Ch. 34 Iron Deficiency Anemia and Vit B12 Deficiency Flashcards

1
Q

Hematology

A

is the study of the blood and the lymphatic system.

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2
Q

Anemia

A

occurs when there is a reduction in the oxygen-carrying capacity through either fewer RBCs or a reduction in hemoglobin.

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3
Q

Which anemia is the most prevalent nutritional deficiency in the world?

A

Iron deficiency anemia

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4
Q

Which group of people does IDA affect the most?

A

African American’s or those in low social status

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5
Q

Risk Factors for IDA

A
Inadequate iron in the diet
Hemorrhage
Chronic blood loss
Gastrointestinal problems (ulcers, esophageal varices)
Colon cancer 
Meds (PPI, NSAIDs)
Pregnancy
Premenopausal women 
Celiac or Chron's disease 
Gastrointestinal surgeries such as gastric bypass surgery and partial and total gastrectomy can lead to poor absorption of iron and IDA
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6
Q

Patho of IDA

A

With an iron deficiency, the body has insufficient hemoglobin to carry adequate oxygen to meet body requirements

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7
Q

What is the late manifestation of iron deficiency?

A

Anemia

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8
Q

Where does the body store iron?

A

in the liver as ferritin

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9
Q

Clinical Manifestations of IDA

A
Hypoxia
Fatigue
Pallor
Tachycardia
Tachypnea 
Spoon-shaped fingernails, or koilonychias
Glossitis
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10
Q

diagnosis of IDA?

A

A complete blood count (CBC) demonstrates decreased hemoglobin and hematocrit levels. Low serum ferritin levels, which reflect the body’s iron stores, are a confirmation of IDA

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11
Q

Diet for medical management of IDA?

A

Good dietary sources of iron include meat (especially red meat), dark green leafy vegetables (spinach, broccoli, peas), beets, dried beans, iron-fortified breakfast cereals and breads, and Cream of Wheat

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12
Q

What is diet alone does not work for IDA and what is the first line of therapy?

A

iron supplementation is needed, and this can be done through iron preparations administered orally, intramuscularly, or intravenously. Oral supplementation is the first line of therapy

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13
Q

Pts on iron therapy should be monitored for?

A

monitored for nausea, abdominal discomfort, constipation, and/or diarrhea

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14
Q

Iron supplementation by parenteral means is indicated only in cases of

A

severe gastrointestinal distress secondary to oral administration, malabsorption disorders, or in acute cases of IDA in which levels need to be increased more rapidly.

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15
Q

How are parenteral iron given and why?

A

Because parenteral iron formulas stain the skin, the Z-track method is used when administering iron intramuscularly. The Z-track prevents leakage of irritating and discoloring medications, such as iron dextran

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16
Q

Complications of IDA and why

A
  • Heart failure- b/c w/o iron do not have the O2 carrying ability to meet demand
  • Renal failure- all blood flows through renal system b/c kidneys filter the waste products and will not produce more RBCs due to lack of erythropoietin
  • Impaired thermoregulation- w/o enough O2 carrying RBCs, blood is shunted to core leading to shivering
  • Impaired immune function -Its deficiency affects the capacity to have an adequate immune response. The role of iron in immunity is necessary for immune cell proliferation
  • Psychomotor and cognitive impairment- b/c in puts body into a inflammatory state and causes tissue damage
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17
Q

Signs/symptoms related to decreased oxygenation

A
  • Decreased hematocrit and hemoglobin levels
  • Decreased serum ferritin levels
  • Tachypnea
  • Shortness of breath
  • Tachycardia
  • Pallor
  • Fatigue
  • Blood loss
  • Changes in level of consciousness
  • Cognitive impairment
  • Glossitis
  • Physical abnormalities such as spoon-shaped fingernails
18
Q

IDA nursing diagnosis

A
  • Inadequate tissue perfusion related to decreased oxygen delivery as a result of decreased iron stores
  • Fatigue related to inadequate oxygenation to body tissues
  • Activity intolerance related to impaired oxygen-carrying capacity secondary to IDA
19
Q

Nursing Interventions for IDA: Assessment

What are you looking for and why?

A

Vital signs Tachycardia and tachypnea are secondary to the heart and lungs compensating for decreased oxygenation of body tissues caused by decreased iron levels, which leads to decreased hemoglobin levels.
• Serum hemoglobin and ferritin levels With an iron deficiency, reflected by low ferritin levels, there is insufficient hemoglobin to deliver oxygen to the body tissues. Decreased hemoglobin and serum ferritin levels indicate IDA.
• Fatigue, pallor, and shortness of breath Fatigue, pallor, and shortness of breath worsen with increasingly decreased levels of iron, resulting in inadequate oxygen-carrying capacity.
• Level of consciousness Alterations in level of consciousness occur as a result of decreased iron levels that cause decreased oxygenation to the brain. If prolonged IDA is present in a child’s developing brain, cognitive impairment could be permanent.
• Blood loss, if present The greater the blood loss, the worse the clinical manifestations are as a result of decreasing iron stores and decreased hemoglobin levels leading to inadequate tissue perfusion.

