MIDTERM EXAM REVIEW NR 507/NR507 ADVANCED
PATHOPHYSIOLOGY|2025
Hematology
Hematopoiesis: -process of blood cell production
-Constant throughout life to replace RBCs that grow old and die, are
killed by disease, or are lost through bleeding
-Occurs in liver and spleen of fetus
-Occurs in bone marrow after birth
-2 stages: 1. Proliferation (mitotic division)
2. Maturation (differentiation)
-Bone marrow: red (hematopoietic/active) & yellow (fatty/inactive)
Hematopoietic stem cells (HSCs)- all blood cells are created from
HSCs
-signaled to undergo differentiation (by cytokines and chemokines,
growth factors) to form RBC, WBC, & platelets
· Lymphoid: T cell (T-lymphocyte) & B cell (B-lymphocyte)
· Myeloid: Monocyte & Granulocytes (WBCs)
· Erythrocyte (RBC)
· Megakaryocyte (Platelets)
Mesenchymal stem cells-develop into osteoclasts, fibroblasts, &
adipocytes
Erythropoietin: -hormone that stimulates erythrocyte production
-Secreted by the kidneys in response to tissue hypoxia
Erythrocyte: -most abundant cells in the body
-primarily responsible for tissue oxygenation
-mature erythrocytes lack a nucleus and mitochondria, cannot
synthesize protein or carry out oxidative reactions. Cannot divide
*anaerobic metabolism only
-life span: 100-120 days
-contains hemoglobin molecules
o Stages: (7-day process)
· Hemocytoblast (stem cell) binds with erythropoietin
· Proerythroblast- committed to morph into RBC
· Erythroblast- ribosome synthesis (2 phases)
· Normoblast- Hgb accumulation & nucleus ejection
· Reticulocyte –(immature RBC) released into circulation, no nucleus,
ribosome, or mitochondria
· RBC (after it has been in bone marrow 1-2 days)
Hemoglobin: oxygen carrying protein of the erythrocyte
-hemoglobin packed blood cells pick up oxygen in the lungs and
exchange it for carbon dioxide in the tissues
,-composed of 2 pairs of polypeptide chains (globins) & 4 colorful iron
complexes (hemes)
-can carry up to 4 molecules of oxygen
Oxyheoglobin- binding of oxygen to Fe in heme molecule, RED
Deoxyhemoglobin- reduced hemoglobin, after it releases the oxygen to
the tissues, BLUE
Risk factors and causes for developing any type of anemia:
-blood loss (acute or chronic)
-impaired erythrocyte production
-increased erythrocyte destruction
-a combination of these factors
Iron Deficiency Anemia- Microcytic-Hypochromic Anemia
-most common nutritional disorder
-occurs when iron stores are depleted Oreduced hemoglobin synthesis
-more common in toddlers, adolescent girls and, women of
childbearing age
-causes:
· Dietary deficiency
· Impaired absorption
· Increased requirement
· Chronic blood loss
Thalassemia-Microcytic-Hypochromic
-inherited autosomal recessive disorder
-impaired synthesis of one of the two chains of adult hemoglobin
(alpha or beta)
-common among Mediterranean descent
-can be minor or major, can be asymptomatic or lethal (Cooley’s)
Sickle Cell Anemia-Normocytic-normochromic/Hemolytic
-inherited autosomal recessive disorder
-presence of atypical hemoglobin-Hemoglobin S
-amino acid change on the beta-globin chain (glutamine replaced for
valine)-distort erythrocytes into sickle shape= cannot properly carry
O2.
-vaso-occlusive crisis (pain), aplastic crisis (anemia), sequestration
crisis (blood pooling in spleen), hyperhemolytic crisis ( accelerated
RBC destruction)
- Stress, hypoxia, anxiety, fever, cold, dehydration = lower O2 binding
-↑ risk of CVA, splenic damage, or kidney damage. Most people with
sickle cell will become asplenic by adulthood.
