NSC 350- Patho Exam 2 (Answered) 100%
Correct. 2025/2026.
Define pernicious anemia?
Macrocytic/normochromic (large size/normal color) anemia from a vitamin B-12 deficiency.
What, in most cases, is the cause of pernicious anemia?
Lack of intrinsic factor, which is essential for absorption of B-12.
Where is B-12 absorbed with the help of intrinsic factor?
The ileum.
What produces intrinsic factor?
Stomach parietal cells.
What is pernicious anemia believed to result from?
Possibly autoimmune, atrophy/destruction of gastric mucosa from chronic inflammation.
Some symptoms of pernicious anemia.
-Fatigue
-Weight loss
-Numbness & tingling in toes and hands
How do they diagnosis pernicious anemia?
Detection of parietal cell and intrinsic factor antibodies.
Treatment for pernicious anemia?
Lifelong intramuscular injections or high oral doses of vitamin B-12 reverses the anemia.
What happens when there is an increase in bilirubin?
There is an increase in RBC destruction and increased urobilinogen in stool/urine.
What are two forms for inherited hemolytic anemias?
Thalassemias and Sickle cell anemia.
What is the etiology of Thalassemias?
Absent or defective production of alpha or beta chains of hemoglobin.
What populations is Thalassemias common in?
The beta-Thalassemias is common among Mediterranean decent. The alpha-Thalassemias is
common among Asian decent. And both are common among people of African decent.
Thalassemias alpha is caused by?
,A gene deletion that results in defective alpha chain synthesis. It shows great variation in severity
related to number of gene deletions.
What age group experiences the most severe form of Thalassemias alpha?
Infants due to very high oxygen affinity of the hemoglobin. Death in utero or early infancy is
common.
What causes Thalassemias beta?
Multiple point mutations in the beta-globin gene causing a defect in beta-chain synthesis.
How many gene mutations are possible with Thalassemias beta?
200 possible gene mutations.
Clinical manifestations of Thalassemias?
-Impaired bone growth
-Splenomegaly (enlargement of spleen)
-Hepatomegaly (enlargement of liver)
-Enlargement of spleen and liver results from extramedullary hematopoiesis and increased RBC
destruction.
What is sickle cell anemia?
An autosomal recessive disorder of defective Hb gene, HbS. When RBCs are exposed to low oxygen,
it becomes rigid and sickles. These sickle cells get trapped in microvascular areas and lead to
ischemia and infarcts.
HbS trait is carried by 10% of what population?
African Americans
Which form of sickle cell anemia, homozygous or heterozygous, may be asymptomatic?
Heterozygous
Which form of sickle cell anemia, homozygous or heterozygous, can develop severe hemolysis?
Homozygous
What clinical sign indicates RBC hemolysis?
Enlarged spleen and liver.
Clinical manifestations of sickle cell anemia?
-Intense pain due to vascular occlusion in sickle episodes
-Frequent bacterial infections
-Organ failure
Example of acute blood loss?
A hemorrhage, which is normocytic and normochromic
Example of chronic blood loss?
,Gastrointestinal bleeding
What does aplastic anemia consist of?
-Decreased RBCs, WBCs, and Platelets
-Reduced bone marrow development and/or function
-Onset is usually gradual, but could be rapid
How is aplastic anemia diagnosed?
It is sometimes found by accident through routine CBC.
What causes aplastic anemia?
-Chemicals
-Toxins: benzene, chloramphenicol
-Radiation
-Chemotherapy
-Virulent infections (viral hepatitis, AIDS)
-Unknown
Clinical manifestations of aplastic anemia?
Signs and symptoms of infection or bleeding often occur before signs of anemia. AIDS, hepatitis, and
mononucleosis can be associated with serious infection.
What is the treatment for aplastic anemia?
-Symptom management
-Stem cell transplant (bone marrow transplant, peripheral blood transplant)
What is polycythemia?
Excess red blood cells
What is relative polycythemia?
Fluid volume deficit: r/t their fluid volume, RBC not actually elevated.
