The University of Alabama
Capstone College of Nursing
NUR 529 Exam 2 Blueprint
Pages referred to below are from Porth’s Pathophysiology: Concepts of Altered States, 10th ed.,
and the current e-book on coursepoint. Older versions are not included, this course does not
utilize older textbook versions. Format for page numbers below is Porth 10th ed “hard copy”
book/ Course Point Porth E-Book. Example: p. 967/975. If the pages correlate between editions
then only one will be listed.
---------------------------------------------------------------------------------------------------------------------
Unit 7. Disorders of the Hematopoietic System. Chapters 22, 23, and 24. There are 6
questions from this unit.
1. Chapter 22. Could talk a client through the Mechanisms of Hemostasis. See page 623,
Understanding hemostasis, three stages.
1. Vessel vasoconstriction- imjury in the vascular smooth muscle, causes the vessel
wall to contract, reducing blood flow from vessel rupture
2. Formation of platelet plug- seconds after vessel injury, vWF is released from the
endothelium and binds to platelet receptors causing adhesions to the platelets to
the collagen fibers. As the platelets adhere to the collagen fibers on the vessel
wall they become activated by release of ADP and TXA, which attracts additional
platelets, leading to platelet aggregation.
3. Blood clot develops as a result of coagulation process. There are two
cogagulation pathways intrinsic and extrinsic. Both lead to theactivation of factor
X, the conversion of prothrombin to thrombin, and conversion of fibrinogen to
fibrin threads that hold the clot together.
2. Chapter 22. Bleeding Disorders: Bleeding Associated with Platelet Disorders.
Bleeding because of platelet disorders reflects a decrease in platelet number because of decreased
production, increased destruction, or impaired function of platelets. Spontaneous bleeding from
platelet disorders most often involves small vessels of the mucous membranes and skin.
Common sites of bleeding are the mucous membranes of the nose, mouth, gastrointestinal
tract, and uterine cavity. Cutaneous bleeding is seen as pinpoint hemorrhages (petechiae) and purple
areas of bruising (purpura) in dependent areas where the capillary pressure is higher (Fig. 22.3).
Petechiae are seen almost exclusively in conditions of platelet deficiency and not platelet dysfunction.
Bleeding of the intracranial vessels is a rare danger with severe platelet depletion.
Thrombocytopenia: A reduction in platelet number, also referred to as thrombocytopenia, is an
important cause of generalized bleeding. Thrombocytopenia usually refers to a decrease in the number
of circulating platelets to a level less than 150,000/μL.19 CO Important 8/15/2022 The greater the
,decrease in the platelet count, the greater the risk of bleeding. Thrombocytopenia can result from a
decrease in platelet production, increased sequestration of platelets in the spleen, or decreased platelet
survival.
3. Chapter 23. Anemia: Red blood cell characteristics seen in different types anemias.
There are four primary causes of anemia:
(1) excessive loss of red blood cells from bleeding,
(2) destruction (hemolysis) of red blood cells,
(3) defective red blood cell production, or
(4) inadequate red blood cell production because of bone marrow failure.
***Anemia is not a disease, but an indication of some disease process or alteration in body function.***
The effects of anemia can be grouped into three categories:
1. Manifestations of impaired oxygen transport and the resulting compensatory mechanisms
2. Reduction in red cell indices and hemoglobin levels
3. Signs and symptoms associated with the pathologic process that is causing the anemia
4. Chapter 23. Anemia: Anemias of Deficient Red Cell Production. Iron deficiency
anemia (IDA). Compare causes of IDA in adults and children. What are the most
common causes in each group?
Iron Deficiency Anemia (IDA) Iron deficiency is a common worldwide cause of anemia affecting people
of all ages. The anemia results from dietary deficiency, loss of iron through bleeding, or increased
demands. Because iron is a component of heme, a deficiency leads to decreased hemoglobin synthesis
and consequent impairment of oxygen delivery.
B12 deficiency can be from diet but more importantly lack of intrinsic factor in the stomach that leads to
failure to absorb vitamin B12. (pernicious anemia). When vitamin B 12 is deficient, the red cells that are
produced are abnormally large because of excess cytoplasmic growth and structural proteins. Thus,
megaloblastic anemia.
Folic acid is required for DNA synthesis and RBC maturation. Because the link between folic acid
deficiency and neural tube birth defects is so well known it is recommended that all women of child-
bearing age are advised to take in 400 mcg per day.
The usual reason for iron deficiency in adults in the western world is chronic blood loss because there
is inadequate iron available for recycling. In men and postmenopausal women, blood loss may occur
from gastrointestinal bleeding because of peptic ulcer, vascular lesions, intestinal polyps, hemorrhoids,
or cancer. In women of child-bearing age, iron demand is increased because of losses from
menstruation. Additionally, in pregnant women, fetal development increases iron requirements for
erythropoiesis.
