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SS- Heme > Structure and Function/ Hematopoiesis > Flashcards

Structure and Function/ Hematopoiesis Flashcards

1
Q

eosinophil

A

< 5% of leukocytes

increase in allergic reactions and parasite infections

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2
Q

basophil

A

< 1% of leukocytes

degranulates in allergic reaction and only rarely increased in non-neoplastic conditions

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3
Q

monocyte

A

3-8% of blood leukocytes
APC and phagocytes
increased numbers in inflammation

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4
Q

macrophages

A

derived from monocyte

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5
Q

lymphocyte

A

20-30% of blood leukocytes
increase in viral syndrome or neoplastic process
predominantly T-cells, then B and NK cells

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6
Q

reactive lymphocytes

A

increase in viral syndromes

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7
Q

neutrophils

A

40-70% of leukocytes
phagocytosis, degranulation (lysozyme), NETs (neutrophil extracellular traps made of chromatin) in bacterial infection
rapid turnover

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8
Q

IL-8

A

attracts neutrophils

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9
Q

CD11a/CD18 complex

A

integrins: grab and hold neutrophils

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10
Q

Leukocyte adhesion defect

A

CD18 defect

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11
Q

Wiskott-Aldrich Syndrome

A

cytoskeleton dysfunction of T cells (some neutrophil dysfunction)

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12
Q

How do neutrophils recognize pathogens?

A
  1. TLR
  2. Complement receptors
  3. Fc receptors
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13
Q

Chemokines secreted by neutrophils

A
  1. CXCL2
  2. IL-8
  3. TNF
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14
Q

chronic granulmatous disease

A

myeloperoxidase deficiency

neutrophils can’t make hypochlorite

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15
Q

left shift

A

lots of new granulocytes due to bacterial infection: bands, metamyelocytes, myelocytes

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16
Q

toxic granulation

A

neutrophils have primary granules suggesting infection

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17
Q

primary granules

A

blue granules

usually only seen in early myeloid precursors in bone marrow

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18
Q

secondary granules

A

salmon pink granules seen in mature neutrophils

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19
Q

platelets

A

concentrations 100x that of white cells
9-10 day lifespan
Function:
1. primary hemostatic plug (adherence/activation/aggregation)
2. stimulate coagulation cascade (fibrin formation/clot retraction)
3. stimulate wound healing (fibroblast growth/migration)
4. immune function (including antigen presentation and pathogen activation)

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20
Q

What happens to platelets in iron deficient patients?

A

increases

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21
Q

PF4

A

platelet factor 4 (platelet cytokine)

kills malaria pathogen

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22
Q

What causes reduced production of all coagulation factors?

A

liver disease (liver makes all the factors)

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23
Q

What causes reduction of coagulation factors (and often platelets)?

A

excessive activation platelets and cascade

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24
Q

giant platelets

A

occurs when platelet production is ramped up or in abnormal production due to disease that effect bone marrow

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25
Q

What happens when RBC hemoglobin precipitates?

A

obstruct vessels, rupture RBC

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26
Q

ankyrin

A

attaches RBC integral membrane protein to spectrin

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27
Q

spectrin

A

links the RBC plasma membrane to the actin cytoskeleton, and functions in the determination of cell shape, arrangement of transmembrane proteins, and organization of organelles

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28
Q

What is the most important micro-organism that thrives on hemoglobin?

A

Plasmodium (protozoa that causes malaria)

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29
Q

What happens if RBCs have impaired ATP production?

A

Na/K ATPase fails

RBC swell and burst

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30
Q

What happens when RBC antioxidant system fails?

A
  1. oxidized-SH groups on hemoglobin crosslink: Hgb denaturation/precipitation
  2. oxide iron (Fe3+++) can’t carry O2: hemoglobin containing Fe3+++ (methemoglobin) and patient is hypoxic
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31
Q

glutathione (GSH)

A

eliminates peroxide

req. NADPH

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32
Q

cytochrome b5 reductase

A

reduces methemoglobin back to hemoglobin

req. NADH

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33
Q

precipitated hemoglobin

A

Can be due to hemoglobinopathy or oxidized hemoglobin
can result in hemolytic anemia
can see heinz bodies, sickle cells, and bite cells

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34
Q

hemolytic anemia

A

excess RBC lysis

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35
Q

bite cells

A

macrophages take hemoglobin clumps our of RBCs in big bites resulting in deformed RBCs

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36
Q

How do RBCs make energy?

A
  1. glycolysis: ATP and NADH

2. pentose shunt: NADPH

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37
Q

Glucose 6 phosphate dehydrogenase deficiency

A

first failure point in pentose shunt pathway

see bite cells

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38
Q

DAF

A

slows down complement fixation

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39
Q

hypochromia

A

lack of color

40
Q

anisocytosis

A

abnormal distribution of RBC sizes

41
Q

poikilocytosis

A

abnormal RBC shape

42
Q

morphology of RBC that don’t have enough hemoglobin

A

hypochromic and/or microcytic

43
Q

polychromasia

A

blue: seen in accelerated production due to residual mRNA

due to rapid RBC loss

44
Q

methylene blue

A

binds negative (nucleic acids)

45
Q

eiosin

A 
red
binds positive (ex: some proteins)
46
Q

reticulocyte

A

immature RBC: lots is polychromes

47
Q

Heinz bodies

A

clumps of oxidized hemoglobin

48
Q

hemoglobinopathy

A

genetic defect in hemoglobin structure

49
Q

Diseases selected for by providing heterozygotes from malaria

A
  1. sickle cell anemia

2. G6PD

50
Q

schistocytes

A

red cell fragments due to mechanical lysis or microangiopathic process

51
Q

hemoglobin: hematocrit ratio

A

1: 3

52
Q

What does a turbid blood specimen indicate?

