lOMoAR cPSD| 67691079
Exam 3 Blueprint
Hematology (~25 questions)
• Types of Anemia
• Types of Lymphoma
• Clotting cascade, intrinsic, extrinsic, and common pathway, all the factors affected
WBC and what things mean when abnormality is present.
• Oxygen hemoglobin dissociation curve
• Hypercoagulability and disease
• TTP, ITP
• Hemophilia
Cardiology (~25 questions)
• Know general cardiology terms and what they mean, e.g., stroke volume, etc.
• General anatomy and blood supply to the heart
• Valvular problems (all of them)
• Atrial and ventricular hypertrophy
• HF (systolic/diastolic), right sided/left sided HF
• Endocarditis
• CAD/ angina
• Atrial fib
• EKG changes with electrolyte abnormalities
• PAD
Prior Content (~10 questions (from modules 1-4)
• Passive immunity, acquired immunity
• Cytokines
• Kinds of IV fluids and when to use
• IgG, IgM, IgE
• Metabolic acidosis and what is seen with acidosis in regard to electrolytes
Metabolic alkalosis
Module 5: Hematology
Types of Anemia
• Macrocytic Anemia o Larger than normal RBCs, indicated by a high MCV >100
Ex: Vit B12 deficiency anemia (pernicious anemia) & folate deficiency
anemia
• Microcytic Anemia o Smaller than normal RBCs, indicated by low MCV <80
Ex: iron deficiency anemia, ACD in later stages, and thalassemia
• Normocytic Anemia o Normal sized RBCs, indicated by a normal MCV (80-100)
Ex: acute blood loss anemia, hemolytic anemia, anemia of chronic disease
(early stages), and aplastic anemia
Sickle cell anemia
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, lOMoAR cPSD| 67691079
• Anemia of Chronic Illness/Chronic Disease (ACD) - NORMOCYTIC o The second most
common type of anemia, often seen in chronic infections, inflammatory conditions, and
chronic diseases
Ex: Rheumatoid Arthritis, Cancer, CKD, AIDS, Chronic hepatitis
o Mechanism
Proinflammatory cytokines inhibit erythropoietin production.
They destroy immature erythroblasts.
Stimulate the release of hepcidin , which controls iron absorption and
blocks iron release, thereby reducing iron availability despite normal or
increased iron stores.
• Hepcidin important in regulating iron and iron stores in liver o controls iron absorption
in blood & secretion of iron in GI tract
o Blocks the release of iron from reticuloendothelial system o
Decreases oral iron absorption – leading to iron deficiency
o Pattern in Iron Studies
Serum Iron: Low
Ferritin: Normal or high (due to inflammation)
TIBC: Low or normal
Transferrin Saturation: Low
• Hemolytic Anemia – NORMOCYTIC o Anemia caused by the premature destruction of
RBCs from the mother’s antibodies
o Causes:
Genetic disorders
• ABO incompatibility
Autoimmune diseases
• ex: Lupus, Rheumatoid Arthritis
Drug Reactions
• ex: NSAIDs, Penicillin, Cephalosporins
Neonatal Hyperbilirubinemia
• This is hemolysis but not anemia*
o Clinical Manifestations:
Symptoms include fatigue, jaundice, dark urine, fever, abdominal pain,
and splenomegaly.
Hemolysis of fetal red blood cells initially leads to increased
erythropoiesis and higher hemoglobin levels, but severe cases can result
in anemia. Neonatal hyperbilirubinemia is a significant manifestation. o
Pathophysiology: The body's immune system (or other mechanisms)
produces antibodies that attack or cause premature destruction of red
blood cells (hemolysis). This rapid destruction leads to a significant
release of hemoglobin and its breakdown products, including
unconjugated bilirubin. The liver then conjugates this bilirubin for
, lOMoAR cPSD| 67691079
excretion, but excessive breakdown can lead to hyperbilirubinemia
(jaundice). The lifespan of RBCs is shortened from the normal 90-120
days.
o Pattern in Iron Studies
Serum Iron: Can be normal or high due to increased iron release from
destroyed RBCs.
Ferritin: Can be normal or high.
TIBC: Typically normal.
Transferrin Saturation: Can be high.
High Bilirubin, High Phosphorus, High Uric Acid, High hemoglobinuria
Positive Coombs test (if autoimmune) – hemolytic anemia
Decreased Haptoglobin
• Hemolytic Disease of the Fetus and Newborn (HDFN) o
Pathophysiology
Results from an ABO or RH incompatibility between the
mother and fetus
• An incompatibility exists if the fetus has a different blood type
than the mother OR if the fetus is Rh positive and the mother is
Rh negative o Most cases are ABO
incompatibility
The first pregnancy primes the immune system
• Then, the second time the female is pregnant with an ABO or Rh
incompatible fetus previously formed IgG antibodies cross the
placenta attack the fetus RBCs and cause them to hemolyze
progressive hemolysis anemia
Erythropoiesis increases in LIVER and SPLEEN and immature red cells
called erythroblastosis fetalis are released into the blood
• The rupture of the RBCs leads to an accumulation of bilirubin
which is cleared by the mother after birth, the baby becomes
jaundiced bc it is no longer being cleared by the mother
Rh incompatibility is more severe anemia than ABO; Rh may cause
intrauterine death, CNS damage, or cardiovascular damage
• Death may result in stillborn babies who exhibit generalized
edema called hydrops fetalis (can occur as early as 17w gestation)
o Clinical Manifestations
Pallor, jaundice, enlarged liver and spleen
Hyperbilirubinemia (icterus neonatorum)
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Exam 3 Blueprint
Hematology (~25 questions)
• Types of Anemia
• Types of Lymphoma
• Clotting cascade, intrinsic, extrinsic, and common pathway, all the factors affected
WBC and what things mean when abnormality is present.