,The manifestations of iron deficiency anemia are related to impaired oxygen transport and lack of
hemoglobin. Depending on the severity of the anemia, fatigability, palpitations, dyspnea, angina, and
tachycardia may occur. Pica, a craving for substances lacking nutritional value such as clay or ice, may
develop.
Diagnosis and Treatment:
Low hemoglobin and hematocrit, decreased iron stores, and low serum iron and ferritin
characterize iron deficiency anemia. The red cells are decreased in number and are microcytic and
hypochromic (see Fig. 23.7). Poikilocytosis (irregular shape) and anisocytosis (irregular size) are also
present. Laboratory values indicate reduced MCHC and MCV.
Prevention of iron deficiency is a primary concern in infants and children. Avoidance of cow’s
milk, iron supplementation at 4 to 6 months of age in breast-fed infants, and use of iron-fortified
formulas and cereals are recommended for infants younger than 1 year of age.17 In the 2nd year, a diet
rich in iron-containing foods and use of iron-fortified vitamins will help prevent iron deficiency. The
treatment of iron deficiency anemia in children and adults is directed toward controlling chronic blood
loss, increasing dietary intake of iron, and administering supplemental iron. Ferrous sulfate, which is the
usual oral replacement therapy, replenishes iron stores in several months.
5. Chapter 24. Nonneoplastic Disorders of White Blood Cells: Infectious Mononucleosis.
Clinical course, most common complication, and laboratory diagnostics.
Infectious Mononucleosis:
• Self-limiting disorder where lymphocytes are produced in excessive quantities.
• Caused by the Epstein-Barr virus.
• Transmitted in saliva.
• Once infected the virus will remain present in the B lymphocytes for a lifetime.
• Characterized by fever, generalized lymphadenopathy, sore throat, and the appearance in
the blood of atypical lymphocytes and several antibodies.
• Highest incidence in adolescents and young adults.
• Treatment is symptomatic and supportive.
• Long term, the Epstein-Barr virus (EBV) may increase the risk of lupus and six other
autoimmune diseases by changing how certain human genes are expressed.
Splenomegaly – most common complication occurs in approximately 50% to 60% of cases.14
The spleen may be enlarged two to three times its normal size, and rupture of the spleen occurs in
less than 0.5% of cases
Blood testing includes the monospot and serologic testing. The monospot tests for heterophile
antibodies, which are considered the hallmark of an EBV infection. The development of the
, heterophile antibodies take time to develop, resulting in false negatives early in the disease. An
increase in IgM and IgG antibodies early in the disease are indicative of an EBV infection.
6. Chapter 24. Neoplastic Disorders of Lymphoid and Hematopoietic Origin: Hodgkin’s
Lymphoma. Clinical manifestations, diagnosis, and treatment.
Hodgkin’s & Non-Hodgkin’s Lymphoma:
Hodgkin’s:
Lymphoma arises in a single node or chain of nodes.
Painless cervical/neck/supraclavicular lymphadenopathy.
Reed- Sternberg cells are present.
Cell of origin: B cells.
Non-Hodgkin’s:
Lymphoma originates at extra-nodal sites and spreads to anatomically contiguous nodes.
Painless disseminated lymphadenopathy.
Reed-Sternberg cells are not present.
Cell of origin: B cells, T cells, NK cells.
Clinical Manifestations:
Hodgkin's lymphoma:
1. Painless Lymphadenopathy: Enlarged lymph nodes, usually in the neck, armpits, or
groin, are a hallmark of Hodgkin's lymphoma. These nodes are often painless.
2. B symptoms: These include fever, night sweats, and unexplained weight loss (usually
more than 10% of body weight within 6 months).
3. Fatigue: Patients with Hodgkin's lymphoma often experience significant fatigue.
4. Pruritus (Itching): Intense itching of the skin is sometimes associated with HL.
5. Alcohol-induced Pain: Some individuals with Hodgkin's lymphoma experience pain in
lymph nodes after consuming alcohol.
Non-Hodgkin's Lymphoma (NHL):
1. Lymph Node Enlargement: Like HL, NHL also presents with painless swelling of
lymph nodes, but it can occur in multiple areas of the body.
2. B Symptoms: Fever, night sweats, and weight loss can also occur in NHL.
3. Fatigue: Similar to HL, NHL patients often complain of fatigue.
4. Pain and Swelling: Depending on the location of the lymphoma, patients may
experience pain, swelling, or pressure in various parts of the body.
5. Frequent Infections: NHL can weaken the immune system, leading to a higher risk of
infections.
6. Gastrointestinal Symptoms: In cases where lymphoma affects the digestive tract,
patients may experience symptoms like abdominal pain, nausea, vomiting, and diarrhea.
