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HEMATOLOGY > Hemoglobin > Flashcards

Hemoglobin Flashcards

1
Q

Normal PO2 level in arterial blood

A

80-100 mmHg

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2
Q

Normal PO2 level in venous blood:

A

30-50 mmHg

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3
Q

Shift in the curve due to changes in pH; demonstrates relationship of blood pH and Hgb-O2 affinity

Facilitates the ability of hemoglobin to exchange oxygen and CO2

A

BOHR EFFECT

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4
Q

Hgb-O2 binding promotes release of CO

A

HALDANE EFFECT

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5
Q

Increased Hgb-O2 affinity, Decreased dissociation, decreased oxygen, increase release

A

SHIFT TO THE LEFT:

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6
Q

Decreased Hgb-O2 affinity, Increased dissociation, increase oxygen, decrease release

A

SHIFT TO THE RIGHT

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7
Q

True or false

Hgb-O2 affinity is inversely proportional with dissociation and oxygen release

A

True

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8
Q

High affinity for oxygen than HgbA1 due to weakened ability to bind 2,3-DPG.

High affinity allows more effective oxygen withdrawal from maternal circulation.

A

Hgb F

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9
Q

• REVERSIBLE oxidation of ferrous iron to the ferric state (Fe3+)

• Cannot bind and transport O2

A

Methemoglobin (MetHb or Hi)

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10
Q

can be acquired or hereditary

Aka toxic methemoglobinemia; occurs in normal individuals after exposure to an exogenous oxidant, such as nitrites, primaquine, dapsone, or benzocaine

A

METHEMOGLOBINEMIA

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11
Q

Toxic level of methemoglobin
<25%

A

Asymptomatic

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12
Q

Toxic levl of methemoglobin 30%

A

Cyanosis

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13
Q

bluish discoloration of skin due to decreased O2 in the tissues) and symptoms of hypoxia

A

Cyanosis

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14
Q

Toxic level of methemoglobin is >50%

A

Coma or death

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15
Q

amount of oxygen needed to saturate 50% of hemoglobin.

A

P50

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16
Q

Shift to the left mmHg?

A

27 mmHg

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17
Q

Normal mmHg of hemoglobin

A

26.52 to 27 mmHg

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18
Q

Autosomal recessive
<50% of total hemoglobin

A

Methemoglobin reductase/Cytochrome B5 reductase deficiency

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19
Q

Hydrogen sulfide derivative of hemoglobin; addition of a sulfur atom to the pyrrole ring of heme

A

Sulfhemoglobin (HgbS

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20
Q

Color of blood is Chocolate brown

A

Methemoglobin

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21
Q

Color of blood is Greenish pigment/ hemochrome * MAUVE-LAVANDER

A

Sulfhemoglobin (HgbS

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22
Q

IRREVERISBLE CHANGE in denatured/precipitated hemoglobin

A

Heinz bodies

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23
Q

colorless, tasteless gas, termed SILENT KILLER

A

Carbon monoxide

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24
Q

COLOR OF BLOOD: CHERRY RED

A

Carboxyhemoglobin (HgbCO)

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25
Q

increased affinity; prevent O2 release to the tissues

A

Shift to left of Carboxyhemoglobin

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26
Q

Absorption peak of hgbS

A

630 nm

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27
Q

Absorption peak of HgbCO

A

540 nm

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28
Q

TOXIC LEVELS of Carboxyhemoglobin (HgbCO)

20-30%

A

headache, dizziness, disorientation

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29
Q

Toxic levels of HgbCO >40%

A

coma, seizure, hypotension, cardiac arrhythmias, pulmonary edema, and death

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30
Q

controversial; it is primarily used to prevent neurologic and cognitive impairment after acute carbon monoxide exposure in patients whose level exceeds 25%

A

hyperbaric oxygen therapy

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31
Q

Reference method/Gold standard for hemoglobin determination because:

