Pediatric Study Guide for Final Exam 2021
Study Guide for “Final” Exam
75% will cover Chapters 43-49 and Integumentary chapters from ATI Book.
25% will include Chapters 40-43.
Utilize your resources too: the handouts/worksheet for endocrine and neuromuscular, Renal/GU disorders,
the objectives I posted for Hematology/Immunology, the Children’s Hospital resources, the cardiology
case study, the Textbook Study Guide Workbook, and ATI Nursing Care of Children book. There will be
65-70 questions total. There will also be bonus questions, 2-3 points possible.
Hematology and Immunology: Chapter 43
Describe the pathophysiology, clinical manifestations, therapeutic and nursing management of each of the
following anemias: iron deficiency anemia, Sickle cell anemia, β-thalassemia, and aplastic anemia.
Describe nursing goals and interventions used when caring for a child with hemophilia or von
Willebrand.
o Iron deficiency anemia:
- Most common nutritional disorder in US.
- Most at-risk are children 12-36 months since milk is low in iron and is
the major staple of the child’s diet.
- Iron fortified formula for first year of life supplied by WIC.
- Prolonged breast feeders with minimal solid food intake also have low
iron.
o Treatment:
- Iron fortified formula and cereals – supplement at 4-6 months. Breast
milk is low in iron.
- Avoid cows milk < 12 months age. Check guiaic.
- Increase dietary sources – Meat, green leafy vegies - (spinach).
- Supplement with ferrous iron.
- Vit C helps facilitate absorption of iron.
- If unsuccessful at increasing hgb, look for bleeding sources,
malabsorption, noncompliance.
- IV iron or transfusion recommended for severe anemia.
o Sickle Cell anemia/disease:
- Sickle cell anemia/disease- hemoglobin A is partly or completely
replaced by abnormal sickle cell hemoglobin S
- Insufficient oxygen causes the cells to assume a sickle shape, and the
cells become rigid and clumped together, obstructing capillary blood
flow
o Treatment:
- Prevent sickling phenomena and treat symptoms of sickle cell crisis.
- Rest to minimize energy expenditures and improve oxygen utilization.
- Adequate Hydration – both oral and IV.
- Support and Analgesia to treat pain during crisis.
- Electrolyte replacement (metabolic alkalosis promotes sickling).
- Vaccines due to functional asplenia/Antibiotics
- Blood transfusions to treat anemia and reduce viscosity.
- Exchange transfusions – replace sickle cells with normal RBC’s.
- Splenomegaly
- Education of family and child
, Pediatric Study Guide for Final Exam 2021
- Prognosis – varies, but most can participate in normal activities
- Highest risk of complications in children < 5 years.
- Hydroxyurea approved medication.
- Stem cell transplant curative for some.
o B-Thalassemia:
- B-Thalassemia: autosomal recessive disorder characterized by the
reduced production of 1 of the globin chains in the synthesis of
hemoglobin. Causes severe anemia requiring transfusion support to
sustain life
- Blood transfusions – foundation of management. Needed to maintain
Hgb levels to prevent bone marrow expansion and bony deformities and
provide sufficient RBC’s for growth.
- Goal of maintaining Hgb above 9.5 g/dL
- Frequent complication is iron overload. Excess iron from hemolysis gets
stored in various organs (hemosiderosis - iron overload) and deposited in
body tissues.
o Aplastic anemia:
- Total bone marrow failure. All formed elements of the blood are
simultaneously depressed. Causes a deficiency of erythrocytes,
leukocytes, and thrombocytes
o Treatment:
- Bone marrow is unable to carry out its hematologic functions. Care is
similar to leukemia treatment
- Immunosuppressive therapy. AA may be autoimmune
- Antithymocyte globulin (ATG) – chemo. ATG suppresses T-cell
dependent autoimmune responses
- Goal is to restore the function of the marrow. Bone marrow or stem cell
transplant – treatment of choice
o Nursing care:
- Prevent bleeding.
- Administer and monitor blood transfusions.
- Screen for infection.
- Encourage mobility
- Educate parents and child
- Supportive care for side effects of treatment. ATG and
chemotherapy cause n/v, alopecia, and mucositis.
- Emotional support
- Prevent potentially fatal outcome.
Describe nursing goals and interventions used when caring for a child with hemophilia.
