Hem/Onc Flashcards
Types of hemoglobin
Hgb F- until 6 months
Hgb A- adult
Hgb A2- subtype of hgb a
How does hematopoiesis differ from infants and adults
Infants: all bones involved
Adulthood: only flat bones
3 types of cells found in blood
Erythrocyte (RBCs)- transport nutrients/oxygen to the tissue and carry waste away from tissue
Thrombocytes (platelets)- clotting
Leukocytes (WBCs)- fight infection
Iron sources
Newborn: maternal stores
Infants: milk or iron fortified formula
Adolescence: physiologic anemia
Who is at increased risk of anemia
Pre-term infants
2-6 months of age=physiologic anemia
(increased growth + increased blood volume + decrease in maternal iron stores = anemia)
Adolescence: increased time of growth
Role of the spleen
Production and destruction of RBCs
Stores platelets
Clinical manifestations of iron-deficiency anemia
Fatigue, lethargy
Pallor of oral mucosa
Nail spooning
Tachycardia
Splenomegaly
Decrease hgb, hct, serum Fe, ferritin levels
Nursing management of iron-deficiency anemia
Dietary intervention
Promote safety
Iron supplementation
Education
Sickle Cell Anemia
Autosomal recessive dz where hemoglobin SS partially or completely replaces normal hemoglobin
Found predominantly in AA
Vaso-occlusive Crisis
Acute pain crisis
Occurs when stasis of blood causes tissue hypoxia leading to ischemia and possible infarction
Severity dependent on the site of the occlusion
Symptoms of VOC include: pain, fever, tissue engorgement, joint swelling, and tachycardia
Pain in joints, hands, feet, abdomen
Enuresis common
Sickle cell dz progression
Decreased oxygen –> Hemoglobin S sickles –>
cells become rigid –> obstruct capillary blood flow –>
congestion of blood –> tissue hypoxia –>
additional sickling –> extensive infarctions –>
vaso-occlusion
What is splenic sequestration in sickle cell crises
When blood pools in the spleen
Profound anemia, hypovolemia, and shock, splenomegaly
What is acute chest syndrome in sickle cell crises
Clumping of the sickle cells in the lungs
Leads to hypoxia
Hypoxia = further sickling
What is aplastic crisis in sickle cell crisis
Increased destruction of fragile RBCs
Leads to temporary cessation of RBC production
Treatment of sickle cell anemia
Bone marrow transplant (only cure- not done very often)
Blood transfusion
Hydroxyurea
New biologics
Nursing management of sickle cell anemia
Full physical assessment
Lab tests include: hgb/hct, platelet count, ESR
Education
Pain management:
-analgesics (NSAIDS, acetaminophen, narcotics)
-distraction, relaxation
-oxygen, if hypoxia present
-fluids (po, IV)
-heat packs, ice packs
What is B-thalassemia Major
Disorder of hemoglobin synthesis
Autosomal recessive
Most common in mediterranean, African, Asian, and Middle Eastern descent
Increased bone marrow with thinning of bony cortex
Manifestations of B-thalassemia
Failure to thrive
Pallor and/or jaundice
Severe anemia
Hemosiderosis
Hepatosplenomegaly
Bone deformities- frontal and maxillary bone bossing
B-thalassemia treatment
Chronic transfusion tx
Chelation therapy
Splenectomy
Education
What is disseminated intravascular coagulopathy (DIC)
Acquired process involving abnormal activation of body’s thrombin mechanism and fibrinolytic system
Secondary illness
Severe and life-threatening
DIC dz process
increased uncontrolled bleeding –>
anemia from excess bleeding –>
organ damage –>
tissue hypoxia and necrosis
Precipitating factors of DIC
Cancer
Hypoxia
Burns
Traums
Sepsis
Shock
Liver dz
NEC
Assessment for DIC
Excessive bruising
Petechiae
Hematuria
Oozing injection sites
Mild GI bleeding
DIC management
Constant assessment especially circulation and neurologic status
Administer clotting factors, platelets
Administer anti-coagulation therapy
Apply pressure and elevate if possible areas of acute bleeding