A

CYANMETHEMOGLOBIN METHOD/HEMIGLOBINCYANIDE (HiCN) METHOD

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32
Q

only standard used in hematology

A

HiCN standard are readily available

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33
Q

Absorption peak (wavelength): of CYANMETHEMOGLOBIN

A

540 nm

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34
Q

Principle of CYANMETHEMOGLOBIN

A

Colorimetric/Indirect/Spectrophotometric

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35
Q

Reagent used in CYANMETHEMOGLOBIN

A

Modified Drabkin’s reagent (contains anhydrous Dihy

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36
Q

light sensitive; contains cyanide which is highly toxic

A

DRABKIN’S REAGENT

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37
Q

DRABKIN’S REAGENT contains?

A

contains sodium bicarbonate

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38
Q

uses sodium lauryl sulfate (SLS) to convert Hgb to SLS-methemoglobin.

A

Automated instruments

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39
Q

HemoCue; converts hgb to azidehemoglobin (read at 570 nm and 880 nm)

A

POCT device

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40
Q

Converts methemoglobin to cyanmethemoglobin

A

Potassium cyanide

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41
Q

Converts hemoglobin (Fe2+) to methemoglobin (Fe3+)

A

Potassium ferricyanide

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42
Q

Improves RBC lysis and decreases turbidity from protein precipitation

A

Non-ionic surfactants/Detergent

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43
Q

Hastens conversion of Hgb to HiCN

A

Dihydrogen potassium phosphate (3 minutes) Sodium

bicarbonate (10 minutes

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44
Q

Hemoglobin molecules assume a negative charge and migrate toward the anode (positive pole

A

CELLULOSE ACETATE

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45
Q

CELLULOSE ACETATE alkaline pH?

A

8.4 to 8.6

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46
Q

Fastest to migrate to the anode in cellulose lactate

A

Hgb H

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47
Q

Slowest to migrate to the anode in cellulose lactate

A

HgbC

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48
Q

Migrates with C: in cellulose lactate

A

Hgb E and O

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49
Q

Migrates with S: in cellulose lactate

A

Hgb D and Hgb G

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50
Q

Hemoglobins assume a negative charge and migrate toward the anode, whereas others are positively charged and migrate toward the cathode

A

CITRATE AGAR

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51
Q

CITRATE AGAR pH

A

(Acid pH 6.0-6.2

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52
Q

Quantification of fetal hemoglobin; used to quantitate the number of fetal Rh-positive cells because of fetomaternal hemorrhage (iFMH

A

KLEIHAUER-BETKE TEST (ACID ELUTION TEST

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53
Q

Maternal blood smear is treated with _________ and then stained with counterstain what stain?

A

Citric acid phosphate buffer (pH 3.2)
Shepard’s stain

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54
Q

Acid hematoxylin and Erythrosine B as counterstain is called

A

Shepar’ds stain

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55
Q

Pink (has fetal Hgb which is resistant to acid elution)

A

Fetal cells (w/ Hgb F)

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56
Q

Ghost cells (appear as pale pink and is susceptible to acid elution)

A

Maternal cells (w/ Hgb A):

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57
Q

Adding sodium metabisulfite, a reducing substance, to blood enhances deoxygenation of Hgb and sickling of Hgb S

A

➢ SODIUM METABISULFTITE TEST

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58
Q

➢ SODIUM METABISULFTITE TEST • Positive result: formation of?

