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Module 5 (Pediatrics) > Hematology/Immunology > Flashcards

Hematology/Immunology Flashcards

1
Q

Anemia is the ?
and in conjuction does what?

A

Reduction in RBCs mass and/or hemoglobin concentration
- Decrease in the Hgb available to carry O2 to cells

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2
Q

Main causes of anemia

A

Inadequate production of RBCs
- Does not enough made
Increased destruction of RBCs
- Kills them too fast
Excessive lossof RBCs (Trauma)

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3
Q

Anemia s/s

A

fatigue, high heart rate and BP, tachypnea, pale and cold, low cap refill, blue extremities (extreme),
blood count – low RBCs

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4
Q

RBCs carry

A

O2 and nutrients

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5
Q

Low RBCs cause the body to

A
  • pumps blood faster
  • causes demand for more O2 in the body
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6
Q

Retic Count

A

what the body does in an anemic state (High = increased RBCs, low = decrease RBCs)

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7
Q

Reticulocyte

A

last stage of development in RBCs

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8
Q

Erythrocyte is

A

RBCs

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9
Q

Erythrocyte life span = _____ days

A

120

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10
Q

homeostatic balance of RBCs

A

RBC production = RBC destruction

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11
Q

RBCs transport what to the cells

A

hemoglobin to cells O2

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12
Q

Hemoglobin is composed of what 4 globulin chains?

A

Fetal Hgb: 2 α and 2 y globin chains
Later in pregnancy, adult Hgb: 2 α and 2 β globin chains

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13
Q

fetal defect in Hgb synthesis present (e.g., Sickle Cell Disease, Beta Thalassemia Major) = Fetal Hgb

A

may be produced into adulthood

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14
Q

What disease kills the erythrocytes too fast and they live less than 120 days?

A

sickle cell anemia

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15
Q

Why is fetal hemoglobin used in hemolytic diseases like sickle cell anemia?

A

Fetal hemoglobin and O2 have a pos. charge joining together and grabbing each other
- help compensation

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16
Q

Basic regulators of RBC production

A

Tissue oxygenation
Kidney production of erythropoietin**

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17
Q

Chronic kidney disease can produce anemia, why?

A

kidney is unable to make erythropoietin and help production of RBCs

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18
Q

As RBCs age, the membrane

A

ruptures

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19
Q

When hemoglobin is broken down, what is released?

A

Iron pigment (Hemosiderin)
Bile pigment (Bilirubin)

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20
Q

Hemosiderin most reused in

A

bone marrow for RBC production

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21
Q

Bilirubin is excreted by what organ after the rupture of hemoglobin?

A

liver in bile

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22
Q

When too many RBCs are broken down, then what can occur in relation to bile and iron?

A

jaundice from too much bile and the body has excess iron in blood leading to organ dysfunction and impact the brain

Elation = getting rid of excess iron = storage = liver

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23
Q

Anemia assessment

A

pallor, fatigue, weakness, tachycardia, increased respiratory rate, dizziness, headache (no O2), irritability

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24
Q

Severe anemia assessment

A

hyperventilation

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25
Q

Children with anemia are prone to

A

infection

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26
Q

Infections worsen

A

anemia

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27
Q

Normal Ranges of Anemia
- newborn
- infant
- child
- adult

A

Newborn – 14-24
Infant – 10-17
Child – 9.5-15.5
Adult – 12-18
- the younger the child the more hemoglobin needed

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28
Q

Iron Deficiency Anemia (IDA)

A

Hgb Levels Below Normal Range
Because Of Body’s Inadequate Supply, decreased Intake, chronic blood loss Or lack of Absorption Of Iron

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29
Q

Iron Deficiency Anemia (IDA) causes

A

Inadequate Supply during fetal development
decreased Intake,
chronic blood loss
Or lack of Absorption Of Iron
- last trimester in pregnant women = iron goes to the baby

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30
Q

Iron Deficiency Anemia (IDA)
children at high risk

A
  • Preterm infants, multiple births (don’t get the iron stores or not getting enough bc sharing with siblings)
  • Mother has iron deficiency
  • Infants 6 to 24 months old (growth spurts)
  • Toddlers (don’t eat enough and picky eaters)
  • Female adolescents (puberty periods and growth spurts, not great diets)
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31
Q

Iron Deficiency Anemia (IDA) s/s

A

Pallor/paleness of mucous membranes
Tiredness/fatigue**

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32
Q

Iron Deficiency Anemia (IDA)
- possible findings

A

Overweight “milk baby”
Dietary intake low in iron
Milk intake > 32 oz./day
Pica habit (eating nonfood substances) = trying to get iron from other sources

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33
Q

Milk baby

A

drinking too much cow’s milk
chunky overweight
not good source of iron

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34
Q

Iron Deficiency Anemia (IDA) Diet

A

Iron fortified formula or cereal
Dietary addition of iron-rich foods

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35
Q

Iron Deficiency Anemia (IDA) Tx

A

Oral iron supplements
- Ferrous sulfate (Fer-in-Sol)

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36
Q

Iron Deficiency Anemia (IDA)
Tx for severe anemia

A

Blood transfusions
Packed RBCs to minimize chance of circulatory overload
Tissue hypoxia – supplemental O2

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37
Q

Iron-rich foods

A

green leafy veggies, red meat (steak and liver), fish, legumes

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38
Q

Ferrous sulfate (Fer-in-Sol)
side effects

A

Upset GI, feces black/tarry/dark green, constipation (increase fluids and fiber),

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39
Q

How long do you take Ferrous sulfate (Fer-in-Sol) until mature RBCs

A

3 months (120 days) for mature RBCs to venture out
1 month have H&H see changes
If not chronic bleeding or iron disorder

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40
Q

Iron supplement Administration

A

Give on empty stomach
Give with citrus juices (vitamin C)
- Increases absorption of iron in bloodstream
Use dropper or straw
Stain the teeth
Stools will be tarry
Safety
No overdose, stored correctly and out of reach
NO milk = Decrease absorption

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41
Q

During iron-deficient anemia, limit milk to

A

< 32 oz per day
and dietary sources of iron

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42
Q

If iron-deficient anemia is severe and longstanding, what is the prognosis?

