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NR 328 PEDS EXAM 2 STUDY GUIDE 2 VERSIONS / NR 328 PEDS EXAM 2 STUDY GUIDE 2 VERSIONS: 100% CORRECT,CHAMBERLAIN COLLEGE OF NURSING CA$32.99   Add to cart
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NR 328 PEDS EXAM 2 STUDY GUIDE 2 VERSIONS / NR 328 PEDS EXAM 2 STUDY GUIDE 2 VERSIONS: 100% CORRECT,CHAMBERLAIN COLLEGE OF NURSING
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NR 328 PEDS EXAM 2 STUDY GUIDE 2 VERSIONS / NR 328 PEDS EXAM 2 STUDY GUIDE 2 VERSIONS: 100% CORRECT,CHAMBERLAIN COLLEGE OF NURSINGNR 328 PEDS EXAM 2 STUDY GUIDE 2 VERSIONS / NR 328 PEDS EXAM 2 STUDY GUIDE 2 VERSIONS: 100% CORRECT,CHAMBERLAIN COLLEGE OF NURSINGNR 328 PEDS EXAM 2 STUDY GUIDE 2 VERSIO...

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  • May 2, 2021
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  • nr 328 peds exam 2 study guide
  • nr328 peds exam 2 study guide

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VERSION 1

NR 328 PEDS EXAM 2 STUDY GUIDE
HEMATOLOGIC DISORDERS: 7-10 questions
 Identify general nursing strategies associated with altered anemia
 Describe the morphology, pathophysiology, clinical manifestations,
therapeutic management and nursing considerations of the following
anemias:
o ***Laboratory norms: 6-12 years of age
 Hemoglobin:
 11.5-15.5 g/dl
 Hematocrit:
 35-45%
 MCV (mean corpuscular volume)
 77-95 fL
 Measure of average size of RBC
 ↓ in microcytic; ↑ in macrocytic
 MCHC (mean corpuscular Hgb concentration)
 31–37 g/dl
 Reflection of Hgb concentration
 Refer to color; in hypo-, values are ↓
 MCH (mean corpuscular Hgb)
 25–33 pg/cell
 Reflection of Hgb concentration
 Refer to color; in hypo-, values are ↓
o Anemia
 Condition where the hemoglobin content of the blood is
insufficient to satisfy bodily needs
 Causes:
 Blood loss
 Accelerated hemolysis
 Decreased production
 Typical Clinical Manifestations:
 Fatigue
 Dizziness
 Weakness
 Pallor
 ↑ heart rate
 ↑ breathing rate
o Types:
 Iron-deficiency anemia—MOST COMMON IN PEDS
 Nutritional anemia
 Microcytic-hypochromic—small, pale RBC
 Who’s at risk?
o Varied
o Premature babies at ↑ risk b/c they don’t get that
blood rush the mom gives the baby late in that 3 rd
trimester, b/c premies are born early—this is why

, premature infants need the iron supplements at 2-3
months, whereas term babies don’t need it until 4-6
months
o Multiples and twins at ↑ because only finite amount
of blood available in that last rush of blood; so not
all the babies get enough iron
o Breast-fed exclusively babies at ↑ risk—breast milk
doesn’t have same iron content as fortified iron
formula
o Kiddos with chronic blood loss—GI bleeders,
hemophiliacs
o Kiddos with poor dietary intake; whole milk doesn’t
have same iron concentration as iron fortified
formula
 Pathophysiology:
o Body stores iron that is used for erythropoiesis
o Iron necessary mineral for erythropoiesis to occur
o Not enough iron to transport to the bone marrow to
make RBCs
o Bone marrow still makes RBCs but they are very
small and have a lower hemoglobin concentration
 Clinical Manifestations:
o Typical signs of anemia plus:
 Irritability—due to tissue hypoxia/O2 craving
 Pica (especially ice, dirt, chalk, powder or
pure starch)—eating of substances that are
not typical of kiddos to eat; however this
could be hard to distinguish from this
occurring normally in toddlerhood
 Poor muscle tone
 Growth retardation
 Headache
 Nail bed deformities called?? Spoon nail
 Tachycardic; possible murmurs
 Lab Values:
o Everything is ↓↓↓↓ b/c its microcytic-hypochromic
 Implementations:
o EDUCATION***
 Prevention*
 High iron foods*
 Foods that a toddler would eat; eggs,
breads
 Whole milk takes up room in belly!!!
So kiddo may not intake enough iron-
rich food b/c they’re not hungry;
remember whole milk does not have
same iron concentration like fortified
formula so if kiddo is drinking equal
amounts of whole milk as he/she used
to drink the formula he/she is not
getting enough iron
 Iron supplements
 Best on an empty stomach
 Best with Vitamin C
 Don’t give with milk

