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Peds Exam 5 > Hematologic > Flashcards

Hematologic Flashcards

1
Q

Erythrocytes or red blood cells (RBCs)

A

Responsible for transporting nutrients and oxygen to the body tissues and waste products from the tissues

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2
Q

Thrombocytes or platelets

A

Responsible for clotting

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3
Q

Leukocytes or white blood cells (WBCs)

A
  • Responsible for fighting infection
  • divided into Granulocytes (neutrophils, eosinophils, and basophils) and agranulocytes (lymphocytes and monocytes)
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4
Q

Assessment of Hematologic Function

A
  • Complete blood count (CBC)
  • Historical data
  • Physical assessment findings
  • Child’s energy and activity level
  • Growth patterns
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5
Q

CBC alterations

A

↓ hemoglobin – evaluate oxygen carrying capacity and effects of hypoxia on tissues

↓ platelets – evaluate for bleeding

↑WBC – evaluate for infection

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6
Q

Historical data

A
  • Ask about birth history – weight, gestational diabetes, vit k given at birth
  • Sleep/wake patterns and bowel patterns – may be affected by alterations in circulating blood volume or changes in oxygenation
  • Family history of hemophilia, sickle cell, thalassemia
  • Diet / lead exposure
  • Ask about: fatigue/malaise, pallor of the skin, unusual bruising, excessive bleeding or difficulty stopping bleeding, pain
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7
Q

Anemia r/t Nutritional deficiency

A

Iron deficiency, folic acid deficiency, pernicious anemia

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8
Q

Anemia r/t Toxin exposure

A

Lead poisoning

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9
Q

Anemia r/t Adverse reaction to medication

A

Aplastic anemia

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10
Q

Hemolytic anemia

A

(Caused by alteration/destruction of RBC) Sickle cell anemia, thalassemia

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11
Q

Anemia

A
  • The most common hematologic disorder of childhood
  • Decrease in the number of red blood cells (RBCs) and/or a hemoglobin (Hgb) concentration that is below normal
  • Diminished oxygen-carrying capacity of blood, so ↓O2
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12
Q

Consequences of Anemia

A
  • Decrease in the oxygen-carrying capacity of the blood leads to a decreased amount of oxygen available to tissues
  • When anemia develops slowly, the child adapts (If quick can’t adapt)
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13
Q

Effects of Anemia on the Circulatory System

A
  • Hemodilution
  • Decreased peripheral resistance
  • Increased cardiac circulation and turbulence (May have murmur, May lead to cardiac failure)
  • Cyanosis
  • Growth retardation
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14
Q

Anemic Kids

A

These kids are pale, tired, tachycardic, dizzy, diaphoretic Infants have poor suck and feeding - Failure to thrive

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15
Q

Diagnostic Evaluation of Anemia

A

• History and physical examination findings • CBC • Other tests can be done to determine the particular type of anemia

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16
Q

CBC for anemia**

A
  • Decreased RBCs
  • Decreased hemoglobin and hematocrit (Hct)
  • Typically, the hemoglobin is less than 10 or 11 g/dL
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17
Q

Therapeutic Management of Anemia

A
  • Treat the underlying cause
  • Supportive care
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18
Q

Treat the underlying cause of anemia

A
  • Transfusion after hemorrhage if needed
  • Nutritional intervention for deficiency anemias
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19
Q

Supportive care of anemia

A
  • Intravenous (IV) fluids to replace intravascular volume
  • Oxygen
  • Bed rest
  • Diet
  • Family education
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20
Q

What type of milk do Fe deficiency anemic kids need?

A
  • These kids need iron fortified formulas, oral iron supplements, cows milk continues substances that bind to iron and interfere with absorption so they should not be administered together.
  • Milk babies are typically over wt and are anemic
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21
Q

Since liquid Fe supplements can stain teeth need to…

A

give with straw or syringe toward back of mouth, brush teeth after administration, can be toxic if overdose

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22
Q

Want kids to take Flintstones but… **

A

Have kids take Flintstones – but put up with lock bc if eat too many than iron overdose

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23
Q

Iron Deficiency Anemia

A
  • Caused by an inadequate supply of dietary iron (cannot produce Hgb)
  • Generally preventable
  • Predictable at developmental periods
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24
Q

Predictable at developmental periods (Iron Deficiency Anemia)