Capstone College of Nursing
NUR 529 Exam 2 Blueprint
Pages referred to below are from Porth’s Pathophysiology: Concepts of Altered States, 10th ed.,
and the current e-book on coursepoint. Older versions are not included, this course does not
utilize older textbook versions. Format for page numbers below is Porth 10th ed “hard copy”
book/ Course Point Porth E-Book. Example: p. 967/975. If the pages correlate between editions
then only one will be listed.
---------------------------------------------------------------------------------------------------------------------
Unit 7. Disorders of the Hematopoietic System. Chapters 22, 23, and 24. There are 6
questions from this unit.
1. Chapter 22. Could talk a client through the Mechanisms of Hemostasis. See page 623,
Understanding hemostasis, three stages.
1. Vessel vasoconstriction- imjury in the vascular smooth muscle, causes the vessel
wall to contract, reducing blood flow from vessel rupture
2. Formation of platelet plug- seconds after vessel injury, vWF is released from the
endothelium and binds to platelet receptors causing adhesions to the platelets to
the collagen fibers. As the platelets adhere to the collagen fibers on the vessel
wall they become activated by release of ADP and TXA, which attracts additional
platelets, leading to platelet aggregation.
3. Blood clot develops as a result of coagulation process. There are two
cogagulation pathways intrinsic and extrinsic. Both lead to theactivation of factor
X, the conversion of prothrombin to thrombin, and conversion of fibrinogen to
fibrin threads that hold the clot together.
2. Chapter 22. Bleeding Disorders: Bleeding Associated with Platelet Disorders.
Bleeding because of platelet disorders reflects a decrease in platelet number because of decreased
production, increased destruction, or impaired function of platelets. Spontaneous bleeding from
platelet disorders most often involves small vessels of the mucous membranes and skin.
Common sites of bleeding are the mucous membranes of the nose, mouth, gastrointestinal
tract, and uterine cavity. Cutaneous bleeding is seen as pinpoint hemorrhages (petechiae) and purple
areas of bruising (purpura) in dependent areas where the capillary pressure is higher (Fig. 22.3).
Petechiae are seen almost exclusively in conditions of platelet deficiency and not platelet dysfunction.
Bleeding of the intracranial vessels is a rare danger with severe platelet depletion.
Thrombocytopenia: A reduction in platelet number, also referred to as thrombocytopenia, is an
important cause of generalized bleeding. Thrombocytopenia usually refers to a decrease in the number
of circulating platelets to a level less than 150,000/μL.19 CO Important 8/15/2022 The greater the
,decrease in the platelet count, the greater the risk of bleeding. Thrombocytopenia can result from a
decrease in platelet production, increased sequestration of platelets in the spleen, or decreased platelet
survival.
3. Chapter 23. Anemia: Red blood cell characteristics seen in different types anemias.
There are four primary causes of anemia:
(1) excessive loss of red blood cells from bleeding,
(2) destruction (hemolysis) of red blood cells,
(3) defective red blood cell production, or
(4) inadequate red blood cell production because of bone marrow failure.
***Anemia is not a disease, but an indication of some disease process or alteration in body function.***
The effects of anemia can be grouped into three categories:
1. Manifestations of impaired oxygen transport and the resulting compensatory mechanisms
2. Reduction in red cell indices and hemoglobin levels
3. Signs and symptoms associated with the pathologic process that is causing the anemia
4. Chapter 23. Anemia: Anemias of Deficient Red Cell Production. Iron deficiency
anemia (IDA). Compare causes of IDA in adults and children. What are the most
common causes in each group?
Iron Deficiency Anemia (IDA) Iron deficiency is a common worldwide cause of anemia affecting people
of all ages. The anemia results from dietary deficiency, loss of iron through bleeding, or increased
demands. Because iron is a component of heme, a deficiency leads to decreased hemoglobin synthesis
and consequent impairment of oxygen delivery.
B12 deficiency can be from diet but more importantly lack of intrinsic factor in the stomach that leads to
failure to absorb vitamin B12. (pernicious anemia). When vitamin B 12 is deficient, the red cells that are
produced are abnormally large because of excess cytoplasmic growth and structural proteins. Thus,
megaloblastic anemia.
Folic acid is required for DNA synthesis and RBC maturation. Because the link between folic acid
deficiency and neural tube birth defects is so well known it is recommended that all women of child-
bearing age are advised to take in 400 mcg per day.
The usual reason for iron deficiency in adults in the western world is chronic blood loss because there
is inadequate iron available for recycling. In men and postmenopausal women, blood loss may occur
from gastrointestinal bleeding because of peptic ulcer, vascular lesions, intestinal polyps, hemorrhoids,
or cancer. In women of child-bearing age, iron demand is increased because of losses from
menstruation. Additionally, in pregnant women, fetal development increases iron requirements for
erythropoiesis.
