoietin (Tpo) made constantly by the liver.

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12
Q

How to Epo/Tpo receptors cause intracellular signalling?

A

through Jak-2 kinases

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13
Q

What molecules are needed to make heme?

A

iron B6 Succinyl CoA Glycine (needs B12 and folate)

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14
Q

What is globin synthesis?

A

the protein portion of hemoglobin, needs non-mutated genes to be made correctly.

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15
Q

What types of RBC do you see in iron deficiency anemia?

A

small read cells without much hemoglobin (hypochromic) anisocytosis poikilocytosis

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16
Q

Anisocytosis

A

variation in size

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17
Q

poikilocytosis

A

variation in shape

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18
Q

A high RDW (red cell distribution width) means

A

that the red cell size distribution is increased (anisocytosis)

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19
Q

iron oxidation state

a. dietary iron
b. heme iron
c. iron:transferrin

A

a. ferric (3+)
b. ferrous
c. ferric

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20
Q

What augments iron uptake?

A

vitamin C, helps turn into ferrous state.

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21
Q

What is included in the iron reserve pool?

A

macrophages in bone marrow, liver, and spleen bound to ferritin

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22
Q

What enterocyte receptor uptakes iron?

A

DMT-1

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23
Q

What is DMT-1 regulated by?

A

physiologic conditions, iron-dependent

24
Q

What receptor exports iron from the enterocyte into the serum?

A

ferroportin (also exports iron from macrophages)

25
Q

What regulates ferroportin activity?

A

hepcidin reduced feroportin expression, made in liver

26
Q

Serum iron levels detect

A

transferrin-bound iron.

27
Q

What is the correlation between serum ferritin and iron storage levels?

A

serum ferritin concentration is proportional to the amount of storage pool iron in the body.

28
Q

How do macrophages sense the need for iron mobilization and how do macrophages respond?

A
  1. iron deficiency means low transferrin bound iron, this leads to decreased hepcidin production.
    a. macrophages upregulate transferrin receptors on their surface (this can be measured as increased “soluble transferrin receptor” level.
    b. macrophages upregulate ferroportin receptor on their surface
29
Q

What is total iron binding capacity?

A

the amount of transferrin circulating. Transferrin production is increased during low iron intake leading to an increased total iron binding capacity.

30
Q

Low dietary iron lab results

a. serum ferritin
b. serum iron
c. transferrin saturation
d. soluble transferrin receptor
e. total iron binding capacity
f. free iron

A

a. low serum ferritin
b. low serum iron (bound to transferrin)
c. low transferrin saturation
d. high soluble transferrin receptor levels
e. high total iron binding capacity
f. low free iron

31
Q

hepcidin function

A

negative regulator of ferroportin expression. High hepcidin means low ferroportin

32
Q

How is hepcidin production regulated?

A

Normal levels of iron increase hepcidin production, and hepcidin reduces ferroportin expression (in macrophages and enterocytes – it becomes internalized and degraded). So at low iron levels, hepcidin expression is reduced, ferroportin expression is increased, and more iron is put into the transport system so as to feed red cell production.

33
Q

What is thalassemia?

A

genetic defects leading to globin production deficiency.

34
Q

What often distinguishes thalassemia from iron deficiency?

A

a. thalassemia has normal or elevated RBC count, while iron deficiency usually leads to decreased RBC count.
b. target cells (however they are also seen in liver disease)
c. thal is more microcytic than IDA

35
Q

What test is diagnostic for thalassemia?

A

hemoglobin electrophoresis test

36
Q

describe the beta globin locus

A

chromosome 11

1 “beta globin” gene 4 beta globin homologues 1 pseudogene

Three are expressed in utero; a fourth, psi-beta, is a pseudogene awaiting an evolutionary assignment; the fifth (delta) is primarily expressed in the fetus, with a low level of expression after birth; and the last is the form expressed in adults. (delta gamma beta is the order of expression)

37
Q

What is the defect in beta thalassemia

A

There is a mutation in the beta globin allele and the relative amount of delta globin (hemoglobin A2) is increased. In severe cases, fetal hemoglobin may also be expressed.

