The University of Alabama
Capstone College of Nursing
NUR 529 Exam 2 Blueprint
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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.
Hemostasis is the stoppage of blood flow
Stage 1: vessel vasoconstriction
o Vascular smooth muscle contraction occurs and Local nervous reflexes + local humoral
factors (TXA2) are released from platelets and contribute to vasoconstriction
Stage 2: Formation of the platelet plug
o vWF (Von Willebrand factor) is released from the endothelium, binds to platelet
receptors and causes adhesion of the platelets to the exposed collagen fibers (inset)
o platelet adhesion to the collagen fibers become activated and release ADP + TXA2 which
attract additional platelets = platelet aggregation.
Stage 3: Development of a blood clot as a result of the coagulation process (blood coagulation) –
activation of several factors through 2 coagulation pathways:
o Intrinsic pathway – begins in circulation, activated by factor XII
o Extrinsic pathway – activated by tissue factor (a cellular lipoprotein that becomes
exposed when tissues are injured)
o Both pathways activate factor X which converts prothrombin thrombin and fibrinogen
insoluble fibrin threads that hold the clot together
Clot retraction
o Pulls the edges of the injured vessel together
Clot dissolution/ Lysis
o Plasmin dissolves the clot and allows blood flow to be reestablished and tissue healing to
take place (t-PA is released slowly)
2. Chapter 22. Bleeding Disorders: Bleeding Associated with Platelet Disorders (p 629).
Disorders result from a decrease in # of platelets from either: decreased platelet production,
increased destruction, or impaired function.
Spontaneous bleeding often involve small vessels of mucous membranes & skin ( mouth,
nose, GI tract, uterine cavity)
Cutaneous bleeding = pinpoint hemorrhages (petechiae) and bruising (purpura)
Petechiae indicates platelet deficiency (not dysfunction)
Thrombocytopenia
o Reduced platelets < 150,000/uL (the lower the platelets the higher the bleeding risk)
Severe is <30,000
o Causes:
decreased production - i.e. loss of bone marrow function
Decreased survival/destruction - i.e. antiplatelet antibodies or mechanical
injury such as prosthetic heart valves or malignant HTN which narrows the
vessels
, abnormal pooling in the spleen (Spleen normally sequesters 30-40% of
platelets before releasing them into circulation but in Splenomegaly it can
hold as much as 90%)
o Tx: Plasmapheresis + plasma infusion
3. Ch 23. Anemia: Red blood cell characteristics seen in different types anemias (p. 648, 654)
Iron deficiency anemia – microcytic (small cell) & hypochromic (decreased color or
decreased MCHC) red cells, also poikilocytosis (irregular shaped), anisocytosis (irregular
size)
o MCHC – concentration of hemoglobin in each cell which accounts for the color of
the cell
Megaloblastic anemia – macrocytic (large cell) & misshaped RBCs
o Caused by impaired DNA synthesis (slow process, S&S occur late)
o Enlarged cell = MCV > 100 fL from impaired maturation & division
o Commonly caused by folic acid and vitamin B12 deficiencies
Sickle cell disease – abnormally shaped RBCs from deoxygenation (becomes sickled) this
increases red cell adhesiveness and adherence to vessel wall (hemolysis, occlusion, ischemia)
Normal – normocytic & normochromic (normal size and color)
4. Chapter 23. Anemia: Anemias of Deficient Red Cell Production. (p. 654) Iron deficiency anemia
(IDA). Compare causes of IDA in adults and children. What are the most common causes in each group?
4 causes of anemia
o Loss of RBCs from bleeding – iron loss/deficiency i.e. GI bleeds & menstrual cycle
disorders
o Destruction (hemolysis) of RBCs – iron is retained i.e. sickle cell
Increased erythropoiesis (Bone marrow is working overtime to produce more
RBCs which means there are more circulating reticulocytes)
Shortened RBC lifespan
o Defective RBC production or Inadequate RBC production from bone marrow failure
Decreased production of erythrocytes
Deficiency in nutrients for production (folic acid and cobalamin)
Cause of IDA in adults:
o Chronic blood loss
o In men and postmenopausal women GI bleeds from peptic ulcer, vascular lesions,
intestinal polyps, hemorrhoids, or cancer
o Child bearing age women require have an increased iron demand because of loss
through menstrual cycle
Cause of IDA in Children:
o Child growth = increased demand
o Iron requirements are highest in infancy (3-24 months) and deficiency is usually
caused by low iron levels at birth because of the mom’s deficiency and a diet
consisting of cows milk
Anemia manifestation: fatigue, irritability, PICA (cravings for things without nutritional
value), dyspnea, tachycardia, angina, palpitations
Diagnosis: decreased MCHC, MCV
5. Chapter 24. Nonneoplastic Disorders of White Blood Cells: Infectious Mononucleosis. Clinical course,
most common complication, and laboratory diagnostics.
, Neutropenia (Agranolucytosis)
o Leukopenia: decrease of leukocytes in blood and often affects the neutrophils (which
engulf, digest, and destroy microorganisms)
o Neutrophils are the granulocytes most responsinle for defense against bacteria
o Higher risk for infection, proportional to the ANC (absolute neutrophil count), if
<500 cells/mm3, neutrophil precutions!
