Hemopath 1 RBC Flashcards

(15 cards)

1
Q

How is anemia classified based on mean cell volume (MCV), and what are the typical ranges?

A

• Microcytic: MCV < 80 fL
• Normocytic: MCV 80–100 fL
• Macrocytic: MCV > 100 fL

This helps determine the underlying mechanism of anemia.

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2
Q

What does hypochromia indicate on a peripheral blood smear, and what causes it?

A

Hypochromia = RBCs with less hemoglobin, appearing pale.
Common in iron deficiency anemia and thalassemia.

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3
Q

What is bilirubin, and how does its accumulation relate to hemolysis?

A

Bilirubin is a breakdown product of heme.
In hemolytic anemia, increased RBC destruction leads to excess unconjugated bilirubin, causing jaundice.

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4
Q

What is extravascular hemolysis, and where does it typically occur?

A

Occurs when macrophages in the spleen or liver destroy damaged or abnormal RBCs.
Common in hereditary spherocytosis and autoimmune hemolytic anemia.

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5
Q

What causes sickling in sickle cell anemia, and what triggers sickle crises?

A

HbS polymerizes under low oxygen, dehydration, or acidosis.
Leads to RBC sickling, hemolysis, and vascular occlusion.

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6
Q

Why are individuals with sickle cell trait usually asymptomatic?

A

They produce both HbA and HbS.
HbA prevents significant polymerization of HbS under normal conditions.

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7
Q

Why is fetal hemoglobin (HbF) protective in sickle cell disease?

A

HbF has no β-chains, so it doesn’t sickle.
Infants with high HbF levels are often asymptomatic until HbF declines around 6 months.

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8
Q

What clinical complications arise from sickle cell crises?

A

Vaso-occlusion causes pain crises, acute chest syndrome, stroke, priapism, and splenic infarction.

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9
Q

What is β-thalassemia major, and how does it affect erythropoiesis?

A

Caused by mutations in both β-globin genes.
Results in excess α-chains, ineffective erythropoiesis, severe anemia, and skeletal deformities from marrow expansion.

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10
Q

How do thalassemias typically appear on CBC and blood smear?

A

Microcytic, hypochromic anemia with target cells and anisopoikilocytosis on smear.

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11
Q

How do reactive oxygen species (ROS) contribute to RBC damage?

A

ROS damage RBC membranes and hemoglobin.
In G6PD deficiency, inability to detoxify ROS leads to episodic hemolysis and bite cells.

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12
Q

What is aplastic anemia, and what are common causes?

A

Bone marrow failure leads to pancytopenia (↓ RBCs, WBCs, platelets).
Causes include idiopathic, drugs, radiation, or viral infections (e.g., parvovirus B19).

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13
Q

What does pancytopenia on a CBC suggest about bone marrow function?

A

Indicates failure or suppression of all cell lineages — often due to aplastic anemia or marrow infiltration (e.g., leukemia, fibrosis).

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14
Q

What are schistocytes, and what condition are they associated with?

A

Schistocytes = fragmented RBCs.
Seen in microangiopathic hemolytic anemia (TTP, HUS, DIC), due to RBCs being sheared by fibrin strands.

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15
Q

What is Disseminated Intravascular Coagulation (DIC), and how does it affect RBCs?

A

DIC causes widespread clotting and bleeding due to consumption of clotting factors and platelets.
Leads to hemolysis and schistocyte formation.

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