NURS 535 EVALUATION TEST QUESTIONS AND
ANSWERS SET A+
✔✔iron deficiency anemia - ✔✔Anemia caused by inadequate iron intake
✔✔iron deficiency anemia - RF, Causes, Diagnosis - ✔✔Age Between 6 mo - 4 yrs and
adolescence
Risk Factors:
-Low socioeconomic status (age 6-24mos)
-Premature infants
-Twins/Triplets
-Adolescents
Causes:
-Excessive whole milk intake in a child over 12 mos. of age
-Impaired iron absorption
-Blood loss
-Inadequate intake of iron
Diagnosis:
-H/H low
-Serum Ferritin low
✔✔iron deficiency anemia treatment - ✔✔Correction of the underlying problem
Replacement of depleted iron stores
-Dietary sources: Counsel foods high in Fe
-Supplements: 6 mg/kg/day of elemental Fe, divided into 1-2 doses
-Give the prescribed medication as ordered
Issues with food:
1. Absorbed best in high acid environment
2. Administer on empty stomach or with citrus juice
,3. Fe can stain teeth: give with a straw or dropper
4. Foods interfere with absorption, but sometimes needed due to unpalatable taste
5. Small frequent feedings if necessary-may decrease N/V/D
Frequent rest periods
-Monitor the child's fatigue level
✔✔Lead Poisoning - ✔✔A medical condition caused by toxic levels of the metal lead in
the blood
✔✔Lead Poisoning Pathophysiology - ✔✔Exposure occurs through inhalation, ingestion
or occasionally skin contact.
Lead may be taken in through direct contact with mouth, nose, and eyes (mucous
membranes), and through breaks in the skin.
Lead absorption is higher in infants and children
The main body compartments that store lead are the blood, soft tissues, and bone; the
half-life of lead in these tissues is measured in weeks for blood, months for soft tissues,
and years for bone.
Lead has no known physiologically relevant role in the body, and its harmful effects are
myriad.
Lead and other heavy metals create reactive radicals which damage cell structures
including DNA and cell membranes.
✔✔S/S of Lead poisoning - ✔✔Drowsiness, clumsiness, ataxia, seizures, coma, resp.
arrest
✔✔Lead poisoning treatment - ✔✔CaEDTA, Dimercaprol (adults), succimer (kids)
✔✔Lead poisoning prevention - ✔✔Prevention: Hand washing, remove shoes,
adequate dietary intake of Ca and Iron, hazards of renovations, clean
✔✔Sickle cell disease - ✔✔A group of genetic disorders characterized by:
-Production of hemoglobin S
-Chronic hemolytic anemia
-Acute & chronic tissue damage secondary to the blockage of blood flow by abnormally
shaped RBCs
✔✔Sickle cell pathophysiology - ✔✔Glutamic acid (hydrophilic) replaced by valine
(hydrophobic) at position 6 in beta globin chain
,✔✔Laboratory analysis for sickle cell - ✔✔Platelet count should be high
ESR is normal
Reticulocyte level should be elevated (>5%)
LDH/AST are elevated secondary to hemolysis
✔✔Sickle cell disease - physical exam - ✔✔Growth
-May be delayed
-"Catch up" growth is common in adolescence
Common findings
-Assess spleen
-Scleral icterus
-Functional murmur
-Mild, generalized lymphadenopathy
-Slightly enlarged liver
✔✔Sickle cell crisis - ✔✔Intense pain because blood vessels can become blocked or
the defective red blood cells can damage organs in the body. HYDRATE
✔✔Types of sickle cell crisis - ✔✔(1) Vasoocclusive crisis (2) Sequestration crisis (3)
Aplastic crisis
✔✔Pain management for sickle cell disease - ✔✔Opioids or NSAIDS
✔✔SCD Infections - ✔✔6 months - 3 years are 400 times more likely to become
infected by Strep Pneumonia
✔✔SCD Fever management - ✔✔Fever > 101 requires treatment
Chemo ppx PCN from 2 months - 5 yeras
✔✔SCD Summary - ✔✔Hydration, Hydration, Hydration!
(Keep the vascular bed open!)