Infectious Mononucleosis (p.670)
o Self-limiting lymphoproliferative disorder usually caused by the Epstein-barr virus
(herpes family) 90% of the time and by cytomegalovirus (CMV) 10% of the time
o Usually in young adults; remains present in the B-lymphs for life
o Clinical course
Incubation 4-6 weeks, gradual/insidious onset
Prodromal period – malaise, anorexia, chills
Day 5-7: Fever, pharyngitis, lymphadenopathy, palatal petechiae
Acute phase: 2-3 weeks with fatigue persisting for 2-3 months post recovery
o Complications
Splenomegaly in 50-60% of cases, hepatitis, myocarditis, hemolytic anemia
o Diagnostics
Monospot & serologic testing – checks for heterophile antibodies, increase of
IgM and IgG (hallmark of EBV infection)
6. Chapter 24. Neoplastic Disorders of Lymphoid and Hematopoietic Origin: Hodgkin’s
Lymphoma. Clinical manifestations, diagnosis, and treatment.
Lymphomas – malignancies that arise in the peripheral lymphoid tissues
Hodgkin’s lymphoma – reed-Sternberg cell (abnormal cell)
S&S: painless enlargement of node/s typically above the diaphragm (neck, axilla), mediastinal
mass (seen on CXR), chest discomfort with SOB or cough, fevers, chills, night sweats, weight
loss, pruritis (itching)
Dx: reed-Sternberg cell present on lymph node biopsy, bipedal lymphangiogram (detects
structural changes in the lymph nodes too small to be seen by CT), bone marrow biopsy is done
on severe cases.
o Staging is based on # of lymph nodes involved, on one of both sides of the diaphragm,
and if there’s mets to bone marrow, lung, liver, skin
Tx: Radiation (most common in localized disease), chemotherapy, biptherapy. All 3 are done in
severe cases (depends on staging!)
Other notes from quiz & PowerPoints:
Cytokines are hormone-like growth factors that stimulate proliferation, differentiation, and
functional activiation of various blood cells
ITP (slide 12) – most common in children
Common form of leukemia caused by Clonal malignancy of B lymphs: slide 26 chronic
lymphocytic leukemia (CLL)
Pernicious anemia – slide 18 – defective secretion of the intrinsic factor which is essential for
absorption of vitamin B12
Unit 8. Chapters 25- 28. There are 19 questions from this unit.
Capstone College of Nursing
NUR 529 Exam 2 Blueprint
---------------------------------------------------------------------------------------------------------------------
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.
Hemostasis is the stoppage of blood flow
Stage 1: vessel vasoconstriction
o Vascular smooth muscle contraction occurs and Local nervous reflexes + local humoral
factors (TXA2) are released from platelets and contribute to vasoconstriction
Stage 2: Formation of the platelet plug
o vWF (Von Willebrand factor) is released from the endothelium, binds to platelet
receptors and causes adhesion of the platelets to the exposed collagen fibers (inset)
o platelet adhesion to the collagen fibers become activated and release ADP + TXA2 which
attract additional platelets = platelet aggregation.
Stage 3: Development of a blood clot as a result of the coagulation process (blood coagulation) –
activation of several factors through 2 coagulation pathways:
o Intrinsic pathway – begins in circulation, activated by factor XII
o Extrinsic pathway – activated by tissue factor (a cellular lipoprotein that becomes
exposed when tissues are injured)
o Both pathways activate factor X which converts prothrombin thrombin and fibrinogen
insoluble fibrin threads that hold the clot together
Clot retraction
o Pulls the edges of the injured vessel together
Clot dissolution/ Lysis
o Plasmin dissolves the clot and allows blood flow to be reestablished and tissue healing to
take place (t-PA is released slowly)
2. Chapter 22. Bleeding Disorders: Bleeding Associated with Platelet Disorders (p 629).
Disorders result from a decrease in # of platelets from either: decreased platelet production,
increased destruction, or impaired function.
Spontaneous bleeding often involve small vessels of mucous membranes & skin ( mouth,
nose, GI tract, uterine cavity)
Cutaneous bleeding = pinpoint hemorrhages (petechiae) and bruising (purpura)
Petechiae indicates platelet deficiency (not dysfunction)
Thrombocytopenia
o Reduced platelets < 150,000/uL (the lower the platelets the higher the bleeding risk)
Severe is <30,000
o Causes:
decreased production - i.e. loss of bone marrow function
Decreased survival/destruction - i.e. antiplatelet antibodies or mechanical
injury such as prosthetic heart valves or malignant HTN which narrows the
vessels
, abnormal pooling in the spleen (Spleen normally sequesters 30-40% of
platelets before releasing them into circulation but in Splenomegaly it can
hold as much as 90%)
o Tx: Plasmapheresis + plasma infusion
3. Ch 23. Anemia: Red blood cell characteristics seen in different types anemias (p. 648, 654)
Iron deficiency anemia – microcytic (small cell) & hypochromic (decreased color or
decreased MCHC) red cells, also poikilocytosis (irregular shaped), anisocytosis (irregular
size)
o MCHC – concentration of hemoglobin in each cell which accounts for the color of
the cell
Megaloblastic anemia – macrocytic (large cell) & misshaped RBCs
o Caused by impaired DNA synthesis (slow process, S&S occur late)
o Enlarged cell = MCV > 100 fL from impaired maturation & division
o Commonly caused by folic acid and vitamin B12 deficiencies
Sickle cell disease – abnormally shaped RBCs from deoxygenation (becomes sickled) this
increases red cell adhesiveness and adherence to vessel wall (hemolysis, occlusion, ischemia)
Normal – normocytic & normochromic (normal size and color)
4. Chapter 23. Anemia: Anemias of Deficient Red Cell Production. (p. 654) Iron deficiency anemia
(IDA). Compare causes of IDA in adults and children. What are the most common causes in each group?