Hemolytic Anemia-
-premature destruction of erythrocytes
-majority occur within phagocyctes in lymphoid tissue
, -congenital (sickle cell or thalassemia) acquired (transfusion reaction,
infection, autoimmune)
-causes elevated erythropoietin to induce accelerated production of
erythrocytes and in increase in the products of hemoglobin catabolism
-transfusion with incorrect blood type: intravascular hemolysis by
activation of complement system; extravascular hemolysis by
phagocytosis of antibody-coated erythrocytes in spleen
Pernicious Anemia-Macrocytic
-vitamin B deficiency
-Autoimmune gastritis-impaired intrinsic factor (transporter needed
for vitamin B12 absorption)
-can be congenital- autosomal recessive inheritance
-gastric bypass, or gastrectomy
- H. Pylori infection= risk factor
-will need Vit B 12 injections for life
Pulmonary
Oxygen O2 transport involves 4 steps:
1. Air is inhaled through the process of Ventilation (mechanical
movement of gas or air into and out of the lungs, necessary to ensure
sufficient perfusion) through the lungs.
2. Oxygen diffuses from alveoli into pulmonary capillaries (dense
network of blood vessels surrounding the alveoli), moving oxygen
from the pulmonary veins (only veins which carry oxygenated blood)
to the left side of the heart (atrium-ventricle) to the aorta into
systemic arterial circulation.
3. Perfusion (exchange of O2 and CO2 in the bloodstream, which
occurs via the alveoli and pulmonary capillaries) of systemic
capillaries with oxygenated blood.
4. Oxygen is diffused from the systemic capillaries to each and
every cell.
Gas CO2 transport involves 4 steps (backwards):
1. Diffusion of blood (deoxygenated) from cells into systemic
capillaries.
2. Perfusion of systemic capillaries with deoxygenated blood
through the venous circulation, to the vena cava, into the right side of
the heart (atrium-ventricle), to pulmonary arteries (only arteries
which carry deoxygenated blood).
3. Diffusion of CO2 from pulmonary arteries into alveoli through
pulmonary capillaries.
PATHOPHYSIOLOGY|2025
Hematology
Hematopoiesis: -process of blood cell production
-Constant throughout life to replace RBCs that grow old and die, are
killed by disease, or are lost through bleeding
-Occurs in liver and spleen of fetus
-Occurs in bone marrow after birth
-2 stages: 1. Proliferation (mitotic division)
2. Maturation (differentiation)
-Bone marrow: red (hematopoietic/active) & yellow (fatty/inactive)
Hematopoietic stem cells (HSCs)- all blood cells are created from
HSCs
-signaled to undergo differentiation (by cytokines and chemokines,
growth factors) to form RBC, WBC, & platelets
· Lymphoid: T cell (T-lymphocyte) & B cell (B-lymphocyte)
· Myeloid: Monocyte & Granulocytes (WBCs)
· Erythrocyte (RBC)
· Megakaryocyte (Platelets)
Mesenchymal stem cells-develop into osteoclasts, fibroblasts, &
adipocytes
Erythropoietin: -hormone that stimulates erythrocyte production
-Secreted by the kidneys in response to tissue hypoxia
Erythrocyte: -most abundant cells in the body
-primarily responsible for tissue oxygenation
-mature erythrocytes lack a nucleus and mitochondria, cannot
synthesize protein or carry out oxidative reactions. Cannot divide
*anaerobic metabolism only
-life span: 100-120 days
-contains hemoglobin molecules
o Stages: (7-day process)
· Hemocytoblast (stem cell) binds with erythropoietin
· Proerythroblast- committed to morph into RBC
· Erythroblast- ribosome synthesis (2 phases)
· Normoblast- Hgb accumulation & nucleus ejection
· Reticulocyte –(immature RBC) released into circulation, no nucleus,
ribosome, or mitochondria
· RBC (after it has been in bone marrow 1-2 days)
Hemoglobin: oxygen carrying protein of the erythrocyte
-hemoglobin packed blood cells pick up oxygen in the lungs and
