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IUHEME > Exam 3 Material > Flashcards

Exam 3 Material Flashcards

1
Q

Identify three areas of red cell metabolism that are crucial for normal erythrocyte survival and function.

A
  1. RBC membrane
  2. Hemoglobin structure and function
  3. RBC metabolic pathways
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2
Q

Discuss the two major proteins of the red cell membrane, glycophorin and spectrin, according to:

a. Integral versus peripheral protein
b. Major functions for each

A

a. Integral protein: extends through the lipid bilayer and is permanently attached to the cell membrane

Peripheral protein: does not extend though the lipid bilayer, has temporary connections to the cell membrane, forms membrane 
cytoskeleton

b. Glycophorin: accounts for most of the membrane’s sialic acid – giving RBCs its negative charge

Spectrin: strengthens membrane (shape and stability), preserves deformability (pliability)
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3
Q

State the mechanism for producing each of the following types of poikilocytosis that are caused by structural membrane defects:

Acanthocytes

Bite cells

Spherocytes

Target cells:

A

Acanthocytes: an absence of low density lipoproteins (LDLs) leading to malabsorption of fats within the body (i.e. abetalipoproteinemia – acanthocytes)

Bite cells: a decrease in spectrin leading to less deformability – when attempting to pass thorough the spleen, it is very “slow” – the RE may try to phagocyte these cells leaving a portion of the RBC membrane removed

Spherocytes: a decrease in spectrin leading to less deformability – when attempting to pass thorough the spleen, it is very “slow” – the RE may try to phagocyte these cells leaving a reduce surface to volume ratio

Target cells: accumulation of cholesterol in RBC membrane leading to an increased surface area and decreased intracellular hemoglobin

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4
Q

State the protein carrier that delivers iron to the RBC membrane for hemoglobin synthesis.

A

Transferrin

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5
Q

List the two major tissues in the body where heme synthesis occurs.

A
  1. Erythroid marrow
  2. Liver
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6
Q

Diagram the sequence leading to heme synthesis … beginning with succinyl coenzyme A + glycine and ending with heme.

A

Succinyl coenzyme A + glycine to ALA to Porphobilinogen to Uroporphyrinogen to Coproporphyrinogen to Protoporphyrinogen IX to Protoporphyrin IX + Fe = Heme

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7
Q

Describe the chemical structure of heme.

A

Porphyrin is made up of four (4) five-member rings bound by methane bridges – the arrangement of the nitrogen atoms allows it to chelate metal atoms (i.e. iron)

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8
Q

Explain the reason why a patient with lead poisoning presents with “ringed sideroblasts”.

A

Lead damages one or more of the enzymes involved in heme synthesis – it blocks the incorporation of iron into the molecule leading to iron buildup in the mitochondria causing the “ringed sideroblasts”

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9
Q

Explain the reason why a freshly voided urine from a patient with a porphyria may not be red.

A

Porphyrin becomes oxidized from porphyrinogen, which is colorless – it oxidizes with exposure to air or acids – this process can take time

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10
Q

List three hemoglobins that are found exclusively in the embryo.

A
  1. Gower 1: Zeta2 – Epislon2
  2. Gower 2: Alpha2 – Epislon2
  3. Portland: Zeta2 – Gamma2 or Zeta2 - Alpha2
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11
Q

State the globin chain composition and percentages for each of the three normal adult hemoglobins.

A
  1. Hemoglobin A: Alpha2 – Beta2 (>95%)
  2. Hemoglobin A2: Alpha2 – Delta2 (1.5-3.0%)
  3. Hemoglobin F: Alpha2 – Gamma2 (~ 2%)
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12
Q

Characterize the oxygen affinity of the relaxed (R) form and the tense (T) form of the hemoglobin molecule.