A

fatty meal: increases scatter

looks like you have more hemoglobin

53
Q

hematocrit

A

RBC/blood volume

54
Q

What will clumping of RBC look like on blood count?

A

red cells counted as one cell

  1. artificially increased MCV
  2. artificially reduced red cell count
  3. reduced hematocrit
55
Q

What will a hematology analyzer count bands as?

A

neutrophils

56
Q

What will a hematology analyzer count blasts as?

A

lymphocytes or monocytes

57
Q

What will a hematology analyzer count red cell fragments as?

A

platelets

58
Q

What will a hematology analyzer count platelet clumps as?

A 
lab artifact (EDTA can expose antigens and cause clumping due to Ab): not always detected: can resolution an artificial thrombocytopenia
use citrate instead for these cases
59
Q

Iron deficiency

  1. morphology
  2. labs
  3. causes
A
  1. microcytic, hypochromia, anisocytosis, poikilocytosis
  2. reduced ferritin, reduced transferrin saturation, increased TIBC, iron reduced, (reduced RBC)
  3. chronic blood loss or deficient diet
60
Q

RDW

A

red cell distribution width

correlates with anisocytosis

61
Q

transferrin

A

binds Fe3+ and transports it

62
Q

ascorbate

A

cofactor for duodenal reductase (ferrireductase)

63
Q

ferrireductase

A

Fe3+ -> Fe2+

conversion needed to absorb iron in intestines

64
Q

DMT-1

A

active transport of iron from GI tract into intestinal cells

regulation: iron dependent

65
Q

ferritin

A

binds iron (Fe2+) for storage

66
Q

ferroportin

A

transport iron out of intestinal cell into plasma
export of iron from iron storage pool
increases in response to low iron

67
Q

hephaestin

A

ferioxidase: Fe2+ -> Fe3+

need oxidized to transport in plasma (keep away from bacteria)

68
Q

iron reservoir in body

A

macrophages in bone marrow, liver, spleen

69
Q

hepcidin

A

increased by: increased levels of transferrin-bound iron and inflammation
decreased in low iron;
action: decreases ferroportin expression in macrophages and enterocytes (internalize and degrades it)

70
Q

serum iron

A

direct measure of transferrin-bound iron

71
Q

total iron binding capacity (TBIC)

A

total amount of transferrin in circulation

72
Q

transferrin saturation

A

serum iron/total transferrin

73
Q

serum ferritin

A

direct measurement of storage pool iron

74
Q

soluble transferrin receptor

A

second line measurement of storage pool iron

increases on macrophages in iron starved state

75
Q

High hepcidin levels

A

results in anemia

76
Q

Low hepcidin levels

A

get too much iron stored: liver disease, cardiomyopathy, diabetes

77
Q

Beta thalassemia

  1. morphology
  2. lab
  3. confirmation
A
  1. very microcytic, hypochromia, target cells
  2. normal or increased RBC, low MCV
  3. hemoglobin electrophoresis: hemoglobin A2; in severe cases hemoglobin F is detected
78
Q

MCV

A

mean cell volume

79
Q

hemoglobin A2

A

two delta globins bound to two alpha globins

migrates differently from hemoglobin A

80
Q

hemoglobin F

A

fetal hemoglobin: two alpha globins and two gamma globins

81
Q

hemoglobin A

A

adult hemoglobin: two alpha and two beta globins

82
Q

Alpha thalassemia 1 trait

A

1 defective alpha allele

no clinical/ lab findings

83
Q

alpha thalassemia 2 trait

  1. morphology
  2. lab
  3. Dx
A 
2 defective alpha alleles
1. mild microcytic anemia
2. normal Hgb electrophoresis as adults
3. PCR based
3% african americans
84
Q

Hgb Bart’s

A

four defective alpha alleles: four gamma chains

lethal in utero or soon after birth

85
Q

Hgb H disease

A

3 defective alpha alleles

  1. variable microcytic anemia
  2. Hgb electrophoresis: 15-30% Hgb H
86
Q

Hgb H

A

four beta chains

87
Q

Folate deficiency

A

megaloblastic anemia

88
Q

B12 deficiency

A

takes years of inadequate dietary intake
megaloblastic anemia
increased homocysteine and methyl malonate
neurological problems

89
Q

cobalamin

A

B12

90
Q

What happens if you give a B12 deficient person folate without B12?

A

worsens neurological symptoms

91
Q

haptocorrin (HC)

A

binds Vit. B12 in saliva

92
Q

IF

A

intrinsic factor: binds B12 in jejunum after HC dissolves away
made by parietal cells in stomach

93
Q

megaloblastic anemia

A

occurs in impaired DNA syntesis: large nucleus and chromatin does not condense down into heterochromatin
cytoplasm continues to mature
RNA that is blue begins to degrade and hemoglobin’s red color predominates

94
Q

How are folate derivatives stored?

A

polyglutamation

95
Q

anemia of chronic inflammation

A

infection increases IL-6 which stimulates the liver to increase hepcidin causing anemia
get decreased transferrin, increased ferritin

96
Q

Erythroferrone (ERFE)

A

Stimulated by EPO
Down regulates hepcidin: iron moves into transport (transferrin) to make it more available for RBC precursors
B-thalassemia: increased ERFE can cause hemochromatosis

SS- Heme (13 decks)

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