A
  • In premature infants, due to low fetal supply
  • At 12 to 36 months, due to ingestion of large amounts of cow’s milk and diet
  • In adolescents, due to rapid growth and poor eating habits
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25
Q

prophylaxis of Iron Deficiency Iron Supplements

A

1 to 2 mg/kg/day, up to a maximum of 15 mg elemental iron per day

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26
Q

Mild to moderate iron deficiency Supplements

A

3 mg/kg/day of elemental iron in one or two divided doses

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27
Q

Severe iron-deficiency anemia Supplements

A

4 to 6 mg/kg/day of elemental iron in three divided doses

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28
Q

Foods High in iron

A

red meat, tuna, salmon eggs, tofu, enriched grains, dried beans and peas, dried fruits, leafy green vegetables, and iron fortified breakfast cereals

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29
Q

Lower levels of lead poisoning

A
  • Behavioral problems
  • Learning difficulties
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30
Q

Higher levels of lead poisoning

A
  • Encephalopathy
  • Seizures
  • Brain damage
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31
Q

Lead poisoning treated with

A

chelating agents- removes heavy metals. Oral or IV

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32
Q

Aplastic Anemia (AA)

A
  • Failure of bone marrow to produce cells
  • All formed elements of the blood are simultaneously depressed (pancytopenia) – decreased numbers of all blood cells
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33
Q

In hypoplastic anemia, ***

A

there is profound depression of RBCs but normal levels of white blood cells (WBCs) and platelets

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34
Q

Aplastic anemia etiology

A
  • is idiopathic
  • Genetic-congenital (autosomal recessive trait)
  • Acquired severe or moderate
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35
Q

Diagnostic evaluation of aplastic anemia

A
  • History and physical examination results
  • Blood and bone marrow examination
36
Q

Nursing assessment of aplastic anemia

A
  • Determine history of exposure to myelosuppressive medications or radiation therapy.
  • Obtain a detailed family, environmental, and infectious disease history.
  • Note history of epistaxis, gingival oozing, or increased bleeding with menstruation.
  • Anemia may lead to headache and fatigue.
  • On physical examination, note ecchymoses, petechiae or purpura, oral ulcerations, tachycardia, or tachypnea.
37
Q

Therapeutic Management of aplastic anemia

A
  • Immunosuppressive therapy
  • Replace bone marrow- transplant
  • Antilymphocyte globulin ALG
  • If problem of RBC is because of where getting from (Bone marrow) so bone marrow transplant to make good RBC
38
Q

Sickle Cell anemia

A
  • A hereditary hemoglobinopathy (condition in which abnormal hemoglobin is present)
  • RBC do not carry the normal adult hemoglobin
39
Q

Ethnicity of sickle cell

A
  • Occurs primarily in African Americans • Occurs in 1 in 375 infants born in the United States • One in 12 has sickle cell trait
  • Occasionally also in persons of Mediterranean descent
  • Also seen in persons of South American, Arabian, and East Indian descent
40
Q

In areas of the world where malaria is common, individuals with sickle cell trait tend

A

tend to have a survival advantage over those without the trait

41
Q

Sickle cell is what type of disorder**

A

Autosomal recessive disorder

42
Q

One in ____ African Americans is a carrier (i.e., has sickle cell trait)

A

12

43
Q

If both parents have sickle cell trait then***

A

each child of theirs will have a 1 in 4 likelihood of having the disease

44
Q

Pathophysiology of Sickle Cell Anemia

A
  • Partial or complete replacement of normal hemoglobin with abnormal hemoglobin S (Hgb S)
  • Hemoglobin in the RBCs takes on an elongated “sickle” shape
  • Sickled cells are rigid and obstruct capillary blood flow – “clog up”
  • Microscopic obstructions lead to engorgement and tissue ischemia
  • Hypoxia occurs and causes sickling, leading to pain - Because can’t carry hemoglobin in sickled cell
  • Large tissue infarctions occur
  • Damaged tissues in organs; impaired function
45
Q

If Splenic sequestration with sickle cell

A
  • May require splenectomy at an early age
  • Results in immunity
46
Q

Organs Affected by Sickle Cell Anemia

A
47
Q

Prognosis for Sickle Cell Anemia

A
  • No cure (except possibly bone marrow transplants)
  • Supportive care; prevention of sickling episodes
  • Frequent bacterial infections may occur due to immunocompromise
  • Bacterial infection is the leading cause of death in young children with sickle cell disease
  • Strokes in 5% to 10% of children with disease
48
Q

