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Hematology 2 Lec > IDA, ACI, SDA > Flashcards

IDA, ACI, SDA Flashcards

1
Q

● Cells are smaller than usual

A

MICROCYTIC

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2
Q

MICROCYTIC

● Size:

A

<6 um

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3
Q

● Caused by 1 or more cell division due to the depression of mean corpuscular hemoglobin concentration (MCHC)

A

MICROCYTIC

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4
Q

● Anemia = division of RBC making the cell

A

MICROCYTIC

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5
Q

● Microcytic also inhibit

A

HYPOCHROMIA

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6
Q

● ↓ MCHC = ↓ overall hemoglobin concentration (no red or pink coloration of blood) =

A

HYPOCHROMIC

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7
Q

● Due to the problem of hemoglobin (there would be an impairment with the hemoglobin in the hemoglobin synthesis or an abnormality to heme or globin)

A

HYPOCHROMIC

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8
Q

● Components of a Hemoglobin:

(any abnormality of the two can cause a defect in the hemoglobin)

A

Heme and Globin

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9
Q

● Under a larger classification of anemia

A
  1. IRON DEFICIENCY ANEMIA (IDA)
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10
Q
  1. IRON DEFICIENCY ANEMIA (IDA)
    ● Etiology: A cause of anemia where in there is an (?)
A

abnormal iron metabolism

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11
Q

ANEMIA OF ABNORMAL IRON METABOLISM:

A
  1. Iron Deficiency Anemia
  2. Anemia of Chronic Disease (Sideroblastic Anemia)
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12
Q

Normal Hgb production and synthesis is dependent on (3 major requirement of Hb to be functional):

A

● Polypeptide chain (Adult Hb: Alpha & Beta chains)
● Protoporphyrin IX
● Iron (needs to be integrated to the Hgb in order to function well)

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13
Q

● Polypeptide chain (?)
● Protoporphyrin IX

A

Adult Hb: Alpha & Beta chains

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14
Q

(needs to be integrated to the Hgb in order to function well)

A

● Iron

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15
Q

The body contains approx:

A

4,000 mg Fe (60%: in form of Hgb)

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16
Q

IRON METABOLISM

A

For storage

For use

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17
Q

 Largest source of iron is from the ingestion of food

A

For storage

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18
Q

For storage

 Diet (?) → Mucosal cell (oxidized by the cells of the (?) to become Fe3+ or ferric form) → passed onto the bloodstream (transported to the bloodstream and(?) where it can be stored; Fe3+ will be bound to a storage protein known as (?) → forms FERRITIN

A

Fe2+ or ferrous form

duodenum and jejunum

liver

Apoferritin

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19
Q

: a storage protein that carries iron up to the bloodstream in which once the Fe3+ will go to bloodstream it will become a Ferritin

A

Apoferritin

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20
Q

: storage form of iron in the liver cells

A

Ferritin

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21
Q

stores metabolically active iron which we can get anytime if our body demands increased iron use

A

Ferritin

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22
Q

Iron → bloodstream → mononuclear phagocytic cells in the BM and other tissues

A

For use

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23
Q

: storage protein that transports Fe2+, Fe3+, and Apoferritin in the blood stream

A

Transferrin

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24
Q

carries iron from the bloodstream to the bm

A

Transferrin

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25
Q

: incorporates the iron to the hemoglobin.

A

Mononuclear phagocytic cells

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26
Q

: process in which the mononuclear phagocytic cells will incorporate the ferrous to rbc (hemoglobin)

A

Ropheocytosis

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27
Q

FACTORS AFFECTING IRON ABSORPTION
Promote Absorption
Reduce Absorption

A
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28
Q

Ferrous form

A

Promote Absorption

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29
Q

Ferric Form

A

Reduce Absorption

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30
Q

Inorganic Form

A

Promote Absorption

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31
Q

Organic Form

A

Reduce Absorption

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32
Q

Acids (HCl, Vit. C)

A

Promote Absorption

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33
Q

Alkalis (antacids, pancreatic juices)

A

Reduce Absorption

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34
Q

Solubilizing agents (Sugar, Amino Acids)

A

Promote Absorption

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35
Q

Precipitating agents: phosphates

A

Reduce Absorption

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36
Q

Iron Deficiency

A

Promote Absorption

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37
Q

Iron Excess

A

Reduce Absorption

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38
Q

Increased erythropoiesis

A

Promote Absorption

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39
Q

Decreased erythropoiesis, infection

A

Reduce Absorption

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40
Q

Iron in [?] form will be stored in ferritin

A

ferric

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41
Q

: stomach; increases the chance of the iron to be absorb

A

HCl

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42
Q

: medications

A

● antacids

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43
Q

: alkaline, so if iron is exposed in this kind of environment, it will have less absorption or decrease absorption rate in the intestines

A

● pancreatic juices

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44
Q

it will have less absorption or decrease absorption rate in the intestines

A

● pancreatic juices

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45
Q

● Iron is absorbed in an increased level

A

Iron Deficiency

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46
Q

● faster absorption because cells needs it

A

Iron Deficiency

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47
Q

● Regulatory hormones will try to block the absorption of iron to the intestines

A

Iron Excess

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48
Q

● absorption should not exceed

A

Iron Excess

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49
Q

● There is a need for you to absorb the iron so that it can be stored also in some parts of the cell

A

Increased erythropoiesis

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50
Q

● Iron absorption is also decreased

A

Decreased erythropoiesis, infection

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51
Q

IDA is caused mainly by 4 reasons:

A
  1. INTAKE OF IRON IS INADEQUATE FROM THE LEVEL OF DEMAND OF THE BODY.
  2. THE NEED FOR IRON EXPANDS AND COMPENSATION IS NOT MET
  3. IMPAIRED ABSORPTION OF IRON
  4. CHRONIC LOSS OF HEMOGLOBIN FROM THE BODY
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52
Q

Fe lost is not replaced

A

1mg/day

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53
Q

● Normally,[?] of Iron is lost and if the lost iron is not replaced by intaking or from the diet, then that could lead to the erythrocyte/ RBC being slowly starved of iron.

A

1mg/day

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54
Q

● Usually, Fe is lost in the

A

mitochondria of desquamated cells.

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55
Q

 when our cells die in the skin, they slough off =

A

desquamate

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56
Q

 the [?] has iron content

A

mitochondria

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57
Q

 inside the cells that was desquamated is the

A

mitochondria

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58
Q

● Although, the body conserves iron from the [?], but it is not enough because the level that was lost is not the same to what the body can conserve

A

senescent RBC

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59
Q

● A replacement of [?] of iron from the diet every day is needed to maintain the RBC production.