Oxygen
Pain management
Prophylactic antibiotics (monitor for infection)
Monitor for complications (neuro/cardio/resp)
Psychosocial support
✔✔Thalassemia - ✔✔Inherited defect in ability to produce hemoglobin
✔✔S/S of Thalassemia - ✔✔1. Pale
2. Tachycardia/Tachypnea
3. Hepatosplenomegaly
, 4. Frontal bossing with bone changes
✔✔Clinical diagnosis of thalassemia - ✔✔CBC
Hg < 6
✔✔Alpha Thalassemia - ✔✔Diseases in which there are insuffiecient alpha-globin
chains due to gene deletions
✔✔Beta Thalassemia - ✔✔Disease in which insufficient beta-globin chains are
produced and there is an excess of alpha chains
✔✔Four types of thalassemia - ✔✔Thalassemia minor: Asymptomatic silent carrier
Thalassemia trait: Mild microcytic anemia
Thalassemia intermediate: Moderate to severe anemia + splenomegaly
Thalassemia major "Cooley anemia": Severe anemia requiring transfusions to survive
✔✔Clinical manifestations of thalassemia - ✔✔Growth, both physical and mental is
often retarded.
Thalassemia major: pale, displays general symptoms of anemia.
Pronounced splenomegaly and hepatomegaly.
Jaundice from RBC lysis.
As the bone marrow responds to the deficit of the oxygen-carrying capcity of blood,
RBC production is stimulated and the marrow becomes packed with immature erythroid
precursors that die >>> stimulates further erythropoiesis leading to the chronic bone
marrow hyperplasia and expansion of the bone marrow space >>> thickening of the
cranium and maxillary cavity.
Pt is in a hypercoagualble state.
Microcytosis (small cells).
Hypochromia (pale cells).
✔✔Treatment of thalaseemia - ✔✔Thalassemia minor No intervention/Monitoring
Thalassemia major
•Goal is to normalize Hgb
•Frequent transfusions
•Splenectomy - eliminate the site of hemolysis
•Blood transfusion to maintain normal Hgb level
•Bone marrow transplant
✔✔Hemophilia A - ✔✔Factor VIII deficiency
✔✔Hemophilia B - ✔✔Factor IX deficiency
ANSWERS SET A+
✔✔iron deficiency anemia - ✔✔Anemia caused by inadequate iron intake
✔✔iron deficiency anemia - RF, Causes, Diagnosis - ✔✔Age Between 6 mo - 4 yrs and
adolescence
Risk Factors:
-Low socioeconomic status (age 6-24mos)
-Premature infants
-Twins/Triplets
-Adolescents
Causes:
-Excessive whole milk intake in a child over 12 mos. of age
-Impaired iron absorption
-Blood loss
-Inadequate intake of iron
Diagnosis:
-H/H low
-Serum Ferritin low
✔✔iron deficiency anemia treatment - ✔✔Correction of the underlying problem
Replacement of depleted iron stores
-Dietary sources: Counsel foods high in Fe
-Supplements: 6 mg/kg/day of elemental Fe, divided into 1-2 doses
-Give the prescribed medication as ordered
Issues with food:
1. Absorbed best in high acid environment
2. Administer on empty stomach or with citrus juice
,3. Fe can stain teeth: give with a straw or dropper
4. Foods interfere with absorption, but sometimes needed due to unpalatable taste
5. Small frequent feedings if necessary-may decrease N/V/D
Frequent rest periods
-Monitor the child's fatigue level
✔✔Lead Poisoning - ✔✔A medical condition caused by toxic levels of the metal lead in
the blood
✔✔Lead Poisoning Pathophysiology - ✔✔Exposure occurs through inhalation, ingestion
or occasionally skin contact.
Lead may be taken in through direct contact with mouth, nose, and eyes (mucous
membranes), and through breaks in the skin.
Lead absorption is higher in infants and children
The main body compartments that store lead are the blood, soft tissues, and bone; the
half-life of lead in these tissues is measured in weeks for blood, months for soft tissues,
and years for bone.
Lead has no known physiologically relevant role in the body, and its harmful effects are
myriad.
Lead and other heavy metals create reactive radicals which damage cell structures
including DNA and cell membranes.