38
Q

What are the three types of hemoglobin

A

Hemoglobin A (normal): alpha2beta2

Hemoglobin A2: alpha2delta2

Fetal hemoglobin: alpha2gamma2

39
Q

Describe the alpha globin locus

A

chromosome 16:

2 adult alpha globin genes

2 fetal zeta globin genes

40
Q

What is the defect in alpha thalassemia?

A

defect in either alpha allele on one or both chromosomes (up to 3 alleles total)

41
Q

Alpha thalassemia 1 trait

A

only 1 alpha allele is mutated, no phenotype

42
Q

Alpha thalassemia 2 trait

A

when both copies of one alpha allele are mutated

a. mild microcytic anemia
b. excess Hgb Barts (gamma) at birth
c. Normal Hgb electrophoresis as adults
d. 3% AAs

43
Q

Hemoglobin H disease

A

(three alpha globin alleles are mutated)

a. variable microcytic anemia
b. 15-30% Hgb H (seen by electrophoresis)

44
Q

Hgb H

A

beta globin tetramers, functional

45
Q

Hgb Bart’s

A

four defective alleles. Fetus/infant dies before beta globin gene can be significantly produced to make Hgb H. Common in southeast asia.

46
Q

How are B12 and folate involved in DNA synthesis?

A

They are needed to make THF, which is a required cofactor for amino acid and nucleic acid synthesis. Also are required specifically to methylate UTP to make TTP (thymidine).

47
Q

How is B12 (cobalamin) absorbed?

A

a. Haptocorrin binds B12 in saliva, intrinsic factor secreted by parietal cells in the stomach binds B12 after haptocorrin is digested away in the ileum.
b. intrinsic factor bound to B12 is absorbed in the ileum, and gets transported to the bloodstream.

48
Q

What happens if DNA synthesis of red blood cells is interrupted?

A

(by B12, folate, intrinsic factor)

a. fewer RBCs produced, production halts after one or two cell divisions (normally 5) so RBCs can have large nuclei, RNA. This appearance is “megaloblastic.”

49
Q

pernicious anemia

A

due to impaired B12 uptake

50
Q

What can cause megaloblastic anemia

A

Impaired B12 uptake (Pernicious anemia)

Impaired folate uptake malabsorption malnutrition

Drug effect

i. nucleoside analogues (HAART)
ii. Ribonucleotide reductase inhibitors (Hydroxyurea)

Intrinsic Bone marrow dysfunction

i. Myelodysplastic syndrome(s)

51
Q

If hepcidin production is increased, what happens to ferroportin level?

A

they are decreased, so reduced availability of iron storage and dietary iron.

52
Q

What biological process leads to increased hepcidin production?

A

infection/inflammation through IL-6

53
Q

Anemia of chronic inflammation has increased/decreased levels of:

a. Serum iron (bound to transferin)
b. Serum ferritin
c. total iron binding capacity
d. transferrin saturation
e. bone marrow iron stores

A

normocytic anemia caused by AIDS, TB, RA, and cancer. (storage can still be high, but will not be mobilized due to inflammation and increased hepcidin)

a. normal/low serum iron (bound to transferrin) because transferrin is taken from the serum by RBC precursors in the bone marrow.
b. increased ferritin
c. decreased TIBC
d. increased transferrin saturation, unknown
e. increased bone marrow iron stores

54
Q

How can you diagnose anemia of chronic inflammation?

A

bone marrow biopsy for increased iron storage

55
Q

You have a problem with your gastric parietal cells. This can cause: a. impaired Hgb synthesis b. impaired epo production c. impaired DNA synthesis d. impaired iron uptake e. rapid red cell lysis

A

C. Parietal cells are needed to make intrinsic factor to absorb B12. Without B12 you will have impaired DNA synthesis.

56
Q

Anemic patient with RA does not respond to iron. His ferritin is 560 (n is

a. TIBC, serum iron
b. serum B12, folate
c. epo level
d. oxygenation status
e. hgb electrophoresis

A

a. in chronic inflammation, increased heparin decreases ferroportin (you cannot mobilize storage iron)

57
Q

if ferritin is increased, do they have an iron deficiency?

A

no, they have a problem with transport!!

Strom - Hematology (6 decks)

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