A

1 mg

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60
Q

● If you have an inadequate intake eventually, [?] will be decreased since it is the source of RBCs iron (not present in the diet)

A

iron stores

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61
Q

● If the [?]:
 ↓ hemoglobin production (hemoglobin needs iron) = not present in the diet = anemia

A

iron stores are decreased

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62
Q

a. Iron needs increase →

A

no compensation

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63
Q

● no compensation for

A

iron needs

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64
Q

Iron needs increase → no compensation

● usually occurs during

A

infancy, childhood, adolescence, pregnancy and nursing (breastfeeding)

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65
Q

● during infancy, childhood, adolescence, the body needs an iron for

A

rapid growth

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66
Q

● need a lot of iron so that the body can grow in synchrony with RBC production.

A

babies

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67
Q

● [?] with no compensation = anemia.

A

↑ iron needs

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68
Q
  1. IMPAIRED ABSORPTION OF IRON
A

a. Malabsorption

b. Genetic mutations

c. Decreased stomach acidity

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69
Q

: most of the nutrition including iron is being malabsorbed (not absorbed properly)

A

Celiac disease

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70
Q

● A mutation in the regulatory protein called

A

matriptase 2 protein

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71
Q

: a regulatory protein which normally would keep hepcidin inactivated or not triggered but in a normal condition, so that it won’t stop ferroprotein to help in iron absorption

A

● Matriptase 2 Protein

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72
Q

: a regulatory/blocking hormone that blocks the absorption of iron in the intestinal lumen by binding to ferroportin

A

 Hepcidin

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73
Q

: helps in the absorption of iron to the intestinal lumen in the absence of hepcidin

A

 Ferroportin

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74
Q

 In the mutation of matriptase 2, it activates

A

hepcidin

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75
Q

: increased in production = ferroportin will be inactivated = iron will not be absorbed in the lumen of the intestine = low iron or absorption

A

 Activation of hepcidin

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76
Q

: continues production of hepcidin

A

● Activation of matriptase

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77
Q

: one of the factors that promote absorption

A

● acidity

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78
Q

 if the stomach has a [?], that means that iron could not be absorbed very well

A

decreased acidity

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79
Q

 example: [?] has something to do with GIT (stomach: acidic part of our body)

A

gastrectomy or bariatric surgery

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80
Q

: ferric is not reduced back to ferrous (Fe2+ or ferrous is the absorbable form of iron)

A

 ↓ stomach acidity

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81
Q

an alkaline; it will bind iron and decrease the rate of iron absorption

A

● Antacids

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82
Q

Loss of small amount of [?] from the body develops over a prolonged period of time.

A

heme iron

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83
Q

● Overtime, [?] decreases until it impairs with heme/iron production

A

iron content

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84
Q
  1. CHRONIC LOSS OF HEMOGLOBIN FROM THE BODY:
A
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85
Q

: the iron in the hemoglobin is passed out in the urine

A

 Hemolysis (Paroxysmal Nocturnal Hemoglobinuria)

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86
Q

Due to hemolysis

A

 Hemolysis (Paroxysmal Nocturnal Hemoglobinuria)

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87
Q

we can detect Hgb in urine

A

 Hemolysis (Paroxysmal Nocturnal Hemoglobinuria)

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88
Q

: due to ulcerations (affects the absorption of iron)

A

 Chronic GIT bleeding

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89
Q

: due to increased alcohol or aspirin ingestion (affects the absorption of iron in the GIT tract)

A

 Gastritis

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90
Q

: specially hookworm, whipworm and schistosoma spp. (involved in causing iron deficiency anemia)

A

 Parasitosis

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91
Q

: means that there is inflamed mucosal lining of the intestines (affects the absorption of iron)

A

 Diverticulitis

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92
Q

: seen in females

A

 Prolonged menorraghia (menstruation)/fibroid tumors/uterine malignancy

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93
Q

loss of RBC overtime = ↓ RBC count and iron stores are pressured to release iron so that the body can produce more Hgb and more RBC

A

 Prolonged menorraghia (menstruation)/fibroid tumors/uterine malignancy

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94
Q

 Renal diseases: such as

A

kidney stones, tumor or chronic UTI

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95
Q

IDA PATHOGENESIS

A
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96
Q

● RBC development is normal

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

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97
Q

● No evidence of iron deficiency in this phase

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

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98
Q

 RBC production continues to rely on iron available in the transport compartment

A

STAGE 2

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99
Q

 Exhaustion of the storage pool of iron (severely decreased iron stores/ferritin)

A

STAGE 2

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100
Q

 Anemia not evident

A

STAGE 1& 2

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101
Q

 Hgb and hct are low

A

STAGE 3

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102
Q

 Iron deficiency: readily display frank anemia

A

STAGE 3

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103
Q

 Compensation is remarkably slow (no iron available)

A

STAGE 3

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104
Q

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON Aka

A

Latent/subclinical IDA

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105
Q

the body’s iron reserve is sufficient to maintain the transport and functional compartments (the iron reserve is still sufficient)

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

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106
Q

● PB: will not exhibit anemia yet

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

STAGE 2

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107
Q

 Iron stores or serum ferritin begins to decrease (first) but the Hgb will still appear Normal

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

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108
Q

 RBC survival is 120 days: before iron is depleted, normal RBCs are already prodyced (RBC has enough iron and normal Hgb)

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

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109
Q

 In 120 days that the iron stores are continuously depleting, it’s still not very obvious because RBC can still compensate with it (iron stores are not yet needed due to the presence iron)

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

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110
Q

 Anemia is not evident (no evidence of IDA)

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

STAGE 2

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111
Q

● BM (iron staining): (-) iron stores

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

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112
Q

: very invasive; not performed unless there are no correlations with the symptoms and signs that a patient present

A

 BM aspiration

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113
Q

 In this stage there is really no evidence of leukemia: test should not be performed (usually skipped)

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

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114
Q

 ongoing decrease in the iron store

A

STAGE 1: PROGRESSIVE LOSS OF STORAGE IRON

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115
Q

: transport compartment.

