module 4 lesson 1.2: anemias

The Red Blood Cell (RBC)

• Primary purpose: carry oxygen

• Oxygen is carried on ___

→Hemoglobin needs (what element) __ for synthesis

• RBC life span is __ days

→ Broken down by the ___

→ Recycled parts: iron and amino acids

→ Heme combines with ___ excreted in bile

• RBCs are produced in ____

→Kidneys respond to (what medical condition) ___

→Erythropoietin is produced by (what organ)___ 

The Red Blood Cell (RBC)

• Primary purpose: carry oxygen

• Oxygen is carried on hemoglobin

→Hemoglobin needs iron for synthesis

• RBC life span is 120 days

→ Broken down by the spleen

→ Recycled parts: iron and amino acids

→ Heme combines with bilirubin excreted in bile

• RBCs are produced in the bone marrow

→Kidneys respond to hypoxemia (Hypoxemia is a low level of oxygen in the arterial blood, while hypoxia is an inadequate supply of oxygen to the body's tissues and organs)

→Erythropoietin is produced by kidneys 

Anemia: 

• Description: ___

→ Impaired __

→ Low ___

• Causes

→___

→___

→ ___

→ ___

Manifestations of anemia

Mild hypoxemia

• Metabolic acidosis

• Increase in heart rate

• Peripheral vasoconstriction

• Diaphoresis

• Increase in blood pressure

• Slight impairment of mental performance

Fatigue

Anemia: 

• Low number of circulating RBCS and/or Low level of hemoglobin

→ Impaired oxygen transport

→ Low H/H (hemoglobin hematocrit)

• Causes

→Blood loss

→Destruction of RBCs (hemolysis)

→ Defective of RBC production

→ Inadequate RBC production (bone marrow suppression)

Manifestations of anemia

Mild hypoxemia

• Metabolic acidosis

• Increase in heart rate

• Peripheral vasoconstriction

• Diaphoresis

• Increase in blood pressure

• Slight impairment of mental performance

Fatigue

Hemolytic anemia

description: ___

→what happens to the RBC? ____

• Body will retain iron and other products of hemoglobin destruction

• An increase in ____

→ Hyperactive ___, increased immature RBCs

Premature destruction of red cells

→Shortened life span of RBC

• Body will retain iron and other products of hemoglobin destruction

• An increase in erythropoiesis

→ Hyperactive bone marrow, increased immature RBCs: Hyperactive bone marrow is the body's attempt to fix hemolytic anemia by working overtime to make new red blood cells and replace the ones being destroyed too quickly

Sickle cell disease

• Recessive genetic disorder (both parents must have the gene in order to pass it to their child)

• Description of the disease: ____

Complications

• ____

• ____

Symptoms

• Triggered by ___

• Acute pain: due to ____

• No treatment, focus on preventing sickling episodes, symptom management

Sickle Cell Anemia - Hydroxyurea (Droxia)

Why	_____
MOA	-helps increase ____ -helps dilute ____
Therapeutic effect	-Reduces the frequency of ___ -Prevents ____
ADE (adverse drug effects)	-___ -can enhance ____
Contraindication	-___

Sickle cell disease

• Recessive genetic disorder (both parents must have the gene in order to pass it to their child)

• Abnormal structure of the hemoglobin

Complications

• Anemia: Reduced oxygen carrying capacity

• Occlusion of vessels with sickled cells (vaso-occlusive crises), forms something similar to blood clot

Symptoms

• Triggered by stress, physical exertion, infection

• Acute pain: due to ischemia

• No treatment, focus on preventing sickling episodes, symptom management

Sickle Cell Anemia - Hydroxyurea (Droxia)

Why	-Increase fetal hemoglobin in bone marrow, slows growth & division of cells while boosting growth of normal cells
MOA	-helps increase fetal hemoglobin in bone marrow -helps dilute abdominal hemoglobin S
Therapeutic effect	-Reduces the frequency of painful sickling episodes -Prevents serious symptoms of disease and reduces pain
ADE (adverse drug effects)	-Bone marrow suppression (bc haults DNA synthesis and stops rapidly dividing blood-forming cells): decreased WBC, decreased plt, anemia -can enhance bleeding in patients: due to lack of platelets made by bone marrow
Contraindication	-severe anemia or leukopenia

Anemia of deficit red cell production types:

• __ deficiency anemia

• ___ anemias

• ___ anemias

• ___ disease anemias

Anemia of deficit red cell production

• Iron deficiency anemia

• Megaloblastic anemias

• Aplastic anemias

• Chronic disease anemias

Iron Deficiency Anemias

• Iron is an essential component of heme

→Deficiency leads to ___

• Caused by iron deficiency in diet: vegetarians, pregnant women, picky children

• Pregnancy: increased iron demand

• Chronic ___ loss

• Clinical manifestations

→___

• Treatment

• Increase dietary intake

• Ferrous sulfate supplement

Iron Supplement - Ferrous sulfate

Why	-___
MOA	-Increase ___ concentration -what form is given IV?
ADE	-GI-constipation*, GI upset, staining of teeth, darkening of stools -may inhibit antibiotics