What is absolute polycythemia?
Consists of primary and secondary polycythemia. RBC is actually elevated.
What is primary polycythemia vera?
-Increased production of all formed elements of blood
-Increased RBC count
-Increased blood volume
-Increased blood viscosity: concentration
-Liver and spleen congested with RBCs
-Hemorrhage: major cause of death
What causes primary polycythemia vera?
Unknown cause.
What is secondary polycythemia?
, Compensatory increase in RBCs
What is secondary polycythemia due to?
Chronic hypoxia- emphysema, chronic bronchitis, COPD
What to consider with RBCs and Pediatrics?
-At birth: hemoglobin is elevated
-1 week: decreased Hb, Hct, RBC, MCV
-2 months- lowest level, physiologic anemia
What is erythroblastosis fetalis?
Hemolytic disease of newborn due to Rh factor discrepancy between mother and baby.
What happens when a mother is Rh negative and the baby is Rh positive?
-Rh positive infant releases RBCs from placenta into mother's circulation during delivery
-1st Rh positive infant is not affected
-Sensitized Rh negative mother transports Rh antibodies during subsequent pregnancies
-Mother's antibodies attack the next Rh positive infant (RBC clumping, hemolysis, severe anemia,
liver failure, Hydrops fetalis: severe edema r/t decreased albumin, Kernicterus: severe neurological
outcome vs. death)
What is hemostasis?
The cessation of bleeding, the prevention of blood loss following vessel injury.
What are platelets?
-Thrombocytes
-150,000-450,000 microliters
-Formed in bone marrow
-Circulation: 70%, Spleen: 30%
-Lifespan is 10 days
How many clotting factors are there?
13
What are clotting factors?
Most are plasma proteins made in liver, and some require Vitamin K for synthesis or function.
What is calcium's role with clotting?
Calcium serves as a clotting factor, so it would be good to monitor calcium levels in bleeding
patients.
What is hypercoagulability?
Consists of increased platelet function (thrombocytosis) and excessive bleeding (inherited or
acquired).
Hemostasis disorders- bleeding?
Correct. 2025/2026.
Define pernicious anemia?
Macrocytic/normochromic (large size/normal color) anemia from a vitamin B-12 deficiency.
What, in most cases, is the cause of pernicious anemia?
Lack of intrinsic factor, which is essential for absorption of B-12.
Where is B-12 absorbed with the help of intrinsic factor?
The ileum.
What produces intrinsic factor?
Stomach parietal cells.
What is pernicious anemia believed to result from?
Possibly autoimmune, atrophy/destruction of gastric mucosa from chronic inflammation.
Some symptoms of pernicious anemia.
-Fatigue
-Weight loss
-Numbness & tingling in toes and hands
How do they diagnosis pernicious anemia?
Detection of parietal cell and intrinsic factor antibodies.
Treatment for pernicious anemia?
Lifelong intramuscular injections or high oral doses of vitamin B-12 reverses the anemia.
What happens when there is an increase in bilirubin?
There is an increase in RBC destruction and increased urobilinogen in stool/urine.
What are two forms for inherited hemolytic anemias?
Thalassemias and Sickle cell anemia.
What is the etiology of Thalassemias?
Absent or defective production of alpha or beta chains of hemoglobin.
What populations is Thalassemias common in?
The beta-Thalassemias is common among Mediterranean decent. The alpha-Thalassemias is
common among Asian decent. And both are common among people of African decent.
Thalassemias alpha is caused by?
,A gene deletion that results in defective alpha chain synthesis. It shows great variation in severity
related to number of gene deletions.
What age group experiences the most severe form of Thalassemias alpha?
Infants due to very high oxygen affinity of the hemoglobin. Death in utero or early infancy is
common.
What causes Thalassemias beta?
Multiple point mutations in the beta-globin gene causing a defect in beta-chain synthesis.
How many gene mutations are possible with Thalassemias beta?
200 possible gene mutations.
Clinical manifestations of Thalassemias?