✔✔S/S of Lead poisoning - ✔✔Drowsiness, clumsiness, ataxia, seizures, coma, resp.
arrest
✔✔Lead poisoning treatment - ✔✔CaEDTA, Dimercaprol (adults), succimer (kids)
✔✔Lead poisoning prevention - ✔✔Prevention: Hand washing, remove shoes,
adequate dietary intake of Ca and Iron, hazards of renovations, clean
✔✔Sickle cell disease - ✔✔A group of genetic disorders characterized by:
-Production of hemoglobin S
-Chronic hemolytic anemia
-Acute & chronic tissue damage secondary to the blockage of blood flow by abnormally
shaped RBCs
✔✔Sickle cell pathophysiology - ✔✔Glutamic acid (hydrophilic) replaced by valine
(hydrophobic) at position 6 in beta globin chain
,✔✔Laboratory analysis for sickle cell - ✔✔Platelet count should be high
ESR is normal
Reticulocyte level should be elevated (>5%)
LDH/AST are elevated secondary to hemolysis
✔✔Sickle cell disease - physical exam - ✔✔Growth
-May be delayed
-"Catch up" growth is common in adolescence
Common findings
-Assess spleen
-Scleral icterus
-Functional murmur
-Mild, generalized lymphadenopathy
-Slightly enlarged liver
✔✔Sickle cell crisis - ✔✔Intense pain because blood vessels can become blocked or
the defective red blood cells can damage organs in the body. HYDRATE
✔✔Types of sickle cell crisis - ✔✔(1) Vasoocclusive crisis (2) Sequestration crisis (3)
Aplastic crisis
✔✔Pain management for sickle cell disease - ✔✔Opioids or NSAIDS
✔✔SCD Infections - ✔✔6 months - 3 years are 400 times more likely to become
infected by Strep Pneumonia
✔✔SCD Fever management - ✔✔Fever > 101 requires treatment
Chemo ppx PCN from 2 months - 5 yeras
✔✔SCD Summary - ✔✔Hydration, Hydration, Hydration!
(Keep the vascular bed open!)
Oxygen
Pain management
Prophylactic antibiotics (monitor for infection)
Monitor for complications (neuro/cardio/resp)
Psychosocial support
✔✔Thalassemia - ✔✔Inherited defect in ability to produce hemoglobin
✔✔S/S of Thalassemia - ✔✔1. Pale
2. Tachycardia/Tachypnea
3. Hepatosplenomegaly
, 4. Frontal bossing with bone changes
✔✔Clinical diagnosis of thalassemia - ✔✔CBC
Hg < 6
✔✔Alpha Thalassemia - ✔✔Diseases in which there are insuffiecient alpha-globin
chains due to gene deletions
✔✔Beta Thalassemia - ✔✔Disease in which insufficient beta-globin chains are
produced and there is an excess of alpha chains
✔✔Four types of thalassemia - ✔✔Thalassemia minor: Asymptomatic silent carrier
Thalassemia trait: Mild microcytic anemia
Thalassemia intermediate: Moderate to severe anemia + splenomegaly
Thalassemia major "Cooley anemia": Severe anemia requiring transfusions to survive
✔✔Clinical manifestations of thalassemia - ✔✔Growth, both physical and mental is
often retarded.
Thalassemia major: pale, displays general symptoms of anemia.
Pronounced splenomegaly and hepatomegaly.
Jaundice from RBC lysis.
As the bone marrow responds to the deficit of the oxygen-carrying capcity of blood,
RBC production is stimulated and the marrow becomes packed with immature erythroid
precursors that die >>> stimulates further erythropoiesis leading to the chronic bone
marrow hyperplasia and expansion of the bone marrow space >>> thickening of the
cranium and maxillary cavity.
Pt is in a hypercoagualble state.
Microcytosis (small cells).
Hypochromia (pale cells).
✔✔Treatment of thalaseemia - ✔✔Thalassemia minor No intervention/Monitoring
Thalassemia major
•Goal is to normalize Hgb
•Frequent transfusions
•Splenectomy - eliminate the site of hemolysis
•Blood transfusion to maintain normal Hgb level
•Bone marrow transplant
✔✔Hemophilia A - ✔✔Factor VIII deficiency
✔✔Hemophilia B - ✔✔Factor IX deficiency
