Quiz 5 RBC Disorders, Upper GI, Lower GI

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N220 Pathophysiology Spring 26 Week 9, 10, 11

Last updated 1:46 AM on 4/14/26
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175 Terms

1
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What is the purpose of a Complete Blood Count (CBC)?

Use the values to assess and identify any abnormalities

  • Blood Cells Quantity (RBCs, WBCs, PLTs)

  • Oxygen Carrying Capacity

  • RBC Morphology

  • Blood Disorders

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What are the 4 main values of CBC? What are normal values of each one?

  • WBC (white blood cells

  • RBC (red blood cells)

  • Hgb (hemoglobin)

  • Hct (hematocrit)

<ul><li><p>WBC (white blood cells</p></li><li><p>RBC (red blood cells)</p></li><li><p>Hgb (hemoglobin)</p></li><li><p>Hct (hematocrit)</p></li></ul><p></p>
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What are the 4 main values of CBC? Description & What are normal values of each one? (WBC)

Description: Total white blood cell count

Normal Value: 5,000 - 10,000 / mm³

<p>Description: <strong>Total white blood cell count</strong></p><p>Normal Value: <strong>5,000 - 10,000 / mm³ </strong></p><p></p>
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What are the 4 main values of CBC? Description & What are normal values of each one? (RBC)

Description: Total Mature Red Blood Cell Count

Normal Value: 4.5 - 5.5 / mm³

<p>Description: <strong>Total Mature Red Blood Cell Count</strong></p><p>Normal Value<strong>: 4.5 - 5.5 / mm³ </strong></p>
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What are the 4 main values of CBC? Description & What are normal values of each one? (Hgb)

Description: Total hemoglobin level

Normal value: 14-17 g/100 mL

<p>Description: <strong>Total hemoglobin level</strong></p><p>Normal value: <strong>14-17 g/100 mL</strong></p>
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What are the 4 main values of CBC? Description & What are normal values of each one? (Hct) What is abnormal Hct?

Description: Proportion of RBCs to plasma

Normal value: 42 - 52%

Anemia: Depressed hematocrit %

Polycythemia: Elevated hematocrit %

<p>Description: <strong>Proportion of RBCs to plasma</strong></p><p>Normal value: <strong>42 - 52%</strong></p><p>Anemia: <strong>Depressed hematocrit %</strong></p><p>Polycythemia: <strong>Elevated hematocrit %</strong></p>
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Explain Erythropoiesis & how red blood cells (RBCs) are monitored?

Process which produces red blood cells (erythrocytes) and monitored by the Complete Blood Count (CBC)

<p>Process which produces red blood cells (erythrocytes) and monitored by the Complete Blood Count (CBC)</p>
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Define Anemia and how does it affect the tissues?

  • Deficit of mature, healthy RBCs in circulation

  • Insufficient delivery of O2 to the tissues

<ul><li><p>Deficit of mature, healthy RBCs in circulation</p></li><li><p>Insufficient delivery of O2 to the tissues</p></li></ul><p></p>
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Define Polycythemia

Over-proliferation of RBCs in the bone marrow

<p>Over-proliferation of RBCs in the bone marrow</p><p></p>
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What is hematopoiesis? What are the two stages?

  • Hemostatic process

  • Bone marrow stem cells → Differentiate blood cells

  • Two stages: Proliferation & Maturation

    • Proliferation: “-poietin” → suffix for growth or multiplication of specific cell types

    • Maturation: Bone marrow stem cells mature to WBCs, RBCs, PLTs

<ul><li><p>Hemostatic process</p></li><li><p>Bone marrow stem cells → Differentiate blood cells</p></li><li><p>Two stages: Proliferation &amp; Maturation</p><ul><li><p>Proliferation: “-poietin” → suffix for growth or multiplication of specific cell types</p></li><li><p>Maturation: Bone marrow stem cells mature to WBCs, RBCs, PLTs</p></li></ul></li></ul><p></p>
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What is purpose of RBCs

Most numerous cell type in circulation: Transporters

  • Deliver O2 to tissues via hemoglobin chains

  • Remove CO2 from tissues for release via lungs

<p>Most numerous cell type in circulation: <strong>Transporters</strong></p><ul><li><p><strong>Deliver O2</strong> to tissues via hemoglobin chains</p></li><li><p><strong>Remove CO2 </strong>from tissues for release via lungs</p></li></ul><p></p>
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Where are RBCs made, lifespan, and what’s it made of

Manufactured in bone marrow by stem cells

  • Lifespan = 120 days

  • Reticulocytes: Immature RBCs

More than one third of an RBC is made of hemoglobin

  • Heme: red pigment, contains iron

  • Globin: protein chain

<p>Manufactured in bone marrow by stem cells</p><ul><li><p>Lifespan = 120 days</p></li><li><p>Reticulocytes: Immature RBCs</p></li></ul><p>More than one third of an RBC is made of hemoglobin</p><ul><li><p>Heme: red pigment, contains iron</p></li><li><p>Globin: protein chain</p></li></ul><p></p>
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What is Erythropoiesis? What is it stimulated by? What adequate nutrition does it need?

Process which produces red blood cells (erythrocytes)

Stimulated by decreased O2 in circulation

  • Detected by the kidneys which then secrete the hormone erythropoietin

  • Triggers bone marrow to produce more RBCs

Requires adequate

  • Protein

  • Vitamin B12

  • Iron

  • Folic Acid

<p>Process which produces red blood cells (erythrocytes)</p><p>Stimulated by decreased O2 in circulation</p><ul><li><p><strong>Detected by the kidneys which then secrete the hormone erythropoietin</strong></p></li><li><p><strong>Triggers bone marrow to produce more RBCs</strong></p></li></ul><p>Requires adequate</p><ul><li><p><strong>Protein</strong></p></li><li><p><strong>Vitamin B12</strong></p></li><li><p><strong>Iron</strong></p></li><li><p><strong>Folic Acid</strong></p></li></ul><p></p>
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What are stages of Erythropoiesis?

