B3.083 Big Case Anemia Flashcards

1
Q

definition of anemia

A

defined as decreased red cell mass

usually decrease hematocrit, hemoglobin, RBC

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2
Q

describe the progression of normal Hb levels at various ages

A

decreases from neonates to 3 months
slowly increases over childhood
levels out at about age 10
men > women

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3
Q

most common cause of anemia worldwide

A

iron deficiency anemia

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4
Q

what given reticulocytes their bluish color

A

RNA in cytoplasm

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5
Q

what are the 3 stages of RBC development

A

normoblast (nucleated RNC)
reticulocyte
mature RBC

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6
Q

what cell type recycles old/damaged RBCs?

A

macrophages

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7
Q

what happens to iron from old RBCs?

A

transported in circulation from macrophages to bone marrow via transferrin

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8
Q

signs and symptoms of anemia

A

pallor
conjunctival pallor
fatigue
chest discomfort, palpitations

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9
Q

3 primary causes of anemia

A
  1. decreased RBC production
  2. increased RBC destruction
  3. bleeding
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10
Q

how do you check to see if bone marrow is working?

A
other blood counts
reticulocyte count (best indicator)
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11
Q

RBC lifespan

A

120 days

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12
Q

how many RBCs normally replaced each day?

A

1/120 or 1%

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13
Q

how long are newly released RBCs identifiable as reticulocytes?

A

a day

1% of circulating RBCs

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14
Q

normal absolute reticulocyte count

A

50,000

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15
Q

why are reticulocytes released earlier in most types of anemia?

A

anemia causes EPO levels to rise

EPO stimulation leads to early release

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16
Q

result of EPO stim on retic count

A

can potentially double reticulocyte count even in absence of increased RBC production

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17
Q

what is an expected retic count for an anemic patient with a normal bone marrow

A

50000 x 2 x 2 = 200000
doubles release rate
live for 2 days instead of 1

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18
Q

retic count >200000

A

adequate marrow function in anemic pt

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19
Q

retic count >300000

A

hemolysis likely

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20
Q

retic count <100000 in anemic

A

suboptimal RBC production

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21
Q

RPI

A

retic production index
makes corrections for Hct and RBC lifespan
RPI = retic % x (HCT/45) x (1/RMT)
where RMT is retic maturation time

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22
Q

RPI = 1

A

individual without hemolysis or blood loss

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23
Q

RPI > 2-3

A

increased

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24
Q

RPI < 2 in an anemic

A

inappropriately low

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25
Q

what are two causes of inadequate RBC production (retic normal or low)

A
  1. hypoproliferative: impaired RBC production, lower than normal RBC precursors in marrow
  2. ineffective erythropoiesis: impaired RBC production despite increased marrow RBC precursors
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26
Q

what are two causes of increased RBC destruction

A

hemolysis

blood loss

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27
Q

red cell indices

A

Hgb
Hct
RBC count

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28
Q

MCV

A

mean corpuscular volume
Hct/RBC count
primary classification of anemia

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29
Q

MCH

A

Hgb/ RBC count

30
Q

MCHC

A

Hgb/Hct

31
Q

macrocytic

A

MCV > 100

defective DNA synthesis or reticulocytosis

32
Q

microcytic

A

MCV < 80

decreased Hgb production

33
Q

normocytic

A

MCV 80-100

34
Q

poikilocytosis

A

variation in RBC shape

35
Q

aniscytosis

A

variation in RBC size

RDW quantifies this variability

36
Q

how much iron/day is eaten/absorbed

A

10-15 mg/day in diet
5-10% absorbed
more absorbed in iron def, pregnancy, erythroid hyperplasia, hypoxia

37
Q

can you absorb Fe2+ or Fe3+ better

A

Fe2+

ability to regulate absorption is limited

38
Q

where does iron absorption occur

A

proximal small intestine

39
Q

describe the pathways of iron transport and storage

A

Fe2+ absorbed and oxidized to Fe3+
Fe3+ bound tightly to transferrin in blood
Fe3+ is transferred to cells and reduced to Fe2+ form, then inserted into heme or stored
storage iron (Fe3+) bound to ferritin

40
Q

ferritin in blood

A

correlated with body iron stores

41
Q

what is hepcidin and what does it do?