4 causes of anemia
o Loss of RBCs from bleeding – iron loss/deficiency i.e. GI bleeds & menstrual cycle
disorders
o Destruction (hemolysis) of RBCs – iron is retained i.e. sickle cell
Increased erythropoiesis (Bone marrow is working overtime to produce more
RBCs which means there are more circulating reticulocytes)
Shortened RBC lifespan
o Defective RBC production or Inadequate RBC production from bone marrow failure
Decreased production of erythrocytes
Deficiency in nutrients for production (folic acid and cobalamin)
Cause of IDA in adults:
o Chronic blood loss
o In men and postmenopausal women GI bleeds from peptic ulcer, vascular lesions,
intestinal polyps, hemorrhoids, or cancer
o Child bearing age women require have an increased iron demand because of loss
through menstrual cycle
Cause of IDA in Children:
o Child growth = increased demand
o Iron requirements are highest in infancy (3-24 months) and deficiency is usually
caused by low iron levels at birth because of the mom’s deficiency and a diet
consisting of cows milk
Anemia manifestation: fatigue, irritability, PICA (cravings for things without nutritional
value), dyspnea, tachycardia, angina, palpitations
Diagnosis: decreased MCHC, MCV
5. Chapter 24. Nonneoplastic Disorders of White Blood Cells: Infectious Mononucleosis. Clinical course,
most common complication, and laboratory diagnostics.
, Neutropenia (Agranolucytosis)
o Leukopenia: decrease of leukocytes in blood and often affects the neutrophils (which
engulf, digest, and destroy microorganisms)
o Neutrophils are the granulocytes most responsinle for defense against bacteria
o Higher risk for infection, proportional to the ANC (absolute neutrophil count), if
<500 cells/mm3, neutrophil precutions!
Infectious Mononucleosis (p.670)
o Self-limiting lymphoproliferative disorder usually caused by the Epstein-barr virus
(herpes family) 90% of the time and by cytomegalovirus (CMV) 10% of the time
o Usually in young adults; remains present in the B-lymphs for life
o Clinical course
Incubation 4-6 weeks, gradual/insidious onset
Prodromal period – malaise, anorexia, chills
Day 5-7: Fever, pharyngitis, lymphadenopathy, palatal petechiae
Acute phase: 2-3 weeks with fatigue persisting for 2-3 months post recovery
o Complications
Splenomegaly in 50-60% of cases, hepatitis, myocarditis, hemolytic anemia
o Diagnostics
Monospot & serologic testing – checks for heterophile antibodies, increase of
IgM and IgG (hallmark of EBV infection)
6. Chapter 24. Neoplastic Disorders of Lymphoid and Hematopoietic Origin: Hodgkin’s
Lymphoma. Clinical manifestations, diagnosis, and treatment.
Lymphomas – malignancies that arise in the peripheral lymphoid tissues
Hodgkin’s lymphoma – reed-Sternberg cell (abnormal cell)
S&S: painless enlargement of node/s typically above the diaphragm (neck, axilla), mediastinal
mass (seen on CXR), chest discomfort with SOB or cough, fevers, chills, night sweats, weight
loss, pruritis (itching)
Dx: reed-Sternberg cell present on lymph node biopsy, bipedal lymphangiogram (detects
structural changes in the lymph nodes too small to be seen by CT), bone marrow biopsy is done
on severe cases.
o Staging is based on # of lymph nodes involved, on one of both sides of the diaphragm,
and if there’s mets to bone marrow, lung, liver, skin
Tx: Radiation (most common in localized disease), chemotherapy, biptherapy. All 3 are done in
severe cases (depends on staging!)
Other notes from quiz & PowerPoints:
Cytokines are hormone-like growth factors that stimulate proliferation, differentiation, and
functional activiation of various blood cells
ITP (slide 12) – most common in children
Common form of leukemia caused by Clonal malignancy of B lymphs: slide 26 chronic
lymphocytic leukemia (CLL)
Pernicious anemia – slide 18 – defective secretion of the intrinsic factor which is essential for
absorption of vitamin B12
Unit 8. Chapters 25- 28. There are 19 questions from this unit.