  1. Kidneys secrete Erythropoietin

    1. Bone marrow stem cell → myeloid stem cell

  2. Proerythroblast → Erythroblast

    1. Huge nucleus

    2. Hemoglobin synthesis begins this phase

  3. Normoblast

    1. Nucleus shrinks

    2. Hemoglobin quantity increases

  4. Reticulocyte

    1. Nucleus ejected

    2. Erythrocyte within 24 - 48 hours

    3. Remain in bone marrow ~ 1 day → released into circulation

    4. Reticulocytes are indication of erythropoietic activity

<ol><li><p><strong>Kidneys secrete Erythropoietin</strong></p><ol><li><p>Bone marrow stem cell → myeloid stem cell</p></li></ol></li><li><p><strong>Proerythroblast → Erythroblast</strong></p><ol><li><p>Huge nucleus</p></li><li><p>Hemoglobin synthesis begins this phase</p></li></ol></li><li><p><strong>Normoblast</strong></p><ol><li><p>Nucleus shrinks</p></li><li><p>Hemoglobin quantity increases</p></li></ol></li><li><p><strong>Reticulocyte</strong></p><ol><li><p>Nucleus ejected</p></li><li><p>Erythrocyte within 24 - 48 hours</p></li><li><p>Remain in bone marrow ~ 1 day → released into circulation</p></li><li><p>Reticulocytes are indication of erythropoietic activity</p></li></ol></li></ol><p></p>
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What organ recycles aged, lysed and dead RBCs? What is it broken down into? Where is it stored?

  • Spleen

  • Broken down into component parts

    • Iron

    • Bilirubin

  • Recycled to make new RBCs, stored in liver or secreted as waste

    • May cause problems for liver, spleen

<ul><li><p>Spleen</p></li><li><p>Broken down into component parts</p><ul><li><p>Iron</p></li><li><p>Bilirubin </p></li></ul></li><li><p>Recycled to make new RBCs, stored in liver or secreted as waste</p><ul><li><p>May cause problems for liver, spleen </p></li></ul></li></ul><p></p>
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Complete Blood Count; Description & Normal Value for MCV

Description: Average red blood cell size

Normal Value: 78 - 100 µm³

<p>Description: <strong>Average red blood cell size</strong></p><p>Normal Value: <strong>78 - 100 µm³</strong></p>
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Complete Blood Count; Description & Normal Value for MCH

Description: Amount of Hgb present per cell

Normal value: 25 - 35 pg

<p>Description: <strong>Amount of Hgb present per cell</strong></p><p>Normal value: <strong>25 - 35 pg</strong></p>
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Complete Blood Count; Description & Normal Value for MCHC

Description: Proportion of cell occupied by Hgb

Normal value: 32 - 36 %

<p>Description: <strong>Proportion of cell occupied by Hgb</strong></p><p>Normal value: <strong>32 - 36 %</strong></p>
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What is RBC morphology? What are the different categories?

Categorized RBC based on appearance on peripheral blood smear

  • Normocytic

  • Normochromic

  • Microcytic

  • Hypochromic

  • Megaloblastic

<p>Categorized RBC based on appearance on peripheral blood smear</p><ul><li><p><strong>Normocytic</strong></p></li><li><p><strong>Normochromic</strong></p></li><li><p><strong>Microcytic</strong></p></li><li><p><strong>Hypochromic</strong></p></li><li><p><strong>Megaloblastic</strong></p></li></ul><p></p>
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Normocytic

Normal cell size

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Normochromic

Normal amount of Hgb

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Microcytic

Small cell size

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Hypochromic

Reduced amount of Hgb

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Megaloblastic

Abnormally large, immature and dysfunctional cells

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What is Folic Acid (Folate) necessary for?

Necessary for RBC production

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What is Vit B12 necessary for?

Necessary for RBC production

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What is Iron needed for?

Needed for Hgb production

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Review Question: Red blood cells differ from other cell types in the body because they

A. Contain cytoplasmic protein

B. Have no cytoplasmic organelles

C. Have a longer life span

D. Contain glycolytic enzymes

B. Have no cytoplasmic organelles

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The primary source of erythropoietin is the

A. Bone marrow

B. Kidney

C. Lung

D. Liver

B. Kidney

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What are the Anemia Etiologies?

Relative Anemia

  • Hemodilution

    • concentration of RBCs low because plasma has increased, RBC count is normal, the plasma is just too much that it dilutes

Absolute Anemia

  • Insufficient production

    • bone marrow cannot produce enough RBCs to meet needs

  • Extrinsic loss of destruction

    • Trauma or surgery; bleeding out; RBCs destroyed faster than produced

  • Inherited disorder

    • Genetic mutation; abnormal hemoglobin or misshapen cells

<p><strong>Relative Anemia</strong></p><ul><li><p><mark data-color="purple" style="background-color: purple; color: inherit;">Hemodilution </mark></p><ul><li><p>concentration of RBCs low because plasma has increased, RBC count is normal, the plasma is just too much that it dilutes</p></li></ul></li></ul><p><strong>Absolute Anemia</strong></p><ul><li><p><mark data-color="purple" style="background-color: purple; color: inherit;">Insufficient production </mark></p><ul><li><p>bone marrow cannot produce enough RBCs to meet needs</p></li></ul></li><li><p><mark data-color="purple" style="background-color: purple; color: inherit;">Extrinsic loss of destruction</mark></p><ul><li><p>Trauma or surgery; bleeding out; RBCs destroyed faster than produced</p></li></ul></li><li><p><mark data-color="purple" style="background-color: purple; color: inherit;">Inherited disorder</mark></p><ul><li><p>Genetic mutation; abnormal hemoglobin or misshapen cells</p></li></ul></li></ul><p></p>
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General effects (Clinical Implications) of Anemia