A

 transferrin

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116
Q

 When the RBC has lost its iron = ↓serum iron & free iron and transferrin

A

STAGE 2

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117
Q

 transferrin in the serum contains iron (used up; no use for it to circulate if no iron is attached)

A

STAGE 2

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118
Q

 because the bulk of circulating RBCs are produced during adequate iron availability so the overall hemoglobin measurement is still present (iron is used up in transferrin, but still attached to Hb)

A

STAGE 2

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119
Q

 Hb: normal (no tests are required)

A

STAGE 1 & 2

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120
Q

: signifies an onset of iron deficient erythropoiesis (but we don’t have a way to know it unless we go to bone marrow to see the reticulocytes and hemoglobin)

A

 ↓ retic hemoglobin in STAGE 2

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121
Q

: smaller RBCs will be released from the bone marrow

A

 ↑ RDW in STAGE 2

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122
Q

 muscles and other iron-dependent tissues will be affected

A

STAGE 2

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123
Q

 ↓ serum iron and serum ferritin

A

STAGE 2

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124
Q

: transferrin is empty (↑ capacity to carry iron)

A

 ↑ TIBC in STAGE 2

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125
Q

: is an indirect measure of transferrin’s binding capacity

A

 Total iron binding-capacity (TIBC) in STAGE 2

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126
Q

: clump at the surface of the RBC to capture more iron

A

 ↑ Transferrin receptors in STAGE 2

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127
Q

 ↓ Transferrin

A

STAGE 2

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128
Q

: is a portion of hemoglobin where iron is integrated so the iron holds onto it; this is where iron is attached; iron will accumulate because there’s no protein attached into it (clumping on empty RBC)

A

 Free erythrocyte protoporphyrin (FEP) in STAGE 2

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129
Q

: decreases because it’s a compensatory mechanism of the body (inactivates due to lack of iron)

A

 Hepcidin in stage 2

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130
Q

a natural response of the body against iron depletion

A

 Hepcidin in stage 2

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131
Q

● BM (Prussian blue BM iron staining): (-) Hemosiderin or any iron containing cells/protein are

A

STAGE 2

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132
Q

: storage protein of iron that is usually stained in the bone marrow; not present due to lack of iron = iron deficient erythropoiesis

A

 hemosiderin in STAGE 2

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133
Q

 Hb: normal

A

STAGE 1 & 2

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134
Q

 Anemia is evident (w/ s&s; cbc shows abnormalities of rbc cells, Hb, and Hct)

A

STAGE 3

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135
Q

 ↑ FEP, ↑ Transferrin receptors , ↑ EPO (very prominent)

A

STAGE 3

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136
Q

: a hormone that compensates to anemia by increasing the amount of rbc (anemia still persist due to lack of iron)

A

 ↑ EPO

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137
Q

No specific signs and symptoms

A

IDA

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138
Q

GENERAL SYMPTOMS AND SIGNS OF ANEMIA

A

● Fatigue
● Shortness of breath
● Palor
● Palmar crease (for dark-skinned individuals)

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139
Q

(for dark-skinned individuals)

A

● Palmar crease

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140
Q

IDA HIGH RISK INDIVIDUALS

A

 Menstruating women/childbearing ages

 Adolescent girls

 Growing children

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141
Q

LOW RISK

A

 Men
 Post menopausal women

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142
Q

: inadequate iron-containing food in the diet w/ loss of rbc, iron and no compensation

A

 Menstruating women

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143
Q

: needs to have adequate iron level otherwise they are predispose to having IDA during pregnancy (needs a lot of iron content because it is needed for fetus’ growth)

A

 Childbearing ages (24 or 25 y/o)

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144
Q

prone to IDA especially during pregnancy

A

 Childbearing ages (24 or 25 y/o)

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145
Q

: breastfeeding w/ low iron (IDA) affects the baby

A

 Nursing newborns

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146
Q

 due to rapid growth (rapid erythropoiesis = more iron = more hemoglobin & more normal rbcs)

A

 Adolescent girls ;  Growing children

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147
Q

 IDA is rare (there is only 1 mg/day that is being lost)

A

 Men ;  Post menopausal women

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148
Q

 there is no rate of association to IDA

A

 Men ;  Post menopausal women

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149
Q

DEVELOPMENT OF IDA IS POSSIBLE IN

A

REGULAR ASPIRIN AND ALCOHOL INGESTION

HOOKWORMS (N. amerricanus, A. duodonale), WHIPWORM (T. trichuria), AND SCHISTOSOMA SPP. (S. mansoni, S. haematobium)

EXERCISE (SOLDIERS W/ PROLONGED MANEUVERS/RUNNERS)

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150
Q

: causes decrease acidity in the stomach = decrease/malabsorption of iron

A

 Gastritis and Chronic bleeding

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151
Q

: attach their sucking/ventral teeth of the lumen of the intestine and suck blood; blood loss is 0.03 ml per day

A

 N. americanus

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152
Q

: blood loss is 0.15-0.25 ml per day

A

 A. duodonale

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153
Q

(normal blood loss: )

A

1mg/day

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154
Q

: least effect on IDA

A

 T. trichuria (whipworm)

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155
Q

blood loss is 0.05 ml per day

A

 T. trichuria (whipworm)

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156
Q

: iron is lost through urine

A

 S. mansoni and S. haematobium

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157
Q

: is an exercise induced-hemoglubinuria

A

 March hemoglubinuria

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158
Q

the rbc`s are hemolysed due to foot pounding trauma (the iron will be salvaged and will be excreted in the urine

A

 March hemoglubinuria

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159
Q

urine is (+) hemoglubinuria)

A

 March hemoglubinuria

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160
Q

CLINICAL FEATURES Aside from general manifestations:

A

PARASTHESIA

GLOSSITIS

AGULAR CHEILOSIS

DIFFICULTY SWALLOWING DUE TO WEBS OF TISSUE IN B/W ESOPHAGUS AND HYPOPHARYNX

CHRONIC GASTRITIS; SPELOMEGALY

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161
Q

: eating disorder for non-edible things

A

 PICA

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162
Q

: due to IDA there is spooning of fingernails (spoonlike/sagging/curvy fingernails attached to the skin)

A

 Koilonychias

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163
Q

 Atrophy (↓size) of the tongue due to excessive soreness

A

GLOSSITIS

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164
Q

 IDA proliferates in the epithelial cells that makes up the tongue = soreness = tongue atrophies

A

GLOSSITIS

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165
Q

 Cracking at the mouth corners

A

AGULAR CHEILOSIS

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166
Q

RBC is Normochromic/Normocytic

A

Early IDA

167
Q

Microcytic/Hypochromic

A

Later stages IDA

168
Q

Anisocytosis/Poikilocytosis (unique shape: pencil shape elliptocytes)