What is idiopathic thrombocytopenia purpura (ITP)
Immune response- produces anti-platelet antibodies
Typically secondary to viral infection
Neonatal d/t maternal platelet issues, placental insufficiency & fetal hypoxia
Symptoms: petechiae, ecchymoses, purpura
Platelets less than 50,000
Typically acute but can become chronic
ITP management
Observe and document
Reassurance
Education: avoid trauma; avoid aspirin, NSAIDs, and antihistamines
Severe cases: corticosteroids IVIG
Chronic cases: splenectomy
What is hemophillia
Group of chronic hereditary bleeding disorders
Deficiency of a specific blood clotting factors
Symptoms of hemophillia
Easy bruising
Prolonged bleeding from wounds
Epistaxis
Hemarthrosis
3 main types of hemophillia
A (classic- 80%)- Factor VIII
B (Christmas dz)- Factor IX
von Willebrand dz- factor vWF
Complications of hemophilia
Intracranial bleeding
GI hemorrhage
Shock
Death
Hemophilia management
Prevent bleeding
NO contact sports
Avoid aspirin & NSAID’s
Education
Factor replacement: VIII or IX concentrate
Desmopressin
Support
What is a neuroblastoma
Abnormal proliferation of neuroblast in the sympathetic nervous system
Most common outside of cranium
Solid tumor
Usual onset ~22 months of age
Unknown cause
Typically a late diagnosis
Prognosis based on staging of tumor, location of tumor and location of metastasis
Neuroblastoma symptoms
Abdominal fullness
Fatigue and fever
Weight loss
Bowel and bladder dysfunction
Neurological symptoms
Dyspnea
Limp
Malaise
Neuroblastoma management
Biopsy & surgical resection
Chemotherapy
Emotional support family and child
Radiation
Palliation
What is leukemia
Cancer of blood-forming tissue
Issue is with the immature and/or abnormal WBCs
Most common malignancy of childhood
ALL (acute lymphoblastic) & AML (acute myelogenous)
Majority of cases are now curable
Leukemia dz process
Bone marrow infiltration of immature WBCs –>
Crowds out stem cells –>
Anemia, thrombocytopenia, immature ineffective WBCs/neutropenia
What is ALL
Unrestrictive proliferation of immature lymphocytes (WBCs)
Classification is based on type of WBC that becomes neoplastic and immaturity of neoplastic cell
Cure rate = greater than 70%
Peak age of 4 years
Exact cause unknown
What is AML
Arrest of bone marrow cells resulting in the proliferation of immature granulocytes (WBCs)
Classification: french-american-british classification
Cure rate = about 50%
Peak age is adolescence
Exact cause is unknown
ALL symptoms
Fatigue
Pallor
Petechiae
Bleeding (bruising)
Fever
Lymphadenopathy
Hepatosplenomegaly
Weight loss
Bone pain/ abd pain
HA
N/V
Papilledema
AML Symptoms
Fatigue
Pallor
Petechiae
Bleeding (bruising)
Fever
Lymphadenopathy
Hepatosplenomegaly
Leukemia management
Corticosteroids
Chemotherapy
Platelet transfusions
Prevent & manage complications
Pain management
Emotional support of family and child
WILMS tumor
Nephroblastoma-intrarenal cancer
Usually unilateral
Peak incidence 2-4 yrs of age
Cause unknown
Survival = about 90%
Prognosis dependent on staging and metastasis
Usually asyptomatic
May have: abd pain, hematuria, hypertension, fever
WILMS tumor management
Nephrectomy
Chemotherapy
Radiation
Emotional support
Osteosarcoma
Most common bone cancer
Arises from osteoblasts
Peak incidence = puberty
Metastasis to lungs
Main symptoms is pain/swelling
Metaphysic of long bone
Osteosarcoma management
Surgical removal of tumor
Chemotherapy
Limb sparing surgery
Emotional support
Rhabdomyosarcoma
Soft tissue tumor
Very fast growing
Peak incidecne = 2-5 yrs of age
Prognosis based on staging
Metastasis is common to lung, bone, and CNS
Survival rate = 39% if metastasized
Symptoms if present based on tumor location
Rhabdomyosarcoma managment
Radiation
Surgery & biopsy
Chemotherapy
Emotional support