  • Reduction in oxygen carrying capacity

    • Tissue hypoxia (tissues don’t get enough oxygen)

    • Hypercarbia (elevated CO2 levels)

  • Compensatory mechanisms to restore tissue oxygenation

    • Increased cardiac output and flow to vital organs

    • Enhanced unloading of oxygen by hemoglobin in tissues

    • Increase in erythropoietin activity

  • Increased Oxygen demands

<ul><li><p><strong>Reduction in oxygen carrying capacity</strong></p><ul><li><p>Tissue hypoxia (tissues don’t get enough oxygen)</p></li><li><p>Hypercarbia (elevated CO2 levels)</p></li></ul></li><li><p><strong>Compensatory mechanisms to restore tissue oxygenation</strong></p><ul><li><p>Increased cardiac output and flow to vital organs</p></li><li><p>Enhanced unloading of oxygen by hemoglobin in tissues</p></li><li><p>Increase in erythropoietin activity</p></li></ul></li><li><p><strong>Increased Oxygen demands</strong></p></li></ul><p></p>
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Anemia General S/S; Mild, Moderate, Severe

Mild

  • Usually no clinical symptoms

Moderate

  • Fatigue, generalized weakness, loss of stamina

  • Tachycardia and exertional dyspnea

Severe

  • Hypotension, vasoconstriction, pallor

  • Tachypnea, dyspnea

  • Tachycardia, angina pectoris, heart failure

  • Intermittent claudication, night cramps in muscles

  • Headache, lightheadedness, faintness

  • Tinnitus, roaring in the ears

  • Enlarged spleen

<p><strong>Mild</strong></p><ul><li><p>Usually no clinical symptoms</p></li></ul><p><strong>Moderate</strong></p><ul><li><p>Fatigue, generalized weakness, loss of stamina</p></li><li><p>Tachycardia and exertional dyspnea</p></li></ul><p><strong>Severe</strong></p><ul><li><p>Hypotension, vasoconstriction, pallor</p></li><li><p>Tachypnea, dyspnea</p></li><li><p>Tachycardia, angina pectoris, heart failure</p></li><li><p>Intermittent claudication, night cramps in muscles</p></li><li><p>Headache, lightheadedness, faintness</p></li><li><p>Tinnitus, roaring in the ears</p></li><li><p>Enlarged spleen</p></li></ul><p></p>
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What CONDITIONS cause Insufficient RBC production?

  • Iron Deficiency Anemia

  • Folic acid Deficiency

  • Pernicious Anemia

  • Aplastic Anemia

  • Chronic Reneal Failure

<ul><li><p>Iron Deficiency Anemia</p></li><li><p>Folic acid Deficiency</p></li><li><p>Pernicious Anemia</p></li><li><p>Aplastic Anemia</p></li><li><p>Chronic Reneal Failure</p></li></ul><p></p>
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Iron Deficiency Anemia: Etiology

Insufficient iron for hemoglobin synthesis

  • Abnormally small RBCs unable to carry sufficient O2 to tissues

<p>Insufficient iron for hemoglobin synthesis</p><ul><li><p>Abnormally small RBCs unable to carry sufficient O2 to tissues</p></li></ul><p></p>
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Iron Deficiency Anemia: Pathogenesis

Leads to production of abnormally small RBCs that are unable to carry sufficient O2 to tissue

  • Hypochromic RBCs

  • Microcytic RBCs

<p>Leads to production of abnormally small RBCs that are unable to carry sufficient O2 to tissue</p><ul><li><p>Hypochromic RBCs</p></li><li><p>Microcytic RBCs</p></li></ul><p></p>
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Iron Deficiency Anemia: Risk Factors

Demographic

  • Elderly

  • Female

  • Pregnancy

Diet

  • Vegan/vegetarian

  • Low Vit C

  • Poor dentition

  • Bowel disease

  • Cancer

Social

  • Poverty

  • ETOH overuse (Alcohol overuse)

  • Stress

  • Depression

<p><strong>Demographic</strong></p><ul><li><p>Elderly</p></li><li><p>Female</p></li><li><p>Pregnancy</p></li></ul><p><strong>Diet</strong></p><ul><li><p>Vegan/vegetarian</p></li><li><p>Low Vit C</p></li><li><p>Poor dentition</p></li><li><p>Bowel disease</p></li><li><p>Cancer</p></li></ul><p><strong>Social</strong></p><ul><li><p>Poverty</p></li><li><p>ETOH overuse (Alcohol overuse)</p></li><li><p>Stress</p></li><li><p>Depression</p></li></ul><p></p>
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Iron Deficiency Anemia: Clinical Manifestations

  • General S/S of Anemia (gradual onset)

  • PICA (craving nonfood substances)

    • Dirt, clay, ice, laundry starch, cardboard, hair

  • Koilonychias (spoon shaped nails)

  • Blue sclerae (white part of eye appears blue)