20
Q

How to see if there is blood loss?

A

Bruising, H&H, and urine

21
Q

Nursing actions to increase iron for IDA

A

Increase dietary iron. Increasing iron intake through dietary sources increases the body’s iron stores and results in increased hemoglobin levels, thus increasing tissue perfusion.
• Increase intake of vitamin C. Increasing vitamin C intake may increase iron absorption.
• Administer iron-supplement therapy. Iron-supplement therapy is necessary if iron stores need to be increased quickly or if malabsorption disorders are present, which interfere with the body’s ability to incorporate iron from dietary sources.
• Minimize blood loss. Any obvious hemorrhaging needs to be controlled immediately to minimize blood loss. Excessive bleeding with menstruation may be controlled by various hormonal medications.

22
Q

Nursing pt teaching for IDA

A

Dietary sources of iron Good dietary sources include meat (especially red), dark green leafy vegetables (spinach, broccoli, peas), beets, dried beans, iron-fortified breakfast cereals and breads, and Cream of Wheat. Many Web sites are available for nutritional information
• Immediately report any signs of bleeding, increasing fatigue, or shortness of breath. Most cases of IDA occur over a prolonged period of time. Therefore, clinical manifestations usually present when iron stores have already been significantly decreased.
• Daily iron supplements must be taken as prescribed. Iron supplements replace the body’s iron stores and increase the production of hemoglobin molecules, leading to improved tissue perfusion. Oral supplements can cause constipation, diarrhea, nausea, or abdominal discomfort. Patients need to be instructed to report these side effects to the healthcare provider. If side effects are too severe, then supplementation via parenteral routes is available.
• Dangers of lead exposure In lower-socioeconomic environments, lead paint is still present in many buildings. Exposure to lead can lead to cognitive impairment and developmental abnormalities in children.
• Prenatal teaching about iron intake Inadequate iron intake by pregnant women has been linked to lower birth weight, preterm labor, and increased mortality of mother and child.

23
Q

Pica

A

When iron levels are low people start to crave non food items

24
Q

Vitamin B12, also called

A

cobalamin

25
Q

Vitamin B12 Deficiency

A

deficiency occurs either when the body has inadequate sources of vitamin B12 or because of malabsorption disorders that make dietary vitamin B12 unavailable for body use

26
Q

Does the body store iron and Vit B12?

A

Body stores iron but not Vit B12 - have to consume daily

27
Q

Risk factors for Vit B12 deficiency

A
Older adults
G I resections
Autoimmune disorders (AIDS)
Crohn’s disease
Celiac disease
Long-term use of medications that decrease gastric acid (PPI and H2)
28
Q

Vit B12 is needed for

A
  • coenzyme required for normal function of the central nervous system, formation of red blood cells, and synthesis and regulation of DNA
  • vitamin B12 because it is essential to the synthesis of fatty acids and energy production
29
Q

What foods have Vit B12?

A

dietary sources of animal proteins, including meat, seafood, eggs, and dairy products

30
Q

Clinical Manifestations of Vit B12 deficiency

A
Spinal cord degeneration
Peripheral neuropathy 
Altered mental status
Depression
Visual changes
Tachycardia
Shortness of breath
Dizziness
Fatigue
31
Q

Diagnosis of Vit B12

A

CBC
Serum Vitamin B12
Schilling’s test

32
Q

What is the Schilling’s test

A

a radionuclide 24-hour urine test that indirectly measures intrinsic factor.

33
Q

What is intrinsic factor?

and where is it made?

A

Intrinsic factor - protein that helps with absorption of vit b 12 and does it small intestine

intrinsic factor made by partial cells in the stomach

34
Q

Medical management of Vit B12 deficiency

A
  • Prevention is key
  • Oral B12 but if severe need weekly injections
  • Diet-meat, seafood, eggs, and dairy products
  • **B12 only made by animal protein
35
Q

Complications of Vit B12 deficiency

A
  • impairs DNA synthesis and the body’s ability to produce RBCs
  • Orthostatic hypotension - causes dizziness
  • impacts on the functional ability of the individual and quality of life
36
Q

Nursing assessment for Vit B12 deficiency

A

Monitor VS for:
• Shortness of breath • Tachypnea • Tachycardia • Pallor • Fatigue • Dizziness

