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NURS 502 > Exam 3 - Hem/Onc > Flashcards

Exam 3 - Hem/Onc Flashcards

1
Q

What is the definition of hematocrit?

A

Amount of space in the blood that is occupied by RBCs

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2
Q

What is the definition of MCV?

A

Average size of RBCs

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3
Q

What is the definition of MCH?

A

Average amount of hemoglobin in each RBC (color)

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4
Q

What does a reticulocyte count indicate?

A

Number of young RBCs → RBC production

  • Higher reticulocyte count = more production
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5
Q

What does a red cell distribution width (RDW) indicate?

A

Measurement of variation in RBC size

  • Higher RDW = more variation (young vs old RBC)
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6
Q

What is the definition of anemia? Is anemia a diagnosis?

A

Decreased RBC and hemoglobin or hematocrit

  • NOT a diagnosis → s/s of an underlying disorder
  • Identify source and treat it appropriately
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7
Q

Causes of anemia → RBC production disorders

A
  • IDA
  • Anemia of chronic disease (ACD)
  • Vitamin B12 and folate deficiency
  • Aplastic anemia
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8
Q

Causes of anemia → RBC destruction disorders

A
  • Sickle cell anemia
  • Hereditary spherocytosis and elliptocytosis
  • G6PD deficiency
  • Autoimmune hemolytic anemia
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9
Q

Causes of anemia → blood loss (acute or chronic)

A

Trauma, hemorrhage, menorrhagia, hematuria, GI bleeding

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10
Q

Normal RBC levels in men and women

A

Men: >13.6 g/dL

Women: >12 g/dL

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11
Q

Anemia clinical manifestations

A
  • If healthy, few s/s until hemoglobin falls below 7.5 g/dL → Fatigue, malaise, HA, dyspnea, irritability, mild decrease in exercise tolerance
  • Moderate to severe anemia: wide pulse pressure, midsystolic or pansystolic murmur, confusion, lethargy, brittle nails, glossitis, angular cheilitis, spoon shaped nails
    • Pallor of mucous membranes, lips, conjunctivae, nail beds, palmar creases
    • Forceful apical pulse, tachycardia with exertion, systolic murmur
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12
Q

Anemia diagnostics

A
  • CBC w/ diff
  • Reticulocyte count
  • Peripheral blood smear
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13
Q

What diagnostic labs are most sensitive for anemia?

A
  • Serum bilirubin
  • Lactate dehydrogenase
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14
Q

What labs should be collected for suspected microcytic anemia or IDA?

A

Iron profile

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15
Q

What is the definition of microcytic anemia?

A

Small RBCs → less hemoglobin, less volume

  • Due to iron deficiency (without iron RBCs cannot grow or be produced)
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16
Q

Microcytic anemia lab results

A
  • Low MCH, low MCV
  • Low/normal reticulocyte count (low RBC production)
  • Increased RDW (newer cells are smaller than old cells)
  • High TIBC (RBCs really want iron)
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17
Q

What is the definition of macrocytic anemia?

A

Large RBCs → more hemoglobin, more volume

  • Due to folate or vitamin B12 deficiency (without either RBCs cannot divide/undergo mitotic division)
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18
Q

Macrocytic anemia lab results

A
  • High MCH, high MCV
  • Low/normal reticulocyte count (low RBC production)
  • Increased RDW
  • Normal TIBC (RBCs have enough iron)
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19
Q

Possible causes of normocytic anemias

A
  • Congenital → sickle cell disease, G6PD deficiency
  • Hemolysis
  • Acute/large volume blood loss
  • Anemia of chronic disease (ACD)
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20
Q

Types of microcytic anemia

A
  • IDA
  • Thalassemia
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21
Q

Types of macrocytic anemia

A

Megaloblastic (vitamin B12/folate deficiency)

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22
Q

IDA peripheral smear findings

A
  • Hypochromia
  • Microcytosis
  • Mild anisocytosis
  • Poikilocytosis
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23
Q

Are microcytic and macrocytic hypo proliferative or hyper proliferative?

A

Hypo proliferative = lack nutrient for proper RBC production

  • Low reticulocyte count
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24
Q

Iron profile findings for IDA

A
  • Low serum iron
  • Low ferritin
  • Low % transferrin saturation
  • Elevated TIBC (looking for iron to bind to)
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25
Q

What is the most sensitive test to assess IDA?