<ul><li><p>General S/S of Anemia (gradual onset)</p></li><li><p>PICA (craving nonfood substances)</p><ul><li><p>Dirt, clay, ice, laundry starch, cardboard, hair</p></li></ul></li><li><p>Koilonychias (spoon shaped nails)</p></li><li><p>Blue sclerae (white part of eye appears blue)</p></li></ul><p></p>
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Iron Deficiency Anemia: Treatments

Treat underlying cause

  • Iron (Fe) replacement

    • Iron supplement tablets

    • Ferrous Sulfate elixir

    • Iron Sucrose Injection

Foods that ENHANCE Iron absorption

  • Citrus fruits

  • Tomatoes

  • Chili peppers

Foods that IMPAIR iron Absorption

  • Tea

  • Cereal (if it contains phytates)

<p>Treat underlying cause</p><ul><li><p>Iron (Fe) replacement</p><ul><li><p>Iron supplement tablets</p></li><li><p>Ferrous Sulfate elixir</p></li><li><p>Iron Sucrose Injection</p></li></ul></li></ul><p>Foods that ENHANCE Iron absorption</p><ul><li><p>Citrus fruits</p></li><li><p>Tomatoes</p></li><li><p>Chili peppers</p></li></ul><p>Foods that IMPAIR iron Absorption</p><ul><li><p>Tea</p></li><li><p>Cereal (if it contains phytates)</p></li></ul><p></p>
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Iron Deficiency Anemia: Nursing Considerations

Monitor for Fe replacement side effects

  • Nausea

  • Black stools

  • Teeth staining

  • Pain upon injection and can cause Orthostatic hypotension (IV forms)

Beware of Iron Toxicity

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Folic Acid Deficiency Anemia: Etiology

  • Inadequate Intake

    • Limited consumption of fresh, minimally cooked food

    • ETOH (alcohol) overuse

  • Malabsorption

    • Malabsorption syndrome (E.g. Celiac Disease)

    • Inflammatory bowel disease (E.g. Crohn’s Disease)

    • Gastric Surgery

  • Increased Demand

    • Pregnancy

    • Lactation

    • Infancy

    • Cancer

    • Hemodialysis

<ul><li><p><strong>Inadequate Intake</strong></p><ul><li><p>Limited consumption of fresh, minimally cooked food</p></li><li><p>ETOH (alcohol) overuse</p></li></ul></li><li><p><strong>Malabsorption</strong></p><ul><li><p>Malabsorption syndrome (E.g. Celiac Disease)</p></li><li><p>Inflammatory bowel disease (E.g. Crohn’s Disease)</p></li><li><p>Gastric Surgery</p></li></ul></li><li><p><strong>Increased Demand</strong></p><ul><li><p>Pregnancy</p></li><li><p>Lactation</p></li><li><p>Infancy</p></li><li><p>Cancer</p></li><li><p>Hemodialysis</p></li></ul></li></ul><p></p>
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Folic Acid Deficiency Anemia: Pathogenesis

Deficiency causes formation of megaloblasts

  • Very similar to Vit B12 deficiency

<p>Deficiency causes formation of megaloblasts</p><ul><li><p>Very similar to Vit B12 deficiency</p></li></ul><p></p>
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Folic Acid Deficiency Anemia: Risk Factors

  • Inadequate Intake

    • Limited consumption of fresh, minimally cooked food

    • ETOH (alcohol) overuse

  • Malabsorption

    • Malabsorption syndrome (E.g. Celiac Disease)

    • Inflammatory bowel disease (E.g. Crohn’s Disease)

    • Gastric Surgery

  • Increased Demand

    • Pregnancy

    • Lactation

    • Infancy

    • Cancer

    • Hemodialysis

<ul><li><p><strong>Inadequate Intake</strong></p><ul><li><p>Limited consumption of fresh, minimally cooked food</p></li><li><p>ETOH (alcohol) overuse</p></li></ul></li><li><p><strong>Malabsorption</strong></p><ul><li><p>Malabsorption syndrome (E.g. Celiac Disease)</p></li><li><p>Inflammatory bowel disease (E.g. Crohn’s Disease)</p></li><li><p>Gastric Surgery</p></li></ul></li><li><p><strong>Increased Demand</strong></p><ul><li><p>Pregnancy</p></li><li><p>Lactation</p></li><li><p>Infancy</p></li><li><p>Cancer</p></li><li><p>Hemodialysis</p></li></ul></li></ul><p></p>
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Folic Acid Deficiency Anemia: Clinical Manifestations

  • General S/S of Anemia

  • Malnutrition

  • Depression

  • Forgetfulness

  • Painful ulcerations of cheeks and tongue

  • Fissuring of lips and mouth

<ul><li><p>General S/S of Anemia</p></li><li><p>Malnutrition</p></li><li><p>Depression</p></li><li><p>Forgetfulness</p></li><li><p>Painful ulcerations of cheeks and tongue</p></li><li><p>Fissuring of lips and mouth</p></li></ul><p></p>
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Folic Acid Deficiency Anemia: Treatments

  • Folic Acid Supplements

  • Dietary Sources of Folate (Vit B9)

    • Spinach

    • Asparagus

    • Avocado

    • Broccoli

    • Eggs

    • Milk

    • Bread & Pasta

    • Etc….