A

Relaxed form (R): when hemoglobin has an affinity and readily binds to oxygen via ALL of the iron molecules (oxyhemoglobin – arterial blood)

Tense form (T): when hemoglobin has a lower affinity and readily unloads the oxygen via ALL of the iron molecules – binding of 2,3 DPG occurs (deoxyhemoglobin – venous blood)

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13
Q

Explain the relationship between pO2 of the surrounding medium and the percent of oxygen saturation of hemoglobin as depicted by an oxygen dissociation curve, including the effects of the following:

A

Hemoglobin’s affinity for oxygen based on its location and condition(s) in/of the body

pH: in the tissues – is decreased due to uptake of CO2, etc.
in the lungs – is increased due to expulsion of CO2

2,3 DPG levels: in the tissues – increased (O2 being squeezed out)
in the lungs – decreased (relaxed form of Hgb)

Temperature: in the tissues – increased (i.e. fever)
in the lungs – decreased

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14
Q

Differentiate “shift-to-the right” and “shift-to-the left” in relation to the hemoglobin-oxygen dissociation curve.

A

“Shift-to-the right:” favors the release of oxygen; therefore, lowering the affinity of hemoglobin for oxygen

“Shift-to-the left:” favors the uptake of oxygen; therefore increasing the affinity of hemoglobin for oxygen

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15
Q

List three abnormal hemoglobins that are unable to transport or deliver oxygen.

A
  1. Carboxyhemoglobin
  2. Methemoglobin
  3. Sulhemoglobin
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16
Q

State the main source of ATP production in the mature RBC.

A

Anaerobic breakdown of glucose

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17
Q

Name the metabolic pathway that generates most of the red cell’s ATP.

A

Embden-Meyerhof

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18
Q

State the major function for each of the following red cell metabolic pathways:

Embden-Meyerhof Pathway

Hexose Monophosphate Shunt

Methemoglobin Reductase Pathway

Leubering-Rapaport Shunt

A

Embden-Meyerhof Pathway
90% of the energy needed for the RBC is generated via this pathway – it produces two (2) molecules of ATP, the majority of glucose production and utilization

Hexose Monophosphate Shunt
5-10% glucose utilization (aerobically), protects against hydrogen peroxide which denatures hemoglobin (inherited defect: G-6-PD deficiency)

Methemoglobin Reductase Pathway
Maintains iron in the ferrous (2+) state

Leubering-Rapaport Shunt
Synthesis of 2,3 DPG – profound effect on hemoglobin’s affinity for oxygen, its stores can serve for additional ATP generation

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19
Q

State the changes in the red cell leading to its demise at 120 days.

A

As enzymes decrease, RBCs lose production of energy and deformability and no longer transverse through the microvasculature

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20
Q

Compare and contrast the steps involved in the extravascular versus intravascular breakdown of senescent RBCs.

A

Extravascular:

  1. RES cells phagocyte RBCs
  2. Iron is transported back to BM via transferrin
  3. Globin is return to AA pool
  4. Protophorphyrin ring dissembled – biliverdin converted to bilirubin
  5. Bilrubin is coupled to albumin and transported to liver
  6. Bilirubin converted to urobilinogen and excretedIntravascular:
  7. RBCs break in the lumen of vessel
  8. Haptoglobin picks up the free Hgb
  9. Hapto-Hgb complex goes to the liver for further metabolism – follows the same process as extravascular
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21
Q

State the characteristic level (decreased, normal, or increased) of haptoglobin in the presence of intravascular hemolysis.

A

Decreased – during intravascular hemolysis, destruction of RBCs are occurring within the blood vessel leaving haptoglobin to the vessel to pick-up the free hemoglobin – it would lower the plasma haptoglobin levels that would lead to hemoglobinemia or hemoglobinuria

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22
Q

State the protein carrier for the following:

Bilirubin
Hemoglobin
Iron

A

Bilirubin: albumin
Hemoglobin: haptoglobin
Iron: transferrin

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23
Q

List two general causes for anemia.

A

• Increased loss of RBCs (hemorrhage or hemolysis)
• Decreased production of RBCs (in the BM)

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24
Q

Describe six (general) clinical symptoms of anemia.