A

Ferritin

  • Levels decline when iron storage depletes
  • Ferritin = storage of iron (body will use this when levels of iron are low)
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26
Q

Causes of IDA

A
  • MCC: chronic blood loss (GI bleed, menorrhagia)
  • Inadequate nutrition in children and pregnant women
  • Malignancy
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27
Q

IDA treatment for adults

A

Iron supplementation (150-200 mg elemental iron daily)

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28
Q

Iron supplementation side effects

A
  • N/D/C (prescribed with stool softeners)
  • Heartburn
  • Upper GI discomfort
  • Black stools
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29
Q

How to best take iron for maximum absorption

A

Taken 30 minutes before meals with ascorbic acid (vitamin C)

  • Decreased with ingestion of MV with calcium or diary products
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30
Q

When should the provider consider parenteral administration of iron supplementation?

  • Referral to hematologist for IV administration
A
  • Severe anemia
  • Iron malabsorption problem
  • Oral iron not tolerated
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31
Q

IDA treatment during pregnancy

A

Prenatal vitamins with iron

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32
Q

IDA treatment for full term healthy infants (breast-feeding considerations)

A

Babies have adequate iron stores for up to 4-6 months of life

  • Exclusively breastfed babies over 4 months or lack iron fortified foods by 6 months need iron supplementation
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33
Q

What is the Mentzer index?

A

Used to differentiate between IDA and beta thalassemia minor

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34
Q

What is hemoglobin electrophoresis?

A

Measures different types of hemoglobin in the blood

  • Screens for genetic conditions
  • Can differentiate between IDA and thalassemia
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35
Q

What is thalassemia?

A

Autosomal recessive inheritance

  • Causes microcytic and hypo chromic anemia similar to IDA
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36
Q

Thalassemia lab findings

A
  • Low MCV and MCH
  • High RBC (different from IDA)
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37
Q

Thalassemia pregnancy and newborn considerations

A
  • Alpha thalassemia can be diagnosed during routine newborn screening
  • Women of childbearing age should be referred to genetic counseling if considering conceiving
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38
Q

Thalassemia clinical manifestations

A
  • Minor (mild) → no hematologic effects or mistaken for IDA
  • Intermedia (moderate) → moderate microcytic and hypochromic anemia that is not transfusion dependent
  • Major (severe) → developmental problems, decreased life expectancy, lifelong chronic RBC transfusions
    • Short stature, abnormal facies (cranial marrow expansion)
    • Diagnosed as early as 3 months of age: severe anemia, pallor, jaundice, enlarged spleen, liver, heart
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39
Q

Thalassemia management

A
  • Regular blood transfusions to maintain adequate hemoglobin level to allow normal growth and development
  • Iron chelation therapy to prevent complications of transfusion-dependent iron overload
40
Q

Causes of vitamin B12 deficiency (macrocytic anemia)?

A
  • Strict vegetarian
  • Pernicious anemia → loss of intrinsic factor, unable to absorb B12 from diet
  • Chronic use of PPIs
  • Other malabsorption problem
41
Q

Vitamin B12 deficiency symptoms

A
  • Neurological deficits (if severe): decreased vibratory sensation, loss of proprioception, peripheral neuropathy, ataxia, spasticity, hyperactive reflexes, positive Romberg sign
  • Beefy red tongue
42
Q

Vitamin B12 deficiency lab findings

A
  • Low hemoglobin
  • Elevated MCV
  • Elevated RDW
  • Low reticulocyte count
43
Q

What is a Schillings test?

A

Previous way of diagnosing pernicious anemia

  • Now use anti-IF or anti-parietal cell antibodies
44
Q

Causes of folate deficiency

A
  • Dietary
  • Alcoholism
  • Malabsorption
  • Increased requirements during pregnancy
45
Q

Folate deficiency lab findings

A
  • Low hemoglobin
  • Elevated MCV
  • Elevated RDW
  • Low reticulocyte count
46
Q

Folate deficiency pregnancy considerations

A

Deficiency during pregnancy can lead to neural tube defects in the fetus

47
Q

Anemia of chronic disease (ACD) definition

A

Mild to moderate anemia that results from inflammatory disorders, infection, or malignancy

48
Q

Causes of anemic of chronic disease (ACD)

A
  • Malignancy
  • Chronic infection
  • Autoimmune conditions (RA, SLE, IBD)
  • Chronic kidney disease
49
Q