Von Willebrand:
o Hereditary bleeding disorder, involving deficiency of von
Willebrand factor (plasma protein) and factor VIII
o von Willebrand factor necessary for platelet adhesion
Hemophilia:
o Hereditary bleeding disorders
, Pediatric Study Guide for Final Exam 2021
o Deficiency in clotting factors
Treatment
Von Willebrand
o Infusion of von Willebrand’s protein concentrate
o DDAVP infusion before surgery or to treat bleeding episode
o Aminocaprioc acid to treat bleeding in mucous membranes (in
some cases)
Hemophilia:
o Replacement of missing clotting factor (Factor VIII
concentration infusion on a regular basis)
o DDAVP: IV infusion - causes 2 to 4 times increase in factor VII
activity, used for mild hemophilia
o Factor VIII Infusions done at home with prompt intervention to
reduce complications following major or minor hemorrhages
Nursing management and teaching
Hemophilia
- Close supervision and safe environment
- Dental procedures in controlled situation
- Shave only with electric razor
- Superficial bleeding-apply pressure for at least 15 minutes + ice
to vasoconstrict
- If significant bleeding occurs, transfuse for factor replacement
- Hemarthrosis management
- Elevate and immobilize joint
- Ice
- Analgesics
- ROM after bleeding prevents contractures
- PT
- Avoid obesity to minimize joint stress
o Bleeding precautions:
- Avoid taking temperatures rectally or giving
suppositories
- Check blood pressure cuff as infrequently as possible
- Avoid intramuscular or subcutaneous injections
- Use only paper or silk tape for dressings
- Except for factor replacement therapy avoid all
venipunctures
- Do not give aspirin
Describe the pathophysiology and nursing goals and interventions when caring for a child with ITP
(Idiopathic Thrombocytopenia Purpura).
i. Pathophysiology:
- Acquired hemorrhagic disorder characterized by Thrombocytopenia: an excessive
destruction of platelets, absence or minimal signs of bleeding (easy bruising, petechiae),
and normal bone marrow with normal or increased number of immature platelets
ii. How it presents – symptoms:
- Easy or excessive bruising.
, Pediatric Study Guide for Final Exam 2021
- Superficial bleeding into the skin that appears as pinpoint-sized reddish-purple spots
(petechiae) that look like a rash, usually on the lower legs.
- Bleeding from the gums or nose.
- Blood in urine or stools.
- Unusually heavy menstrual flow.
iii. Managing symptoms:
- Primarily supportive. Think: low platelet precautions
- Prednisone (need to rule out leukemia first)
- IVIG (expensive)
- Anti D antibody (newer therapy, one dose). Anti-D (also known as Rho(D) immune globulin
intravenous or anti-D IGIV) is a blood product consisting of antibodies to the RH factor on red
blood cells. It achieves a temporary rise in the platelet count in about 80 percent of people and
occasionally has a longer term effect. Following a treatment with anti-D, there is removal of
antibody-coated RBC’s. Since red blood cells are eliminated, the process often causes a mild
anemia. However, it is usually successful in keeping the antibody-coated platelets of the ITP
patient in circulation. Takes 48 hours to be effective. After an infusion of anti-D antibody, the
platelet count does not increase for 48 hours. It is not the appropriate choice of treatment for
patients who are actively bleeding. Intravenous γ-globulin or prednisone would be the more
appropriate choice.
- Splenectomy for chronic ITP not responsive to management.
Describe the pathophysiology and diagnostic criteria for disseminated intravascular coagulation
(DIC).
- Occurs as a secondary disorder of coagulation that occurs as a complication of different
pathologic processes such as hypoxia, shock, systemic diseases
- Bleeding and clotting that occurs at the same time
- diffuse fibrin deposits in the microvasculature, consumption of coagulation factors and generation
of thrombin and plasmin
- s/s: petechiae, bleeding from openings, GI bleed, hypotension
- occurs when the first stage of the coagulation process is abnormally stimulated
- clotting mechanism is triggered: thrombin is generated in greater amounts than can be neutralized
- rapid conversion of fibrinogen to fibrin with platelet destruction
- Diagnostic criteria:
Increased tendency to bleed.
Prolonged PT, PTT, and thrombin time.
Depressed platelets and depleted fibrinogen.
Increased D-dimer antigen
Describe the pathophysiology and nursing goals and interventions used when caring for a child with HIV,
SCIDs, or Wisckott-Aldrich disease.
o HIV:
- Adolescents are the fastest growing group of newly infected
- Retrovirus, from RNA to DNA, can only replicate in cells. Transmits through body fluids. CD4
cells get infected
- RNA virus. HIV enters the CD4 T cell where it is transcribed into a single strand of viral DNA.
This strand copies itself, becoming double stranded viral DNA, which then enters the cell’s
nucleus and using another enzyme spices itself into the human genome becoming permanent part
of the cell’s genetic structure. Because all genetic material is replicated during cell division, all
daughter cells are also infected and viral DNA in the genome directs the cell to make new HIV.