Iron Deficiency Anemias

• Iron is an essential component of heme

→Deficiency leads to decreased hemoglobin

• Caused by iron deficiency in diet: vegetarians, pregnant women, picky children

• Pregnancy: increased iron demand

• Chronic blood loss

• Clinical manifestations

→Fatigue, palpitations, dyspnea, angina, tachycardia

• Treatment

• Increase dietary intake

• Ferrous sulfate supplement

Iron Supplement - Ferrous sulfate

Why	-People deficient in iron for oxygen transport
MOA	-Increase serum iron concentration -IV: pure elemental iron: Sodium Ferric-Gluconate
ADE	-GI-constipation*, GI upset, staining of teeth, darkening of stools -may inhibit antibiotics

Megaloblastic Anemia

• Description: ____

→Caused by ___

Vitamin B12

• Malabsorption caused by ___

• Dietary sources: ___

• Pernicious anemia: failure to produce ____ needed for ___

• Symptoms include ___

Folic acid

• Dietary sources: vegetables, fruit, meats, fortified cereals

• Malabsorption: associated with ___

Pernicious Anemia - Cyanocobalamin = B12

Why	• Essential for ___ • Necessary for ___
MOA	• ___
Consideration	• PO: ____ • IM: ___
SE	___
CI	___

Folate Acid Deficiency - Folic Acid

Why	• ___ • ___ during pregnancy
MOA	• Essential for ___ • Replacement of ___
CI	Hypersensitivity, leavers disease
ADE	Long term folic acid: ___

Megaloblastic Anemia

• Enlarged but impaired red blood cells

→Caused by deficiencies (in Vitamin b12 & folate for normal DNA synthesis)

Vitamin B12

• Malabsorption: caused by gastrointestinal disease, use of certain medications

• Dietary sources: animal origin

• Pernicious anemia: failure to produce factors needed to absorb B12

• Symptoms include anemia, mild jaundice, neurologic changes

Folic acid

• Dietary sources: vegetables, fruit, meats, fortified cereals

• Malabsorption: associated with ETOH

Pernicious Anemia - Cyanocobalamin = B12

Why	• Essential for cell growth and division • Necessary for myelin sheath
MOA	• Replacement of essential vitamin
Consideration	• PO: poor absorption, need high dose • IM: might be required, monthly injections
SE	NVD
CI	Allergy

Folate Acid Deficiency - Folic Acid

Why	• Treat folic acid deficiency anemia • Prophylaxis during pregnancy
MOA	• Essential for cell growth and division • Replacement of essential vitamin
CI	Hypersensitivity, leavers disease
ADE	Long term folic acid: may worsen symptoms, antileptic meds can decrease efficiency of folic acid

Anemia and nutrition

Nutritional Sources

• Folic Acids: fortified cereals, animal (beef and liver), plant (leafy greens, citrus fruits, beans)

• Iron: animal (red meat, poultry, seafood), plant (lentils, spinach, dried fruits)

• Vitamin B12: animal (fish, meats, eggs, dairy), fortified cereals

Diets with increased risk for nutritional deficits

• Vegetarian or Vegan

• Diets low in red meat

Other considerations

• Alcohol Use Disorder

.

Aplastic anemia: 

issue with the _____

• lab values: everything is high or low? ___ high/ low on what values? ___

• Pancytopenia (everything’s low)

Causes	• ___ • ___ • ___
Clinical manifestations	• Weakness • Fatigue • Pallor • Petechiae • Bleeding • Risk for infection

Aplastic anemia: 

Bone marrow issue

• Low RBCs, Low WBCs and Plts

• Pancytopenia (everything’s low)

Causes	• Radiation and chemotherapy • Medication adverse effect • Infection: viral infections (hepatitis, mononucleosis)
Clinical manifestations	• Weakness • Fatigue • Pallor • Petechiae • Bleeding • Risk for infection

Chronic disease anemia: chronic renal failure

description: ___

Erythropoiesis Stimulating Agent- Epoetin Alfa (Epogen)

Why	• Treat ____ • Reduce the need for ___
MOA	• Stimulates ___ • Controls ___
Evaluation	• Consider assessment measures:  • How will you know your treatment has been effective? ___

as kidney cells decline, long term inability to synthesize erythropoietin

Erythropoiesis Stimulating Agent- Epoetin Alfa (Epogen)

Why	• Treat anemia of chronic kidney disease • Reduce the need for blood transfusions
MOA	• Stimulates bone marrow to make more RBCS: acts as synthetic replacement for missing hormone, directly restoring the chemical signal needed to manufacture red blood cells • Controls rate of RBC production
Evaluation	• Consider assessment measures:  • more RBC