A

Sickle cells holly leaf appearance

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59
Q

Other positive result for sodium metabisulfate

A

Rare sickling hemoglobins (Hbs S Travis, C Harlem), Hgb I, Hgb Bart’s

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60
Q

False negative results is sodium metabisulfite test

A

Hgb S concentration is less than 10% (as in very young infants) or if deoxygenation is inadequate (e.g., deterioration of reagent)

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61
Q

Most common screening test for Hgb S

A

DITHIONITE TUBE TEST/SICKLE SOLUBILITY TEST/HGB SOLUBILITY TEST

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62
Q

Positive result to DITHIONITE TUBE TEST/SICKLE SOLUBILITY TEST/HGB SOLUBILITY TEST

A

Turbidity
Turbud Deoxygenated polymerized Hgb S)

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63
Q

Negative result to DITHIONITE TUBE TEST/SICKLE SOLUBILITY TEST/HGB SOLUBILITY

A

Negative: Clear (non-sickling hemoglobin)

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64
Q

converts ferrous to ferric iron; ferric iron is unable to bind oxygen, converting hemoglobin to the deoxygenated form

A

Dithionite

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65
Q

dissolves membrane lipids, causing release of hemoglobin from RBCs

A

Saponin

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66
Q

Central pallor/pallor area occupies 1/3 of the cell Normal MCHC: 32-36 g/dL

A

Normochromic RBC

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67
Q

Central pallor/pallor area is >1/3 of cell Decreased MCHC: <32 g/dL of hypochromic rbc

A

Target cells and elliptocytes

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68
Q

Example of Hypochromic RBC

A

Target cells, Elliptocytes

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69
Q

Central pallor/pallor area is <1/3 of the cell Increased MCHC: >36 g/dL

A

Hyperchromic RBC (De facto)

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70
Q

Example of Hyperchromic RBC (De facto)

A

Spherocytes and stomaticytes

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71
Q

RBC with a thin rim of hemoglobin and a large clear center Seen in Iron deficiency anemia

A

Anulocyte/Pessary cell/Ghost cell

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72
Q

variation in cell shape
Abnormal shape rbc

A

POIKILOCYTOSIS

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73
Q

RBC Membrane abnormalities -

A

Intrinsic defect

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74
Q

Trauma/Physical damage

A

Extrinsic defect

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75
Q

Developmental macrocytosis
➢ RBC Membrane abnormalities - intrinsic defect
➢ Abnormal hemoglobin content
➢ Trauma/Physical damage

A

POIKILOCYTOSIS

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76
Q

common cells in hemolytic anemias

A

SPHEROCYTES

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77
Q

Thinner variant of a Target cell

A

Leptocyte

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78
Q

oval macrocytes

A

Megablolastic anemia

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79
Q

Large RBC, mostly oval (MCV= >100 fL

A

Macrocytic RBCs

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80
Q

Small, round, RBC with no central pallor (increased MCHC)
Hyperchromic red cells
Decreased surface area to volume ratio (increased OFT

A

Spherocytes/Bronze cells

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81
Q

Hereditary spherocytosis Pre & post splenectomy HDN WAIHA, MAHA Severe burns Jaundice

A

Spherocytes/Bronze cells

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82
Q

Megaloblastic anemia (Vit B12 and B9 deficiency) Chronic liver disease Myelodysplastic syndromes
Bm failure

A

Macrocytic RBCs

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83
Q

Hemoglobinopathies Thalassemia

Hepatic disease with or without jaundice

A

Target cells/Codocytes/ Mexican Hat cell

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84
Q

Central area of hemoglobin surrounded by colorless ring and a peripheral ring of hemoglobin (Maldistribution of hemoglobin

A

Target cell
Codocytes
Mexican hat cell

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85
Q

Seen in IDA

A

Pencil shape rbc

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86
Q

Gerbich null (Ge: -2,-3,-4)

A

Leach phenotype

87
Q

Have a cigar, elliptical, pencil, egg shape Hemoglobin are concentrated at the two ends of the cell with normal pallor area

A

Elliptocyte

88
Q

Hereditary elliptocytosis Iron deficiency anemia Thalassemia major Sickle cell anemia Pernicious anemia Myelofibrosis