Precipitating factors of sickle cell crisis

A
  • Anything that increases the body’s need for oxygen or alters the transport of oxygen
  • Trauma
  • Fever, infection
  • Physical and emotional stress
  • Increased blood viscosity due to dehydration
  • Hypoxia (Results from high altitude, poorly pressurized airplanes, hypoventilation, vasoconstriction due to hypothermia)
49
Q

Vaso-occlusive (VOC) thrombotic ***

A
  • Most common type of crisis and is very painful
  • Stasis of blood with clumping of cells in the microcirculation leads to ischemia and then infarction
  • Signs are fever, pain, and tissue engorgement
50
Q

Splenic sequestration

A
  • Life-threatening type; death can occur within hours
  • Blood pools in the spleen
  • Signs are profound anemia, hypovolemia, and shock
51
Q

Aplastic crises

A
  • Diminished production and increased destruction of RBCs
  • Triggered by viral infection or depletion of folic acid
  • Signs include profound anemia and pallor
52
Q

Diagnosis of Sickle Cell Anemia

A
  • Cord blood in newborns
  • Newborn screening - Genetic testing to identify carriers and children who have the disease
  • Sickle turbidity test - Quick screening in children over 6 months of age
  • Hemoglobin electrophoresis
53
Q

sickle cell crisis pic

A
54
Q

Most important tx for sickle cell**

A
  • Remember HOP – hydration, oxygenation, and pain relief
55
Q

Hemoglobin with sickle cell:

A

baseline is usually 7 to 10 mg/dL; will be significantly lower with splenic sequestration, acute chest syndrome, or aplastic crisis

56
Q

Reticulocyte count with sickle cell:

A

greatly elevated

57
Q

Peripheral blood smear with sickle cell:

A

presence of sickle-shaped cells and target cells

58
Q

Platelet count with sickle cell:

A

increased

59
Q

Erythrocyte sedimentation rate with sickle cell:

A

elevated because cells clumped causes inflammation

60
Q

liver function tests with sickle cell

A

Abnormal liver function tests with elevated bilirubin

61
Q

Therapeutic Management of sickle cell

A
  • Prevent sickling
  • Treat emergencies of crisis
62
Q

Medical Management of sickle cell

A
  • Rest to minimize energy expenditure and to improve O2 use (O2 to prevent additional cell sickling)
  • Hydration
  • Electrolyte replacement- hypoxia = met. Acidosis
  • Pain management- No Demerol, now using Dilaudid, Ketamine and Narcan – typically use morphine but now giving those drugs (Demoerol increases risk of seizures in sickle cell kids)
  • Blood transfusion- tx anemia and reduce viscosity of sickled blood
  • Antibiotics- for infection
63
Q

Thalassemia (Cooley Anemia)

A
  • Inherited blood disorders of hemoglobin synthesis
  • Classified by the hemoglobin chain affected and by the amount of effect
  • Autosomal recessive disorder with varying expressivity
    • Both parents must be carriers to have offspring with the disease
    • Occurred in those who live around Mediterranean sea
    • Occurs all over as a result of migration
64
Q

Thalassemia is what type of disorder**

A

Autosomal recessive

65
Q

Thalassemia occurs where**

A

Occurred in those who live around Mediterranean sea

66
Q

b-Thalassemia four types

A
  • Thalassemia minor: Asymptomatic silent carrier
  • Thalassemia trait: Mild microcytic anemia
  • Thalassemia intermediate: Moderate to severe anemia plus splenomegaly
  • Thalassemia major (Cooley anemia): Severe anemia requiring transfusions for survival
67
Q

Pathophysiology of Thalassemia

A
  • Anemia results from defective synthesis of hemoglobin, structurally impaired RBCs, and a shortened life of RBCs
  • Chronic hypoxia - Headache, irritability, precordial and bone pain, exercise intolerance, anorexia, epistaxis
  • Detected in infancy or toddlerhood - Pallor, failure to thrive (FTT), hepatosplenomegaly,
68
Q