Neuro exam:
• Numbness, tingling, or burning in hands or feet • Altered mental status (confusion, dementia) • Depression • Mood swings • Coordination and balance • Impaired taste, stinging sensation on the tongue (can cause glossitis) • Visual disturbances

37
Q

Nursing diagnosis for Vit B12 Deficiency

A
  • Inadequate tissue perfusion related to decreased oxygenation as a result of decreased hemoglobin and hematocrit
  • Activity intolerance related to impaired oxygen-carrying capacity secondary to vitamin B12 deficiency
  • Chronic pain related to inadequate vitamin B12 levels as evidenced by peripheral neuropathy
38
Q

Nursing interventions: assessment for Vit B12

A

• Vital signs

Vitamin B12 deficiency impairs RBC production, with a resulting decrease in tissue perfusion. Tachycardia and tachypnea occur as the heart attempts to compensate for the decrease in tissue perfusion.

• Fatigue, pallor, and shortness of breath

Fatigue, pallor, and shortness of breath worsen with increasingly decreased levels of RBCs, causing inadequate tissue perfusion.

• Numbness, tingling, or burning of the hands or feet; confusion; mood swings

Neurological clinical manifestations occur because of the impairment of DNA synthesis of myelin sheath and neurotransmitters.

• Decreased hemoglobin/hematocrit levels, decreased vitamin B12 levels, elevated serum and urine MMA levels

A CBC shows decreased hemoglobin and hematocrit levels. The serum vitamin B12 assay is decreased due to the lack of vitamin B12 needed for synthesis.

• Fall risk (safety)

Confusion, dementia, coordination and balance impairment, and visual disturbances make these patients at risk for falls. Paresthesia and tingling (peripheral neuropathy) can affect ambulation, gait, and stability. Severe neuropathy may take time to recover.

• Intake and output

Constipation, diarrhea, and/or anorexia affect the absorption of vitamin B12 and may worsen the problem.

39
Q

Nursing Interventions: Actions for Vit B12

A

• Ensure adequate vitamin B12 intake.

Ensuring that the patient has an adequate intake of vitamin B12 prevents clinical manifestations of anemia and degenerative neurological changes (see Table 34.3).

• Administer vitamin B12 therapy.

Oral supplementation in mild cases of vitamin B12 deficiency may be helpful. In more severe cases, supplementation with parenteral therapy is required. Parenteral supplementation may be necessary for patients who lack intrinsic factor and cannot absorb oral supplementation. Vegetarians can prevent or treat this deficiency with oral supplements, vitamins, or fortified soy milk. When the deficiency is due to pernicious anemia or the absence of intrinsic factor, the replacement of vitamin B12 involves I-mg IM injections of cyanocobalamin vitamin B12.

• Monitor use of folic acid.

Before starting a patient on folic acid, confirm that the patient does not have a vitamin B12 deficiency. Folic acid resolves the anemia by escaping the methylfolate trap, but neurological degeneration due to vitamin B12 deficiency continues.

• Monitor use of nitrous oxide.

Nitrous oxide inactivates vitamin B12 in the body. Prior to using for anesthesia, confirm that the patient is not vitamin B12 deficient.

• Assess pain and activity levels due to peripheral neuropathy.

Peripheral neuropathy may develop because of vitamin B12 deficiency. Increasing pain may interfere with functional abilities. Because position sense, coordination, and balance are affected, physical therapy and occupational therapy should be considered along with the use of assistive devices.

40
Q

Nursing interventions: pt teaching Vit B12

A
  • Dietary sources of vitamin B12 Dietary sources of vitamin B12 include meat, seafood, eggs, and dairy products.
  • Need for vitamin B12 supplementation Because of the lack of vitamin B12 in plants, vegans/vegetarians may need daily oral supplementation. Patients may have a sore tongue and need bland, soft food frequently, along with mouth care.
  • Immediately report any clinical manifestations of fatigue, shortness of breath, paresthesias, and confusion. Clinical manifestations usually present after prolonged vitamin B12 deficiency. Resolution of the anemia does not stop neurological degeneration unless the deficiency is resolved.
  • Prenatal teaching Pregnancy may increase the demand for vitamin B12. Prophylactic oral supplementation is recommended.
  • Radiation for advanced cancers Radiation therapy may increase the need for vitamin B12 supplementation. Patients with anemia do not respond as well to radiotherapy because of impairment of oxygen transport to cancer cells.
  • Actions of acid-reducing medications Patients using these medications may develop vitamin B12 deficiency because of a decrease in the function of the parietal cells of the stomach, which produce intrinsic factor.