A

Diminished cognitive function
Behavioral changes
Delayed growth and development
(extreme = death)

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43
Q

Sickle Cell Anemia

A

Autosomal Recessive Genetic Disorder That Results In The Formation Of Abnormal Hemoglobin Chains
- Normal Adult Hemoglobin A (HbA) Is Partly Or Completely Replaced By Abnormal Sickle Hemoglobin (HbS)

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44
Q

Under Certain Circumstances, Abnormal RBC “Sickles” cell anemia, results in

A

Occlusion Of Small Blood Vessels, Ischemia, And Damage To Affected Organs

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45
Q

If both parents have the sickle cell trait, what are the percentages of the child?

A

is 25% not have it at all, 50% trait carrier, 25% have disease
90,000-100,000 in the US have it

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46
Q

What race and gender is more likely to have sickle cell?

A

AA at risk, males more than females,
lifelong

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47
Q

What causes the cells to sickle?

A

stress

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48
Q

Sickle cell anemia causes

A

occlusion of small vessels (pile up)
leads to ischemia and damage cells

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49
Q

HbS changes the molecular structure of an RBC to form what?

A

elongated crystals
- Cresent and distorted

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50
Q

Sickled RBC lifespan

A

less than 40 days
- leads to chronic anemia

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51
Q

Sicle cell anemia s/s are not usually seen until

A

after 1st 6 months of life

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52
Q

Fetal hemoglobin does not

A

sickle
- reason to continue giving in later years

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53
Q

Triggers to sickling

A

Dehydration
Acidosis
Hypoxia/Hypoxemia
Temperature changes (winter cold)
Emotional stress
Infection

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54
Q

Effects of Sickling

A

Abnormal adhesion, entanglement, and enmeshing of rigid sickle-shaped RBCs
↓
Inflammatory process
↓
Intermittent blocking of microcirculation
↓
Vaso-occlusion
↓
Absence of blood flow to adjacent tissues
↓
Local hypoxia
↓
Tissue ischemia and infarction

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55
Q

Infarctions can occur

A

anywhere

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56
Q

Dx of Sickle cell prenatally

A

Chorionic villus sampling from prenatal tissue
Amniocentesis

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57
Q

Dx of Sickle cell after birth

A

1st = Newborn screening – heel stick
If positive
2nd = Sickledex (sickle turbidity test)
3rd = If positive, hemoglobin electrophoresis = confirms (electricity to the RBCs to see sickling

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58
Q

S/S of Sickle cell anemia

A

asymptomatic until 6 months
general chronic hemolytic anemia s/s
- Frequent infections
- Fatigue
- Delayed physical growth – smaller ht and wt than peers

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59
Q

Sickle Cell CRISES

A

acute exacerbations triggered
- Vaso-occlusive
- Splenic Sequestration
Aplastic
Hyper hemolytic

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60
Q

Vaso-occlusive crisis (VOC) in sickle

A

observed with 4-6 days
- peripheral
- pain crisis by anemia

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61
Q

Splenic sequestration crisis in sickle cell

A

6 months to 5 y/o
Pooling of large amount of blood in the spleen and liver causing drastic decrease of blood volume
Hypovolemic and life threatening with death within hours without treatment

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62
Q

Aplastic crisis in sickle cell

A

Child has a viral illness
Causing Decreased RBCs

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63
Q

Hyper hemolytic crisis in sickle cell

A

Body unknown = Accelerates destruction of RBCs

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64
Q

Vaso-occlusive crisis (VOC) classic s/s

A

Acute Pain – 15/10
Fever
Severe abdominal pain
Painful edematous hands and feet
Hand-Foot Syndrome (infants)
Arthralgia = pain In joints
Leg ulcers (adolescents) – low circulation
Cerebrovascular accident (CVA)

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65
Q

What could mask as appendicitis if the pain is in the stomach area?

A

Vaso-occlusive crisis

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66
Q

Vaso-occlusive crisis chronic signs

A

Splenomegaly (enlarged spleen) → auto splenectomy (infarction of the spleen killing it)
Hepatomegaly → liver failure
Kidney abnormalities → hematuria, inability to concentrate urine, enuresis, possible renal failure
Bone changes → osteoporosis, skeletal deformities
Retinal detachment → blindness

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67
Q

When the spleen is in failure (auto splenectomy), the person has an increase of

A

infection

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68
Q

Additional complications of sickle cell in Chest Syndrome s/s

A

Fever ≥ 101.3°
Cough
Chest pain
Tachypnea
Dyspnea
Wheezing
Decreased O2 saturations

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69
Q

Acute Chest Syndrome

A

blockage of blood flow to the lungs

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70
Q

If the acute Chest Syndrome is untreated, then

A

respiratory distress and death

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71
Q

Acute Chest Syndrome tx with

A

Antibiotics, O2, and blood transfusion

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72
Q

VOC Mgmt

A

Hydration
Electrolyte replacement
Strict I & O
Monitor kidneys
Analgesics – PCA pumps and narcotics
- Warm compresses
Blood transfusion – RBCs are in to treat
Antibiotics if infection
Hydroxyurea
- Increases fetal hemoglobin production bc it does not sickle

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73
Q

What is contraindicated in VOC management?

A

cold compresses - vasoconstriction and extreme cold is a trigger for crisis

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74
Q

How do you reverse sickling of sickle cell anemia?

A

prevent dehydration with hydration

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75
Q

VOC Pain mgmt

A

mild to moderate = tylenol and ibuprofen
severe = opioids (morphine, hydromorphine, hydrocodone and ketorolac)

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76
Q

ORAL AND IV pain management for VOC need to be administered when

A

schedule with PCA if appropriate

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77
Q

Meperidine is contraindicated in children due to

A

seizures

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78
Q

Education to prevent hypoxia in Sickle cell anemia by avoiding

A

Avoid strenuous exercise = dehydration
Avoid high altitudes = cold environment
Avoid being around anyone who is sick and seek care at first sign of infection

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79
Q

Education to prevent hypoxia in Sickle cell anemia by

A

prophylactic penicillin if prescribed
Prevent strep
If allergic then azithromycin
Keep child well hydrated (do not withhold fluids at night)
Up-to-date immunizations
Refer family for genetic counseling
Provide emotional support

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80
Q

Prognosis of Sickle cell anemia

A

depending upon severity of disease
Typically live to 50
Greater risk is < 5 with crises
- Death is related to overwhelming infection
Stem cell transplantation

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81
Q

Beta Thalassemia Major aka

A

“Cooley’s Anemia”
Autosomal Recessive Disorder
- both parents are carriers

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82
Q

Beta Thalassemia Major is deficiency (partial or complete)

A

Synthesis Of The β Chain Of The Hemoglobin Molecule

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83
Q

Beta Thalassemia Major results in

A

Life-Threatening Anemia Requiring Lifelong Blood Transfusions That Lead To Iron Overload

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84
Q

Why do transfusions not work for Beta Thalassemia Major?