A

Severe IDA

169
Q

Decreased reticulocytes

A

Retiulocytopenia

170
Q

Slightly increased platelet

A

Slight thrombocytosis

171
Q

Decreased

A

Serum Iron

172
Q

Reduced to 0 (stage 1: decreased, stage 2: cont. decreasing; stage 3: depleted)

A

Serum ferritin

173
Q

SREENING TESTS FOR IRON DEFICIENCY ANEMIA

A
  1. CLASSIC PICTURE
174
Q

IRON PROFILE TESTS

A
  1. SERUM FERRITIN
  2. SERUM IRON
  3. TOTAL IRON BINDING CAPACITY (TIBC)
  4. % SATURATION OF TIBC
  5. FREE ERYTHROCYTE PROTOPORPHYRIN (FEP)
  6. BONE MARROW ASSESSMENT
175
Q

IDA 1. CLASSIC PICTURE

A

● Anisocytosis (varying size and volume of RBCs)
o Increased RDW: >15 %
● Microcytosis
● Hypochromia
● RBC indices o Decreased MCV, MCH, MCHC
● RBC count: decreased
● Hematocrit: decreased

176
Q

For differential diagnosis of Iron Deficiency Anemia (important test to differentiate anemia)

A

IRON PROFILE TESTS

177
Q

● Reflects body’s iron stores

A
  1. SERUM FERRITIN
178
Q
  1. SERUM FERRITIN ● Normal value:
A

12-300 ug/dL

179
Q

● Sensitive indicator of iron depletion

A
  1. SERUM IRON
180
Q
  1. SERUM IRON ● Normal value:
A

50-160 ug/dL

181
Q

● Assay for serum transferrin

A
  1. TOTAL IRON BINDING CAPACITY (TIBC)
182
Q
  1. TOTAL IRON BINDING CAPACITY (TIBC) ● Normal value:
A

250-400 ug/dL

183
Q

● Ratio of serum iron: TIBC (transferrin)

A
  1. % SATURATION OF TIBC
184
Q
  1. % SATURATION OF TIBC ● Normal value:
A

20-55%

185
Q

● Builds up in RBC

A
  1. FREE ERYTHROCYTE PROTOPORPHYRIN (FEP)
186
Q
  1. FREE ERYTHROCYTE PROTOPORPHYRIN (FEP) ● Normal value:
A

10-99 ug/dL

187
Q

Intracellular storage for metabolically active iron which can be readily integrated to hemoglobin

A
  1. SERUM FERRITIN
188
Q

Decreased in Stage I (first one to deplete)

A
  1. SERUM FERRITIN
189
Q

 A little bit difficult to measure due to the marked diurnal measurement (normally increased in the morning)

A
  1. SERUM IRON
190
Q

 There is 30% difference: it is highest in the morning, lowest in the afternoon or night time

 E.g. Morning: 80 ug/dL, Afternoon/Night: 50 ug/dL

A
  1. SERUM IRON
191
Q

 Very sensitive indicator (assessment in the right time)

A
  1. SERUM IRON
192
Q

 Decreased in IDA Stage I and esp. Stage II

A
  1. SERUM IRON
193
Q

 Increased in IDA Stage II (capacity of transferrin increases because there is no longer iron stored)

A
  1. TOTAL IRON BINDING CAPACITY (TIBC)
194
Q

 Decreased in Stage II (<15%; the important tests are TIBC and % Saturation of TIBC)

A
  1. % SATURATION OF TIBC
195
Q

: a part in hemoglobin where iron is integrated

A

FEP

196
Q

 Increased in IDA Stage 3

A
  1. FREE ERYTHROCYTE PROTOPORPHYRIN (FEP)
197
Q

● Other specialized test

A
  1. BONE MARROW ASSESSMENT
198
Q

● Not performed unless required

A
  1. BONE MARROW ASSESSMENT
199
Q

● Decreased M:E ratio

A
  1. BONE MARROW ASSESSMENT
200
Q

has the most dramatic morphological change in the cytoplasm and nucleus

A

● Rubricytes/Polychromatic Normoblast (Stage IV)

201
Q

● N:C Asynchrony (structure of bm)

A
  1. BONE MARROW ASSESSMENT
202
Q

● Decreased production of hemoglobin (due to absence of iron)

A
  1. BONE MARROW ASSESSMENT
203
Q

o cytoplasm matures slower compared to the nucleus (cytoplasm maturation is lagging)

A
  1. BONE MARROW ASSESSMENT
204
Q

o cytoplasm is bluish due to decreased hemoglobin caused by IDA (no Hb = no pink coloration)

A
  1. BONE MARROW ASSESSMENT
205
Q

o second and third stage:

A

hemoglobin production

206
Q

o fourth stage (rubricyte):

A

dawn hemoglobinization (normal: cytoplasm is pinkish)

207
Q

 Aside from the iron deficiency anemia, anemia is also commonly associated with systemic diseases including CHRONIC INFLAMMATORY CONDITIONS

A
  1. ANEMIA OF CHRONIC INFLAMMATION
208
Q
  1. ANEMIA OF CHRONIC INFLAMMATION Older name:
A

Anemia of Chronic Disease

209
Q

the most common anemia among hospitalized patients (due to the long term running disease)

A
  1. ANEMIA OF CHRONIC INFLAMMATION
210
Q

Overtime you can developed this kind of anemia

A
  1. ANEMIA OF CHRONIC INFLAMMATION
211
Q

CHRONIC INFLAMMATORY CONDITIONS

A

o Rheumatoid arthritis
o Chronic infections (i.e., Tuberculosis)
o Human Immunodeficiency Virus Infection
o Malignancy

212
Q

● Originally called as “Anemia of Chronic Disease”

A

ANEMIA OF CHRONIC INFLAMMATION

213
Q

thought to be caused by blood loss (only limited to IDA)

A

ANEMIA OF CHRONIC INFLAMMATION

214
Q

inflammation is the unified factor among the aforementioned general type of conditions

A

ANEMIA OF CHRONIC INFLAMMATION

215
Q

ANEMIA OF CHRONIC INFLAMMATION CHARACTERIZED BY

A

“Sideropenia”

216
Q

 ↑ iron stores (serum ferritin) but ↓ serum iron (used for Hgb synthesis)

A

ACI

217
Q

: both iron stores and serum iron are both decreased

A

 IDA

218
Q

● Acute phase reactant

A
  1. HEPCIDIN
219
Q

 Aside for being the hormone that are being produced by the hepatocyte which regulates the absorption/realease of iron