<ul><li><p>Folic Acid Supplements</p></li><li><p>Dietary Sources of Folate (Vit B9)</p><ul><li><p>Spinach</p></li><li><p>Asparagus</p></li><li><p>Avocado</p></li><li><p>Broccoli</p></li><li><p>Eggs</p></li><li><p>Milk</p></li><li><p>Bread &amp; Pasta</p></li><li><p>Etc….</p></li></ul></li></ul><p></p>
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Folic Acid Deficiency Anemia: Nursing Considerations

  • Associate low folate with neural tube deficits (spina bifida) in infants

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Vitamin B12 Anemia: Etiology

  • Inadequate intake

  • Malabsorption

  • Genetic Mutation

    • Intrinsic factor deficiency (pernicious)

<ul><li><p>Inadequate intake</p></li><li><p>Malabsorption</p></li><li><p>Genetic Mutation</p><ul><li><p>Intrinsic factor deficiency (pernicious)</p></li></ul></li></ul><p></p>
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Vitamin B12 Anemia: Pathogenesis

  • Disruption in DNA synthesis of blast cells;

  • RBCs cannot be properly synthesized → Megaloblastic RBCs

    • Poor oxygen carrying capacity

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Vitamin B12 Anemia: Risk Factors

Malabsorption

  • Gastritis

  • Gastrectomy

  • Crohn’s Disease

Inadequate Intake

  • Veganism

  • ETOH overuse

Genetic Mutation

  • Intrinsic factor deficiency (pernicious)

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Vitamin B12 Anemia: Clinical Manifestations

  • General S/S of Anemia

  • Brain fog memory issues, lack of motivation or prolonged feelings of apathy

  • Mood swings and grouchiness

  • Fatigue, low energy

  • Neuropathy (tingling in extremities)

  • Muscle weakness

  • Depression, dementia, blindness, or brain damage

<ul><li><p>General S/S of Anemia</p></li><li><p>Brain fog memory issues, lack of motivation or prolonged feelings of apathy</p></li><li><p>Mood swings and grouchiness</p></li><li><p>Fatigue, low energy</p></li><li><p>Neuropathy (tingling in extremities)</p></li><li><p>Muscle weakness</p></li><li><p>Depression, dementia, blindness, or brain damage</p></li></ul><p></p>
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Vitamin B12 Anemia: Treatments

  • Treat underlying cause

    • B12 Supplements or B12 Rich diet

  • Cyanocobalamin (Vitamin B12)

    • Usually administered via IM injection

    • Also available in PO and intranasal spray

<ul><li><p>Treat underlying cause</p><ul><li><p>B12 Supplements or B12 Rich diet</p></li></ul></li><li><p>Cyanocobalamin (Vitamin B12)</p><ul><li><p>Usually administered via IM injection</p></li><li><p>Also available in PO and intranasal spray</p></li></ul></li></ul><p></p>
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Vitamin B12 Anemia: Nursing Considerations

  • Patient education on dietary sources of B12

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Aplastic Anemia: Etiology

Caused by toxic, radiant or immunologic injury to the bone marrow stem cells

  • Diagnosed via bone marrow biopsy

    • 10-15% of severe aplastic anemia cases evolve into myelodysplastic syndrome and leukemia

<p>Caused by toxic, radiant or immunologic injury to the bone marrow stem cells</p><ul><li><p>Diagnosed via bone marrow biopsy </p><ul><li><p>10-15% of severe aplastic anemia cases evolve into myelodysplastic syndrome and leukemia</p></li></ul></li></ul><p></p>
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Aplastic Anemia: Pathogenesis

Stem cell disorder characterized by reduction of hematopoietic tissue, fatty marrow replacement and pancytopenia

  • Damaged bone marrow and hematopoietic stem cells are unable to sufficiently produce mature cells

    • Low WBCs

    • Low Plts

    • Low RBCs

    • Low Retic count (indicates failure of bone marrow response)

<p>Stem cell disorder characterized by reduction of hematopoietic tissue, fatty marrow replacement and pancytopenia</p><ul><li><p>Damaged bone marrow and hematopoietic stem cells are unable to sufficiently produce mature cells</p><ul><li><p>Low WBCs</p></li><li><p>Low Plts</p></li><li><p>Low RBCs</p></li><li><p>Low Retic count (indicates failure of bone marrow response)</p></li></ul></li></ul><p></p>
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Aplastic Anemia: Clinical Manifestations

Onset of S/S may be abrupt or insidious

  • General S/S of anemia due to low RBCs

  • Additional S/S include those to low Plts (bleeding)

  • May also include S/S due to low WBCs

<p>Onset of S/S may be abrupt or insidious</p><ul><li><p>General S/S of anemia due to low RBCs</p></li><li><p>Additional S/S include those to low Plts (bleeding)</p></li><li><p>May also include S/S due to low WBCs</p></li></ul><p></p>
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Aplastic Anemia: Treatments

  • Blood Transfusions

    • RBCs, PLTs, Plasma

  • Bone Marrow Transplants

  • Bone Marrow Stimulants

    • NEUPOGEN (Stimulates WBC production)

    • EPOGEN or ARANESP (Stimulates RBC production)

  • Prophylactic antibiotics

<ul><li><p>Blood Transfusions</p><ul><li><p>RBCs, PLTs, Plasma</p></li></ul></li><li><p>Bone Marrow Transplants</p></li><li><p>Bone Marrow Stimulants</p><ul><li><p>NEUPOGEN (Stimulates WBC production)</p></li><li><p>EPOGEN or ARANESP (Stimulates RBC production)</p></li></ul></li><li><p>Prophylactic antibiotics</p></li></ul><p></p>
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Aplastic Anemia: Nursing Considerations

Precautions to minimize risk for injury, blood loss, and infection

<p>Precautions to minimize risk for injury, blood loss, and infection</p>
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Chronic Renal Failure: Etiology

Impaired renal endocrine function

<p>Impaired renal endocrine function</p>
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Chronic Renal Failure: Pathogenesis