A

Elliptocyte

89
Q

Liver disease Renal insufficiency (uremia) Pyruvate kinase deficiency

A

Echinocytes/ Crenated RBC/ Sea urchin cell / Burr cells

90
Q

not evenly distributed blunt serrated edges/short projections

A

Burr cell

91
Q

Evenly distributed blunt serrated edges/short projections

A

Echinocytes

92
Q

Due to plasma abnormalities, osmotic changes; decreased ATP

A

In vivo

93
Q

❖ prolonged standing of blood film with AC, moist slide, and stored blood
May be an artifact

A

In vitro

94
Q

Acute, severe hemolytic anemia
G6PD deficiency
Hereditary lipoprotein deficiency

A

Pyknocytes (Turgeon)

95
Q

Are distorted, contracted erythrocytes that are similar to burr cells

A

Pyknocytes (Turgeon)

96
Q

Contains uneven spaced, pointed projections without central pallor

A

Acanthocytes/Spur cells/Thorn cells

97
Q

Abetalipoproteinemia/ Bassen-Kornzweig syndrome McLeod syndrome

A

Acanthocytes
Spur cells
Thorn cells

98
Q

absence of Kx gene,
Due to the changes in the ratio of plasma lipids (lecithin and sphingomyelin) absence of Kell antigens

A

McLeod syndrome

99
Q

Due to the changes in the ratio of plasma lipids ________
_________

A

lecithin and

sphingomyelin)

100
Q

Characterized by elongated/slit/mouth like pallor area instead of circular pallor

A

Stomatocytes

101
Q

Piezo type” ➢ Increased membrane permeability to
potassium leading to loss of water from cell water efflux

A

Dehydrated stomatocytosis

102
Q

increased membrane permeability to sodium and potassium (water influx) __________

A

Rh null disease

103
Q

➢ increased membrane permeability to
sodium and potassium (water influx)
Rh null disease

A

Overhydrated stomatocytosis

104
Q

Rh Null disease/Rh deficiency syndrome

A

Stomatocytes

105
Q

Can appear as an artifact
Can be seen with puddled hemoglobin at the periphery of cells with spicules

A

Stomatocytes

106
Q

Fragmented RBC (about half the size of a normal RBC

A

Schistocytes/ Schizocyte

107
Q

Helmet/Hornlike

A

Kerocyte

108
Q

Triangular, resemble

“pinch-bottle”, RBC with 2 central pallors

A

Knizocyte

109
Q

➢ Variety of small, irregular shapes

A

Blister cells

110
Q

Causes of fragmentation:

❖ Altered vessel walls
❖ Presence of fibrin
❖ Prosthetic heart valves
❖ Renal transplant rejections

A

Schistocytes

111
Q

Moschcowitz syndrome, UpshawSchülman syndrome
Microangiopathic hemolytic anemia (MAHA)
TTP
HUS
DIC

A

Schistocytes

112
Q

Disk shaped cells with smaller volume Due to thermal damage to cell membrane protein spectrin, no pallor area

A

Pyropoikilocytes/ Microspherocytes

113
Q

Severe burns Hereditary pyropoikilocytosis

A

Pyropoikilocytes/ Microspherocytes

114
Q

Laboratory results:
❖ 2-3um in
diameter
❖ MCV = <60fL

A

Pyropoikilocytes/ Microspherocytes

115
Q

Tear drop, pear drop shaped with blunt pointed projection
Due to squeezing of red cells through small openings or splenic sinuses and remains behind

A

Dacryocytes

116
Q

Myeloid metaplasia Primary myelofibrosis
MMM
Myelopthisic anemia
Pernicious anemia
Beta thalassemia Tuberculosis
Heinz body formation

A

Dactocytes

117
Q

Halfmoon cell, half crescent cell Large, pale pink staining ghost of red cell

A

Semilunar bodies

118
Q

Malaria

Causes overt hemolysis

A

Semilunar bodies

119
Q

Long, rod, crescent shaped, with thin and elongated with pointed ends
Polymerization of deoxygenated hemoglobin (Hgb S)