,  If taking efficiently they will have
black/green tarry stools
 Lab values best indicator
 Use a straw to prevent staining of
teeth
 Monitor for constipation & treat




 Beta-Thallasemia
 Hemolytic anemia; bone marrow issue is the underlying
patho—blood cells are extremely unstable, RBCs lyse very
easily
 Not producing correct beta chains of hgb—alpha and
gamma attempt to take over and produce RBCs that are
fragile and prone to lysing
 ***kiddos BM is not making right hemoglobin
chains—they break down very quickly and easily
 Microcytic-hypochromic
 Defective synthesis of the protein component of
hemoglobin
 Who’s at Risk
o Mediterranean descent—Italians and Greeks
 Pathophysiology:
o Hemoglobin synthesis is impaired
o Fragile RBC w/short life
o Severe anemia
 Types:
o Major
 Most severe
 Occurs in infancy
 If kiddo doesn’t receive freq. transfusions
and treatments they rarely survive childhood
 Without treatment they die before age 7
o Intermediate
 Develop normally into adulthood
 Need to be treated
 Delayed puberty
o Minor
 Carry the trait, don’t have it
 Have normal life-span
 Clinical Manifestations:
* occurring b/c of BM involvement
o Frequent epistaxis*
o Osteoporosis*
o Pathologic fractures*
o Chronic CHF
o Myocardia fibrosis
o Murmurs
o Hepatosplenomegaly—b/c spleen has to work
harder to clean up dysfunctional RBCs
o Diabetes mellitus

, Darkening of the skin—indication of iron toxicity
o
that’s occurring
 Therapeutic Management:
o Frequent blood transfusion
 Subsequent iron chelation therapy
 ***Enough transfusions to maintain the Hgb
greater than 9.5
 Monitor for iron overload
o Splenectomy
 Nursing Management:
o Promote compliance
o Assist w/ coping strategies
o Observe for complications of multiple transfusions
o Differentiate between Iron Deficiency Anemia & Thalassemia

IDA Thalassemia
Ferritin Levels
Serum iron
TIBC
MCHC
Hemoglobin
Electrophoresis
Ethnic Background

 Sickle-cell anemia
 Hemolytic anemia
 Autosomal recessive condition where normal hemoglobin
is partially or completely replaced by the sickle-shaped,
abnormal S Hgb
 Won’t see manifestations until about 6-12 months after
birth b/c kiddo still had fetal hemoglobin circulating; fetal
hemoglobin does not sickle!
 Who’s at Risk?
 Pathophysiology:
o Biggest trigger is hypoxia—stress, high altitudes,
cold, not breathing well, excessive exercises, low
body or environment temp, anesthesia—watch
closely in OR, dehydration, infection, acidosis
o Hemoglobin S becomes elongated and rigid
o Cells clump together and obstruct capillary blood
flow
o Ischemia and tissue infarction occur beyond the
obstruction
o Hypoxia continues which leads to tissue infarcts—
ischemia of tissue is extremely painful
 Crisis experienced:
o Vaso-occlusive crisis
 Norm/MC—typically non-life threatening;
associated with a lot of pain
 Seriousness depends upon where occlusion
occurs; ex: brain vs. hand
 Manifestations
 Severe pain #1
 Tissue engorgement
 Fever

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