A

• Pallor
• Lightheadedness
• Muscle weakness
• Vertigo
• General lethargy
• Dyspnea (shortness of breath)
• Tachycardia (increased heart rate)

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25
Q

Describe the characteristic results you would find in the workup of an anemic patient with regard to the following laboratory tests:

Cell profile
RBC indices (microcytic-hypochromic anemia)
RBC indices (macrocytic anemia)
RBC indices (normocytic-normochromic anemia)
Reticulocyte count (aplastic anemia)
Reticulocyte count (extracorpuscular hemolytic anemia)

A

Cell profile: decreased RBC count and/or decreased hemoglobin
RBC indices (microcytic-hypochromic anemia): MCV< 80 fL, MCHC< 32 g/dL
RBC indices (macrocytic anemia): MCV> 100 fL
RBC indices (normocytic-normochromic anemia): MCV 80-100 fL, MCHC 32-36 g/dL
Reticulocyte count (aplastic anemia): decreased retic count
Reticulocyte count (extracorpuscular hemolytic anemia): increased retic count

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26
Q

Describe the characteristic RBC morphology you would find with regard to the following diseases/anemias:

Extracorpuscular hemolytic anemia
Hereditary spherocytosis
Liver disease
Pernicious anemia
Sickle cell anemia
Thalassemia
Hemoglobinopathy

A

Extracorpuscular hemolytic anemia: schistocytes and spherocytes
Hereditary spherocytosis: spherocytes
Liver disease: round macrocytes, targets, stomatocytes, spur cells
Pernicious anemia: oval macrocytes and teardrops
Sickle cell anemia: sickle cells
Thalassemia: M/H w/marked morphology and basophilic stippling
Hemoglobinopathy: “targets plus…” – sickle cells, C crystals, SC crystals

27
Q

List the anemias found under the following “morphologic classification of anemias” categories:

Microcytic-hypochromic (list four)

Macrocytic (list two)

Normocytic-normochromic (list three)

A

Microcytic-hypochromic (list four)

• Iron Deficiency Anemia
• Anemia of Chronic Inflammation (Disease)
• Sideroblastic Anemia
• Thalassemias

Macrocytic (list two)

• Non-megaloblastic Anemia
• Megaloblastic Anemia

Normocytic-normochromic (list three)

• Aplastic Anemia
• Hemoglobinpathies
• Hemolytic Anemias (other than hemoglobinopathies)

28
Q

State three criteria for accepting a CBC profile.

A

• H & H in balance
• MCHC < 37
• Make sure results make sense!!

29
Q

State the primary function of iron in the body.

A

Oxygen transport

30
Q

State the six iron compartments of the body (from largest to smallest).

A

• Hemoglobin
• Storage
• Myoglobin
• Labile Pool
• Tissue Iron Department
• Transport Compartment

31
Q

List four factors that influence iron absorption.

A

• Amount and type of iron accessible from food
• Functional state of GI mucosa and pancreas
• Current iron stores
• Erythropoietic needs

32
Q

List three conditions that result in an increased need for iron.

A

• Growth periods
• Blood loss
• Diversion of iron to the fetus

33
Q

Name the anatomic site at which iron is absorbed most efficiently.

A

Duodenum

34
Q

State the function of transferrin.

A

Iron transport protein

35
Q

Name the organelle that contains iron in the erythrocyte precursors.

A

Mitochondria

36
Q

Describe what is being measured for each of the following laboratory determinations:

Serum iron:

TIBC:

Serum ferritin:

BM macrophage iron:

BM sideroblasts:

ZPP:

A

Serum iron: amount of iron (bound to transferrin) in the serum/plasma

TIBC: amount of iron that transferrin can bind

Serum ferritin: the amount of iron located in the body’s storage

BM macrophage iron: iron held by the RE cells in the erythroblastic island that is used to supply the developing RBC precursors in the BM

BM sideroblasts: nRBCs in the BM that contain iron

ZPP: insufficient iron availability to developing nRBCs – erythrocyte protoporphyrin accumulates in the cell

37
Q

State the relationship between serum ferritin levels and bone marrow iron stores in a healthy individual.

A

In a healthy person, serum ferritin is equivalent to the body’s storage of iron, in BM

38
Q

Describe the peripheral smear RBC morphology that would prompt the ordering of iron studies.