Study Guide for “Final” Exam
75% will cover Chapters 43-49 and Integumentary chapters from ATI Book.
25% will include Chapters 40-43.
Utilize your resources too: the handouts/worksheet for endocrine and neuromuscular, Renal/GU disorders,
the objectives I posted for Hematology/Immunology, the Children’s Hospital resources, the cardiology
case study, the Textbook Study Guide Workbook, and ATI Nursing Care of Children book. There will be
65-70 questions total. There will also be bonus questions, 2-3 points possible.
Hematology and Immunology: Chapter 43
Describe the pathophysiology, clinical manifestations, therapeutic and nursing management of each of the
following anemias: iron deficiency anemia, Sickle cell anemia, β-thalassemia, and aplastic anemia.
Describe nursing goals and interventions used when caring for a child with hemophilia or von
Willebrand.
o Iron deficiency anemia:
- Most common nutritional disorder in US.
- Most at-risk are children 12-36 months since milk is low in iron and is
the major staple of the child’s diet.
- Iron fortified formula for first year of life supplied by WIC.
- Prolonged breast feeders with minimal solid food intake also have low
iron.
o Treatment:
- Iron fortified formula and cereals – supplement at 4-6 months. Breast
milk is low in iron.
- Avoid cows milk < 12 months age. Check guiaic.
- Increase dietary sources – Meat, green leafy vegies - (spinach).
- Supplement with ferrous iron.
- Vit C helps facilitate absorption of iron.
- If unsuccessful at increasing hgb, look for bleeding sources,
malabsorption, noncompliance.
- IV iron or transfusion recommended for severe anemia.
o Sickle Cell anemia/disease:
- Sickle cell anemia/disease- hemoglobin A is partly or completely
replaced by abnormal sickle cell hemoglobin S
- Insufficient oxygen causes the cells to assume a sickle shape, and the
cells become rigid and clumped together, obstructing capillary blood
flow
o Treatment:
- Prevent sickling phenomena and treat symptoms of sickle cell crisis.
- Rest to minimize energy expenditures and improve oxygen utilization.
- Adequate Hydration – both oral and IV.
- Support and Analgesia to treat pain during crisis.
- Electrolyte replacement (metabolic alkalosis promotes sickling).
- Vaccines due to functional asplenia/Antibiotics
- Blood transfusions to treat anemia and reduce viscosity.
- Exchange transfusions – replace sickle cells with normal RBC’s.
- Splenomegaly
- Education of family and child
, Pediatric Study Guide for Final Exam 2021
- Prognosis – varies, but most can participate in normal activities
- Highest risk of complications in children < 5 years.
- Hydroxyurea approved medication.
- Stem cell transplant curative for some.
o B-Thalassemia:
- B-Thalassemia: autosomal recessive disorder characterized by the
reduced production of 1 of the globin chains in the synthesis of
hemoglobin. Causes severe anemia requiring transfusion support to
sustain life
- Blood transfusions – foundation of management. Needed to maintain
Hgb levels to prevent bone marrow expansion and bony deformities and
provide sufficient RBC’s for growth.
- Goal of maintaining Hgb above 9.5 g/dL
- Frequent complication is iron overload. Excess iron from hemolysis gets
stored in various organs (hemosiderosis - iron overload) and deposited in
body tissues.
o Aplastic anemia:
- Total bone marrow failure. All formed elements of the blood are
simultaneously depressed. Causes a deficiency of erythrocytes,
leukocytes, and thrombocytes
o Treatment:
- Bone marrow is unable to carry out its hematologic functions. Care is
similar to leukemia treatment
- Immunosuppressive therapy. AA may be autoimmune
- Antithymocyte globulin (ATG) – chemo. ATG suppresses T-cell
dependent autoimmune responses
- Goal is to restore the function of the marrow. Bone marrow or stem cell
transplant – treatment of choice
o Nursing care:
- Prevent bleeding.
- Administer and monitor blood transfusions.
- Screen for infection.
- Encourage mobility
- Educate parents and child
- Supportive care for side effects of treatment. ATG and
chemotherapy cause n/v, alopecia, and mucositis.
- Emotional support
- Prevent potentially fatal outcome.
Describe nursing goals and interventions used when caring for a child with hemophilia.