A

Sickle cells/ Drepanocytes/ Menisocytes

120
Q

Decreased blood pH
Influx of sodium ions
Increased intracellular calcium

A

Polymerization of deoxygenated hemoglobin (Hgb S)

121
Q

Can be due to amino acid substitution resulting to cell membrane alterations (glutamic acid to valine ; 6 th A.A. of the beta chain

A

Hemoglobin S

122
Q

Homogeneous: hexagonal with blunt ends
Bar of gold/Clam shell appearance

A

Hemoglobin CC crystals

123
Q

Hgb CC disease

A

Hemoglobin cc crystals

124
Q

Confirmed with hemoglobin electrophoresis

A

Hemoglobin CC crystals

125
Q

Dark-hued crystals of condensed hemoglobin

A

Hemoglobin SC crystals

126
Q

Crystals appear straight with parallel sides and one blunt, point, protruding end, fingerlike (Washington’s monument appearance

A

Hemoglobin SC crystals

127
Q

Hgb SC disease

A

Hemoglobin SC crystals

128
Q

Small, 1-2 um in size, nuclear fragments of DNA Normally pitted by splenic macrophages and are not seen in normal RBCs

A

Howell-Jolly bodies

129
Q

Reddish blue; Dark blue-purple with Wright’s stain (same with supravital

A

Howell-Jolly bodies

130
Q

Feulgen positive reaction

A

Howell-Jolly bodies

131
Q

Congenital absence of spleen
Splenic atrophy
Sickle cell anemia

A

Howell jolly bodies

132
Q

Multiple, tiny, fine or coarse rRNA aggregates/precipitates
rRNA inclusions aggregates in drying & staining

A

Basophilic stippling/Punctuate basophilia

133
Q

Hemoglobin appears homogeneous;
“Blueberry gel appearance”

A

Basophilic stippling/Punctuate basophilia

134
Q

Dark-blue to purple with Wright’s stain (same with supravital

A

Basophilic stipplings

135
Q

Thalassemia Lead Toxicity (plumbism)
Arsenic toxicity
Pyrimidine-5’-nucleotidase deficiency

A

Basophilic stippling

136
Q

Aggregates of mitochondria, ribosomes, and IRON PARTICLES (unused iron)
Appears in the periphery of the erythrocytes

A

Pappenheimer bodies/ Siderotic granules

137
Q

Stains with Perl’s Prussian blue (Rous test)

A

Pappenheimer bodies/ Siderotic granules

138
Q

Pappenheimer bodies

A

Wright’s stains

139
Q

Siderotic granules

A

Prussian blue stain

140
Q

Sideroblastic anemia
Hemoglobinopathies
Thalassemias

A

Pappenheimer bodies/ Siderotic granules

141
Q

Wright’s stain: Bluish tinge; also called

A

polychromasia

142
Q

Dark blue RNA remnants in the cytoplasm

A

reticulocytes

143
Q

Young cells with no nucleus but contains RNA remnants

A

Diffuse basophilia/ Diffusely basophilic RBC

144
Q

Hemolytic anemia After treatment of iron, Vitamin B12 or folate deficiency

A

Diffuse basophilia/ Diffusely basophilic RBC

145
Q

Thin ring like, circular, figure of eight, incomplete rings

A

Cabot rings

146
Q

Remnants of microtubules from the mitotic spindle

Associated with Howell jolly bodies in the same RBC

A

Cabot ring

147
Q

Reddish-violet (Wright’s stain)

A

Cabot ring

148
Q

Megaloblastic anemia
Myelodysplastic syndromes

A

Cabot ring

149
Q

Precipitated/denatured globin attached to the RBC membrane
Round, 0.2 to 2.0 um, seen with a supratival stains