exchange it for carbon dioxide in the tissues
,-composed of 2 pairs of polypeptide chains (globins) & 4 colorful iron
complexes (hemes)
-can carry up to 4 molecules of oxygen
Oxyheoglobin- binding of oxygen to Fe in heme molecule, RED
Deoxyhemoglobin- reduced hemoglobin, after it releases the oxygen to
the tissues, BLUE
Risk factors and causes for developing any type of anemia:
-blood loss (acute or chronic)
-impaired erythrocyte production
-increased erythrocyte destruction
-a combination of these factors
Iron Deficiency Anemia- Microcytic-Hypochromic Anemia
-most common nutritional disorder
-occurs when iron stores are depleted Oreduced hemoglobin synthesis
-more common in toddlers, adolescent girls and, women of
childbearing age
-causes:
· Dietary deficiency
· Impaired absorption
· Increased requirement
· Chronic blood loss
Thalassemia-Microcytic-Hypochromic
-inherited autosomal recessive disorder
-impaired synthesis of one of the two chains of adult hemoglobin
(alpha or beta)
-common among Mediterranean descent
-can be minor or major, can be asymptomatic or lethal (Cooley’s)
Sickle Cell Anemia-Normocytic-normochromic/Hemolytic
-inherited autosomal recessive disorder
-presence of atypical hemoglobin-Hemoglobin S
-amino acid change on the beta-globin chain (glutamine replaced for
valine)-distort erythrocytes into sickle shape= cannot properly carry
O2.
-vaso-occlusive crisis (pain), aplastic crisis (anemia), sequestration
crisis (blood pooling in spleen), hyperhemolytic crisis ( accelerated
RBC destruction)
- Stress, hypoxia, anxiety, fever, cold, dehydration = lower O2 binding
-↑ risk of CVA, splenic damage, or kidney damage. Most people with
sickle cell will become asplenic by adulthood.
Hemolytic Anemia-
-premature destruction of erythrocytes
-majority occur within phagocyctes in lymphoid tissue
, -congenital (sickle cell or thalassemia) acquired (transfusion reaction,
infection, autoimmune)
-causes elevated erythropoietin to induce accelerated production of
erythrocytes and in increase in the products of hemoglobin catabolism
-transfusion with incorrect blood type: intravascular hemolysis by
activation of complement system; extravascular hemolysis by
phagocytosis of antibody-coated erythrocytes in spleen
Pernicious Anemia-Macrocytic
-vitamin B deficiency
-Autoimmune gastritis-impaired intrinsic factor (transporter needed
for vitamin B12 absorption)
-can be congenital- autosomal recessive inheritance
-gastric bypass, or gastrectomy
- H. Pylori infection= risk factor
-will need Vit B 12 injections for life
Pulmonary
Oxygen O2 transport involves 4 steps:
1. Air is inhaled through the process of Ventilation (mechanical
movement of gas or air into and out of the lungs, necessary to ensure
sufficient perfusion) through the lungs.
2. Oxygen diffuses from alveoli into pulmonary capillaries (dense
network of blood vessels surrounding the alveoli), moving oxygen
from the pulmonary veins (only veins which carry oxygenated blood)
to the left side of the heart (atrium-ventricle) to the aorta into
systemic arterial circulation.
3. Perfusion (exchange of O2 and CO2 in the bloodstream, which
occurs via the alveoli and pulmonary capillaries) of systemic
capillaries with oxygenated blood.
4. Oxygen is diffused from the systemic capillaries to each and
every cell.
Gas CO2 transport involves 4 steps (backwards):
1. Diffusion of blood (deoxygenated) from cells into systemic
capillaries.
2. Perfusion of systemic capillaries with deoxygenated blood
through the venous circulation, to the vena cava, into the right side of
the heart (atrium-ventricle), to pulmonary arteries (only arteries
which carry deoxygenated blood).
3. Diffusion of CO2 from pulmonary arteries into alveoli through
pulmonary capillaries.