A
  1. HEPCIDIN
220
Q

● Level usually responds to IL-6 during inflammation

A
  1. HEPCIDIN
221
Q

● Iron level in the serum is affected due to inhibited absorption, and release

A
  1. HEPCIDIN
222
Q

: a cytokine that responds to an inflammation

A

 Interleukin-6

223
Q

= ↑ Hepcidin (↓ iron level)

A

 ↑ IL-6

224
Q

Hepcidin: Iron level (normal)

A

↓ Hepcidin: ↓ Iron level

↑ Iron: ↑ Hepcidin

225
Q

■ The body responds to [?] by decreasing hepcidin

A

↓ Iron level

226
Q

: ferroportin will not be affected

A

■ ↓ Hepcidin

227
Q

: extracts the iron from the hepatocytes to store it from the plasma so that it can be utilized by the hemoglobin

A

● Ferroportin

228
Q

gets the iron from the hepatocyte (the cell that stores iron)

A

● Ferroportin

229
Q

■ To prevent overloading of iron

A

↑ Hepcidin

230
Q

: ferroportin will be inactivated = the absorption and release of iron in the plasma will be inhibited as well (normal)

A

↑ Hepcidin

231
Q

■ Inflammation = [?] Hepcidin (APR)

A

↑

232
Q

 storage from ferritin is not released

A

↑ Hepcidin

233
Q

■ Hepcidin level: corresponds to low iron level and inflammation (stimulation of IL-6) = ↓ Iron level in serum

A

↑ Hepcidin

234
Q

● Available iron in the serum before inflammation in the body will be sequestered by the macrophage and hepatocytes → disable its use for foreign organisms (their metabolism)

A
  1. HEPCIDIN
235
Q

● Chronic inflammation → chronic increase → diminished erythropoiesis

A
  1. HEPCIDIN
236
Q

o Bacteria, parasites or other foreign materials that could harm the body needs iron for their metabolism

A
  1. HEPCIDIN
237
Q

o Macrophage and hepatocytes try to get all the available iron = ↓ serum iron.

A
  1. HEPCIDIN
238
Q

o Therefore, the Hgb will now be deprived of Hgb synthesis

A
  1. HEPCIDIN
239
Q

o Overtime, both hemoglobin and erythropoiesis are affected because hemoglobin needs iron and if there is no more iron, the rate of erythropoiesis will be decreased

A
  1. HEPCIDIN
240
Q

● Second Acute Phase Reactant

A
  1. LACTOFERRIN
241
Q

● Iron binding protein in the granules of neutrophils

A
  1. LACTOFERRIN
242
Q

● Prevents phagocytized bacteria from using intracellular iron for their use

A
  1. LACTOFERRIN
243
Q

● During inflammation, it is released into the plasma-> scavenges the iron at the expense of the transferrin

A
  1. LACTOFERRIN
244
Q

● Causing RBCs to be deprived of plasma iron source

A
  1. LACTOFERRIN
245
Q
  1. LACTOFERRIN

o (?) salvaged all the available iron in the serum. The bacteria will then target the iron in the(?). [?] will try to protect the iron content intracellularly, so it will prevent the bacteria to use the(?). Macrophages engulf the (?). (?) also acts on the bacteria.

A

Macrophage and hepatocytes

RBCs/ WBCs

Lactoferrin

intracellular iron

phagocytized bacteria

Neutrophil

246
Q

o If the bacterial component enters the cell, due to phagocytosis, it can use the iron inside but if there is [?] inside them, it can’t be used.

A
  1. LACTOFERRIN
247
Q

o Inflammation = ↑ neutrophil, WBC value, and leukocytosis

A
  1. LACTOFERRIN
248
Q

o has a higher affinity for iron than transferrin. Thus, when it will be released into the plasma, it will scavenge all the iron available in the plasma at the expense of the transferrin.

A
  1. LACTOFERRIN
249
Q

o However, during inflammation because of the release of lactoferrin, it will get all the iron because it has a higher affinity to iron. Thus, it cannot utilize/transfer the iron to the BM because after collecting the iron in the plasma, the [?] will bind to macrophages and hepatocytes

A
  1. LACTOFERRIN
250
Q

o Macrophage and hepatocytes are also trying to get all the available iron in the circulation so that the foreign materials could not use it.

A
  1. LACTOFERRIN
251
Q

o The RBC does not have a receptor for [?] that is why they don’t have access to the iron that was scavenged by [?]

A
  1. LACTOFERRIN
252
Q

● Increased level of [?] → binds some iron

A
  1. FERRITIN
253
Q

: gets the iron, bring it to the BM, so that it can be incorporated to the hemoglobin of the developing RBCs.

A

o Transferrin

254
Q

● Although high in level → release of iron to developing RBC’s → slowed

A
  1. FERRITIN
255
Q

● Although high in level → release of iron to developing RBC’s → slowed

A
  1. FERRITIN
256
Q

● Similar to IDA → iron restricted erythropoiesis

A
  1. FERRITIN
257
Q

Aside from the problem with hepcidin and with lactoferrin because usually, if hepcidin is increased in level, the release of iron from the [?] will be inhibited or inactivated.

A
  1. FERRITIN
258
Q

The developing RBCs do not have a receptor for (?). Thus, it does not have access to [?]. Thus, iron now is not available for hemoglobin synthesis.

A
  1. FERRITIN
259
Q

As erythrocytes mature, there is no iron. The hemoglobin is defective.

A
  1. FERRITIN
260
Q

: contains a lot of iron derived from hepcidin and lactoferrin

A

o (+) macrophages

261
Q

signifies that the iron level, iron stores or stored iron is normal or in high level

A

o (+) macrophages

262
Q

: because it does not have access to the stored iron

A

o (-) erythrocytes

263
Q

it does not have a receptor for lactoferrin and ferritin

A

o (-) erythrocytes

264
Q

lactoferrin steals iron from transferrin

A

o (-) erythrocytes

265
Q

stored iron is not released because hepcidin is increased and ferritin could not be accessed by RBC because they don’t have the receptor for ferritin (problem in ACI)

A

o (-) erythrocytes

266
Q
  1. SERUM IRON:
     no serum available (stolen by macrophage and lactoferrin)
A

ACI

LOW

267
Q
  1. TOTAL IRON BINDING CAPACITY:
     Because it cannot bind to transferrin because there is no serum iron in the circulation
A

