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Hem/Onc Flashcards

1
Q

Types of hemoglobin

A

Hgb F- until 6 months
Hgb A- adult
Hgb A2- subtype of hgb a

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2
Q

How does hematopoiesis differ from infants and adults

A

Infants: all bones involved
Adulthood: only flat bones

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3
Q

3 types of cells found in blood

A

Erythrocyte (RBCs)- transport nutrients/oxygen to the tissue and carry waste away from tissue
Thrombocytes (platelets)- clotting
Leukocytes (WBCs)- fight infection

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4
Q

Iron sources

A

Newborn: maternal stores
Infants: milk or iron fortified formula
Adolescence: physiologic anemia

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5
Q

Who is at increased risk of anemia

A

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

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6
Q

Role of the spleen

A

Production and destruction of RBCs
Stores platelets

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7
Q

Clinical manifestations of iron-deficiency anemia

A

Fatigue, lethargy
Pallor of oral mucosa
Nail spooning
Tachycardia
Splenomegaly
Decrease hgb, hct, serum Fe, ferritin levels

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8
Q

Nursing management of iron-deficiency anemia

A

Dietary intervention
Promote safety
Iron supplementation
Education

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9
Q

Sickle Cell Anemia

A

Autosomal recessive dz where hemoglobin SS partially or completely replaces normal hemoglobin
Found predominantly in AA

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10
Q

Vaso-occlusive Crisis

A

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

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11
Q

Sickle cell dz progression

A

Decreased oxygen –> Hemoglobin S sickles –>
cells become rigid –> obstruct capillary blood flow –>
congestion of blood –> tissue hypoxia –>
additional sickling –> extensive infarctions –>
vaso-occlusion

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12
Q

What is splenic sequestration in sickle cell crises

A

When blood pools in the spleen
Profound anemia, hypovolemia, and shock, splenomegaly

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13
Q

What is acute chest syndrome in sickle cell crises

A

Clumping of the sickle cells in the lungs
Leads to hypoxia
Hypoxia = further sickling

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14
Q

What is aplastic crisis in sickle cell crisis

A

Increased destruction of fragile RBCs
Leads to temporary cessation of RBC production

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15
Q

Treatment of sickle cell anemia

A

Bone marrow transplant (only cure- not done very often)
Blood transfusion
Hydroxyurea
New biologics

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16
Q

Nursing management of sickle cell anemia

A

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

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17
Q

What is B-thalassemia Major

A

Disorder of hemoglobin synthesis
Autosomal recessive
Most common in mediterranean, African, Asian, and Middle Eastern descent
Increased bone marrow with thinning of bony cortex

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18
Q

Manifestations of B-thalassemia

A

Failure to thrive
Pallor and/or jaundice
Severe anemia
Hemosiderosis
Hepatosplenomegaly
Bone deformities- frontal and maxillary bone bossing

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19
Q

B-thalassemia treatment

A

Chronic transfusion tx
Chelation therapy
Splenectomy
Education

20
Q

What is disseminated intravascular coagulopathy (DIC)

A

Acquired process involving abnormal activation of body’s thrombin mechanism and fibrinolytic system
Secondary illness
Severe and life-threatening

21
Q

DIC dz process

A

increased uncontrolled bleeding –>
anemia from excess bleeding –>
organ damage –>
tissue hypoxia and necrosis

22
Q

Precipitating factors of DIC

A

Cancer
Hypoxia
Burns
Traums
Sepsis
Shock
Liver dz
NEC

23
Q

Assessment for DIC

A

Excessive bruising
Petechiae
Hematuria
Oozing injection sites
Mild GI bleeding

24
Q

DIC management

A

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

25
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
26
ITP management
Observe and document Reassurance Education: avoid trauma; avoid aspirin, NSAIDs, and antihistamines Severe cases: corticosteroids IVIG Chronic cases: splenectomy
27
What is hemophillia
Group of chronic hereditary bleeding disorders Deficiency of a specific blood clotting factors
28
Symptoms of hemophillia
Easy bruising Prolonged bleeding from wounds Epistaxis Hemarthrosis
29
3 main types of hemophillia
A (classic- 80%)- Factor VIII B (Christmas dz)- Factor IX von Willebrand dz- factor vWF
30
Complications of hemophilia
Intracranial bleeding GI hemorrhage Shock Death
31
Hemophilia management
Prevent bleeding NO contact sports Avoid aspirin & NSAID's Education Factor replacement: VIII or IX concentrate Desmopressin Support
32
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
33
Neuroblastoma symptoms
Abdominal fullness Fatigue and fever Weight loss Bowel and bladder dysfunction Neurological symptoms Dyspnea Limp Malaise
34
Neuroblastoma management
Biopsy & surgical resection Chemotherapy Emotional support family and child Radiation Palliation
35
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
36
Leukemia dz process
Bone marrow infiltration of immature WBCs --> Crowds out stem cells --> Anemia, thrombocytopenia, immature ineffective WBCs/neutropenia
37
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
38
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
39
ALL symptoms
Fatigue Pallor Petechiae Bleeding (bruising) Fever Lymphadenopathy Hepatosplenomegaly Weight loss Bone pain/ abd pain HA N/V Papilledema
40
AML Symptoms
Fatigue Pallor Petechiae Bleeding (bruising) Fever Lymphadenopathy Hepatosplenomegaly
41
Leukemia management
Corticosteroids Chemotherapy Platelet transfusions Prevent & manage complications Pain management Emotional support of family and child
42
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
43
WILMS tumor management
Nephrectomy Chemotherapy Radiation Emotional support
44
Osteosarcoma
Most common bone cancer Arises from osteoblasts Peak incidence = puberty Metastasis to lungs Main symptoms is pain/swelling Metaphysic of long bone
45
Osteosarcoma management
Surgical removal of tumor Chemotherapy Limb sparing surgery Emotional support
46
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
47
Rhabdomyosarcoma managment
Radiation Surgery & biopsy Chemotherapy Emotional support

Peds (14 decks)

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