UAMS Hematology Exam 3
"thalassemia belt" - ANS-Types of Thalassemia Mediterranean east thru the Middle East and
India to Southeast Asia and south through Africa
» B Thalassemia silent provider - ANS-Heterozygous country and not using a hematologic
abnormalities or scientific symptoms
(STFR) Increased in - ANS-IDA,
(STFR) Normal in - ANS-Normal in Anemia of Chronic Inflammation
(STFR) Normal Range: - ANS-1.15-2.75mg/L
• % Transferrin Saturation - ANS-Since the TIBC represents the whole range of sites for iron
binding, and the SI represents the with iron, the diploma to which the available web sites are
occupied by means of iron is calculated
• ↑ urine hemoglobin • ↑ urine hemosiderin - ANS-Intravascular Hemolysis
• ⬇️Haptoglobin - ANS-Hemolytic Anemia
• A measure of anisocytosis - ANS-RDW
• Beta Chain replacement Mild Hemolytic Anemia - ANS-• Hgb E
• C crystals • Target cells - ANS-Hgb C
• Due to a slowdown in DNA synthesis in developing cells - ANS-Megaloblastic Anemia
• Haptoglobin • ↑ urine and stool urobilinogen - ANS-Hemolytic Anemia
• Heinz our bodies visible with Methylene Blue - ANS-G-6-PD
• Heinz Body: - ANS-Body: Precipitated Hemoglobin; visible in G6PD deficiency Can
handiest be visible with supravital stain
• In a normal bone marrow, what number of white blood cells are the mature cells? - ANS-•
50% of neutrophils are myelocytes, metamyleocytes, bands and segs
• In aplastic anemia, what is the bone marrow fats to mobile ratio? - ANS-90:10
• Iron is carried to - ANS-· Bone marrow and released to developing cells • Liver where
stored as ferritin
,• is intravascular prominent from extravascular hemolysis? - ANS-Urine Hemosiderin
• Most are due to inadequate production of hemoglobin - ANS-Microcytic Anemia
• Most intrinsic defects are inherited, maximum extrinsic defects are received Except -
ANS-Paroxymal Nocturnal Hemoglobinuria
• Transmitted by using a intercourse-linked, mutant gene • More not unusual in men -
ANS-G-6-PD Deficiency
• What is a bonus of the use of automated devices? - ANS-Increased precision
• What microscopic energy is used to look BM megakaryocytes? - ANS-Low power, 10X
• When frame Iron Increases, - ANS-hepcidin increases Enterocytes export less iron into
plasma, macrophages hold iron • Iron will NOT be available for cell production • Cell
becomes hypochromic microcytic
• When G6PD poor: - ANS-• No NADPH Reduced glutathione Hemoglobin aggregates or
precipitates (Heinz Bodies) • Premature destruction of crimson cells (intracellular,
extravascular hemolysis)
2 CATEGORIES OF NORMOCYTIC, NORMOCHROMIC ANEMIA - ANS-Hemolytic
Aplastic Anemia
2 gene deletion trans: - ANS-no scientific; mild hypo, micro Blacks
3 gene deletion - ANS-Causes Hemoglobin H disorder
Severe hemolytic anemia with tetramers
Hgb H (beta4) •
Non-purposeful tetramers reason precipitation in cells •
Found more often than not in Asians
3 gene deletions: - ANS-intense hemolytic anemia; known as Hgb H disease; patient has
usually Hgb H which is a tetramer of beta chains (Ba). Observed in Asians
four gene deletion: - ANS-Hydrops Fetalis; continually deadly; no Hgb A, A2 or F; all Hgb is
Bart's Hgb that is a tetramer of gamma chains or (y4). Observed in Asians
70% of all instances of autoimmune hemolytic anemia - ANS-Warm-Reactive Autoantibodies
ninety% of ordinary purple cellular destruction - ANS-Extravascular Destruction
Abnormal Tests for Hemolytic Anemia - ANS-•↑ unconjugated bilirubin • ↑ LD
Abnormal Tests in Intravascular Hemolysis - ANS-• ↑ urine hemoglobin • ↑ urine hemosiderin
, Abnormality of hematopoietic cellular membranes. Caused by using somatic mutation -