ACI

LOW

268
Q
  1. TRANSFERRIN SATURATION:
A

ACI

LOW TO NORMAL

269
Q
  1. TRANSFERRIN RECEPTOR:
     It signifies that the transferrin receptors are present in the cells because the transferrin receptor is a determinant that intracellular iron is still intact.
A

ACI

270
Q
  1. SERUM FERRITIN:
     Iron is stored but not used up due to hepcidin, lactoferrin and even increased in ferritin, no receptor for developing RBCs.
A

ACI

NORMAL TO HIGH

271
Q
  1. FREE ERYTHROCYTE PROTOPORPHYRIN:
     Due to failure to incorporate iron to heme
     Like IDA, failure to incorporate iron to FEP (accumulation)
A

ACI

ELEVATED

272
Q
  1. RETIC HGB:
     Due to iron restricted erythropoiesis
A

ACI

DECREASED

273
Q

● Mild anemia

A

ACI

274
Q

● Hgb concentration: 8-10g/ dL without reticulocytosis
 Due to iron restricted erythropoiesis

A

ACI

275
Q

● N/N: normochromic, normocytic

A

ACI

276
Q

● May co-exist with IDA
 IDA w/ ACI: contributes to having more iron deficiency

A

ACI

277
Q

● Leukocytosis thrombocytosis (or both)
 also manifested due to chronic inflammation probably a bacterial or viral infection

A

ACI

278
Q

BONE MARROW ● Hypoproliferation

A

ACI

279
Q

BONE MARROW ● Not usually required for diagnostic evaluation.

A

ACI

280
Q

● Therapeutic administration of Erythropoeitin → to correct ACI

A

ACI

281
Q

● Concurrently, iron is administered because serum ferritin remains unavailable.

A

ACI

282
Q

There is no iron, the Hgb cannot be developed. The developing RBCs are starved of the iron that’s needed.

A

ACI

283
Q

 The serum profile itself is enough unless there are special cases you like to confirm.

A

ACI

284
Q

: can cause a dilemma in diagnosis because iron deficiency might be missed
o: ↑ serum ferritin
o (?) Diagnosis for (?) requires ↓ serum ferritin since it is first to decline = confusion in diagnosis

A

 IDA w/ ACI

ACI

IDA

285
Q

: used to distinguish IDA from ACI

A

 Soluble transferrin receptor

286
Q

: intracellular cpt cannot acquire iron
o Transferrin receptor usually accumulates in the surface of the cells so that it can get more iron
o ↓ iron = ↓ iron store
o ↑ transferrin receptor: accumulation in the cell

A

 IDA

287
Q

: normal intracellular iron
o ↓ to normal (v/v) transferrin receptor: intracellular iron is normal

A

 ACI

288
Q

 ↑ RBC (hyperproliferative) = administer erythropoietin to raise RBC

A

ACI

289
Q

 Even though the erythropoietin can increase RBC, the RBC still lacks iron.

A

ACI

290
Q

 RBC do not have access to ferritin, so you need to administer it together with iron so that iron can be incorporated in the RBC that was stimulated by the erythropoietin therapy

A

ACI

291
Q
  1. SIDEROBLASTIC ANEMIA (SDA) CLASSIFICATION
A

A. X LINKED AND AUTOSOMAL HEREDITARY FORM
B. ACQUIRED
1. PRIMARY SIDEROBLASTIC ANEMIA (REFRACTORY)
2. SECONDARY SIDEROBLASTIC ANEMI

292
Q

 Refractory anemia: (+) sideroblastic rings/sideroblasts

A
  1. PRIMARY SIDEROBLASTIC ANEMIA (REFRACTORY)
293
Q

 Problem in the bone marrow

A
  1. PRIMARY SIDEROBLASTIC ANEMIA (REFRACTORY)
294
Q

 Usually acquired, drugs or toxins that affects bone marrow

A
  1. SECONDARY SIDEROBLASTIC ANEMIA
295
Q
  1. SECONDARY SIDEROBLASTIC ANEMIA  Example:
A

o Antitubercular drugs
o Chloramphenicol
o Alcohol
o Lead (usually and very important)
o Chemotherapeutic agents

296
Q

● Iron is abundant in the bone marrow

A
  1. SIDEROBLASTIC ANEMIA (SDA)
297
Q

● Iron → heme: defective

A
  1. SIDEROBLASTIC ANEMIA (SDA)
298
Q
  1. SIDEROBLASTIC ANEMIA (SDA)
    ● Hallmark of the disease:
A

Ringed sideroblasts

299
Q

 There is no problem in iron

A
  1. SIDEROBLASTIC ANEMIA (SDA)
300
Q

 The problem here is that iron cannot be incorporated to heme

A
  1. SIDEROBLASTIC ANEMIA (SDA)
301
Q

 Normoblast: will have iron deposits in the mitochondria; it will surround the nucleus (sideroblastic ring appearance/ ringed sideroblast)

A
  1. SIDEROBLASTIC ANEMIA (SDA)
302
Q

 The most important relationship of sideroblastic anemia to iron is that [?] will be incorporated into the [?] by [?] to the [?] (last stage of heme synthesis)

A

Fe2+

protoporphyrin rings

ferrochelatase

heme

303
Q
  1. X LINKED RECESSIVE TRAIT:
A

male (more common)

304
Q
  1. AUTOSOMAL RECESSIVE TRAIT:
A

(rare)

305
Q
  1. HEREDITARY TYPE PATHOPHYSIOLOGY
A

 decreased delta aminolevulinic acid synthase activity

306
Q

Delta aminolevulinic acid synthase problems:

A

A. Reduced affinity for pyridoxal cofactor

B. Increased sensitivity to degrading mitochondrial protease

307
Q
  1. HEREDITARY TYPE CLINICAL PRESENTATION/CONSEQUENCE
A

Hereditary sideroblastic anemia: infancy, early adulthood

308
Q
  1. HEREDITARY TYPE Patient manifests:
A

a. Iron overload
b. Mild to moderate splenomegaly and hepatomegaly
c. Diabetes related to iron deposits in pancreatic cells (Type 2)
d. Cardiac arrhythmia due to accumulating iron in myocardial cells

309
Q

 due to the disruption of the steps in heme production = accumulation of iron (60% of the iron: to be incorporated to hemoglobin and accumulated to the RBCs)

A

a. Iron overload

310
Q

 both in the serum and intracellularly

A

a. Iron overload

311
Q

● Anemia: severe

A
  1. HEREDITARY TYPE SDA
312
Q
  1. HEREDITARY TYPE SDA ● Hgb concentration:
A

6.0 g/dL (very low)