Anemia of chronic disease (ACD) clinical manifestations

A
  • Mild and asymptomatic
  • Have symptoms associated with underlying diseases (gradual onset)
    • Fatigue, pallor, tachycardia, dyspnea with exertion
50
Q

Anemia of chronic disease (ACD) treatment

A
  • Manage underlying condition
  • Recombinant human erythropoietin or darbepoetin alfa → EPO triggers production of RBC
  • Blood transfusions
51
Q

Sickle cell disease (SCD) vs sickle cell trait

A

Sickle cell trait: only carry one copy of the altered hemoglobin gene (do not have clinical symptoms)

Sickle cell disease: carry two copies of altered hemoglobin gene

  • Autosomal recessive inheritance
52
Q

SCD (hemolytic anemia)- moderate to severe clinical manifestations

A
  • Jaundice
  • Systolic flow murmur (grade 1 or 2)
  • Scleral icterus
  • Cardiomegaly
53
Q

At what age do symptoms of SCD emerge?

A

Around 6 months of age

54
Q

Multisystem symptoms of SCD

A
  • Fatigue
  • Pain
  • Bacterial infections (functional asplenia)
55
Q

SCD lab findings

A
  • Low HCT and Hgb
  • High reticulocyte count
  • Elevated LDH and bilirubin
56
Q

Gold standard method of diagnosis for SCD

A

Hemoglobin electrophoresis

57
Q

Triggers that lead to SCD vaso-occlusive crisis

A
  • Physical stresses → infection, change of weather (exposure to cold), dehydration, fatigue, overexertion
  • Emotional stress
58
Q

Nonpharmacologic management of SCD

A
  • Oral analgesics (NSAIDs)
  • Hydration
  • Rest, heat, gentle massage
  • Illness prevention (immunizations), monitor growth and development
59
Q

Pharmacologic management of SCD

A
  • ER admission (work with pediatric hematologist)
  • IV narcotic analgesics and fluids
  • Antibiotic prophylaxis for infants and young children
60
Q

SCD complications

A
  • Chronic pain → confused for narcotic dependence
  • Infants and toddlers → dactylitis
  • Children → acute splenic sequestration (higher risk of infection, life threatening)
  • Adults → pulmonary HTN, renal failure, priapism, skin ulcerations, stroke
61
Q

What is aplastic anemia?

A

Life threatening condition resulting from bone marrow stem cell failure → pancytopenia

  • Sudden onset
62
Q

Causes of aplastic anemia

A

Secondary to infection, exposure to toxins or medications, immune mediated

63
Q

Aplastic anemia - clinical presentation and physical examination

A

Clinical presentation → abnormal bleeding, infection, anemia

Physical exam → petechiae, ecchymosis, purpura, pallor of skin and mucous membranes, lymphadenopathy (late stages)

64
Q

True/false: The early stages of aplastic anemia may show no significant changes on physical exam

A

True

65
Q

Aplastic anemia CBC findings

A
  • Pancytopenia with normocytic and normochromic RBCs
  • Normal reticulocyte count
66
Q

Gold standard diagnosis of aplastic anemia

A

Bone marrow biopsy

67
Q

Aplastic anemia management

A
  • Referral to hematologist
  • Non severe cases can be observed with supportive care
  • Avoid infections → hand hygiene, avoid ill contacts, immunizations
68
Q

What is the definitive treatment of aplastic anemia?

A
  • Immunosuppressive therapy
  • Bone marrow transplant
69
Q

What is von willebrand disease (vWD)?

A

Deficiency or abnormality of vWF (coagulopathy) → most common congenital bleeding disorder

  • Autosomal dominant inheritance
70
Q

vWD clinical manifestations

A
  • Epistaxis
  • Menorrhagia
  • Excessive bruising
  • Prolonged bleeding with cuts or dental extractions and in intraoperative or immediate postoperative period
71
Q

vWD management

A
  • Hematology consultation → interdisciplinary
  • Treatment for bleeding episodes
  • Prophylaxis for invasive procedures
    • DDAVP or plasma-derived factor VIII concentrate
72
Q

What is hemophilia?