A

Transfusions = RBCs breakdowns = iron overload
- fetal hemoglobin into adulthood

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85
Q

What si the Tx for Beta Thalassemia Major?

A

Keylation

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86
Q

Beta Thalassemia Major Patho

A

Dramatically decreased or complete deficiency
in the synthesis of β-chain in Hgb molecule
▼
An unbalanced polypeptide unit is very unstable
▼
The Hgb molecule disintegrates
and damages the RBC
▼
The RBC prematurely breaks down
▼
Causing severe hemolytic anemia

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87
Q

Hemolytic Anemia life span of RBC is

A

30-60 days

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88
Q

Beta Thalassemia Major s/s

A

Severe anemia (pale, fussy, won’t eat, and infection)
Chronic hypoxia
Small stature - FFT
In some adolescents – delayed puberty
Bronzed skin tone, possibly = High Bilirubin
Hepatosplenomegaly (liver –stores extra iron and spleen = pooling of cells and stuck))
Cardiomegaly
Bone Changes – frontal boxing, maxilla, and jaw bones (untx older children) - general osteoporosis

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89
Q

Beta Thalassemia Major s/s is shown within how many years of life?

A

2 y/o

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90
Q

Labs of Beta Thalassemia Major

A

High retic count
hypoxia (low O2 sat)

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91
Q

Beta Thalassemia Major Dx prenatal

A

Chorionic villus sampling from prenatal tissue
Amniocentesis

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92
Q

Beta Thalassemia Major Dx after birth

A

1st Newborn screening
2nd CBC
3rd Hemoglobin electrophoresis
X-rays for bone involevement

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93
Q

The goal for Beta Thalassemia Major is to

A

maintain adequate Hgb via transfusion program

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94
Q

What is the goal level of hemoglobin for Beta Thalassemia Major

A

> 9.5
checked every 3-5 weeks for PRBCs

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95
Q

Tranfuse to do what in a patient with Beta Thalassemia Major?

A

Improve well being (physical/mental)
Normal activity
Decrease cardiomegaly/hepatosplenomegaly
Prevent bone changes
Promote normal or near-normal growth and development
Decrease infections

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96
Q

Hemosiderosis

A

iron overload secondary to transfusion
- deposit to tissues

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97
Q

What could possible go wrong during a transfusion?

A

Hemosiderosis
chelation
Hypersplenism
- Splenectomy

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98
Q

Chelating agents

A

Desferal (deferoxamine)
Exjade (Deferasirox)

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99
Q

Desferal (deferoxamine)

A

IM or IV at infusion center
SQ
Portable infusion pump for 8 hours
4 - 6 nights a week
Bind with iron and excrete in urine (rusty colored)

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100
Q

Exjade (Deferasirox) FOR CHILDREN AGE

A

PO to children ≥ 2 years of age

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101
Q

Chelation can cuase what problems and need yealry check ups/

A

hearing and vision

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102
Q

What is given with iron

A

Vitamin C

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103
Q

Splenectomy

A

removal of spleen
- Treats severe splenomegaly and increases life span of transfused RBCs
- Increases susceptibility to overwhelming infection

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104
Q

Splenectomy Interventions

A

Prophylactic antibiotics lifelong**
Up to date Routine immunizations**
s/s of infection call HCP immediately

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105
Q

Prognosis of Beta Thalassemia Major with tx

A

children living into adulthood with decrease life span
- death is usually heart disease, post splenectomy sepsis, or multi-organ failure
secondary to hemochromatosis
Usually have a heart attack or failure by 35 y/o

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106
Q

Beta Thalassemia Major possible cure

A

stem cell transplant

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107
Q

Lead poisoning have what amount of lead in their system?

A

> 5 mcg

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108
Q

What is the safe level of lead in the blood system?

A

NONE in children

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109
Q

Lead exposure and elevated levels have been linked to

A

low IQs

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110
Q

Lead causes

A

anemia

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111
Q

Lead exposure

A

Ingestion – most common route
Inhalation

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112
Q

Ingestion routes of lead

A

Crib rails
Windowsills
Older plumbing (water source)
Contaminated soil
Paint chips (sweet taste)
And many other sources

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113
Q

Inhalation routes of lead

A

renovation of old homes in nearby areas

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114
Q

Risk factors of Lead Poisoning

A

Children < 6 years old (oral) PICA
Living in poverty
Living in urban areas
Living in older homes
Children with anemia
Lead binds to hemoglobin and retains the lead

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115
Q

Who retains more lead?

A

children due to WT TO BSA ration

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116
Q

Lead poisoning s/s

A

Anemia + s/s
Cramping, abdominal pain
Vomiting
Constipation
Anorexia
Headache
Lethargy
Impaired growth

117
Q

Early (toddlers) CNS S/S of lead poisioning

A

Hyperactivity
Aggression**
Impulsiveness**
Decreased interest in play
Irritability
Short attention span

118
Q

Late CNS S/S of lead poisoning

A

Mental retardation= decreased IQ
Paralysis
Blindness
Convulsions
Coma
Death

119
Q

Testing for lead poisoning

A

BLL TEST (Blood lead level)

120
Q

Universal screening of BLL

A

All children at ages 1 - 2 years
Any child between 3 -6 years if never screened
PRN if at high-risk environment

121
Q

Target screening for lead poisoning in

A

If reside in high-risk geographic areas
If in “at risk” group
If family cannot respond “no” to personal risk questions
- low IQs

122
Q

Lead poisoning Interventions

A

Identify sources of lead in the child’s environment
Then rid them of the source
- no vacuum windows or sill - wet mop
- wash and dry hands, toys, and pacifiers

123
Q

Occupations with the most exposure to lead poisoning?