A

peptide produced in the liver

interacts with ferroportin to inhibit iron release from villus enterocytes and macrophages (less iron in blood)

42
Q

what is ferroportin

A

iron transport channel that moves iron from cells into blood

43
Q

what modulates hepcidin levels

A

high plasma iron or inflamm = more hepcidin
low iron = less hepcidin (more iron let into blood)
HFE gene modulates production

44
Q

reasons for decreased hepcidin

A

iron def
HFE mutation
ineffective erythropoiesis
liver disease

45
Q

why does hepcidin increase in inflammation

A

make less iron available to pathogen

46
Q

lab tests used to assess iron status

A

serum iron
TIBC
serum ferritin

47
Q

serum iron

A

transferrin

bound iron being transported in the blood

48
Q

TIBC

A

total iron binding capacity

total amount of transferrin in the blood

49
Q

transferrin saturation

A

serum iron/TIBC (%)

50
Q

serum ferritin

A

reflect body iron stores

51
Q

when is serum iron low

A

iron def

inflammation

52
Q

when is TIBC high

A

iron def

53
Q

when is TIBC normal or low

A

inflammation

54
Q

when is serum ferritin low

A

iron def

55
Q

when does serum ferritin increase

A

inflammation

acute phase reactant

56
Q

sTfR

A

soluble transferring receptor

circulating protein derived from cleavage of the membrane transferrin receptor on erythroid precursor cells

57
Q

what does sTfR concentration in serum indicate

A

directly proportional to erythropoietic rate
inversely proportional to tissue iron availability
similar to serum transferrin
usually increased in iron def patients

58
Q

what is the sTfR-ferritin index

A

sTfR/log[ferritin]
sTfR reflects erythropoiesis
ferritin reflects tissue iron stores
high index - sign of iron deficiency

59
Q

sTfR-ferritin index in patients with ACD

A

<1

60
Q

sTfR-ferritin index in patients with iron def anemia or iron def plus ACD

A

> 2

61
Q

where is most of your iron located

A

RBCs

62
Q

how much iron / day is required for erythropoiesis

A

20 mg
most recycled from old RBCS
1-2 mg new from gut
1-2 mg lost via sloughing of enterocytes

63
Q

what are 3 pathogeneses of iron def

A
  1. blood loss
  2. failure to meet increased requirements
  3. inadequate absorption
64
Q

what is the usual cause of iron def anemia

A

chronic blood loss

women - menstrual blood

65
Q

characteristics of iron def anemia

A
microcytic, hypochromic
retic count not increased
anis- and poik- in more severe cases
serum ferritin usually low
serum iron low, TIBC high
66
Q

describe the evolution of iron def anemia

A
  1. depletion from stores
  2. depletion or stores and transport
  3. all stores and transport gone, erythron iron starts to decrease
67
Q

treatment for iron def anemia

A

most patients are initially with oral iron unless there is an absorptive problem
dietary sources + FeSO4 BID
severe = RBC transfusion

68
Q

indication for iv iron

A

severe symptomatic anemia requiring accelerated erythropoiesis
failure of oral from gi intolerance of absorption issues
cancer w chemo associated anemia
chronic renal disease
heavy ongoing bleeding

69
Q

when do different lab tests reflect oral iron therapy

A

peak retic count 7-10 d
increased Hb and Hct 14-21 d
normal Hb and Hct 2 mo
normal iron stores 4-5 mo

70
Q

other causes of microcytic anemia

A

iron withheld from red cell precursors (inflamm)
globin gene defects (thalassemias)
defects in heme synthetic pathways (sideroblastic)

71
Q

lab findings in anemia of inflamm

A

normocytic or mild microcytic
not many shift cells
low serum iron, normal or low TIBC, normal or high ferritin
relatively low EPO level for degree of anemia