• Oxygen hemoglobin dissociation curve
• Hypercoagulability and disease
• TTP, ITP
• Hemophilia
Cardiology (~25 questions)
• Know general cardiology terms and what they mean, e.g., stroke volume, etc.
• General anatomy and blood supply to the heart
• Valvular problems (all of them)
• Atrial and ventricular hypertrophy
• HF (systolic/diastolic), right sided/left sided HF
• Endocarditis
• CAD/ angina
• Atrial fib
• EKG changes with electrolyte abnormalities
• PAD
Prior Content (~10 questions (from modules 1-4)
• Passive immunity, acquired immunity
• Cytokines
• Kinds of IV fluids and when to use
• IgG, IgM, IgE
• Metabolic acidosis and what is seen with acidosis in regard to electrolytes
Metabolic alkalosis
Module 5: Hematology
Types of Anemia
• Macrocytic Anemia o Larger than normal RBCs, indicated by a high MCV >100
Ex: Vit B12 deficiency anemia (pernicious anemia) & folate deficiency
anemia
• Microcytic Anemia o Smaller than normal RBCs, indicated by low MCV <80
Ex: iron deficiency anemia, ACD in later stages, and thalassemia
• Normocytic Anemia o Normal sized RBCs, indicated by a normal MCV (80-100)
Ex: acute blood loss anemia, hemolytic anemia, anemia of chronic disease
(early stages), and aplastic anemia
Sickle cell anemia
messages.downloaded_by
, lOMoAR cPSD| 67691079
• Anemia of Chronic Illness/Chronic Disease (ACD) - NORMOCYTIC o The second most
common type of anemia, often seen in chronic infections, inflammatory conditions, and
chronic diseases
Ex: Rheumatoid Arthritis, Cancer, CKD, AIDS, Chronic hepatitis
o Mechanism
Proinflammatory cytokines inhibit erythropoietin production.
They destroy immature erythroblasts.
Stimulate the release of hepcidin , which controls iron absorption and
blocks iron release, thereby reducing iron availability despite normal or
increased iron stores.
• Hepcidin important in regulating iron and iron stores in liver o controls iron absorption
in blood & secretion of iron in GI tract
o Blocks the release of iron from reticuloendothelial system o
Decreases oral iron absorption – leading to iron deficiency
o Pattern in Iron Studies
Serum Iron: Low
Ferritin: Normal or high (due to inflammation)
TIBC: Low or normal
Transferrin Saturation: Low
• Hemolytic Anemia – NORMOCYTIC o Anemia caused by the premature destruction of
RBCs from the mother’s antibodies
o Causes:
Genetic disorders
• ABO incompatibility
Autoimmune diseases
• ex: Lupus, Rheumatoid Arthritis
Drug Reactions
• ex: NSAIDs, Penicillin, Cephalosporins
Neonatal Hyperbilirubinemia
• This is hemolysis but not anemia*
o Clinical Manifestations:
Symptoms include fatigue, jaundice, dark urine, fever, abdominal pain,
and splenomegaly.
Hemolysis of fetal red blood cells initially leads to increased
erythropoiesis and higher hemoglobin levels, but severe cases can result
in anemia. Neonatal hyperbilirubinemia is a significant manifestation. o
Pathophysiology: The body's immune system (or other mechanisms)
produces antibodies that attack or cause premature destruction of red
blood cells (hemolysis). This rapid destruction leads to a significant
release of hemoglobin and its breakdown products, including
unconjugated bilirubin. The liver then conjugates this bilirubin for
, lOMoAR cPSD| 67691079
excretion, but excessive breakdown can lead to hyperbilirubinemia
(jaundice). The lifespan of RBCs is shortened from the normal 90-120
days.
o Pattern in Iron Studies
Serum Iron: Can be normal or high due to increased iron release from
destroyed RBCs.
Ferritin: Can be normal or high.
TIBC: Typically normal.
Transferrin Saturation: Can be high.
High Bilirubin, High Phosphorus, High Uric Acid, High hemoglobinuria
Positive Coombs test (if autoimmune) – hemolytic anemia
Decreased Haptoglobin
• Hemolytic Disease of the Fetus and Newborn (HDFN) o
Pathophysiology
Results from an ABO or RH incompatibility between the
mother and fetus
• An incompatibility exists if the fetus has a different blood type
than the mother OR if the fetus is Rh positive and the mother is
Rh negative o Most cases are ABO
incompatibility
The first pregnancy primes the immune system
• Then, the second time the female is pregnant with an ABO or Rh
incompatible fetus previously formed IgG antibodies cross the
placenta attack the fetus RBCs and cause them to hemolyze
progressive hemolysis anemia
Erythropoiesis increases in LIVER and SPLEEN and immature red cells
called erythroblastosis fetalis are released into the blood
• The rupture of the RBCs leads to an accumulation of bilirubin
which is cleared by the mother after birth, the baby becomes
jaundiced bc it is no longer being cleared by the mother
Rh incompatibility is more severe anemia than ABO; Rh may cause
intrauterine death, CNS damage, or cardiovascular damage
• Death may result in stillborn babies who exhibit generalized
edema called hydrops fetalis (can occur as early as 17w gestation)
o Clinical Manifestations
Pallor, jaundice, enlarged liver and spleen
Hyperbilirubinemia (icterus neonatorum)
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