Von Willebrand:
o Hereditary bleeding disorder, involving deficiency of von
Willebrand factor (plasma protein) and factor VIII
o von Willebrand factor necessary for platelet adhesion
Hemophilia:
o Hereditary bleeding disorders
, Pediatric Study Guide for Final Exam 2021
o Deficiency in clotting factors
Treatment
Von Willebrand
o Infusion of von Willebrand’s protein concentrate
o DDAVP infusion before surgery or to treat bleeding episode
o Aminocaprioc acid to treat bleeding in mucous membranes (in
some cases)
Hemophilia:
o Replacement of missing clotting factor (Factor VIII
concentration infusion on a regular basis)
o DDAVP: IV infusion - causes 2 to 4 times increase in factor VII
activity, used for mild hemophilia
o Factor VIII Infusions done at home with prompt intervention to
reduce complications following major or minor hemorrhages
Nursing management and teaching
Hemophilia
- Close supervision and safe environment
- Dental procedures in controlled situation
- Shave only with electric razor
- Superficial bleeding-apply pressure for at least 15 minutes + ice
to vasoconstrict
- If significant bleeding occurs, transfuse for factor replacement
- Hemarthrosis management
- Elevate and immobilize joint
- Ice
- Analgesics
- ROM after bleeding prevents contractures
- PT
- Avoid obesity to minimize joint stress
o Bleeding precautions:
- Avoid taking temperatures rectally or giving
suppositories
- Check blood pressure cuff as infrequently as possible
- Avoid intramuscular or subcutaneous injections
- Use only paper or silk tape for dressings
- Except for factor replacement therapy avoid all
venipunctures
- Do not give aspirin
Describe the pathophysiology and nursing goals and interventions when caring for a child with ITP
(Idiopathic Thrombocytopenia Purpura).
i. Pathophysiology:
- Acquired hemorrhagic disorder characterized by Thrombocytopenia: an excessive
destruction of platelets, absence or minimal signs of bleeding (easy bruising, petechiae),
and normal bone marrow with normal or increased number of immature platelets
ii. How it presents – symptoms:
- Easy or excessive bruising.
, Pediatric Study Guide for Final Exam 2021
- Superficial bleeding into the skin that appears as pinpoint-sized reddish-purple spots
(petechiae) that look like a rash, usually on the lower legs.
- Bleeding from the gums or nose.
- Blood in urine or stools.
- Unusually heavy menstrual flow.
iii. Managing symptoms:
- Primarily supportive. Think: low platelet precautions
- Prednisone (need to rule out leukemia first)
- IVIG (expensive)
- Anti D antibody (newer therapy, one dose). Anti-D (also known as Rho(D) immune globulin
intravenous or anti-D IGIV) is a blood product consisting of antibodies to the RH factor on red
blood cells. It achieves a temporary rise in the platelet count in about 80 percent of people and
occasionally has a longer term effect. Following a treatment with anti-D, there is removal of
antibody-coated RBC’s. Since red blood cells are eliminated, the process often causes a mild
anemia. However, it is usually successful in keeping the antibody-coated platelets of the ITP
patient in circulation. Takes 48 hours to be effective. After an infusion of anti-D antibody, the
platelet count does not increase for 48 hours. It is not the appropriate choice of treatment for
patients who are actively bleeding. Intravenous γ-globulin or prednisone would be the more
appropriate choice.
- Splenectomy for chronic ITP not responsive to management.
Describe the pathophysiology and diagnostic criteria for disseminated intravascular coagulation
(DIC).
- Occurs as a secondary disorder of coagulation that occurs as a complication of different
pathologic processes such as hypoxia, shock, systemic diseases
- Bleeding and clotting that occurs at the same time
- diffuse fibrin deposits in the microvasculature, consumption of coagulation factors and generation
of thrombin and plasmin
- s/s: petechiae, bleeding from openings, GI bleed, hypotension
- occurs when the first stage of the coagulation process is abnormally stimulated
- clotting mechanism is triggered: thrombin is generated in greater amounts than can be neutralized
- rapid conversion of fibrinogen to fibrin with platelet destruction
- Diagnostic criteria:
Increased tendency to bleed.
Prolonged PT, PTT, and thrombin time.
Depressed platelets and depleted fibrinogen.
Increased D-dimer antigen
Describe the pathophysiology and nursing goals and interventions used when caring for a child with HIV,
SCIDs, or Wisckott-Aldrich disease.
o HIV:
- Adolescents are the fastest growing group of newly infected
- Retrovirus, from RNA to DNA, can only replicate in cells. Transmits through body fluids. CD4
cells get infected
- RNA virus. HIV enters the CD4 T cell where it is transcribed into a single strand of viral DNA.
This strand copies itself, becoming double stranded viral DNA, which then enters the cell’s
nucleus and using another enzyme spices itself into the human genome becoming permanent part
of the cell’s genetic structure. Because all genetic material is replicated during cell division, all
daughter cells are also infected and viral DNA in the genome directs the cell to make new HIV.