313
Q

● Blood picture:
 Microcytosis/hypochromia with anisocytosis (change in shape: dimorphic), poikilocytosis (predominance of target cells)
 Normochromic/normocytic

A
  1. HEREDITARY TYPE SDA
314
Q

● Bone marrow: remarkable hyperplasia

A
  1. HEREDITARY TYPE SDA
315
Q

● BM (Prussian blue BM iron staining): (+) excessive iron stored in macrophages

A
  1. HEREDITARY TYPE SDA
316
Q

● 40% are ringed sideroblastic (seen in polychromatophilic and orthochromatophilic stages)

A
  1. HEREDITARY TYPE SDA
317
Q
  1. HEREDITARY TYPE SDA
  2. SERUM FERRITIN:
A

high (because it is not used up)

318
Q
  1. HEREDITARY TYPE SDA
  2. SERUM IRON:
A

high (because there’s no need for the ferritin to compensate since the iron in the serum is high and not used in hemoglobin synthesis)

319
Q
  1. HEREDITARY TYPE SDA
  2. TRANSFERRIN SATURATION:
A

high

320
Q
  1. HEREDITARY TYPE SDA
  2. TIBC:
A

normal

321
Q
  1. HEREDITARY TYPE SDA
  2. FEP:
A

low to normal (differentiatial study for ACI and IDA)

322
Q

: ↑ FEP
o doesn’t have the serum iron which can incorporated to FEP to complete heme resulting in the accumulation of FEP

A

 IDA and ACI

323
Q

: ↓ FEP
o FEP is made up of protoporphyrin 9 (disruption in the previous stages = protoporphyrin 9 will not be formed)
o protoporphyrin 9 → poryphyrin rings → FEP
 porphyrin rings that makes up the FEP

A

 SDA

324
Q

 Pyroxidine theraphy

A
  1. HEREDITARY TYPE SDA
325
Q

 Delta aminolevulinic acid synthase has reduced affinity for pyridoxal cofactor

A
  1. HEREDITARY TYPE SDA
326
Q

: common acquired cause of SDA

A
  1. LEAD POISONING
327
Q

Lead interferes with porphyrin synthesis during these steps:

A

A. CONVERSION OF AMINOLEVULINIC ACID TO PHORPHOBILINOGEN BY ALA DEHYDRATASE (1st step)

B. INCORPORPATION OF IRON INTO PROTOPORPHYRIN IX BY FERROCHELATASE (2nd and last step)

328
Q

 Interference of the delta-aminolevulinic conversion to phorphobilinogen by using aminolevulinic acid (ALA) dehydrase = accumulation of amino levulinic acid because it does not convert to phorphobilinogen

A

A. CONVERSION OF AMINOLEVULINIC ACID TO PHORPHOBILINOGEN BY ALA DEHYDRATASE (1st step)

329
Q

: usually measurable/excreted in urine

A

 Aminolevulinic acid

330
Q

 Lead interferes in the incorporpation of iron into protoporphyrin IX to form heme

A

B. INCORPORPATION OF IRON INTO PROTOPORPHYRIN IX BY FERROCHELATASE (2nd and last step)

331
Q

 Accumulates iron and protoporphyrin IX, because protoporphyrin IX needs iron to complete heme synthesis

A

B. INCORPORPATION OF IRON INTO PROTOPORPHYRIN IX BY FERROCHELATASE (2nd and last step)

332
Q

will then be measurable in the RBC as FEP

A

 Protoporphyrin IX

333
Q

: ↓ FEP (because protoporphrins are not formed)

A

 Hereditary sideroblastic anemia

334
Q

: ↑ FEP (because it accumulates and the iron cannot be incorporated in it)

A

 Lead Poisoning

335
Q

 Early onset: Normocytic/Normochromic

A
  1. LEAD POISONING
336
Q

 Chronic exposure: Microcytic/Hypochromic

A
  1. LEAD POISONING
337
Q

: highest risk of lead poisoning (shows dramatic degree of anemia due to increase rate of erythropoiesis and developing rbcs)

A

 Children

338
Q

: mild effect of lead poisoning

A

 Adults

339
Q

CLASSICAL FINDING:

A

BASOPHILIC STIPPLING

340
Q

 Usually related to lead poisoning but it cannot be diagnostic because basophilic stippling can also be seen in other anemias, however there is higher degree of basophilic stippling in lead poisoning

A

BASOPHILIC STIPPLING

341
Q

: caused by the inhibition of an enzyme called Pyrimidine 59 nucleotidase

A

 Basophilic stippling

342
Q

 breakdowns ribosomal ribonucleic acid (present in reticulocytes)

A

 Basophilic stippling

343
Q

 non-nucleated → Pyrimidine 59 nucleotidase will finish off the maturation by removing the ribosomal RNA in the reticulocyte

A

 mature rbc

344
Q

 stained as pinkish salmon pink

A

 mature rbc

345
Q

: inhibits Pyrimidine 59 nucleotidase → ribosomal RNA will then aggregate in the cytoplasm of reticulocytes causing stippling appearance (remnants are left instead of being removed by Pyrimidine 59 nucleotidase)

A

 Lead poisoning

346
Q

Reticulocyte count: Increased

A
  1. LEAD POISONING
347
Q

 Suggest a hemolytic component (hemolysis during lead poisoning because heme cannot be formed)

A
  1. LEAD POISONING
348
Q

 Iron cannot be incorporated into protoporphyrin IX, therefore no heme will be formed, which in turn results to no hemoglobin causing low levels of oxygen

A
  1. LEAD POISONING
349
Q

: is usually shut down during lead poisoning; the distribution of oxygen via this pathway is inhibited; cells become sensitive to oxidant stress causing hemolysis (PPP is responsible for releasing antioxidants together with the Rapoport pathway) = oxidative environment : hemolysis

A

 Pentose Phosphate Pathway (PPP)

350
Q

● Removal of drug (poisoning)

A
  1. LEAD POISONING
351
Q

: used to chelate the lead present in the body so it can be excreted in the urine

A
  1. LEAD POISONING

● EDTA salt

352
Q

• Diseases characterized by impaired production of heme (can be hereditary or acquired)

A

PORPHYRIAS

353
Q

• Acquired types are usually associated with enzyme deficiency.

A

PORPHYRIAS

354
Q

The products from earlier stages (?) in the pathway accumulate in the cells that actively produce heme proteins such as RBC and hepatocytes. These [?] can also be excreted in the urine or feces or be deposited in body tissues.