ANS-Paroxysmal Nocturnal Hemoglobinuria • All cell traces worried purple cells, white cells
(granulocytes), and platelets
Acanthocytes - ANS-May be inherited or acquired
Acanthocytes membrane defect - ANS-Membranes have altered lipid content • Imbalance of
cholesterol and phospholipid Observed in:
Liver sickness Congenital
Abetalipoproteinemia
Acquired - ANS-• Develop in those who had been previously normal however occurs after
publicity to an chemical/agent/circumstance
Acute Examples: - ANS-• Paroxymal Nocturnal Hemoglobinuria Hemolytic Transfusion
Reaction
After maturation, cells enter the sinus - ANS-via fenestrations in the lining cells of the sinus
Agglutination will affect - ANS-MCV
Alpha Thalassemia - ANS-Only two genes control beta, gamma, and delta chains on
chromosome eleven
Alpha Thalassemia 1 gene deletion: - ANS-no clinical; normal hematology values 30% of all
African Americans
Alpha Thalassemia 2 gene deletion - ANS-no medical; moderate hypo, micro Asians
Also known as sports anemia - ANS-March Hemoglobinuria
An obtained Intracellular Defect with Intravascular Hemolysis - ANS-Paroxysmal Nocturnal
Hemoglobinuria
Anemia of Chronic Disease/Inflammation - ANS-maximum not unusual anemia among
hospitalized patients • Cells are frequently hypochromic microcytic · Also mentioned in N/N
anemia
Anemia of Chronic Disease/Inflammation Stimulated - ANS-Stimulated macrophages will
NOT release iron after normal breakdown in the spleen Liver produces a hormone:
Hepcidin
· An acute phase reactant ·
Regulates: Absorption of iron inside the intestines • Release of iron from macrophages
ANEMIA OF CHRONIC DISORDERS MECHANISM - ANS-Cytokines are produced via the
immune machine in reaction to immune or tumor stimulus Erythropoietin is inhibited
Macrophages come to be stimulated
Will no longer release iron after ordinary RBC break down within the spleen
"thalassemia belt" - ANS-Types of Thalassemia Mediterranean east thru the Middle East and
India to Southeast Asia and south through Africa
» B Thalassemia silent provider - ANS-Heterozygous country and not using a hematologic
abnormalities or scientific symptoms
(STFR) Increased in - ANS-IDA,
(STFR) Normal in - ANS-Normal in Anemia of Chronic Inflammation
(STFR) Normal Range: - ANS-1.15-2.75mg/L
• % Transferrin Saturation - ANS-Since the TIBC represents the whole range of sites for iron
binding, and the SI represents the with iron, the diploma to which the available web sites are
occupied by means of iron is calculated
• ↑ urine hemoglobin • ↑ urine hemosiderin - ANS-Intravascular Hemolysis
• ⬇️Haptoglobin - ANS-Hemolytic Anemia
• A measure of anisocytosis - ANS-RDW
• Beta Chain replacement Mild Hemolytic Anemia - ANS-• Hgb E
• C crystals • Target cells - ANS-Hgb C
• Due to a slowdown in DNA synthesis in developing cells - ANS-Megaloblastic Anemia
• Haptoglobin • ↑ urine and stool urobilinogen - ANS-Hemolytic Anemia
• Heinz our bodies visible with Methylene Blue - ANS-G-6-PD
• Heinz Body: - ANS-Body: Precipitated Hemoglobin; visible in G6PD deficiency Can
handiest be visible with supravital stain
• In a normal bone marrow, what number of white blood cells are the mature cells? - ANS-•
50% of neutrophils are myelocytes, metamyleocytes, bands and segs
• In aplastic anemia, what is the bone marrow fats to mobile ratio? - ANS-90:10
• Iron is carried to - ANS-· Bone marrow and released to developing cells • Liver where
stored as ferritin
,• is intravascular prominent from extravascular hemolysis? - ANS-Urine Hemosiderin
• Most are due to inadequate production of hemoglobin - ANS-Microcytic Anemia
• Most intrinsic defects are inherited, maximum extrinsic defects are received Except -