Decreased erythropoietin production leads to decreased RBC production

<p>Decreased erythropoietin production leads to decreased RBC production</p>
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Chronic Renal Failure: Risk Factors

Long term hemodialysis

<p>Long term hemodialysis</p>
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Chronic Renal Failure: Clinical Manifestations

  • General S/S of anemia

  • Normocytic

  • Normochromic cells

<ul><li><p>General S/S of anemia</p></li><li><p>Normocytic</p></li><li><p>Normochromic cells</p></li></ul><p></p>
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Chronic Renal Failure: Treatments

  • Epogen

  • Aranesp

  • May also require PRBC transfusions

<ul><li><p>Epogen</p></li><li><p>Aranesp</p></li><li><p>May also require PRBC transfusions</p></li></ul><p></p>
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Chronic Renal Failure: Nursing Considerations

Monitor and assess for signs of Renal Failure when long-term hemodialysis

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Blood Work: Signs of Iron Deficiency Anemia

  • Hypochromic, Microcytic RBCs

  • Low MCV, MCH, and MCHC

  • Serum ferritin level decreased

  • Serum Iron level decreased

  • Total Iron binding capacity (TIBC) increased

<ul><li><p>Hypochromic, Microcytic RBCs</p></li><li><p>Low MCV, MCH, and MCHC</p></li><li><p>Serum ferritin level decreased</p></li><li><p>Serum Iron level decreased</p></li><li><p>Total Iron binding capacity (TIBC) increased</p></li></ul><p></p>
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Blood work: Sign of Vitamin B12 Anemia

  • Megaloblastic (enlarged, oval shaped)

  • Serum B12 decreased

  • Serum Folate decreased

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Blood Work: Signs of Folic Acid Deficiency Anemia

  • Serum Folate <4 ng/mL

  • Low Hgb/Hct level

<ul><li><p>Serum Folate &lt;4 ng/mL</p></li><li><p>Low Hgb/Hct level</p></li></ul><p></p>
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Blood Work: Signs of Aplastic Anemia

  • Low WBCs

  • Low Plts

  • Low RBCs

  • Low Retic count indicates failure of marrow response

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Blood work: Sign of Chronic Renal Failure

  • Leads to decreased RBC production

  • Normocytic, Normochromic

  • Low EPO levels

  • General S/S Anemia

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Extrinsic RBC loss/destruction conditions

  • Hemorrhagic Anemia

  • Hemolytic Anemia

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Hemorrhagic Anemia Etiology (Acute & Chronic)

Acute

  • Moderate to large volume of total circulating blood loss in short time period

    • Surgery

    • Trauma

    • Acute GI bleed

Chronic

  • Small to moderate volume of total circulating blood loss over long time period

    • Menorrhagia

    • Chronic GI bleed

<p>Acute</p><ul><li><p><strong>Moderate to large volume of total circulating blood loss in short time period</strong></p><ul><li><p>Surgery</p></li><li><p>Trauma</p></li><li><p>Acute GI bleed</p></li></ul></li></ul><p>Chronic</p><ul><li><p><strong>Small to moderate volume of total circulating blood loss over long time period</strong></p><ul><li><p>Menorrhagia</p></li><li><p>Chronic GI bleed</p></li></ul></li></ul><p></p>
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Hemorrhagic Anemia Pathogenesis (Acute & Chronic)

Deficiency in total circulating blood volume Acute or Chronic

<p>Deficiency in total circulating blood volume Acute or Chronic</p>
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Hemorrhagic Anemia Risk Factors (Acute & Chronic)

Acute

  • Surgery

  • Trauma

  • Acute GI bleed

Chronic

  • Menorrhagia

  • Chronic GI bleed

<p></p><p>Acute</p><ul><li><p><strong>Surgery</strong></p></li><li><p><strong>Trauma</strong></p></li><li><p><strong>Acute GI bleed</strong></p></li></ul><p>Chronic</p><ul><li><p><strong>Menorrhagia</strong></p></li><li><p><strong>Chronic GI bleed</strong></p></li></ul><p></p>
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Hemorrhagic Anemia Clinical Manifestations (Acute & Chronic)

Stages of Hemorrhagic Shock

Mild: (<20% Blood Volume Loss)

  • Cool Extremities

  • Pallor

  • Diaphoresis

  • Increased capillary refill time

  • Anxiety

Moderate: (20-40% Blood Volume Loss)

  • Tachycardia

  • Tachypnea

  • Oliguria

  • Orthostatic Hypotension

  • Confusion or Lethargy

Severe: (>40% Blood Volume Loss)

  • Severe tachycardia

  • Severe hypotension

  • Hemodynamic instability

  • Obtunded or Comatose

<p>Stages of Hemorrhagic Shock</p><p><strong>Mild: (&lt;20% Blood Volume Loss)</strong></p><ul><li><p>Cool Extremities</p></li><li><p>Pallor</p></li><li><p>Diaphoresis</p></li><li><p>Increased capillary refill time</p></li><li><p>Anxiety</p></li></ul><p><strong>Moderate: (20-40% Blood Volume Loss)</strong></p><ul><li><p>Tachycardia</p></li><li><p>Tachypnea</p></li><li><p>Oliguria</p></li><li><p>Orthostatic Hypotension</p></li><li><p>Confusion or Lethargy</p></li></ul><p><strong>Severe: (&gt;40% Blood Volume Loss)</strong></p><ul><li><p>Severe tachycardia</p></li><li><p>Severe hypotension</p></li><li><p>Hemodynamic instability</p></li><li><p>Obtunded or Comatose</p></li></ul><p></p>
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Hemorrhagic Anemia Treatments (Acute & Chronic)