A

Hypochromia, Microcytes, Aniso, some poik, variable

39
Q

Discuss, in detail, iron deficiency anemia, including:

Causes (infants vs. adults)

Clinical signs and symptoms

RBC count and/or HGB:
PLT count:
RBC morphology
MCV:
MCHC:
RDW:
Reticulocyte count:
Treatment:

A

Infants: milk anemia – being fed cow’s milk can make it more difficult to absorb iron
Adults: poor diet, GI bleeds, malabsorption, mental blood loss, pregnancy

Pallor, fatigue, lethargy, SOB – Koilonychia (an abnormal thinness and concavity of the fingernails), heart murmur, peculiar cravings

RBC count and/or HGB: decreased
PLT count: increased
RBC morphology: Hypochromia, Microcytes, Aniso, some poik, variable
MCV: decreased
MCHC: decreased
RDW: increased
Reticulocyte count: increased
Treatment: treat underlying cause, supplemental iron

40
Q

Discuss the mechanism (pathology) for developing a hypochromic-microcytic anemia for each of the following conditions:

Iron deficiency anemia

Anemia of chronic inflammation (disease)

Sideroblastic anemia

A

Malabsorption, decreased dietary intake, and increase loss of iron leads to:
Decreased iron – decreased Hgb – hypochromia – extra cell divisions – microcytosis

BM macrophages fail to give up iron to the RBC precursors; therefore RBCs develop iron deficient

An accumulation of iron in the mitochondria of nRBCs that “gets trapped” – porphyria

40
Q

Discuss the mechanism (pathology) for developing a hypochromic-microcytic anemia for each of the following conditions:

Iron deficiency anemia

Anemia of chronic inflammation (disease)

Sideroblastic anemia

A

Malabsorption, decreased dietary intake, and increase loss of iron leads to:
Decreased iron – decreased Hgb – hypochromia – extra cell divisions – microcytosis

BM macrophages fail to give up iron to the RBC precursors; therefore RBCs develop iron deficient

An accumulation of iron in the mitochondria of nRBCs that “gets trapped” – porphyria

41
Q

Differentiate iron deficiency anemia, anemia of chronic inflammation (disease), and sideroblastic anemia according to the following iron studies:

Serum iron

Iron deficiency anemia: decreased

Anemia of chronic inflammation (disease): decreased

Sideroblastic anemia: increased

TIBC

Iron deficiency anemia: increased

Anemia of chronic inflammation (disease): decreased

Sideroblastic anemia: decreased

Ferritin levels

Iron deficiency anemia: decreased

Anemia of chronic inflammation (disease): increased

Sideroblastic anemia: increased

BM macrophage iron

Iron deficiency anemia: decreased

Anemia of chronic inflammation (disease): increased

Sideroblastic anemia: increased

BM sideroblasts

	   Iron deficiency anemia: decreased

       Anemia of chronic inflammation (disease): decreased

	   Sideroblastic anemia: increased
A

Serum iron

Iron deficiency anemia: decreased

Anemia of chronic inflammation (disease): decreased

Sideroblastic anemia: increased

TIBC

Iron deficiency anemia: increased

Anemia of chronic inflammation (disease): decreased

Sideroblastic anemia: decreased

Ferritin levels

Iron deficiency anemia: decreased

Anemia of chronic inflammation (disease): increased

Sideroblastic anemia: increased

BM macrophage iron

Iron deficiency anemia: decreased

Anemia of chronic inflammation (disease): increased

Sideroblastic anemia: increased

BM sideroblasts

Iron deficiency anemia: decreased

Anemia of chronic inflammation (disease): decreased

Sideroblastic anemia: increased

42
Q

State the reason why long-term iron therapy should not be given to a patient with anemia of chronic inflammation (disease).

A

The amount of iron isn’t the issue – it’s the release of iron made available to the cells

43
Q

Discuss the reason for the presence of “ringed sideroblasts” upon bone marrow iron exam of a patient with lead poisoning.

A

Excess iron-laden in the mitochondria form a ring around the nucleus

44
Q

State the characteristic RBC histogram appearance one would expect to see in a patient with sideroblastic anemia, especially a hereditary form.

A

Two (2) peaks due to the presence of two RBC populations

45
Q

Discuss hereditary hemochromatosis according to complications and treatment.