ANS-Paroxymal Nocturnal Hemoglobinuria
• Transmitted by using a intercourse-linked, mutant gene • More not unusual in men -
ANS-G-6-PD Deficiency
• What is a bonus of the use of automated devices? - ANS-Increased precision
• What microscopic energy is used to look BM megakaryocytes? - ANS-Low power, 10X
• When frame Iron Increases, - ANS-hepcidin increases Enterocytes export less iron into
plasma, macrophages hold iron • Iron will NOT be available for cell production • Cell
becomes hypochromic microcytic
• When G6PD poor: - ANS-• No NADPH Reduced glutathione Hemoglobin aggregates or
precipitates (Heinz Bodies) • Premature destruction of crimson cells (intracellular,
extravascular hemolysis)
2 CATEGORIES OF NORMOCYTIC, NORMOCHROMIC ANEMIA - ANS-Hemolytic
Aplastic Anemia
2 gene deletion trans: - ANS-no scientific; mild hypo, micro Blacks
3 gene deletion - ANS-Causes Hemoglobin H disorder
Severe hemolytic anemia with tetramers
Hgb H (beta4) •
Non-purposeful tetramers reason precipitation in cells •
Found more often than not in Asians
3 gene deletions: - ANS-intense hemolytic anemia; known as Hgb H disease; patient has
usually Hgb H which is a tetramer of beta chains (Ba). Observed in Asians
four gene deletion: - ANS-Hydrops Fetalis; continually deadly; no Hgb A, A2 or F; all Hgb is
Bart's Hgb that is a tetramer of gamma chains or (y4). Observed in Asians
70% of all instances of autoimmune hemolytic anemia - ANS-Warm-Reactive Autoantibodies
ninety% of ordinary purple cellular destruction - ANS-Extravascular Destruction
Abnormal Tests for Hemolytic Anemia - ANS-•↑ unconjugated bilirubin • ↑ LD
Abnormal Tests in Intravascular Hemolysis - ANS-• ↑ urine hemoglobin • ↑ urine hemosiderin
, Abnormality of hematopoietic cellular membranes. Caused by using somatic mutation -
ANS-Paroxysmal Nocturnal Hemoglobinuria • All cell traces worried purple cells, white cells
(granulocytes), and platelets
Acanthocytes - ANS-May be inherited or acquired
Acanthocytes membrane defect - ANS-Membranes have altered lipid content • Imbalance of
cholesterol and phospholipid Observed in:
Liver sickness Congenital
Abetalipoproteinemia
Acquired - ANS-• Develop in those who had been previously normal however occurs after
publicity to an chemical/agent/circumstance
Acute Examples: - ANS-• Paroxymal Nocturnal Hemoglobinuria Hemolytic Transfusion
Reaction
After maturation, cells enter the sinus - ANS-via fenestrations in the lining cells of the sinus
Agglutination will affect - ANS-MCV
Alpha Thalassemia - ANS-Only two genes control beta, gamma, and delta chains on
chromosome eleven
Alpha Thalassemia 1 gene deletion: - ANS-no clinical; normal hematology values 30% of all
African Americans
Alpha Thalassemia 2 gene deletion - ANS-no medical; moderate hypo, micro Asians
Also known as sports anemia - ANS-March Hemoglobinuria
An obtained Intracellular Defect with Intravascular Hemolysis - ANS-Paroxysmal Nocturnal
Hemoglobinuria
Anemia of Chronic Disease/Inflammation - ANS-maximum not unusual anemia among
hospitalized patients • Cells are frequently hypochromic microcytic · Also mentioned in N/N
anemia
Anemia of Chronic Disease/Inflammation Stimulated - ANS-Stimulated macrophages will
NOT release iron after normal breakdown in the spleen Liver produces a hormone:
Hepcidin
· An acute phase reactant ·
Regulates: Absorption of iron inside the intestines • Release of iron from macrophages
ANEMIA OF CHRONIC DISORDERS MECHANISM - ANS-Cytokines are produced via the
immune machine in reaction to immune or tumor stimulus Erythropoietin is inhibited
Macrophages come to be stimulated
Will no longer release iron after ordinary RBC break down within the spleen