  • Treat underlying cause

  • Transfusion of blood products

<ul><li><p>Treat underlying cause</p></li><li><p>Transfusion of blood products</p></li></ul><p></p>
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Hemorrhagic Anemia Nursing Considerations (Acute & Chronic)

  • Monitor Closely for changes from baseline

  • Mental status changes can be early sign

  • Correlation between palpable pulses and systolic BP

<ul><li><p>Monitor Closely for changes from baseline</p></li><li><p><strong>Mental status changes can be early sign</strong></p></li><li><p>Correlation between palpable pulses and systolic BP</p></li></ul><p></p>
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Hemolytic Anemia Etiology

Implanted Devices (Mechanical)

  • Mechanical heart valves

  • Cardiopulmonary bypass machines

Immune Response (Autoimmune response)

  • Transfusion reaction to incompatible blood type

  • Hemolytic disease of the Newborn

Hypersplenism (Organ Dysfunction)

  • Long term or excessive ETOH ingestion

  • SLE

  • RA

Substances (Chemical)

  • Snake venom

  • Hypotonic infusion

  • Chemicals (arsenic)

  • Heavy metals (lead)

  • Infection (malaria)

<p><strong>Implanted Devices (Mechanical)</strong></p><ul><li><p>Mechanical heart valves</p></li><li><p>Cardiopulmonary bypass machines</p></li></ul><p><strong>Immune Response (Autoimmune response)</strong></p><ul><li><p>Transfusion reaction to incompatible blood type</p></li><li><p>Hemolytic disease of the Newborn</p></li></ul><p><strong>Hypersplenism (Organ Dysfunction)</strong></p><ul><li><p>Long term or excessive ETOH ingestion</p></li><li><p>SLE</p></li><li><p>RA</p></li></ul><p><strong>Substances (Chemical)</strong></p><ul><li><p>Snake venom</p></li><li><p>Hypotonic infusion</p></li><li><p>Chemicals (arsenic)</p></li><li><p>Heavy metals (lead)</p></li><li><p>Infection (malaria)</p></li></ul><p></p>
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Hemolytic Anemia Pathogenesis

RBCs are destroyed faster than they are replaced

<p>RBCs are destroyed faster than they are replaced</p>
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Hemolytic Anemia Risk Factors

Malaria infection

Transfusion reactions

Hypersplenism (SLE, RA)

Mechanical Heart Valves

Cardiopulmonary bypass machines

<p>Malaria infection</p><p>Transfusion reactions</p><p>Hypersplenism (SLE, RA)</p><p>Mechanical Heart Valves</p><p>Cardiopulmonary bypass machines</p>
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Hemolytic Anemia Clinical Manifestations

S/S vary mild or severe

  • Dark or bloody urine

  • Jaundice

  • Splenomegaly

<p>S/S vary mild or severe</p><ul><li><p>Dark or bloody urine</p></li><li><p>Jaundice</p></li><li><p>Splenomegaly</p></li></ul><p></p>
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Hemolytic Anemia Treatment

  • Treat underlying cause

  • Transfusion of blood products only when critically necessary

<ul><li><p>Treat underlying cause</p></li><li><p>Transfusion of blood products only when critically necessary</p></li></ul><p></p>
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Blood Work: Signs of Hemorrhagic Anemia

  • Low RBC level

  • Normocytic, Normochromic

  • Low Hgb/Hct levels

<ul><li><p>Low RBC level</p></li><li><p>Normocytic, Normochromic</p></li><li><p>Low Hgb/Hct levels</p></li></ul><p></p>
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Blood work: Signs of Hemolytic Anemia

  • Low RBC level

  • Low Hgb/Hct levels

  • Elevated Reticulocyte count

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What are the inherited blood anemia disorders?

Sickle Cell Anemia

Thalassemia

<p>Sickle Cell Anemia</p><p>Thalassemia </p>
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Sickle Cell Anemia: Etiology

Inherited genetic mutation

  • African American, Arab, Asian descent

<p>Inherited genetic mutation</p><ul><li><p>African American, Arab, Asian descent</p></li></ul><p></p>
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Sickle Cell Anemia: Pathogenesis

Abnormal HGB (hemoglobin) production resulting in decreased O2 carrying capacity

Misshaped RBCs leading to increased RBC hemolysis (destruction)

  • Dysmorphic

<p>Abnormal HGB (hemoglobin) production resulting in decreased O2 carrying capacity</p><p>Misshaped RBCs leading to increased RBC hemolysis (destruction)</p><ul><li><p>Dysmorphic</p></li></ul><p></p>
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Sickle Cell Anemia: Risk Factors

  • Genetics, family hx

  • Ancestry

<ul><li><p>Genetics, family hx</p></li><li><p>Ancestry</p></li></ul><p></p>
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Sickle Cell Anemia: Clinical Manifestations

  • May be asymptomatic

  • General S/S anemia

  • Jaundice

  • Pain episodes (mild to severe)

  • Splenomegaly

  • Stunted growth

<ul><li><p>May be asymptomatic</p></li><li><p>General S/S anemia</p></li><li><p>Jaundice</p></li><li><p>Pain episodes (mild to severe)</p></li><li><p>Splenomegaly</p></li><li><p>Stunted growth</p></li></ul><p></p>
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Sickle Cell Anemia: Treatment

Rx to prevent RBC sickling

  • Voxelotor

  • Hydroxyurea

Folic Acid Supplement

Reduce Risk for exacerbation (SCC)

  • Vaccinations

Allogenic Bone Marrow Transplant

Gene Therapy (limited availability)