A

Heinz bodies

150
Q

RBC with pitted Heinz bodies

A

Bite cell / degmacyte

151
Q

NOT VISIBLE ON WRIGHT’S STAIN Dark-blue purple (Supravital stain

A

Heinz bodies

152
Q

Heinz body preparation

A

Crystal violet

153
Q

Fava beans (Favisim

G-6-PD deficiency
Presence of unstable hemoglobins
Exposure to oxidizing agents

Oxidant drugs (Anti-malarial drugs)

A

Heinz body

154
Q

Small, precipitated beta-globin chains of hemoglobin (4β)
Pitted golf ball appearance of RBC

Results to unstable, easily oxidized and easily precipitated hemoglobi

A

Hgb H

155
Q

NOT VISIBLE ON WRIGHT’S STAIN dark blue or greenish granules (Supratival stain – BCB)

A

Hgb H

156
Q

Hgb H disease

A

Alpha thalassemia

157
Q

Granulo filamentous pattern in hgb H

A

Reticulocyte

158
Q

Hgh H inclusions

A

Single body

159
Q

morphologic classification of anemia

A

RBC indices

160
Q

assess RBC production on response to anemia

A

Reticulocyte count –

161
Q

morphological abnormalities

A

Peripheral blood film examination

162
Q

– for unexplained anemia

A

Bone marrow examination

163
Q

for microcytic, hypochromic anemias

A

Iron studies

164
Q

hemolytic anemia

A

Urinalysis

165
Q

occult blood and blood parasites

A

Fecalysis

166
Q

Hemolytic anemia

A

Chemistry test

167
Q

differentiate autoimmune anemias for other hemolytic anemia

A

DAT

168
Q

are characterized by an MCV greater than 100 fL

A

Macrocytic anemia

169
Q

characterized by an MCV of less than 80 fL

A

Microcytic anemia

170
Q

characterized by an MCV in the range of 80 to 100 fL

A

Normocytic anemias

171
Q

Ineffective erythropoiesis -

A

RPI <2.0

172
Q

Decreased or ineffective RBC production (decreased reticulocyte count) –

A

w/o BM compensation

173
Q

Excessive RBC loss (increased reticulocyte count) – w

A

/ BM compensation

174
Q

Effective erythropoiesis -

A

RPI - >3.0

175
Q

reacts with freed iron forming a colored complex that can be detected spectrophotometrically

A

Ferrozine

176
Q

Indicator of available iron for transport Measures iron bounded to transferrin

Specimen – fasting specimen and collected early in the morning (highest levels)

A

Serum Iron (SI)

177
Q

Indirect indicator of iron stores Measures total number of available transferrin sites for iron binding

A

Total Iron Binding Capacity (TIBC)

178
Q

Serum iron (SI) represents the number of transferrin sites bound with iron

TIBC represents the total number of transferrin sites for iron binding

A

% Transferrin Saturation

179
Q

Indicator of iron storage status
Quantitative assessment of body iron stores

A

Serum ferritin

180
Q

Uses acidic potassium ferrocyanide Prussian blue stain of the bone marrow is considered the

GOLD STANDARD for assessment of body iron stores

A

Prussian Blue staining of bone marrow

181
Q

readily seen as dark blue granules or precipitate

A

Ferric iron

182
Q

stains readily, distinct blue granules

A

Hemosiderin

183
Q

Indicator of functional iron available in cells Major advantage – IDA and ACD differentiation

A

Soluble transferrin receptor (sTfR) level/ Serum transferrin receptor

184
Q
  • associated with increased serum levels of
A

IDA

185
Q

Ida- associated with increased serum level of tfrs because of increased membrane TfR1

A

Stfr

186
Q

Indicator of functional iron available in cells

A

Ferritin index/ stfr

187
Q

Increased binding of zinc to protoporphyrin IX when iron is not incorporated to heme

A

Free Erythrocyte Protoporphyrin (FEP)/ Zinc protoporphyrin level (ZPP)

188
Q

BM iron store : decreased
Hgb: normal
SI: Normal
Ferritin: Decreased
TIBC: normal