A

construction
paint
ceramics
pottery

124
Q

When BLL is >45, what Tx needs to be done?
What is the chelator used?

A

Chelation → Protect Kidneys
Succimer (Chemet)
PO for 19 days
Capsule or sprinkle
Calcium disodium (EDTA) IM
Very painful
Atraumatic care with rotation of site, EMLA,
Multiple treatments if necessary, after blood level tests

125
Q

The Tx for BLL over 45, does not counteract the

A

CNS effects already in place

126
Q

Hemophilia

A

Inherited X-Linked Recessive Bleeding Disorder
- maternal with males having the disease

127
Q

Hemophilia is not passed to

A

females do to another X chromosome to cancel out the disease one

128
Q

Hemophilia results in

A

Deficiency, Dysfunction, Or Absence Of
Coagulation Factor VIII Or Factor IX

129
Q

Where is the bleeding of a hemophilia pt?

A

anywhere in the body
- mild to severe

130
Q

Hemophilia A

Aka?
Deficiency type?

A

classic neoplastic
Factor 8 Deficiency (75%)

131
Q

Hemophilia B
Aka?
Deficiency type?

A

Christmas disease
Factor 9 deficiency (25%)

132
Q

Mild Hemophilia factor production

A

6-50%

133
Q

Moderate Hemophilia factor production

A

1-5%

134
Q

Severe Hemophilia factor production

A

less than 1% most common

135
Q

Dx of Hemophilia

A

hx of bleeding episodes
genetic testing

136
Q

Labs for Hemophilia

A

PTT less than 25%

137
Q

Hemophilia Assessment

A

Male child: prolonged bleeding (Vit. K, umbilical cord, post-circumcision)
Hemarthrosis (most frequent site of bleeding)
Knees, elbows, ankles - loss of motion in joints
“Target joints”
- tingling sensation
Spontaneous bleeding subcutaneous tissues and muscles
- brusing excess, pooling hematoma
Spontaneous hematuria or blood in stool
Coffee grounds in vomiting
Frequent and no stop nosebleeds

138
Q

What is the most frequent site of bleeding in hemophilia?

A

Hemarthrosis
Knees, elbows, ankles - loss of motion in joints
“Target joints”
- severe pain

139
Q

How do you stop hemophilia nosebleed?

A

head down with pressure for at least 10 mins with cotoon or tissue in nostril – not back) – ice to constrict vessels try to remain calm of the child

140
Q

If repeated bleeding episodes in the joints, then

A

, synovial thickens and becomes target joints leading to chronic arthritis
- Joint immobility and crippling deformities

141
Q

How to Recognize & Control Bleeding in hemophilia

A

Believe child (feel pressure of tingling but not outward s/s bc faster = better outcome)
RICE then medical tx - help joints only
Factor replacement per bleeding episode and prophylactically

142
Q

Factor replacement per bleeding episode and prophylactically
how many times per week?

A

2-3 times

143
Q

Factor replacement starts when

A

2-3 y/o done by family after a while
- more often if severe
- impanted port with edu when older
expensive only good for 2 hours after reconstituted

144
Q

Factor Replacement is

A

Genetically engineered recombinant factor VIII and IX
Recommended over factor concentrate from pooled plasma

145
Q

When the hemophilia pt is 8-12 y/o then they are able to

A

self-administer factor by themselves
- port-a-cath

146
Q

DDAVP (synthetic vasopressin is used for

A

mild Fcator 8 deficiency
and RA

147
Q

How to prevent bleeding in hemophilia?

A

Regular exercise
Soft bristle toothbrush under warm water
Water pick instead of floss
Med ID bracelet
Avoid IM injections if possible
Venipunctures instead of heel sticks/finger sticks
Educate to recognize early signs and symptoms of hemorrhage
Medication to avoid Aspirin and aspirin mixed meds
(Ibuprofen) (give acetaminophen)

148
Q

Complication of hemophilia

A

Inhibitors risk
Factor specific antibodies
Give slower
Develop after the child has received factor replacement

149
Q

Prognosis of Hemophilia

A

no cure
average life expect

150
Q

Activity acceptable for hemophilia

A

Swimming, golf, cross country, bowling, band, archery, discuss
No contact sports (football, basketball, hockey)

151
Q

Immune Thrombocytopenia (ITP)

A

Autoimmune Disorder
Characterized By Thrombocytopenia

152
Q

Immune Thrombocytopenia (ITP) occurs when

A

Immune System
Mistakenly Attacks And Destroys Platelets

153
Q

Immune Thrombocytopenia (ITP) caused by

A

Unknown Etiology** But Most Often
Presents After Viral Infection

Etiology Unknown – Often Presents After A
Viral Infection

154
Q

Thrombocytopenia

A

low platelets

155
Q

ITP bone marrow aspiration (conscious sedation) results in

A

normal
if abnormal then leukemia

156
Q

ITP S/S

A

spots on skin
Petechiae (spider spots)
easy Bruising
Bleeding from mucus membranes
Nosebleeds, bleeding gums
Prolonged bleeding from abrasions

157
Q

ITP peaks

A

2-6 y/o

158
Q

s/s of ITP disappear within

A

3 weeks

159
Q

If ITP is chronic then persists for

A

years

160
Q

Testing for ITP

A

No definitive tests due to mimic of other disease
HMP
CBC
Platelets < 20,000/mcL

161
Q

What is the platelet count of ITP

A

Platelets < 20,000/mcL

162
Q

Normal platelet count

A

150,000-200,000

163
Q

Suportive Care of ITP

A

Restrict activities while platelets < 50,000

Monitor for s/s bleeding (increase HR, RR, drop in BP if enough)
Everywhere for bleeding sites
Prednisone, immune globulin (IVIG), Anti-D Antibody (Wintho)
Decrease activity destroying the platelets

164
Q

A ITP pt should restrict activity while platelets are

A

< 50000

165
Q

Chronic ITP can cause what in over 5 y/o

A

Splenectomy
If > 5 y/o bc of bacterial infection with sepsis
Penicillin prophylaxis

166
Q

Vertical Transmission of HIV

A

Late in pregnancy
Labor and delivery
Breastfeeding

ART
for pregnant mothers with HIV

167
Q

Horizontal Transmission of HIV

A

Sexual contact
HIV-infected blood products (transfusion)
Adolescents - high risk behavior
Drug use
Sharing needles

168
Q

Dx of HIV

A

Maternal antibodies persist up to 18 months
Infants born to HIV mothers will test positive
Even if they don’t have HIV,

169
Q

If an HIV pregnant mother has a baby and the baby tests positive for HIV, does the baby have HIV?