,The manifestations of iron deficiency anemia are related to impaired oxygen transport and lack of
hemoglobin. Depending on the severity of the anemia, fatigability, palpitations, dyspnea, angina, and
tachycardia may occur. Pica, a craving for substances lacking nutritional value such as clay or ice, may
develop.
Diagnosis and Treatment:
Low hemoglobin and hematocrit, decreased iron stores, and low serum iron and ferritin
characterize iron deficiency anemia. The red cells are decreased in number and are microcytic and
hypochromic (see Fig. 23.7). Poikilocytosis (irregular shape) and anisocytosis (irregular size) are also
present. Laboratory values indicate reduced MCHC and MCV.
Prevention of iron deficiency is a primary concern in infants and children. Avoidance of cow’s
milk, iron supplementation at 4 to 6 months of age in breast-fed infants, and use of iron-fortified
formulas and cereals are recommended for infants younger than 1 year of age.17 In the 2nd year, a diet
rich in iron-containing foods and use of iron-fortified vitamins will help prevent iron deficiency. The
treatment of iron deficiency anemia in children and adults is directed toward controlling chronic blood
loss, increasing dietary intake of iron, and administering supplemental iron. Ferrous sulfate, which is the
usual oral replacement therapy, replenishes iron stores in several months.
5. Chapter 24. Nonneoplastic Disorders of White Blood Cells: Infectious Mononucleosis.
Clinical course, most common complication, and laboratory diagnostics.
Infectious Mononucleosis:
• Self-limiting disorder where lymphocytes are produced in excessive quantities.
• Caused by the Epstein-Barr virus.
• Transmitted in saliva.
• Once infected the virus will remain present in the B lymphocytes for a lifetime.
• Characterized by fever, generalized lymphadenopathy, sore throat, and the appearance in
the blood of atypical lymphocytes and several antibodies.
• Highest incidence in adolescents and young adults.
• Treatment is symptomatic and supportive.
• Long term, the Epstein-Barr virus (EBV) may increase the risk of lupus and six other
autoimmune diseases by changing how certain human genes are expressed.
Splenomegaly – most common complication occurs in approximately 50% to 60% of cases.14
The spleen may be enlarged two to three times its normal size, and rupture of the spleen occurs in
less than 0.5% of cases
Blood testing includes the monospot and serologic testing. The monospot tests for heterophile
antibodies, which are considered the hallmark of an EBV infection. The development of the
, heterophile antibodies take time to develop, resulting in false negatives early in the disease. An
increase in IgM and IgG antibodies early in the disease are indicative of an EBV infection.
6. Chapter 24. Neoplastic Disorders of Lymphoid and Hematopoietic Origin: Hodgkin’s
Lymphoma. Clinical manifestations, diagnosis, and treatment.
Hodgkin’s & Non-Hodgkin’s Lymphoma:
Hodgkin’s:
Lymphoma arises in a single node or chain of nodes.
Painless cervical/neck/supraclavicular lymphadenopathy.
Reed- Sternberg cells are present.
Cell of origin: B cells.
Non-Hodgkin’s:
Lymphoma originates at extra-nodal sites and spreads to anatomically contiguous nodes.
Painless disseminated lymphadenopathy.
Reed-Sternberg cells are not present.
Cell of origin: B cells, T cells, NK cells.
Clinical Manifestations:
Hodgkin's lymphoma:
1. Painless Lymphadenopathy: Enlarged lymph nodes, usually in the neck, armpits, or
groin, are a hallmark of Hodgkin's lymphoma. These nodes are often painless.
2. B symptoms: These include fever, night sweats, and unexplained weight loss (usually
more than 10% of body weight within 6 months).
3. Fatigue: Patients with Hodgkin's lymphoma often experience significant fatigue.
4. Pruritus (Itching): Intense itching of the skin is sometimes associated with HL.
5. Alcohol-induced Pain: Some individuals with Hodgkin's lymphoma experience pain in
lymph nodes after consuming alcohol.
Non-Hodgkin's Lymphoma (NHL):
1. Lymph Node Enlargement: Like HL, NHL also presents with painless swelling of
lymph nodes, but it can occur in multiple areas of the body.
2. B Symptoms: Fever, night sweats, and weight loss can also occur in NHL.
3. Fatigue: Similar to HL, NHL patients often complain of fatigue.
4. Pain and Swelling: Depending on the location of the lymphoma, patients may
experience pain, swelling, or pressure in various parts of the body.
5. Frequent Infections: NHL can weaken the immune system, leading to a higher risk of
infections.
6. Gastrointestinal Symptoms: In cases where lymphoma affects the digestive tract,
patients may experience symptoms like abdominal pain, nausea, vomiting, and diarrhea.