<p>Rx to prevent RBC sickling</p><ul><li><p>Voxelotor</p></li><li><p>Hydroxyurea</p></li></ul><p>Folic Acid Supplement</p><p>Reduce Risk for exacerbation (SCC)</p><ul><li><p>Vaccinations</p></li></ul><p>Allogenic Bone Marrow Transplant</p><p>Gene Therapy (limited availability)</p><p></p>
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Sickle Cell Anemia: Nursing Consideration

SCD Crisis Management

  • Identify and treat cause

  • Pain management

  • Supplemental O2

  • Blood transfusions

  • Hydration

<p>SCD Crisis Management</p><ul><li><p>Identify and treat cause</p></li><li><p>Pain management</p></li><li><p>Supplemental O2</p></li><li><p>Blood transfusions</p></li><li><p>Hydration</p></li></ul><p></p>
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What is polycythemia? What are the two types of conditions?

Excess production of blood cells

  • Polycythemia vera (Primary)

  • Induced Polycythemia (Secondary)

<p>Excess production of blood cells</p><ul><li><p>Polycythemia vera (Primary)</p></li><li><p>Induced Polycythemia (Secondary)</p></li></ul><p></p>
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Polycythemia Vera: Etiology

Idiopathic genetic mutation

<p>Idiopathic genetic mutation</p>
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Polycythemia Vera: Pathogenesis

Genetic mutation of bone marrow stem cells causes overproduction of RBCs, WBCs, and PLTs

<p>Genetic mutation of bone marrow stem cells causes overproduction of RBCs, WBCs, and PLTs</p>
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Polycythemia Vera: Risk Factors

  • Viruses

  • Autoimmune

<ul><li><p>Viruses</p></li><li><p>Autoimmune</p></li></ul><p></p>
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Polycythemia Vera: Clinical Manifestations

Usually insidious onset of S/S

  • Pruritus

  • HA

  • Weakness

  • Fatigue

  • Dyspnea

  • Dizziness

  • Visual disturbances

  • Weight loss

  • Enlarged spleen

  • Abdominal discomfort

  • Erythromelalgia

    • Increased PLT aggregation → tiny blood clots in extremities vessels

<p>Usually insidious onset of S/S</p><ul><li><p>Pruritus</p></li><li><p>HA</p></li><li><p>Weakness</p></li><li><p>Fatigue</p></li><li><p>Dyspnea</p></li><li><p>Dizziness</p></li><li><p>Visual disturbances</p></li><li><p>Weight loss</p></li><li><p>Enlarged spleen</p></li><li><p>Abdominal discomfort</p></li><li><p>Erythromelalgia</p><ul><li><p>Increased PLT aggregation → tiny blood clots in extremities vessels</p></li></ul></li></ul><p></p>
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Polycythemia Vera: Treatment & Nursing Considerations

  • Therapeutic phlebotomy

  • Radiation

  • Chemotherapy

  • Interferon alpha: off label use now being researched

<ul><li><p>Therapeutic phlebotomy</p></li><li><p>Radiation</p></li><li><p>Chemotherapy</p></li><li><p>Interferon alpha: off label use now being researched</p></li></ul><p></p>
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Secondary Polycythemia: Etiology

Chronic hypoxia

<p>Chronic hypoxia</p>
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Secondary Polycythemia: Pathogenesis

Compensatory response to chronic hypoxia causes overproduction of erythropoietin → high RBC levels

<p>Compensatory response to chronic hypoxia causes overproduction of erythropoietin → high RBC levels</p>
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Secondary Polycythemia: Risk Factors

  • High altitude

  • Lung Disease (COPD, ILD)

  • Renal tumors

  • Heart failure

<ul><li><p>High altitude</p></li><li><p>Lung Disease (COPD, ILD)</p></li><li><p>Renal tumors</p></li><li><p>Heart failure</p></li></ul><p></p>
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Secondary Polycythemia: Clinical Manifestations

Usually insidious onset of S/S

  • Pruritus

  • HA

  • Weakness

  • Fatigue

  • Dyspnea

  • Dizziness

  • Visual disturbances

  • Weight loss

  • Enlarged spleen

  • Abdominal discomfort

  • Erythromelalgia

    • Increased PLT aggregation → tiny blood clots in extremities vessels

<p>Usually insidious onset of S/S</p><ul><li><p>Pruritus</p></li><li><p>HA</p></li><li><p>Weakness</p></li><li><p>Fatigue</p></li><li><p>Dyspnea</p></li><li><p>Dizziness</p></li><li><p>Visual disturbances</p></li><li><p>Weight loss</p></li><li><p>Enlarged spleen</p></li><li><p>Abdominal discomfort</p></li><li><p>Erythromelalgia</p><ul><li><p>Increased PLT aggregation → tiny blood clots in extremities vessels</p></li></ul></li></ul><p></p>
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Secondary Polycythemia: Treatment & Nursing Considerations

  • Treat underlying cause

  • Admin O2

<ul><li><p>Treat underlying cause</p></li><li><p>Admin O2</p></li></ul><p></p>
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Blood Product Administration S/S

Monitor closely for S/S of transfusion reaction

  • Urticaria

  • Pruritis

  • Fever/Chills

  • Respiratory Disease/Dyspnea

  • Hypotension

  • Hematuria

<p>Monitor closely for S/S of transfusion reaction</p><ul><li><p>Urticaria</p></li><li><p>Pruritis</p></li><li><p>Fever/Chills</p></li><li><p>Respiratory Disease/Dyspnea</p></li><li><p>Hypotension</p></li><li><p>Hematuria</p></li></ul><p></p>