A

NOT ALWAYS

170
Q

When are extra tests done to verify if the baby is HIV positive?

A

18 months
Elisa or wesern blot test

171
Q

If the baby is less than 18 months what test is run to see if they are HIV +

A

HIV polymerase chain reaction test

172
Q

HIV S/S

A

Failure to thrive (low wt, no growth)
Lymphadenopathy (swollen nodes)
Hepatosplenomegaly (enlarged)
Neuropathy (nerve pain)
Cardiomyopathy (enlarged heart)
Chronic/recurrent infections
Oral thrush (white fuzzy in mouth)
Unexplained fevers

173
Q

HIV Tx goals

A

Slow growth of HIV virus
Prevent and treat opportunistic infections
Provide nutritional support
Promote normal growth

174
Q

Medication therapy of HIV

A

Antiretroviral medications
Prevent opportunistic infections (avoid crows, prophylactic antibiotics)
IV gamma globulin (IVIG)
Antibiotics = Bactrum combination : trimethoprim – sulfamethoxazole

175
Q

Interventions of HIV

A

Standard precautions
Nutritional support
HIV can lead to FTT
Protect privacy (HIPAA)
Immunizations – no live vaccines

176
Q

Childhood CA typically grow

A

Faster

177
Q

T/F: Lifestyle-related behaviors have little to no effect on childhood cancer

A

True
not smoking, drinking, or bad diet

178
Q

Classic s/s of childhood CA

A

Unusual mass or swelling, enlarged lymph nodes
Unexplained paleness & loss of energy
Sudden tendency to bruise
Persistent, localized pain or limping - bones
Prolonged, unexplained fever or illness
Frequent headache, often with vomiting-brain tumor
Sudden eye or vision changes – brain or eye
Excessive, rapid weight loss

179
Q

Leukemia charcterized by

A

an unrestricted proliferation of immature white blood cells in the blood-forming tissues
Bone marrow

180
Q

What is the ost common form of CA?

A

LEUKEMIA

181
Q

What are the most common type of Leukemia

A

Acute lymphocytic leukemia (ALL)
AML as well

182
Q

Tx of Leukemia

A

primary chemo

183
Q

Leukemia Patho

A

Competition for nutrients, infiltration, replacement in bone marrow
▼
Decreased RBCs, WBCs, platelets (bone marrow suppression)
▼
Anemia, risk for infection, bleeding, bruises, bone & joint pain, weakening of the bone, physiologic fractures

184
Q

Leukemia blast cells migrate to what other organs

A

Spleen
Liver
Lymph glands
CNS
areas with high blood flow

185
Q

S/S of Leukemia

A

Minor infection that fails to completely disappear
Infection, fever (r/t neutropenia)
Pallor, fatigue, weakness, lethargy (r/t anemia)
Petechiae, bleeding, bruising (r/t thrombocytopenia)
Bone joint pain (r/t leukemic infiltration of bone marrow)
Enlarged nymph nodes, hepatosplenomegaly
Anorexia, weight loss
Headache, vomiting (if CNS involvement)

186
Q

Leukemia is supected if

A

History and physical manifestations
Labs including CBC with differential
Low WBC, RBC, and platelets

187
Q

Dx of leukemia

A

Bone marrow biopsy and aspiration (BMA)
Positive leukemia
Lumbar puncture

188
Q

Higher leukocyte count at diagnosis =

A

worse prognosis

189
Q

what percentage of children relapse with leukemia within the year

A

15-20%

190
Q

what is the 5 year survival rate of leukemia

A

85-90%

191
Q

what may occur later in life in all CA and other cells being affected by the chemo therapies?

A

secondary malignancies

192
Q

When are children usually dx with leukemia

A

1-9 y/o

193
Q

High WBCs count means what for tx

A

higher dose of chemo and higher dosage cycle

194
Q

Neuroblastoma

A

Solid tumor that forms in the developing nerve cells, or neurons, of the sympathetic nervous system
Most develop in the adrenal glands, abdomen or nerve cell next to the spinal cord

195
Q

Neuroblastoma can be seen in

A

head
neck
chest
pelvis

196
Q

What is the Most common extracranial solid tumor of childhood?

A

neuroblastoma

197
Q

What is the Most diagnosed cancer in children younger than 1 year of age?

A

neuroblastoma
1-2 y/o dx median age but can be 0-14 y/o

198
Q

In a CT scan the neuroblaoma look like

A

Big dark and crosses the midline of the body (different from other tumor)
in abd

199
Q

S/S of Neuroblastoma

A

Firm nontender irregular mass in the abdomen
“Silent” tumor
grow rapidly and space in the abdomen to grow

200
Q

Survival depends on what in neuroblastoma

A

age
stage

201
Q

If the child is under 1 y/o, the chance of survival is

A

80%

202
Q

if the child is greater than 1, there chance of survival is

A

50%

203
Q

If the child is in the 1st stage of neuroblastoma, then curative rate is

A

90%

204
Q

____ already metastasized by found (lymph nodes, bone marrow, skeletal, and liver)
Typ. found late and prognosis is bad

A

70%

205
Q

Tx of Neuroblastoma

A

chemo
radiation depending on where and stage

206
Q

Wilms Tumor

A

Nephroblastoma

207
Q

Wilms Tumor is

A

Fast growing, asymptomatic, firm, encapsulated mass located to one side of abdomen
- 1 kidney RARE ON BOTH

208
Q

Wilms Tumor occurs most frequently in

A

2-5

209
Q

Wilms Tumor grows _______ before being noticed because of

A

LARGE; ABD space

210
Q

Wilms Tumor is typically found before

A

metastasis

211
Q

DO NOT ___________ Wilms Tumor or what could happen?