A

X-linked recessive bleeding disorder → low factor VIII or IX → defective fibrin clot formation

73
Q

Hemophilia diagnostic lab findings

A
  • Normal PT, thrombin time, PFA-100
  • Prolonged aPTT
  • Diagnosis requires finding of low level of factor VIII (A) or factor IX (B)
74
Q

Hemophilia management (mild and severe cases)

A
  • Mild → coagulation factor replacement (DDAVP)
  • Moderate/severe → replacement of coagulation factor via infusions
75
Q

Hemophilia patient education

A
  • Avoid high contact sports, aspirin and NSAIDs
  • Evaluate coagulation status before dental procedures or surgeries
  • Genetic counseling for family planning
76
Q

Hemophilia complications

A
  • Bleeding into joints can lead to joint swelling, joint immobility, and limb contractures
  • Anemia
  • Bleeding into various organs
77
Q

What is idiopathic thrombocytopenia purpura?

A

Most common thrombocytopenic purpura in childhood (ages 1-4 years)

  • Believed to be autoimmune response in which circulating platelets are destroyed
  • Usually preceded by a viral illness
78
Q

Acute vs chronic ITP

A

Acute: most cases resolve within 6 months

Chronic: >12 months

79
Q

ITP clinical manifestations

A

Symptoms do not present until platelet count is <20,000

  • Acute onset petechiae, purpura, bleeding/bruising (usually over legs)
  • Recent viral illness 1-4 weeks ago
  • Nosebleeds
  • Hemorrhage of gums and lips
80
Q

Lab findings in ITP

A
  • Low platelet count
  • Normal PT and aPTT
  • Normal WBC and RBC count
  • Megathrombocytes on peripheral smear
  • Severe thrombocytopenia
  • Decreased Hgb with normal MVC
81
Q

ITP management - mild cases

A

If platelet count >20,000 and no bleeding observed → avoid contact sports, aspirin and NSAIDs, other agents that could interfere with platelet function

82
Q

ITP management - severe cases (platelets <20,000)

A
  • Short course corticosteroid therapy
  • IVIG - for active severe bleeding and those with contraindications for steroid therapy
  • Thrombopoiesis stimulants → romiplostim, eltrombopag
83
Q

What is the function of neutrophils?

A

Bacterial or fungal infections (most common)

  • Neutrophilia (elevated) → “left shift”
84
Q

What is the function of eosinophils?

A

Parasitic infections and allergic reactions (inflammatory)

85
Q

What is the function of basophils?

A

Allergic and antigen response (release histamines)

  • Rare, but should be concerned about malignancy
86
Q

What is the function of lymphocytes?

A

Include B cells, helper T cells, cytotoxic T cells

  • Operate in lymphatic system (viral illnesses)
87
Q

What is the function of monocytes?

A

Phagocytosis of pathogens

  • Presentation of antigens to T cells
  • Eventually become macrophages
88
Q

What is leukemia?

A

Hematologic malignant neoplasms that affect the bone marrow and lymphatic tissue

89
Q

What is acute leukemia?

A

Abnormal production of immature WBC (blasts) with rapid disease progression → AML, ALL

90
Q

What is chronic leukemia?

A

Overabundance of mature appearing but ineffective WBCs with slow disease progress → CML, CLL

91
Q

Leukemia red flags

A
  • WBC 500-30,000 cells/mm3
  • Leukopenia with >20% blasts
  • Enlarged, non tender lymph nodes present for >1 month
92
Q

Diagnostic tests for leukemia

A
  • CBC w/ differential
  • Bone marrow biopsy
  • Blood smear → will see increased blasts
  • CT scan or PET scans
93
Q

Leukemia management

A
  • Hematology/oncology referral
  • Chemotherapy, immunotherapy, targeted therapy
  • Stem cell transplantation for high risk disease
94
Q

What is lymphoma?

A

Clonal disorder that arises from lymphocytes (B or T cells) → Hodgkins or Non Hodgkin’s lymphoma

95
Q

Lymphoma clinical manifestations

A
  • Lymphadenopathy → lymph nodes persisting for more than 4 weeks or larger than normal (up to 1.5 cm)
  • Fever higher than 38 degrees C
  • B symptoms: drenching night sweats, unintentional weight loss or more than 10% body weight, fatigue
  • Absence of palpable liver and spleen
96
Q

Hodgkin vs Non Hodgkins lymphoma clinical presentation

A

Hodgkins → Reed-Steinberg cells, adenopathy in neck (usually involves mediastinum)

Non Hodgkins → cytopenia, can have rapid or insidious onset of symptoms

NURS 502 (43 decks)

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