Anemia Flashcards

1
Q

What is anemia?

A

It is a reduction in the:

  • the number of RBCs
  • the amount HgB
  • the amount of Hct

It is a clinical condition not a disease

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2
Q

What are the causes of anemia?

A
Dietary conditions
Genetic disorders
Bone marrow disease 
Excessive bleeding
GI bleed - most common cause
Decreased RBC production
Increased RBC destruction
Chronic RBC loss
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3
Q

What will you find on assessment with anemia?

A

Clinical manifestations are associated with Impaired Tissue Perfusion and Impaired Gas Exchange

  • Fatigue – most common symptom
  • Skin – pallor, cyanosis, signs of bleeding.
  • Head and Neck – pallor, ulceration, or fissure
  • Respiratory – tachypnea, SOB at rest or with exertion
  • Cardiovascular – weak pulses, hypotension, tachycardia, palpitations
  • Renal/Urinary – hematuria, proteinuria
  • CNS – lethargy, forgetfulness
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4
Q

What are some lab values that relate to anemia?

A

Hgb ↓, Hct ↓ , RBCs ↓
Hemoglobin S (HbS) 80-100% (Sickle Cell Disease)
Serum Ferritin <10 ng/mL (Iron deficiency anemia)
presence of microcytic RBC (Iron deficiency anemia)
presence of macrocytic RBC (Folic Acid and Vit. B12 deficiency anemia), presence of sickling cells (Sickle Cell Disease)
reticulocyte count ↑, Total-Iron Binding Capacity (TIBC) ↑

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5
Q

What are some other diagnostic tests for anemia?

A

Bone marrow aspiration - positive for anemia
Blood loss - chronic or acute
Medical history of chronic kidney, cardiac, respiratory disorders
Physical symptoms increase as a compensatory mechanism. Cardiac output increases when Hgb drops below 7g/dl.
Imaging: Radioisotopic imaging, Xrays, CT, MRI

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6
Q

What are some risk factors for anemia?

A

Diet high in fats and carbohydrates but lacking in iron, protein, or vitamins or vegan diet.
Poor nutrition or malabsorption
Family history of blood disorder or genetic disease such as sickle cell.
Medication history of anemia-producing drugs – refer to Table 39-3 on p. 801 (FYI only)
GI surgery or GI disorders

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7
Q

What are some nursing diagnoses related to anemia?

A
Ineffective tissue perfusion
Impaired gas exchange
Activity intolerance 
Anxiety 
Impaired Immunity
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8
Q

What are some types of anemias?

A

Sickle cell disease (formerly called Sickle cell anemia)

Iron deficiency anemia

Vitamin B 12 deficiency

Folic acid deficiency

There are others -don’t need to know for now: Aplastic anemia, Glucose-6-phosphate Dehydrogenase Deficiency anemia(G6PD), Immune hemolytic anemia

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9
Q

What is sickle cell disease?

A

A genetic disorder that results in abnormal formation of hemoglobin chains (HbS).
In decreased oxygen states, the RBCs with large amount of HbS become sickle shaped  rigid and clump together  causing blockage or stoppage of the blood flow (vaso-occlusive event).
Vaso-occlusive event (VOE) leads to cycle of more sickling cell due to hypoxia  blood vessel obstruction, inadequate tissue perfusion, ischemia  tissue/organ damage (mostly affects the spleen, liver, heart, kidney, brain, joints, bones, retina).
Sickle cells go back to normal once the precipitating factor has been removed but “revived” cells are more fragile and break easily  anemia.

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10
Q

What is the prevalence and complications of SCD?

A

Prevalence
Approximately 90,000-100,000 people in the US have SCD.
Most common in African Americans (1 in 500 have SCD and 8% to 10% are carriers), but can include people from Middle east, the Mediterranean, and aboriginal tribes India.

Complication
Acute chest syndrome – VOE causes infiltration and damage to the pulmonary system – leading cause of death in SCD

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11
Q

What is a sickle cell crisis?

A

Periodic episodes of extensive cellular sickling.

Has a sudden onset and occurrence vary from weekly to once a year.

Crisis occur in response to conditions such as hypoxemia, strenuous exercise, dehydration, venous stasis, acidosis, anesthesia, low body temperature.

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12
Q

What are the clinical manifestations of SCD?

A
Pain – most common during a crisis
Refer to Physical Assessment/Signs and Symptoms
- Cardiovascular changes
- Respiratory changes
- Skin changes
- Abdominal changes
- Renal changes
- Musculoskeletal changes
- CNS changes
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13
Q

How is SCD diagnosed?

A

Lab results
Higher percentage of hemoglobin S (80%- 100%), percent of cells with permanent sickling (5% - 90%)
Hematocrit may be low (between 20% and 30%), reticulocyte count ↑, white blood cells ↑, Total bilirubin ↑

Other findings
Changes in bone tissues on x-ray ( such as joint necrosis or destruction ), ECG changes, CT or MRI changes in soft tissues from poor oxygenation and chronic inflammation.

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14
Q

How is SCD managed?

A

Collaboratively:

Pain management

  • History – past pain history, previous drug use, disease complication
  • Pain Assessment
  • Drug therapy
  • –> Opioid analgesia
  • IV opioid for at least 48 hours – given on a routine schedule or PCA (patient controlled analgesia)
  • Oral opioid – once relief obtained
  • Avoid “as needed” schedule – not as effective
  • –> Hydroxyurea – stimulates fetal HgB production to reduce sickling cells and pain – can increase risk for leukemia, bone marrow suppression – monitor CBC and drug toxicity
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15
Q

What are the complications of SCD and how are these complications prevented?