A

palpate or manipulate the abd
- rupture and CA cells go everywhere

212
Q

Wilms Tumor is what type of mass

A

encapsulated mass

213
Q

Wilms Tumor Tx

A

surgery, chemo, radiation depending on protocol

Tumor, kidney and adrenal gland are removed in surgery
- can live on 1 kidney

214
Q

Retinoblastoma

A

Cancerous tumor arising out of the retina
Usually unilateral
May be inherited

215
Q

Retinoblastoma primarily in children

A

<5 y/o

216
Q

Retinoblastoma s/s

A

Opaque white area in pupil* (Leukocoria, Cat’s Eye Reflex, White Pupil with flash)
the other eye has a red dot
Strabismus (cross eye)*
Decreased vision in one eye
Eye pain
Larger than normal eyeball*
Lazy eye*
Redness of the eye

217
Q

Retinoblastoma is seen by and dx by

A

Ophthalmology scope stages

Ophthalmologist sees the pt as soon as possible with s/s even if unrelated to retinoblastoma

218
Q

Retinoblastoma Treatment

A

Laser treatment
Cryotherapy
Chemotherapy
Radiation
Enucleation surgery (removal of the eye)
- Fitted for ocular implant and later artificial eye
- Cleaning eye (take out with warm water and mild soap and put back)
- Parent education

219
Q

Tx of Retinoblastoma priority

A

Save child life
Save the eye
Save the vision

220
Q

CA Dx

A

History
Physical examination
Lab tests
Imaging (Xray, CT, MRI, PET)
Procedures
Surgical pathology - Bone Marrow Aspiration and LP)

221
Q

Spinal Tap/LP To Collect CSF Or
To Give

A

Intrathecal Chemotherapy

222
Q

Phase 1 of Chemotherapy

A

Goal – remission
Time of high risk because medications cause myelosuppression
Risk of septic
CNS prophylaxis
Goal – kill or prevent leukemic cells in CSF
Intrathecal administration (tx or prevent CNS)
Cranial radiation reserved for high-risk patients

223
Q

Chemo Phases

A

Induction
Consolidation
Maintenance

224
Q

In the induction phase they want to kill what % of leukemic cells in the 1st month

A

99.9

225
Q

Phase 2 of Chemotherapy

A

Consolidation (Intensification) (1-2 months)
Goal - destroy any residual leukemia (last 100 million left)
combo of chemos
After completion of remission therapy

226
Q

Phase 3 of Chemotherapy

A

Miantenance (2-3 years)
Goal - remain in remission
After successful completion of induction & consolidation therapy
- boys have a high chance of remission

227
Q

Risk For Injury Related To Malignant Process & Treatment

A

Chemotherapy - suppression infections
Radiation Therapy damage to tissue and decrease immune system
Skin breakdown and infection and bleeding

Procedures

228
Q

Chemotherapy is used through

A

Central line (Broviac or Implanted Port)

229
Q

Extravasation

A

(chemo leaking out into surrounding tissue)
- Pain, swelling, itchy, necrosis

230
Q

Anaphylaxis
Signs and Symptoms
of chemo

A

Cyanosis
Hypotension
Wheezing
Urticaria
emergency ready - ambu bag anf suction

231
Q

If reaction with the chemo isuspected then

A

stop and call

232
Q

You need to watch chemo for how long during tx

A

1st 20 minutes

233
Q

Radiation

A

Uses high-energy beams to destroy cancer cells

Changes DNA in neoplastic cells so that it cannot reproduce

Usually scheduled over 1 - 6 weeks

234
Q

Radiation Checks and cautions teachings

A
  • change linen daily
  • internal (potect visits)
    Targeted area/site is marked with indelible ink

No soaps, creams, lotions or powders on area
Irritate skin and misdirect the radiation

Wear soft, loose cotton clothing
No rubbing
Keep area/site protected from the sun

235
Q

Neutrophils

A

fight bacterial infections

236
Q

Each chemotherapy agent that causes bone marrow suppression has a point of

A

NADIR

237
Q

NADIR is

A

Bone marrow suppression at its greatest, neutrophil count at its lowest
- weakest point of immune system
7-14 days

238
Q

WBC calculation for 9000-10000

A

highe the infection

239
Q

Absolute neutrophil count (ANC)

A

Measures the body’s ability to fight infection

240
Q

Segs

A

mature neutrophils

241
Q

Bands

A

immature neutrophils

242
Q

Calculate the ANC formula

A

Neutrophils (Segs + Bands) x WBC x 10

243
Q

If the ANC is less than 1500 then

A

evaluation

244
Q

If the ANC is less than 500

A

greatest risk for infection

245
Q

Remember that when we place a patient with a low ANC in isolation

A

, we are protecting them from us, not us from them.

246
Q

Normal ANC

A

1500

247
Q

Infection Prevention

A

Monitor for signs and symptoms of infection
Private room with restricted visitors
Reverse/protective isolation is prescribed
No fresh fruits or vegetables
NO Pets at home or flowers
No live vaccines - immunosuppression
Administer prescribed prophylactic medications
Antibiotics
Antifungals

248
Q

Nurse considerations when taking care of a CA t

A

Nurse can not be pregnant
Other patients should not be infectious

249
Q

T/F: Family members should get live vaccines to protect the child

A

True

250
Q

Risk for bleeding Preventions

A

Monitor for signs of bleeding
Avoid unnecessary skin punctures
Use aseptic technique
For fingersticks, venipunctures, IM injections
Meticulous mouth care
Soft toothbrushes, toothette, no alcohol or listerine
Avoid activities that might cause injury or bleeding
No contact sports
Nosebleeds (hold pressure 10 mins, head forward, ice)
Platelets transfusion
Monitor for HA (brain bleed)
For active bleeding episodes
No ibuprofen or aspirin

251
Q

Normal platelet count

A

150000-450000

252
Q

N/V treatment

A

Serotonin-receptor antagonists before chemotherapy
Ondansetron (Zofran)
Granisetron (Kytril)
Aprepitant (Emend)
Administered up to 1 hour before chemo
Often combined with Dexamethasone

