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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
What happens when RBC hemoglobin precipitates?
obstruct vessels, rupture RBC
26
ankyrin
attaches RBC integral membrane protein to spectrin
27
spectrin
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
28
What is the most important micro-organism that thrives on hemoglobin?
Plasmodium (protozoa that causes malaria)
29
What happens if RBCs have impaired ATP production?
Na/K ATPase fails | RBC swell and burst
30
What happens when RBC antioxidant system fails?
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
31
glutathione (GSH)
eliminates peroxide | req. NADPH
32
cytochrome b5 reductase
reduces methemoglobin back to hemoglobin | req. NADH
33
precipitated hemoglobin
Can be due to hemoglobinopathy or oxidized hemoglobin can result in hemolytic anemia can see heinz bodies, sickle cells, and bite cells
34
hemolytic anemia
excess RBC lysis
35
bite cells
macrophages take hemoglobin clumps our of RBCs in big bites resulting in deformed RBCs
36
How do RBCs make energy?
1. glycolysis: ATP and NADH | 2. pentose shunt: NADPH
37
Glucose 6 phosphate dehydrogenase deficiency
first failure point in pentose shunt pathway | see bite cells
38
DAF
slows down complement fixation
39
hypochromia
lack of color
40
anisocytosis
abnormal distribution of RBC sizes
41
poikilocytosis
abnormal RBC shape
42
morphology of RBC that don't have enough hemoglobin
hypochromic and/or microcytic
43
polychromasia
blue: seen in accelerated production due to residual mRNA | due to rapid RBC loss
44
methylene blue
binds negative (nucleic acids)
45
eiosin
``` red binds positive (ex: some proteins) ```
46
reticulocyte
immature RBC: lots is polychromes
47
Heinz bodies
clumps of oxidized hemoglobin
48
hemoglobinopathy
genetic defect in hemoglobin structure
49
Diseases selected for by providing heterozygotes from malaria
1. sickle cell anemia | 2. G6PD
50
schistocytes
red cell fragments due to mechanical lysis or microangiopathic process
51
hemoglobin: hematocrit ratio
1: 3
52
What does a turbid blood specimen indicate?
fatty meal: increases scatter | looks like you have more hemoglobin
53
hematocrit
RBC/blood volume
54
What will clumping of RBC look like on blood count?
red cells counted as one cell 1. artificially increased MCV 2. artificially reduced red cell count 3. reduced hematocrit
55
What will a hematology analyzer count bands as?
neutrophils
56
What will a hematology analyzer count blasts as?
lymphocytes or monocytes
57
What will a hematology analyzer count red cell fragments as?
platelets
58
What will a hematology analyzer count platelet clumps as?
``` 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
Iron deficiency 1. morphology 2. labs 3. causes
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
RDW
red cell distribution width | correlates with anisocytosis
61
transferrin
binds Fe3+ and transports it
62
ascorbate
cofactor for duodenal reductase (ferrireductase)
63
ferrireductase
Fe3+ -> Fe2+ | conversion needed to absorb iron in intestines
64
DMT-1
active transport of iron from GI tract into intestinal cells | regulation: iron dependent
65
ferritin
binds iron (Fe2+) for storage
66
ferroportin
transport iron out of intestinal cell into plasma export of iron from iron storage pool increases in response to low iron
67
hephaestin
ferioxidase: Fe2+ -> Fe3+ | need oxidized to transport in plasma (keep away from bacteria)
68
iron reservoir in body
macrophages in bone marrow, liver, spleen
69
hepcidin
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
serum iron
direct measure of transferrin-bound iron
71
total iron binding capacity (TBIC)
total amount of transferrin in circulation
72
transferrin saturation
serum iron/total transferrin
73
serum ferritin
direct measurement of storage pool iron
74
soluble transferrin receptor
second line measurement of storage pool iron | increases on macrophages in iron starved state
75
High hepcidin levels
results in anemia
76
Low hepcidin levels
get too much iron stored: liver disease, cardiomyopathy, diabetes
77
Beta thalassemia 1. morphology 2. lab 3. confirmation
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
MCV
mean cell volume
79
hemoglobin A2
two delta globins bound to two alpha globins | migrates differently from hemoglobin A
80
hemoglobin F
fetal hemoglobin: two alpha globins and two gamma globins
81
hemoglobin A
adult hemoglobin: two alpha and two beta globins
82
Alpha thalassemia 1 trait
1 defective alpha allele | no clinical/ lab findings
83
alpha thalassemia 2 trait 1. morphology 2. lab 3. Dx
``` 2 defective alpha alleles 1. mild microcytic anemia 2. normal Hgb electrophoresis as adults 3. PCR based 3% african americans ```
84
Hgb Bart's
four defective alpha alleles: four gamma chains | lethal in utero or soon after birth
85
Hgb H disease
3 defective alpha alleles 1. variable microcytic anemia 2. Hgb electrophoresis: 15-30% Hgb H
86
Hgb H
four beta chains
87
Folate deficiency
megaloblastic anemia
88
B12 deficiency
takes years of inadequate dietary intake megaloblastic anemia increased homocysteine and methyl malonate neurological problems
89
cobalamin
B12
90
What happens if you give a B12 deficient person folate without B12?
worsens neurological symptoms
91
haptocorrin (HC)
binds Vit. B12 in saliva
92
IF
intrinsic factor: binds B12 in jejunum after HC dissolves away made by parietal cells in stomach
93
megaloblastic anemia
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
How are folate derivatives stored?
polyglutamation
95
anemia of chronic inflammation
infection increases IL-6 which stimulates the liver to increase hepcidin causing anemia get decreased transferrin, increased ferritin
96
Erythroferrone (ERFE)
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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