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NURS 313R > Exam 1: Hematology: Anemias > Flashcards

Exam 1: Hematology: Anemias Flashcards

1
Q

Anemia

A

A deficiency in the number of erythrocytes, quantities of hemoglobin and volume of packed RBCs.

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2
Q

Causes of Anemia

A
  1. Blood loss
  2. Impaired production of erythrocytes (could be d/t deficiency of nutrients such as iron, folic acid, vit B12, etc. which are needed for a production of erythrocytes.)
  3. Increased destruction of erythrocytes (could be d/t hemolysis, medications, the shape of the RBC)
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3
Q

2 General Types of Anemia

A
  1. Morphological

2. Etiological

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4
Q

Morphologic

A

Based on shape and size

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5
Q

Etiologic

A

Based on underlying issue

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6
Q

Types of Morphologic anemia includes

A
  1. Microcytic (small), hyprochomic (pale)

2. Macrolytic (megoblastic)

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7
Q

Types of Etiologic Anemia includes

A
  1. Decreases RBC production
  2. Blood Loss
  3. Increased RBC destruction
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8
Q

What can cause decreased RBC production?

A
  1. Decreases hgb synthesis (could be d/t iron deficiency)
  2. Detective DNA synthesis (could be d/t vitamin B12 deficiency, folic acid deficiency or cobalamin deficiency)
  3. Decreases number of RBC precursors (could be d/t decreased erythropoietin (released by kidneys, liver, and bone marrow), medications (chemotherapy).)
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9
Q

What can cause blood loss?

A
  1. Acute: trauma, surgery or rupture of blood vessels

2. Chronic: chronic illness (check audio for rest)

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10
Q

Increased RBC destruction can be caused by

A
  1. Intrinsic factors -..

2. Extrinsic factors - ..

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11
Q

Clinical Manifestations of Anemia

A
  1. Decreases hemoglobin level
  2. Palpitations
  3. Dyspnea, fatigue
  4. Skin changes (pallor, jaundice, pruritus secondary to bile salts.
  5. Cardiopulmonary Manifestations: murmurs, bruit (d/t low viscosity of blood), risk for angina pectoris, MI and HF
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12
Q

Nursing Management of Anemia: Goals

A

Assume normal ADL’s
Maintain adequate nutrition
Prevent complications

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13
Q

Nursing Interventions

A
  1. Blood Transfusion
  2. Drug therapy (vitamin supplements such as iron)
  3. Volume Replacement
  4. O2 therapy
  5. Dietary and Lifestyle changes
  6. Assess for safety
  7. Energy Conservation (plan periods of rest to maintain oxygen supply)
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14
Q

3 Alterations in Erythropoises

A
  1. Decreases hgb synthesis
  2. Detective DNA synthesis in RBC
  3. Diminished availability of erythrocytes precursor
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15
Q

Iron Deficiency Anemia

A

Most common chronic hematologic disorder.

Developed from inadequate dietary iron intake, malabsorption, blood loss and hemolysis.

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16
Q

Who are more susceptible to iron deficiency anemia?

A

Women in reproductive years are most susceptible

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17
Q

Clinical Manifestations of Anemia

A

Early can be asymptomatic.

  1. Pallor (most common)
  2. Glossitis (second most common)
  3. Headache
  4. Parasthesia
  5. Burning sensation of the tongue
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18
Q

Collaborative Care for Anemia: Goal

A

Treatment of the underlying cause

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19
Q

Collaborative Care: Interventions

A
  1. Educate what foods are a good source of iron (meat, green leafy vegetables, fruits)
  2. Oral and Parenteral Iron Supplements
  3. Blood Transfusion
  4. Drug therapy
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20
Q

When taking iron, stool can become

A

Dark and tarry

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21
Q

Nursing management

A
  • Recognize at risk individual.
  • Dietary Teaching
  • Reassess Hgb and RBC
  • Iron therapy 2-3 after Hgb return to normal
  • Monitor liver function (long term use can affect liver function)
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22
Q

Thalassemia

A

Group disease that has an autosomal recessive genetic basis; it involves inadequate production of normal hemoglobin

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23
Q

2 Forms of Thalassemia

A
  1. Heterozygous

2. Homozygous

24
Q

Heterozygous (Thalassemia minor)

A

1 Thalassemia gene and 1 normal gene from one parent.
Minimal to no symptoms, BUT there is a potential for it.
Can be inherited.

25
Q

Homozygous (Thalassemia Major)

A

Symptoms are the same but life threatening.

26
Q

Clinical Manifestations of Thalassemia

A
  1. Retarded growth (physical and mental)
  2. Paleness, Jaundice
  3. Pronounced splenomegaly and hepatomegaly
  4. Bone marrow hyperplasia (bone marrow tries to compensate by producing more RBC’s causing an overgrowth)
  5. Hyper-coagulable blood
27
Q

Collaborative Care for Thalassemia

A
  1. Blood Transfusion
  2. Chelating Therapy: binds iron (prevents an over abundance of iron). (*more info in recording)
  3. Folic Acid (more info in recording)*
  4. Splenectomy (enlarged spleen destroys normal RBC’s, therefore a splenectomy may be needed)
  5. Monitor cardiac (d/t viscosity of blood and decreased O2 -> HR increases (listen to recording for more info.), hepatic and pulmonary functions)
  6. Hematopoietic stem cell transplant: although it is considered a cure, it is extremely expensive.
28
Q

Megaloblastic Anemia

A

Caused by impaired DNA synthesis characterized by the presence of large RBC

29
Q

Megaloblastic Anemia: What can cause it?