A

porphyrins

355
Q

PORPHYRIAS
• Clinical features:

A

Photosensitivity & Psychosis due to deposition of porphyrins.

356
Q

PORPHYRIAS
• Hematologic manifestations:

A

congenital erythropoietic porphyria & erythropoietic protoporphyria

357
Q

• Urine may appear portwine red in color

A

PORPHYRIAS

358
Q

● Diseases characterized by impaired production of the porphyrin component of heme due to enzyme deficiencies

A

PORPHYRIAS

359
Q

● Maybe acquired (lead poisoning/hereditary)

A

PORPHYRIAS

360
Q

: one of the most common cause of enzyme problems because it affects the function of enzymes in converting one compound to another (accumulation of Delta aminolevulinic acid)

A

Lead poisoning

361
Q

 When an enzyme in heme synthesis is missing, the earlier stages in the pathway will accumulate in the erythrocyte and hepatocyte.

A

PORPHYRIAS

362
Q

 Excess porphyrins leak from cells as they die and this will be excreted in the urine and feces which allows diagnosis

A

PORPHYRIAS

363
Q

 The enzymes in porphobilinogen, hydroxymethylbilane, Uroporphyrinogen III, Coproporphyrinogen III, and Protoporphyrinogen IX has the porphyrins but because of the deficiency.

A

PORPHYRIAS

364
Q

 Enzyme deficiency: 1) uroporphyrinogen III cosynthase is deficient, the hydroxymethylbilane will accumulate, 2) uroporphyrinogen decarboxylase is deficient, uroporphyrinogen III will accumulate

A

PORPHYRIAS

365
Q

 These accumulations of porphyrins will accumulate in the erythrocytes → porphyrins leaks out of the rbc, especially to those that are already old (near to die: 120 days) → excreted in the urine which can be used to diagnose

A

PORPHYRIAS

366
Q

TYPES OF PORPHYRIAS

A

A. CONGENITAL ERYTHROPOIETIC PORPHYRIA (CEP)

B. ERYTHROPOIETIC PROTOPORPHYRIA (EPP)

C. X-LINKED ERYTHROPOIETIC PROTOPORPHYRIA (XLPEP)

367
Q

 Porphyrins accumulate in the cells/tissue when you view it under the microscope = [?] = patient having porphyrias is photosensitive (burning sensation when exposed to sunlight)

A

(+) fluorescence

368
Q

 The fluorescence of accumulated compound can be diagnostic (usually used to diagnose FEP in SDA =[?])

A

(+) rbc fluorescence

369
Q

 BM testing: RBC will appear as [?] under a fluorescent microscope (ability to fluoresce/photosensitivity is used to differentiate the porphyrias)

A

bright red

370
Q

● Photosensitive + Hemolytic anemia

A

A. CONGENITAL ERYTHROPOIETIC PORPHYRIA (CEP)

371
Q

● Photosensitive but mild

A

B. ERYTHROPOIETIC PROTOPORPHYRIA (EPP)

372
Q

● Most severe

A

C. X-LINKED ERYTHROPOIETIC PROTOPORPHYRIA (XLPEP)

373
Q

● Photosensitive + microcytic + hypochromic + reticulocyte is seen

A

C. X-LINKED ERYTHROPOIETIC PROTOPORPHYRIA (XLPEP)

374
Q

 Reticulocytes will try to respond to the problem in the heme (BM compensation)

A

C. X-LINKED ERYTHROPOIETIC PROTOPORPHYRIA (XLPEP)

375
Q

 Hereditary: abnormal reticulocytes

A

C. X-LINKED ERYTHROPOIETIC PROTOPORPHYRIA (XLPEP)

376
Q

 Lead poisoning: reticulocytes can compensate unless in heavy cases that it affects the bone marrow

A

C. X-LINKED ERYTHROPOIETIC PROTOPORPHYRIA (XLPEP)

377
Q

Results when the body’s state of iron acquisition exceeds the rate of iron loss.

A

HEMOCHROMATOSIS

378
Q

It can be acquired or hereditary (mutations affecting the proteins of iron metabolism).

A

HEMOCHROMATOSIS

379
Q

The body’s first reaction is to store excess iron in the form of ferritin, then in the form of hemosiderin within cells.

A

HEMOCHROMATOSIS

380
Q

In the presence of Oxygen, free ferrous iron initiates the generation of superoxide and other free radicals, which results in the PEROXIDATION of membrane lipids.

A

HEMOCHROMATOSIS

381
Q

Results to damage of cell membrane, nuclear membrane, mitochondrial and lysosomal membranes.

A

PEROXIDATION

382
Q

These events ultimately affect cellular respiration, enzyme digestion, cell death and organ damage.

A

PEROXIDATION

383
Q

Hemosiderin also deposits into tissues and organs leading to further organ damage.

A

HEMOCHROMATOSIS

384
Q

• Skin-

A

golden color

385
Q

• Liver -

A

cirrhosis-induced jaundice and subsequent cancer

386
Q

• Pancreas -

A

diabetes mellitus •

387
Q

Heart -

A

congestive heart failure

388
Q

Screening Test: transferrin saturation

A

HEMOCHROMATOSIS

389
Q

Treatment: Iron-chelating drugs to bind excess iron for excretion; Desferrioxamine

A

HEMOCHROMATOSIS

390
Q

IDA Serum iron

A

↓

391
Q

ACI Serum iron

A

↓

392
Q

SDA Serum iron

A

↑

393
Q

IDA Serum TIBC

A

↑

394
Q

SDA Serum TIBC

A

↓

395
Q

ACI Serum TIBC

A

N-↓

396
Q

IDA Serum ferritin

A

↓

397
Q

ACI Serum ferritin

A

N-↑

398
Q

SDA Serum ferritin

A

↑

399
Q

IDA Iron stores

A

↓

400
Q

ACI Iron stores

A

N-↑

401
Q

SDA Iron stores

A

↑

402
Q

IDA Hb A2

A

N-↓

403
Q

ACI Hb A2

A

N

404
Q

SDA Hb A2

A

N

405
Q

IDA Hb F

A

N

406
Q

ACI Hb F

A

N

407
Q

SDA Hb F

A

N-↑

408
Q

IDA % sideroblasts

A

↓

409
Q

ACI % sideroblasts

A

↓

410
Q

SDA % sideroblasts

A

↑

411
Q

IDA ZPP

A

↑

412
Q

ACI ZPP

A

↑

413
Q

SDA ZPP

A

↑(↓)

Hematology 2 Lec (29 decks)

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