253
Q

Anxiety Tx for chemo

A

Adivan or benadryl

254
Q

With chemo and CA pts you should avoid food with

A

strong odors

255
Q

Anorexia/Loss Of Appetite Interventions with CA complications

A

Avoid Pressure To Eat

Do Not Let Food Become A Control Issue

Small, Appealing Meals With Increased Calories and Protein
- Sores in mouth
Tube feeding
- Gives options and frequent eating
- ice cream and chicken nuggets are okay if that’s what they want
- but not no fruits and veggies

Dietary help and high protein shakes

256
Q

Preventing Mucosal Ulceration

A

Offer bland, soft foods
Use a soft sponge toothbrush (toothette)
Provide frequent mouthwashes (coat)
For discomfort
Local anesthetics or nonprescription preparations without alcohol
To prevent or treat mucositis
Moisten lips
Things to avoid
Rectal ulcers (stool softeners not suppositories)
- no rectal temps
Meticulous perineal hygiene
Barrier cream

257
Q

Do not give __________ bc suppress gag reflex avoid hydrogen peroxide and lemon glycerin swabs

A

Lidocaine

258
Q

If they have mucousal ulceration then it is

A

althoughout there GI tract mouth to anus

259
Q

Alopecia in child CA

A

Hair falls out in clumps and regrows in 3 - 6 months
May be darker, thicker, curlier
different than when fell out
Cotton cap, scarf, hat, or wig
Protect scalp from cold and sun
No burn and lose heat that way
Scalp hygiene – soap and water

260
Q

Alopecia in child CA hair will grow back

A

3-6 months with different than fell out

261
Q

Infants and Toddlers Developmental View Of Death

A

No concept of death (temp separation and death are the same)
Toddlers = Recognizes death in terms of immobility often viewed as reversible, temporary, or foreign

262
Q

Infants primary fears

A

“Separation
Strangers”

263
Q

Toddlers primary fears

A

“Separation
Loss of control”

264
Q

Early school-age child primary fears

A

“Bodily injury and mutilation
Loss of control
The unknown
The dark
Being left alone”

265
Q

school-age child primary fears

A

“Loss of control
Bodily injury and mutilation
Failure to live up to expectations of important others
Death”

266
Q

Adolscent primary fears

A

“Loss of control
Altered body image
Separation from peer group”

267
Q

Preschoolers Developmental View Of Death

A

Death as temporary, a departure, a kind of sleep
- “Recognizes death in terms of immobility often viewed as reversible, temporary, or foreign
Begins to question and develop a mature concept
“

268
Q

School Age Developmental View Of Death

A

Death is irreversible but not necessarily inevitable and may fear mutilation
- Recognizes all the components of irreversibility, universality, nonfunctionality, and causality

269
Q

Adolescent Developmental View Of Death

A

Death is inevitable, irreversible
- “Speculates on the implication and ramifications of death
Understands effect of death on other people and society as a whole
Future-oriented, difficult to understand reality of death as a present possibility”

270
Q

Infant spiritual interventions of death

A

“Provide consistent caregivers
Minimize separation from significant others
Decrease parental anxiety
Maintain crib/nursery as ““safe place”” no procedures
encourage parental presence
Facilitate spiritual support system for family”

271
Q

Palliative Care Principles

A

Guide realistic goal setting that includes the physical, emotional, social, and spiritual distress

Multidisciplinary approach
Child life, pastoral, social service

Child and family are the unit of care

272
Q

Nursing Care in end of life

A

Whatever they want and encourage parental involvement
Assess level of pain/administer pain med
minimal
Provide soothing surroundings, avoid excessive light
Music desired, aroma therapy
Limit care to essentials
Last hour or day
Ensure pleasant smell, touch, temperature
Unusual Smell to death so aromatherapy
Encourage family to continuous touching the child and assist
Encourage child to talk about feelings (questions on death) - dreams talk through them
Explain all procedures/therapies
Structure hospital/home environment to allow for max self control/independence
- spiritual and privacy
Stay with the family
Family becomes close to nurse (TMIs)
Accept family’s grief reactions
Anger, denial, crying, depressed, betrayal
Avoid artificial consolation
Do not say outloud
Allow parents to be with the child at the moment of death
Accept if don’t
Remember siblings (developmental)

273
Q

Warn about the surge

A

phenomenon comatose and wake up say goodbye then go back into coma
- get excited family

274
Q

Toddler spiritual interventions of death

A

“Minimize separation from significant others
Keep security objects at hand
Provide simple, brief explanations
explain and maintain consistent limits
Encourage participation in daily care
Provide opportunities for play and play therapy
Reassure the child that disease is not punishment”

275
Q

Early school-age child
spiritual interventions

A

“Don’t underestimate level of comprehension
Provide simple, concrete explanations
Use pictures, models, actual equipment, medical play when providing explanations
When appropriate, initiate discussion of love and caring from Higher Power to relieve anxiety and loneliness
Show behavioral qualities of love, trust, respect, caring and setting of firm limits”

276
Q

school-age child spiritual interventions

A

“Provide choices whenever possible
Stress contact with school, sports, religious peer groups
Use diagrams, pictures and models for explanations
Emphasize the ““normal”” things the child can do
Reassure child he/she has done nothing wrong (Hospitalizat6ions isn’t a punishment)
be alert to anxiety about being punished by deity
Provide appropriate concrete explanations in response to questions regarding spiritual beliefs
Continue spiritual rituals when appropriate
Model behaviors that show forgiveness and acceptance”

277
Q

adolescent spiritual interventions

A

“Allow Adolescent to be an integral part of decision making regarding care
Give information sensitively
Allow as many choices and as much control as possible
Be honest about treatment and consequences
Stress what the adolescent can do for themselves
Stress the importance of cooperation and compliance
Assist in maintaining contact with peer groups
Provide answers without bias and enable participation in discussion of illness in terms of philosophical or spiritual beliefs
Encourage contact with friends and use of spiritual rituals if appropriate
Observe and document verbalizations of adolescent’s values and beliefs”

278
Q

Which statement best describes iron-deficiency anemia in infants?
A. Clinical manifestations result from a decreased intake of milk and the preterm addition of solid foods.
B. It is easily diagnosed because of an infant’s emaciated appearance.
C. Preterm infants are particularly at risk.
D. It is caused by depression of the hematopoietic system.