A
  1. Vit B12 and Folic Acid deficiency (are essential for synthesis of DNA)
  2. Drugs
  3. Inborn Error Metabolism (error in metabolizing folic acid)
  4. Malignancy
30
Q

2 Types of Megaloblastic Anemia

A
  1. Cobalamin Deficiency (Vit B12): includes pernicious anemia
  2. Folic Acid Deficiency
31
Q

Intrinsic Factor

A

Essential for absorption of Vit B12 (most common cause for pernicious anemia)

32
Q

Causes of Cobalamin Deficiency Anemia

A
  1. Pernicious anemia
  2. Gastrectomy
  3. Chronic Gastritis
  4. Nutritional Deficiency
  5. Chronic Alcoholism
  6. Hereditary
33
Q

Clinical Manifestations of Megaloblastic Anemia

A
  1. Sore red beefy and shiny tongue
  2. Anorexia
  3. Nausea/Vomiting, abdominal pain
  4. Weakness/muscle weakness
  5. Paresthesia of feet and hands (vit B12 is needed for sensation)
  6. Decrease vibratory and position senses
  7. Ataxia
  8. Confusion/dementia
34
Q

Collaborative Care for patients with Megaloblastic Anemia

A

Parenteral Intranasal Administration of Cyanocobalamin (without cyanocobalamin, patient may die within 1-3 years)

35
Q

Nursing Management of Megaloblastic Anemia

A
  1. Evaluate pt. With family history of anemia
  2. Early detection and treatment
  3. Report signs and symptoms of PCP
  4. Protect from falls, burns and trauma
  5. Assess for neurological difficulties.
  6. GI cancer screening.
36
Q

How do parietal cells effect intrinsic factor?

A

Secreted by parietal cells.

Parietal cells also secrete HCL to create an acidic environment for IF to thrive.

37
Q

If you decrease intrinsic factor, what happens to Vit B12 absorption?

A

It decreases.

38
Q

Pernicious anemia

A

Absence of intrinsic factor d/t mucosal atrophy or autoimmune destruction of parietal cells. (Decreased IF and decreased HCL - needed for secretion of IF)

39
Q

How does GI surgery such as gastrecotomy/gastric bypass effect Vit B12 absorption?

A

B12 site of absorption is the duodenum of SI. Removal of distal ileum impairs cobalamin absorption.

40
Q

How does Chronic Gastritis effect Vitamin B12 absorption?

A

Inflamed lining causes decreased IF and therefore decreased Vit B12 absorption.

41
Q

How does chronic alcoholism effect Vitamin B12 absorption?

A

B12 is metabolized and absorbed in the liver. -> alcohol causes a defect in the storage of Vit B12.

42
Q

How do Proton Pump Inhibitors and H2 Histamine Receptor blockers effect the absorption of Vitamin B12?

A

Decreases acidity -> acidic environment is needed for IF -> decreased IF -> decreased Vitamin B12 absorption

43
Q

Why are vegetarians more susceptible to Vit B12 deficiency?

A

Meat is high in Vitamin B12

44
Q

Why are their neuromuscular manifestations in pernicious anemia (Vit B12 deficiency)?

A

Vitamin B12 is necessary for the synthesis of myelin on neurons.

45
Q

Folic Acid can be found in

A

Dark green vegetables

Citrus fruits

46
Q

What are clinical manifestations of folic acid deficiency?

A

GI: smooth, beefy red tongue; dyspepsia (indigestion).

NO NEUROLOGIC PROBLEMS

47
Q

The general problem with Cobalamin Deficiency is that

A

The body cannot absorb Vit B12. (Therefore it is NOT beneficial to take PO B12 supplements. Needs nasal or IV supplements to bypass GI system.)

48
Q

Why is splenomegaly a clinical manifestation of Thalassemia?

A

Spleen continuously tries to remove damaged RBC (function of spleen is to hold these RBC) -> enlarging it

49
Q

Why is hepatomegaly/cardiomyopathy a clinical manifestation of thalessemia?

A

Fe deposition.

50
Q

Signs and Symptoms of Fe Toxicity

A

Abdominal Pain
Bloody diarrhea
Emesis (bloody vomit)
Late Signs (decreased LOC, BP, HR; shock; metabolic acidosis)

51
Q

Moderate states of anemia

A

Hgb 10-12

Asymptomatic or Symptomatic (palpitations, dyspnea, mild fatigue)

52
Q

Moderate States of Anemia

A

Hgb 6-10

Cardiopulmonary symptoms increase (at rest or during activity): bounding pulse, increased palpitations, dyspnea.

53
Q

Severe Anemia

A

Hgb <6

Involves multiple body systems.

54
Q

Clinical Manifestations of Severe Anemia

A

Skin:

 - Pallor (reduced Hgb = decreased BF to skin)
 - Jaundice (d/t hemolysis of RBC = increase in bilirubin)
 - Pruritus (d/t bile salts excrete through skin when sweating)

Cardiopulmonary:

  - heart and lungs work harder to provide adequate amounts of O2 to tissues
  - low viscosity of blood -> systolic murmurs and bruit; 
  - MI or angina may occur if O2 needs aren’t met 
 - Tachycardia, dyspnea, tachypnea
 - If heart is overworked for extended period -> HF, cardiomegaly, pulmonary/systemic congestion, ascites and edema.

Glossitis, smooth tongue

55
Q

Anti seizure drugs and oral contraceptives place a patient at risk for what kind of anemia?

A

Folic acid deficiency anemia because these drugs affect the absorption of folic acid.

56
Q

Colloid osmotic pressure

A

Need to know more!!!

NURS 313R (18 decks)

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