A

Storage Iron depletion (Pre-Latent iron deficiency

189
Q

BM stores: Absent
Hgb: normal
SI: decreased
Ferritin: Decreased
TIBC: Increase

A

Transport iron depletion (Latent iron deficiency)

190
Q

BM iron stores: absent
Hgb: decreased
Serum iron: decreased
Ferritin: decrease
Tibc: increased

A

Iron deficiency anemia/ Frank’s anemia

191
Q

➢ Cracks at the corners of the mouth

A

angular cheilosis

192
Q

Spooning or clubbing of the fingernails

A

Koilonychias

193
Q

severe iron deficiency, neurologic problems

A

➢ Pica/Pica syndrome

194
Q

• most common in pica syndrome

A

craving for ice

195
Q

Craving for ice is known as

A

Pagophagia

196
Q

Aka Patterson Kelly / Plummer

A

Vinson syndrome

197
Q

Impaired ferrokinetics (most significant cause)

A

Anemia of a chronic disease or inflammation

198
Q

Acute phase reactant of Anemia of a chronic disease

A

Hepcidin

199
Q

Other acute phase reactants (APR):

A

Ferritin, and lactoferrin

200
Q

inhibits iron release of ferroportin from enterocytes → decreased serum iron

A

Increased hepcidin

201
Q

promotes iron release of ferroportin from enterocyte increased serum iron

A

Decreased hepcidin

202
Q

Caused by blocks in the protoporphyrin pathway resulting in defective hemoglobin synthesis and iron over

A

Sideroblastic anemia

203
Q

Excess iron accumulates in the mitochondrial region of the sideroblasts (metarubricyte) in the bone marrow and siderocytes in the blood and encircles the nucleus

A

Sideroblast anemia

204
Q

aka: PLUMBISM

A

Lead poisoning

205
Q

Gum lead line that forms from blue/black deposits of lead sulfate

A

Lead poisoning

206
Q

Hallmark of the sideroblastic anemias
➢ Contains at least 5 iron granules per cell, and these iron containing mitochondria must circle at least 1/3 of the nucleus
➢ 10-40% of nucleated cells in the bone marrow

A

Ringed sideroblast

207
Q

❖ HEREDITARY: ➢ Common in males ➢ X-linked and autosomal - d-ALA synthase deficiency

A

Sideroblast anemia

208
Q

❖ Are named according to the chain (alpha or beta) with reduced or absent synthesis

A

Thalassemias

209
Q

Mild anemia; sufficient alpha and beta chains produced to make normal hemoglobins A, A2 , and F, but may be in abnormal amounts

A

Thalassemia minor/trait

210
Q

Severe anemia; either no alpha or no beta chains produced

A

Thalassemia major

211
Q

This underproduction of beta chains contributes to a decrease in the total erythrocyte hemoglobin production, ineffective erythropoiesis, and a chronic hemolytic process

❖ Unpaired, excess alpha chains precipitate in developing erythroid precursors forming Heinz bodies

A

Beta thalassemia

212
Q

(COOLEY’S ANEMIA)

➢ Characterized by a severe anemia that requires regular transfusion

➢ Markedly decreased rate of synthesis or absence of both beta chains results in an excess of alpha chains; no

Hgb A can be produced; compensate with up to 90% Hgb

A

Beta thalassemia major

213
Q

Decreased rate of synthesis of one beta chains
➢ Hemoglobin level – 11-15 g/dL
➢ Hemoglobin electrophoresis: Hgb A 1 is slightly decreased, but Hgb A 2 is slightly increased to compensate

A

BETA-THALASSEMIA MINOR/TRAIT ➢

214
Q

Hereditary recessive microcytic anemia, which does not respond to oral iron therapy ➢ Mutation in the TMPRSS6 gene – encodes for matriptase-2 (MT-2) ✓ MT-2 – involved in downregulation of hepcidin

A

IRON-REFRACTORY IDA (IRIDA)

HEMATOLOGY (2 decks)

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