A

Iron overload – major concern is location of iron deposits – occurring in certain organs of the body can initiate a fibrotic response

46
Q

State the hemoglobin molecule defect found in a thalassemia.

A

Defect in the rate of synthesis of one or more of the globin chains

47
Q

Describe the suspected reasoning for the (same) geographic distribution pattern that coincide with the incidence of malaria and the heterozygous state(s) of the thalassemia syndromes.

A

Being heterozygous is advantageous against malaria – having one altered Hgb gene makes infections with Malaria less likely, but sickle cell and thalassemias can occur within the same individual

48
Q

State the globin chain composition and percentages of the three normal adult hemoglobins.

A

• Hemoglobin A: Alpha2 – Beta2 (>95%)
• Hemoglobin A2: Alpha2 – Delta2 (1.5-3.0%)
• Hemoglobin F: Alpha2 – Gamma2 (~ 2%)

49
Q

Describe what is meant by the following nomenclatures as they pertain to the production of globin chains:

β0 thalassemia:
β+ thalassemia:
α0 thalassemia:

A

β0 thalassemia: beta chains ARE NOT being formed
β+ thalassemia: decreased production of beta chains
α0 thalassemia: alpha chains ARE NOT being formed

50
Q

List the four genetic possibilities that may occur with an alpha thalassemia.

A

• No alpha chain production
• One alpha chain functioning – 3 deleted
• Two alpha chain functioning – 2 deleted
• Three alpha chain functioning – 1 deleted

51
Q

Discuss, in detail, Beta Thalassemia Major, including:

Pathology

Ethnic distribution

Clinical features and course of disease

CBC results

RBC morphology

Retic count

BM exam

Hemoglobin electrophoretic pattern

Treatment

A

Pathology

Reduced and/or absent beta chain production – alpha chain synthesis occurs at a normal rate creating an imbalance and leading to precipitation of excess alpha chains resulting in Heinz bodies

Ethnic distribution

Mediterranean area and SE Asia

Clinical features and course of disease

• Onset in early childhood
• Severe hemolytic anemia
• “too many RBCs for Hgb”
• Shorten life span

CBC results

“Too many RBCs for the Hgb”

RBC morphology

Mk’d aniso, poly, hypo, and micro
Mk’d poik w/ targets, schistos, spheres, tears
Inclusions
nRBCs

Retic count

Increased

BM exam

Marked erythroid hyperplasia (a lot of immature RBCs)
Increase in iron stores

Hemoglobin electrophoretic pattern

40-60% F
Increased A2
Decreased A (or absent)

F > A2 – has an greater affinity for oxygen so we observe an increase F before A2

A2/C, S, F, A (shortest to longest distance)

Treatment

Regular transfusions
Iron chelation therapy
Splenectomy
Diet restrictions
Vitamin B & Folate supplementation

52
Q

Discuss the two mechanisms responsible for the early RBC destruction (hemolysis) as seen in Beta Thalassemia Major.

A

• Cells in the BM w/ Heinz bodies leads to ineffective erythropoiesis

• Cells in the circulation w/ Heinz bodies leads to intravascular hemolysis

53
Q

Discuss the reason(s) why patients with Beta Thalassemia Major have the following findings: “hair-on-end” appearance on skull x-rays and Mongoloid appearance to face

A

Due to an increase in hematopoiesis that has caused an expansion of the BM

54
Q

State the results of the following chemistry tests as expected during any hemolytic process… including Beta Thalassemia Major:

A

Plasma haptoglobin: decreased
Serum bilirubin: increased
Serum ferritin: increased
Serum iron: increased

55
Q

Discuss, in detail, Beta Thalassemia Minor, including:

Pathology

Ethnic origin:

Clinical features and course of disease:

CBC results:

RBC morphology:

Retic count:

BM exam:

Hemoglobin electrophoretic pattern

Treatment:

A

Pathology: reduced rate of beta chain production

Ethnic origin: Mediterranean area, SE Asia, Black population of North America and West Africa

Clinical features and course of disease: mild, asymptomatic hemolytic anemia, slight splenomegaly, normal life span

CBC results: “Too many RBCs for the Hgb”