-Impaired bone growth
-Splenomegaly (enlargement of spleen)
-Hepatomegaly (enlargement of liver)
-Enlargement of spleen and liver results from extramedullary hematopoiesis and increased RBC
destruction.
What is sickle cell anemia?
An autosomal recessive disorder of defective Hb gene, HbS. When RBCs are exposed to low oxygen,
it becomes rigid and sickles. These sickle cells get trapped in microvascular areas and lead to
ischemia and infarcts.
HbS trait is carried by 10% of what population?
African Americans
Which form of sickle cell anemia, homozygous or heterozygous, may be asymptomatic?
Heterozygous
Which form of sickle cell anemia, homozygous or heterozygous, can develop severe hemolysis?
Homozygous
What clinical sign indicates RBC hemolysis?
Enlarged spleen and liver.
Clinical manifestations of sickle cell anemia?
-Intense pain due to vascular occlusion in sickle episodes
-Frequent bacterial infections
-Organ failure
Example of acute blood loss?
A hemorrhage, which is normocytic and normochromic
Example of chronic blood loss?
,Gastrointestinal bleeding
What does aplastic anemia consist of?
-Decreased RBCs, WBCs, and Platelets
-Reduced bone marrow development and/or function
-Onset is usually gradual, but could be rapid
How is aplastic anemia diagnosed?
It is sometimes found by accident through routine CBC.
What causes aplastic anemia?
-Chemicals
-Toxins: benzene, chloramphenicol
-Radiation
-Chemotherapy
-Virulent infections (viral hepatitis, AIDS)
-Unknown
Clinical manifestations of aplastic anemia?
Signs and symptoms of infection or bleeding often occur before signs of anemia. AIDS, hepatitis, and
mononucleosis can be associated with serious infection.
What is the treatment for aplastic anemia?
-Symptom management
-Stem cell transplant (bone marrow transplant, peripheral blood transplant)
What is polycythemia?
Excess red blood cells
What is relative polycythemia?
Fluid volume deficit: r/t their fluid volume, RBC not actually elevated.
What is absolute polycythemia?
Consists of primary and secondary polycythemia. RBC is actually elevated.
What is primary polycythemia vera?
-Increased production of all formed elements of blood
-Increased RBC count
-Increased blood volume
-Increased blood viscosity: concentration
-Liver and spleen congested with RBCs
-Hemorrhage: major cause of death
What causes primary polycythemia vera?
Unknown cause.
What is secondary polycythemia?
, Compensatory increase in RBCs
What is secondary polycythemia due to?
Chronic hypoxia- emphysema, chronic bronchitis, COPD
What to consider with RBCs and Pediatrics?
-At birth: hemoglobin is elevated
-1 week: decreased Hb, Hct, RBC, MCV
-2 months- lowest level, physiologic anemia
What is erythroblastosis fetalis?
Hemolytic disease of newborn due to Rh factor discrepancy between mother and baby.
What happens when a mother is Rh negative and the baby is Rh positive?
-Rh positive infant releases RBCs from placenta into mother's circulation during delivery
-1st Rh positive infant is not affected
-Sensitized Rh negative mother transports Rh antibodies during subsequent pregnancies
-Mother's antibodies attack the next Rh positive infant (RBC clumping, hemolysis, severe anemia,
liver failure, Hydrops fetalis: severe edema r/t decreased albumin, Kernicterus: severe neurological
outcome vs. death)
What is hemostasis?
The cessation of bleeding, the prevention of blood loss following vessel injury.
What are platelets?
-Thrombocytes
-150,000-450,000 microliters
-Formed in bone marrow
-Circulation: 70%, Spleen: 30%
-Lifespan is 10 days
How many clotting factors are there?
13
What are clotting factors?
Most are plasma proteins made in liver, and some require Vitamin K for synthesis or function.
What is calcium's role with clotting?
Calcium serves as a clotting factor, so it would be good to monitor calcium levels in bleeding
patients.
What is hypercoagulability?
Consists of increased platelet function (thrombocytosis) and excessive bleeding (inherited or
acquired).
Hemostasis disorders- bleeding?
