Hematologic Flashcards
(87 cards)
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
2
Q
Thrombocytes or platelets
A
Responsible for clotting
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)
4
Q
Assessment of Hematologic Function
A
- Complete blood count (CBC)
- Historical data
- Physical assessment findings
- Child’s energy and activity level
- Growth patterns
5
Q
CBC alterations
A
↓ hemoglobin – evaluate oxygen carrying capacity and effects of hypoxia on tissues
↓ platelets – evaluate for bleeding
↑WBC – evaluate for infection
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
7
Q
Anemia r/t Nutritional deficiency
A
Iron deficiency, folic acid deficiency, pernicious anemia
8
Q
Anemia r/t Toxin exposure
A
Lead poisoning
9
Q
Anemia r/t Adverse reaction to medication
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Aplastic anemia
10
Q
Hemolytic anemia
A
(Caused by alteration/destruction of RBC) Sickle cell anemia, thalassemia
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
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)
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
14
Q
Anemic Kids
A
These kids are pale, tired, tachycardic, dizzy, diaphoretic Infants have poor suck and feeding - Failure to thrive
15
Q
Diagnostic Evaluation of Anemia
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• History and physical examination findings • CBC • Other tests can be done to determine the particular type of anemia
16
Q
CBC for anemia**
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- Decreased RBCs
- Decreased hemoglobin and hematocrit (Hct)
- Typically, the hemoglobin is less than 10 or 11 g/dL
17
Q
Therapeutic Management of Anemia
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- Treat the underlying cause
- Supportive care
18
Q
Treat the underlying cause of anemia
A
- Transfusion after hemorrhage if needed
- Nutritional intervention for deficiency anemias
19
Q
Supportive care of anemia
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- Intravenous (IV) fluids to replace intravascular volume
- Oxygen
- Bed rest
- Diet
- Family education
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
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
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
23
Q
Iron Deficiency Anemia
A
- Caused by an inadequate supply of dietary iron (cannot produce Hgb)
- Generally preventable
- Predictable at developmental periods
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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prophylaxis of Iron Deficiency Iron Supplements
1 to 2 mg/kg/day, up to a maximum of 15 mg elemental iron per day
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Mild to moderate iron deficiency Supplements
3 mg/kg/day of elemental iron in one or two divided doses
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Severe iron-deficiency anemia Supplements
4 to 6 mg/kg/day of elemental iron in three divided doses
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Foods High in iron
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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Lower levels of lead poisoning
* Behavioral problems
* Learning difficulties
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Higher levels of lead poisoning
* Encephalopathy
* Seizures
* Brain damage
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Lead poisoning treated with
chelating agents- removes heavy metals. Oral or IV
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Aplastic Anemia (AA)
* 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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In hypoplastic anemia, \*\*\*
there is profound depression of RBCs but normal levels of white blood cells (WBCs) and platelets
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Aplastic anemia etiology
* is idiopathic
* Genetic-congenital (autosomal recessive trait)
* Acquired severe or moderate
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Diagnostic evaluation of aplastic anemia
* History and physical examination results
* Blood and bone marrow examination
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Nursing assessment of aplastic anemia
* 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.
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Therapeutic Management of aplastic anemia
* 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
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Sickle Cell anemia
* A hereditary hemoglobinopathy (condition in which abnormal hemoglobin is present)
* RBC do not carry the normal adult hemoglobin
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Ethnicity of sickle cell
* 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
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In areas of the world where malaria is common, individuals with sickle cell trait tend
tend to have a survival advantage over those without the trait
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Sickle cell is what type of disorder\*\*
Autosomal recessive disorder
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One in ____ African Americans is a carrier (i.e., has sickle cell trait)
12
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If both parents have sickle cell trait then\*\*\*
each child of theirs will have a 1 in 4 likelihood of having the disease
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Pathophysiology of Sickle Cell Anemia
* 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
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If Splenic sequestration with sickle cell
* May require splenectomy at an early age
* Results in immunity
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Organs Affected by Sickle Cell Anemia
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Prognosis for Sickle Cell Anemia
* 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
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Precipitating factors of sickle cell crisis
* 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)
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Vaso-occlusive (VOC) thrombotic \*\*\*
* 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
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Splenic sequestration
* Life-threatening type; death can occur within hours
* Blood pools in the spleen
* Signs are profound anemia, hypovolemia, and shock
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Aplastic crises
* Diminished production and increased destruction of RBCs
* Triggered by viral infection or depletion of folic acid
* Signs include profound anemia and pallor
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Diagnosis of Sickle Cell Anemia
* 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
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sickle cell crisis pic
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Most important tx for sickle cell\*\*
* Remember HOP – hydration, oxygenation, and pain relief
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Hemoglobin with sickle cell:
baseline is usually 7 to 10 mg/dL; will be significantly lower with splenic sequestration, acute chest syndrome, or aplastic crisis
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Reticulocyte count with sickle cell:
greatly elevated
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Peripheral blood smear with sickle cell:
presence of sickle-shaped cells and target cells
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Platelet count with sickle cell:
increased
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Erythrocyte sedimentation rate with sickle cell:
elevated because cells clumped causes inflammation
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liver function tests with sickle cell
Abnormal liver function tests with elevated bilirubin
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Therapeutic Management of sickle cell
* Prevent sickling
* Treat emergencies of crisis
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Medical Management of sickle cell
* 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
Thalassemia (Cooley Anemia)
* 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
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Thalassemia is what type of disorder\*\*
Autosomal recessive
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Thalassemia occurs where\*\*
Occurred in those who live around Mediterranean sea
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b-Thalassemia four types
* 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
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Pathophysiology of Thalassemia
* 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,
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Medical Management of Thalassemia \*\*
* **_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
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Prognosis for Thalassemia
* 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
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Hemophilia
* 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)
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Hemophilia 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
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Hemophilia B
Christmas disease (deficiency of factor IX)
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von Willebrand disease (vWD)
* Deficiency, abnormality, or absence of vWF and factor VIII
* Affects both males and females
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Manifestations of Hemophilia
* 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
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If bleeding with hemophilia A then inject
factor 8
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Hemarthrosis
* 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
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Bleeding after procedures for hemophilia 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
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Medical Management of Hemophilia
* Replacement of missing clotting factors
* Desmopressin (DDAVP)
* Transfusions - Prompt intervention to reduce complications
* Medications
* Exercise and physical therapy
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Desmopressin (DDAVP)
* IV
* Increases factor VIII activity by two to four times
* Used for mild hemophilia
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Interventions for Hemophilia
* 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
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hemophilia pic
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Idiopathic Thrombocytopenic Purpura (ITP)
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
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Two forms of Idiopathic Thrombocytopenic Purpura (ITP)
* Acute, self-limiting (usually following a viral illness)
* Chronic (lasting longer than 12 months)
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Platelet count for Idiopathic Thrombocytopenic Purpura (ITP)
less than 20,200/mm
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Management of acute Idiopathic Thrombocytopenic Purpura (ITP) \*\*
prednisone, IVIG, anti-D antibody
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Diagnositic of Idiopathic Thrombocytopenic Purpura (ITP)
* Platelet count is less than 20,200/mm
* Rule out other diseases and conditions
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Management of Idiopathic Thrombocytopenic Purpura (ITP)
* Supportive- because self limiting
* Acute-prednisone, IVIG, anti-D antibody
* Chronic- splenectomy