Medical Management of Thalassemia **

A
  • Blood transfusion to maintain normal hemoglobin levels (DIC if don’t)
  • Side effect is hemosiderosis (excessive supply of iron) - Treat with iron-chelating drugs such as deferoxamine (Desferal) - Binds excess iron for excretion by the kidney
69
Q

Prognosis for Thalassemia

A
  • Delayed growth
  • Delayed or absent secondary sex characteristics
  • Expect to live well into adulthood with proper clinical management
  • Bone marrow transplant is a potential cure
70
Q

Hemophilia

A
  • A group of hereditary bleeding disorders that result from deficiencies of specific clotting factors
  • Typically, an X-linked recessive pattern (so mothers are carriers and give to their sons)
71
Q

Hemophilia A**

A
  • Classic hemophilia (deficiency of factor VIII)
    • Factor VIII – essential for activation of factor X – required for the conversion of prothrombin into thrombin
  • Accounts for 80% of cases of hemophilia
72
Q

Hemophilia B

A

Christmas disease (deficiency of factor IX)

73
Q

von Willebrand disease (vWD)

A
  • Deficiency, abnormality, or absence of vWF and factor VIII
  • Affects both males and females
74
Q

Manifestations of Hemophilia

A
  • Bleeding tendencies range from mild to severe
  • Symptoms may not occur until 6 months of age
  • Hemarthrosis
  • Epistasis
  • Bleeding in the gastrointestinal tract
  • Bleeding after procedures
75
Q

If bleeding with hemophilia A then inject

A

factor 8

76
Q

Hemarthrosis

A
  • Bleeding into joint spaces of the knee, ankle, or elbow leads to impaired mobility and, eventually, bony changes and disability
  • Symptoms include warmth, pain, bruising, and decreased movement
  • These kiddos must be careful when playing sports, hitting the knees can cause a joint bleed and immense pain, must be careful brushing teeth. Need soft bristle brush or water pick
77
Q

Bleeding after procedures for hemophilia A

A
  • Minor trauma, tooth extraction, minor surgeries
  • Large subcutaneous and intramuscular hemorrhages may occur
  • Bleeding into the neck, chest, or mouth may compromise the airway
  • Bleeding in the spinal cord may cause paralysis
78
Q

Medical Management of Hemophilia

A
  • Replacement of missing clotting factors
  • Desmopressin (DDAVP)
  • Transfusions - Prompt intervention to reduce complications
  • Medications
  • Exercise and physical therapy
79
Q

Desmopressin (DDAVP)

A
  • IV
  • Increases factor VIII activity by two to four times
  • Used for mild hemophilia
80
Q

Interventions for Hemophilia

A
  • Close supervision and safe environment - Let them play but watch
  • Dental procedures in a controlled situation – done at hospital
  • Shave only with an electric razor
  • For superficial bleeding, apply pressure for at least 15 minutes and ice to promote vasoconstriction
  • If significant bleeding occurs, transfusion for factor replacement
  • Families are taught RICE- rest ice compression elevation
81
Q

hemophilia pic

A
82
Q

Idiopathic Thrombocytopenic Purpura (ITP)

A

An acquired hemorrhagic disorder characterized by:

  • Thrombocytopenia (excessive destruction of platelets)
  • Purpura blood collection under skin (are purplish)
  • discoloration caused by petechiae beneath the skin, with no other signs of bleeding (pinpoint hemorrhages, do not blanche)
  • NORMAL bone marrow
83
Q

Two forms of Idiopathic Thrombocytopenic Purpura (ITP)

A
  • Acute, self-limiting (usually following a viral illness)
  • Chronic (lasting longer than 12 months)
84
Q

Platelet count for Idiopathic Thrombocytopenic Purpura (ITP)

A

less than 20,200/mm

85
Q

Management of acute Idiopathic Thrombocytopenic Purpura (ITP) **

A

prednisone, IVIG, anti-D antibody

86
Q

Diagnositic of Idiopathic Thrombocytopenic Purpura (ITP)

A
  • Platelet count is less than 20,200/mm
  • Rule out other diseases and conditions
87
Q

Management of Idiopathic Thrombocytopenic Purpura (ITP)

A
  • Supportive- because self limiting
  • Acute-prednisone, IVIG, anti-D antibody
  • Chronic- splenectomy

Peds Exam 5 (5 decks)

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