RBC morphology: Slt.-Mod for all morphology relative to Major (aniso, poly, hypo, and micro – poik w/ targets, schistos, spheres, tears – inclusions and nRBCs

Retic count: slightly increased

BM exam:

Mild – mod. erythroid hyperplasia (a lot of immature RBCs)
Increase in iron stores

Hemoglobin electrophoretic pattern

Hgb A predominates – increase in A2 (greater than %5) – increase in F (1-5%)

Treatment: Not usually required

56
Q

Compare and contrast Beta Thalassemia Minor with Iron Deficiency Anemia according to the following parameters:

RBC count:

Beta Thalassemia Minor:

Iron Deficiency Anemia:

Hemoglobin value

Beta Thalassemia Minor:

Iron Deficiency Anemia:

Hgb A2 level

Beta Thalassemia Minor

Iron Deficiency Anemia

ZPP

Beta Thalassemia Minor:

Iron Deficiency Anemia:

A

RBC count:

Beta Thalassemia Minor: increased

Iron Deficiency Anemia: decreased

Hemoglobin value

Beta Thalassemia Minor: >10 g/dL

Iron Deficiency Anemia: <10 g/dL

Hgb A2 level

Beta Thalassemia Minor: >5%

Iron Deficiency Anemia: normal

ZPP

Beta Thalassemia Minor: normal

Iron Deficiency Anemia: increased

57
Q

Discuss Hydrops Fetalis Syndrome according to:

Pathology of the hemoglobin molecule:
Globin chain makeup:
Ethnic distribution:
Compatibility with life:

A

Pathology of the hemoglobin molecule: no alpha chain production
Globin chain makeup: Bart’s = gamma4
Ethnic distribution: SE Asia & Filipino population
Compatibility with life: Death in utero/shortly after delivery

58
Q

Discuss Hemoglobin H disease according to:

Pathology of the hemoglobin molecule
Globin chain makeup:
Unusual characteristic of Heinz bodies:

A

Pathology of the hemoglobin molecule: one functioning alpha chain
Globin chain makeup: Hgb H = beta4
Unusual characteristic of Heinz bodies: RBCs so full of Heinz bodies – “raspberry” appearance

59
Q

Discuss Hemoglobin Lepore according to:

Pathology of the hemoglobin molecule:
Hemoglobins being produced in homozygous state:

A

Pathology of the hemoglobin molecule: fused delta and beta chain
Hemoglobins being produced in homozygous state: produces ~80% Hgb F and make a Lepore with the fused delta and beta chains ~20%

60
Q

Describe the condition known as Hereditary Persistence of Hemoglobin F (HPFH).

A

Persistence of fetal hemoglobin in adult life
Homozygous state (rare) – 100% Hemoglobin F
Heterozygous – A > Hgb F (15-30%)

61
Q

Discuss the Kleihauer-Betke stain according to:

Principle:
Normal values:
Staining pattern with HPFH:
Staining pattern with hemoglobinopathies (other than HPFH):
Appearance of hemoglobin A (adult) cells on smear:
Appearance of hemoglobin F (fetal) cells on smear:

A

Principle: assess the distribution of Hgb F in the RBC
Normal values: adults < 0.01%,
Staining pattern with HPFH: consistently dark pink
Staining pattern with hemoglobinopathies (other than HPFH): “speckled”
Appearance of hemoglobin A (adult) cells on smear: “Ghost cells”
Appearance of hemoglobin F (fetal) cells on smear: Dark pink

62
Q

Describe Heinz bodies with regard to:

Three supravital stain used to detect them:
Appearance on Wright stain:
Composition in: homozygous beta thalassemia:
homozygous alpha0 thalassemia:
hemoglobin H disease:

A

Three supravital stain used to detect them: crystal violet, new methylene blue, brilliant cresyl blue
Appearance on Wright stain: CAN NOT SEE
Composition in: homozygous beta thalassemia: precipitated Hgb – all alpha globins
homozygous alpha0 thalassemia: precipitated Hgb – all gamma globins
hemoglobin H disease: precipitated Hgb – all beta globins

IUHEME (11 decks)

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