A

C. Preterm infants are particularly at risk.Iron is transferred from the mother to the fetus during the last trimester of pregnancy. Maternally derived iron stores are usually adequate for the first 5-6 months in a full-term infant, but only 2-3 months in preterm infants. In iron-deficiency anemia, the child’s clinical appearance is a result of the anemia, not the underlying cause. Usually the hematopoietic system is not depressed in iron-deficiency anemia. The bone marrow produces red cells that are smaller and contain less hemoglobin than normal red cells. Children who are iron deficient from drinking excessive quantities of milk are usually pale and overweight. They are receiving sufficient calories, but are deficient in essential nutrients. The clinical manifestations result from decreased intake of iron-fortified solid foods and an excessive intake of milk.

279
Q

Which clinical manifestation would the nurse expect when a child with sickle cell anemia experiences an acute vasoocclusive crisis?
A. Cardiomegaly
B. Painful swelling of hands and feet
C. Hepatomegaly
D. Circulatory collapse

A

B. Painful swelling of hands and feetA vasoocclusive crisis is characterized by severe pain in the area of involvement. If in the extremities, painful swelling of the hands and feet is seen; if in the abdomen, severe pain resembles that of acute surgical abdomen; and if in the head, stroke and visual disturbances occur. Circulatory collapse results from sequestration crises. Cardiomegaly, systolic murmurs, hepatomegaly, and intrahepatic cholestasis result from chronic vasoocclusive phenomena.

280
Q

What is the purpose of chelation therapy in the treatment of beta-thalasemia?

A. Manages nausea and vomiting

B. Eliminates excess iron

C. Treats the disease

D. Decreases risk of hypoxia

A

B. Eliminates excess ironA complication of the frequent blood transfusions in thalassemia is iron overload. Chelation therapy with deferoxamine (an iron-chelating agent) is given with oral supplements of vitamin C to increase iron excretion. Chelation therapy treats the side effect of the disease management. Decreasing the risk of hypoxia and managing nausea and vomiting are not the purposes of chelation therapy.

281
Q

Parents of a hemophiliac child ask the nurse, “Can you describe hemophilia to us?” Which response by the nurse is descriptive of most cases of hemophilia?

Y-linked recessive inherited disorder in which the red blood cells become moon-shaped

B. X-linked recessive inherited disorder in which a blood-clotting factor is deficient

C. Autosomal dominant disorder causing deficiency in a factor involved in the blood-clotting reaction

D. X-linked recessive inherited disorder causing deficiency of platelets and prolonged bleeding

A

B. X-linked recessive inherited disorder in which a blood-clotting factor is deficient. The inheritance pattern in 80% of all of the cases of hemophilia is X-linked recessive. The two most common forms of the disorder are factor VIII deficiency, hemophilia A or classic hemophilia; and factor IX deficiency, hemophilia B or Christmas disease. The inheritance pattern is X-linked recessive. The disorder involves coagulation factors, not platelets, and does not involve red cells or the Y chromosomes.

282
Q

Which describes the pathology of immune thrombocytopenia?

A. Diffuse fibrin deposition in the microvasculature

B. Deficiency in the production rate of globin chains

C. Bone marrow failure in which all elements are suppressed

D. An excessive destruction of platelets

A

D. An excessive destruction of plateletsITP involves the evolution of antibodies against multiple platelet antigens and cytotoxic T cells that cause platelet destruction in blood and spleen and/or inhibition of platelet production in the bone marrow. Bone marrow failure is associated with aplastic anemia. Deficient production of globin chains is associated with Thalassemia. Diffuse fibrin deposition in the microvascular is associated with disseminated intravascular coagulation.

283
Q

Which is caused by a virus that primarily infects a specific subset of T lymphocytes, the CD4+ T cells?

A. Wiskott-Aldrich syndrome

B. Acquired immunodeficiency syndrome (AIDS)

C. Idiopathic thrombocytopenic purpura

D. Severe combined immunodeficiency disease

A

B. Acquired immunodeficiency syndrome (AIDS)AIDS is caused by the human immunodeficiency virus (HIV), which primarily attacks the CD4+T cells. Wiskott-Aldrich syndrome, idiopathic thrombocytopenic purpura, and severe combined immunodeficiency disease are not viral illnesses.

284
Q

A toddler with leukemia is on intravenous chemotherapy treatments. The toddler’s lab results are WBC: 1000; neutrophils: 7%; nonsegmented neutrophils (bands): 7%. Which is this child’s absolute neutrophil count (ANC)?

(Record your answer in a whole number.)

A

The correct answer is: 140
To calculate an ANC for a WBC = 1000; neutrophils = 7%; and nonsegmented neutrophils (bands) = 7%, the steps are

Step 1: 7% + 7% = 14%

Step 2: 0.14 × 1000 = 140

285
Q

Which immunization would not be given to a child receiving chemotherapy for cancer?

A. Tetanus vaccine

B. Measles, rubella, mumps

C. Pertussis

D. Inactivated poliovirus vaccine

A

B. Measles, rubella, mumpsThe vaccine used for measles, mumps, and rubella is a live virus and can result in an overwhelming infection. Tetanus vaccine, inactivated poliovirus vaccine, and diphtheria, pertussis, tetanus (DPT) are not live virus vaccines.

286
Q

The nurse is admitting a child with a Wilms tumor. Which is the initial assessment finding associated with this tumor?

A. Abdominal distension

B. Weight gain

C. Increased urinary output

D. Hypotension

A

A. Abdominal distension The initial assessment finding with a Wilms (kidney) tumor is abdominal swelling. Weight loss, not weight gain, may be a finding. Hypertension occasionally occurs with a Wilms tumor. Urinary output is not increased, but hematuria may be noted.

287
Q

What does chelation do?

A

binds with iron to be excreted in the urine (rusty)
Used in Iron overload

288
Q

Which chelator is extremely painful? A traumatic care for it?

A

Calcium disodium (EDTA) IM
Very painful
Atraumatic care with rotation of site, EMLA,
Multiple treatments if necessary, after blood level tests

Module 5 (Pediatrics) (27 decks)

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