A
  • Prevention and Early Detection Strategies
    Thorough and frequent handwashing
    Monitoring for infection
    Strict aseptic techniques for invasive procedures
    Appropriate precautions
  • Drug therapy
    Prophylactic antibiotic
    Immunization
  • Preventing vaso-occlusive event (VOE) and promoting perfusion
    Hydration – oral or IV
    Oxygenation – O2 therapy, monitor saturation
    Transfusion – to dilute HbS levels
    Assess for adequate perfusion to all body areas
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16
Q

What is the patient teaching for SCD?

A

Avoid activities that lead to hypoxia or hypoxemia
Report signs of crisis or infection
Correct use of opioid at home
Refer to Gender Health Considerations box on p. 813
Avoid restrictive clothing
Avoid flexing knees and hips

17
Q

What is iron deficiency anemia (IDA)?

A

Adults usually have about 2g to 6g of iron

Once the iron stores (bone marrow, spleen, liver, muscle) are depleted, the hemoglobin in the RBCs is also depleted.

The RBCs become microcytic and are fewer in number.

Serum Ferritin value is decreased.

Most common type of anemia

More common in women, older adults, and people with poor diets

18
Q

What are the causes of iron deficiency anemia (IDA)?

A

Inadequate iron in diet
Blood loss
Poor intestinal absorption

19
Q

What are the clinical manifestations of IDA?

A

Symptom severity increases as iron decreases

Mild anemia- weakness, pallor, SOB, cold intolerance, headache, activity intolerance, fissures in corners of mouth

Severe anemia- pica, glossitis, gastric atrophy, stomatitis, pagophagia, leg cramps

20
Q

What does the collaborative management of IDA look like?

A

Focus on addressing immediate problems, such as hypoxia.
Evaluate for the cause of anemia, especially abnormal bleeding from the GI tract.
Oral iron supplementation – for mild cases - to increase hemoglobin about 2g/dL in 4 weeks
- Must be taken between meals for better absorption and avoid GI distress.
- Can make the stool black and cause constipation.
Severe iron deficiency anemia- iron solutions can be given IM and IV
- Administer deep IM using Z track in buttock (never in arm).
- Change needle between drawing up medication and administration to decrease subcutaneous staining (staining is usually permanent).
Intake of iron-rich food such as red meat, organ meat, egg yolks, kidney beans, leafy green vegetables, raisins.
Taking iron rich foods with a source of vitamin C increases iron absorption.
Monitor laboratory values.

21
Q

What is Vitamin B12 Deficiency Anemia (VB12DA)?

A

Vitamin B12 failed to activate enzymes that move folic acid across the cell membrane for cell division and growth to occur  improper DNA synthesis.
Types:
- Megaloblastic (macrocytic) Anemia- improper DNA synthesis occurs and produces large, abnormal RBCs.
- Pernicious Anemia- caused by a deficiency of intrinsic factor which is necessary to absorb Vitamin B12
Causes
- Poor intake of Vitamin B12 rich foods (such as in vegan, vegetarian diets or lack of dairy), small bowel resection, chronic diarrhea, diverticula, tapeworms, and overgrowth of intestinal bacteria.

22
Q

What are the clinical manifestations of VB12DA?

A

May be mild or severe and develops slowly. Refer to Chart 40-3 – Key Features on p. 814
Neurologic symptoms: Paresthesia in hands and feet, poor balance (difficulty ambulating)
Glossitis – figure 40-3 on p. 815
Fatigue, weight loss

23
Q

What are the lab findings of VB12DA?

A

Megaloblastic changes - hallmark finding is MCV over 110 µm³, macrocytic cells
Decreased hemoglobin
Decreased reticulocytes
Decreased serum vitamin B12 <100pg/mL - diagnostic of Vitamin B12 Deficiency Anemia

24
Q

What does the collaborative management of VB12DA look like?

A

Identify risk factors
Increase Vitamin B12 rich foods –animal protein, fish, eggs, yeast, green leafy vegetables, milk, cheese, citrus, nuts, dried beans
Vitamin supplements
Monitor levels
Those with Pernicious Anemia are tested using the Schilling test for Vitamin B12 absorption - Vitamin B12 injections given if necessary.

25
Q

What is Folic Acid Deficiency Anemia (FADA)

A

Develops slowly and the symptoms are often attributed to other problems or diseases.
Common causes:
Poor nutrition- the most common cause- due to lack of folic acid rich foods, such as green leafy vegetables, liver, yeast, citrus, nuts, beans, etc.
Malabsorption- syndromes such as Crohn’s disease or alcoholism- the second most common cause.
Drugs- anticonvulsants and oral contraceptives slow or prevent the absorption or conversion of folic acid to its active form.

26
Q

How is FADA diagnosed and what are the clinical manifestations?

A

Labs
Similar to Vitamin B12 Deficiency Anemia
Serum folate level <5ng/mL is diagnostic for Folic Acid Deficiency Anemia

Clinical manifestations are similar to Vitamin B12 Deficiency Anemia but without the neurological symptoms.

27
Q

What does the collaborative management of FADA look like?

A

Identify high risk clients- those who are older, debilitated, have alcoholism, those who are susceptible to malnutrition, those with increased folic acid demands.

Encourage a diet high in folic acid and Vitamin B12

Folic acid supplements

28
Q

What is a vaso-occlusive event?

A

In decreased oxygen states, the RBCs with large amount of HbS become sickle shaped  rigid and clump together  causing blockage or stoppage of the blood flow