CLASS 7 - RBCS, ANEMIA, POLYCYTHEMIA, AND RELATED THERAPIES Flashcards

1
Q

What is anemia?

A

Decreased RBCs and

decreased oxygen carrying capacity of the blood which can result in tissue hypoxia.

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2
Q

How much Hgb indicates anemia in men?

How much Hgb indicated anemia in women?

A

< 135 mmol / L Hgb in men

< 120 mmol / L Hgb in women

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3
Q

What are the normal ranges of Hgb in men? Women?

A

Men: 140-180 mmol / L
Women: 120-160 mmol / L

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4
Q

What are the normal ranges of Hct in men? Women?

A

Men: 42-52%
Women: 37-47%

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5
Q
Which symptoms appear if Hct drops below:
30-35%
25-30%
20-23%
15-20%
less than 15%
A
30-35% - no symptoms
25-30% - fatigue, malaise
20-23% - SOBOE, dyspnea
15-20% - light-headedness, confusion
less than 15% - death, MI, etc.
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6
Q

What are the 5 types of anemia related to decreased RBC production?

A
  • Iron Deficiency Anemia
  • Megaloblastic anemia (B12, Folic Acid deficiency)
  • Thalassemia
  • Chronic Disease
  • Aplastic Anemia
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7
Q

What are the 3 types of anemia related to RBC destruction?

A
  • Hemolytic anemia
  • Intrinsic anemia
  • Extrinsic anemia
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8
Q

What are the 2 types of anemia related to blood loss?

A
  • Acute bleeding

- Chronic bleeding

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9
Q

What is iron deficiency anemia?

A

decreased iron impedes synthesis of Hgb –> less O2 transported

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10
Q

Describe the etiology of iron-deficiency anemia

A
  1. Inadequate dietary intake of iron, especially during growth spurts or pregnancy
  2. Chronic blood loss from GI ulcer, hemorrhoids, cancer, or excessive menstrual flow
  3. Impaired absorption of iron resulting from gastritis, chronic inflammatory bowel disease, or diarrhea
  4. Severe liver disease
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11
Q

What is the most common nutritional disorder in the world?

A

Iron-deficiency anemia

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12
Q

Are RBCs small, normal, or large in iron deficiency anemia? Are they hypochronic or normochromic?

A

Microcytic, hypochromic (pale cell)

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13
Q

Outline if the following laboratory results would be low, normal, or high in iron deficiency anemia:

  • hemoglobin
  • hematocrit
  • platelets
  • MCV (Mean Corpuscular Volume)
  • MCHC (Mean Corpuscular Hemoglobin Concentration)
  • MCH (Mean Corpuscular Hemoglobin)
  • Ferritin
  • Serum Iron
  • Total Iron Binding Capacity
A
  • hemoglobin: LOW
  • hematocrit: LOW
  • platelets: NORMAL
  • MCV (Mean Corpuscular Volume): LOW
  • MCHC (Mean Corpuscular Hemoglobin Concentration): LOW
  • MCH (Mean Corpuscular Hemoglobin): LOW
  • Ferritin: LOW
  • Serum Iron: LOW
  • Total Iron Binding Capacity: HIGH
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14
Q

What is Mean Corpuscular Volume (MCV)?

A

RBC size + volume

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15
Q

What would be assessment findings in a client w iron deficiency anemia?

A
  • pallor
  • glottis (inflammation of tongue)
  • cheilitis (inflamed lips)
  • headache, paresthesia, burning sensation in tongue
  • poor dietary intake of iron
  • heavy menstrual flow
  • PICA
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16
Q

Why would chronic blood loss result in iron loss from the body?

A

Loss of iron occurs as blood is lost + not recycled.

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17
Q

Why does iron deficiency in the body result in decreased RBC production?

A

Iron is needed to synthesize hemoglobin.

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18
Q

Which patient populations are at a greater risk of iron deficiency anemia?

A

The very young, those w poor diets, women in reproductive years

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19
Q

What conditions result in impaired absorption of iron?

A

Gastritis, chronic inflammatory bowel disease, diarrhea

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20
Q

Why does severe liver disease result in iron deficiency?

A

The liver performs a major role in iron homeostasis (storage + regulation of iron)

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21
Q

What is elemental iron?

A

The total amt of iron in the supplpement available for absorption by your body.

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22
Q

What are side effects of elemental iron?

A

GI adverse events such as heartburn, constipation, diarrhea

black / deep green stool

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23
Q

What client teaching would the nurse do prior to administering elemental iron? Why is it not recommended to be taken w food?

A

Teaching should include dietary choices to increase iron absorption.
Food helps protect against iron-induced GI distress, but decreases iron absorption by 50-70%.

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24
Q

Why is vitamin C recommended when administering elemental iron?

A

Vit C and iron combine to form an iron chelate complex which increases solubility of iron in the SI.

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25
Q

Why is the z-track method used for IM injection of elemental iron?

A

prevents leakage of the medication which irritates + stains the skin, also helps “seal” the drug into the muscle

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26
Q

What is megaloblastic anemia?

A

Anemia in which RBCs are larger than normal (macrocytic) due to impaired DNA formation. The cells are marked for early destruction.

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27
Q

Which 2 vitamins are most closely linked to megaloblastic anemia?

A

B12 (cobalamin) and FA

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28
Q

Outline if the following lab results would be low, normal, or high in megaloblastic anemia:

  • hemoglobin
  • hematocrit
  • platelets
  • MCV
  • MCHC
  • MCH
  • Folic Acid
  • Cobalamin
A
  • hemoglobin: LOW
  • hematocrit: LOW
  • platelets: NORMAL
  • MCV: HIGH
  • MCHC: HIGH
  • MCH: NORMAL
  • Folic Acid: LOW
  • Cobalamin: LOW
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29
Q

What is the role of VIT B12 and FA in erythropoeisis?

A

These vitamins are required for DNA synthesis and maturation of cells.

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30
Q

why are macrocytic RBCs easily destroyed?

A

b/c they have fragile cell membranes resulting from DNA mutation

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31
Q

Is the MCV high or low in macrocytic anemias? Why?

A

High because macrocytic anemia involves enlarged cells

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32
Q

What is pernicious anemia? How is different from other megaloblastic anemias?

A

Pernicious anemia is caused by an absence of intrinsic factor (IF). The gastric mucose doesn’t secrete IF due to either gastric mucosal atrophy or automimmune destruction of parietal cells that produce IF .

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33
Q

What are general signs of cobalamin deficiency? Do they develop right away or over time?

A
  • Sore, red, shiny tongue
  • anorexia
  • nausea
  • vomiting
  • abdominal pain
  • weakness
  • paresthesia of feet + hands
  • reduced vibratory and position senses
  • ataxia
  • muscle weakness
  • impaired thought processes

slow onset.

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34
Q

What is the relationship between IF and vitamin B12?

A

IF allows vit b12 to move past the GI tract to the plasma mem and into the blood

35
Q

The use of which medications increase the risk of developing pernicious anemia? Why?

A

Long term H2-receptor and proton pump inhibitors. They decrease gastric acid secretion in the stomach and decrease parietal cell function.

36
Q

How do we treat vit B12 deficiency anemia?

A
  • nutritional education to treat underlying condition
  • if chronic deficiency related to malabsoprtion, then administer IM B12 daily for 2 wks, then weekly until Hct reaches normal levels, and then monthly for life.
37
Q

How do we treat FA deficiency anemia?

A

Test for b12 prior to treating for FA for neurological concerns.
Nutritional education to treat underlying condition, FA po daily, increase dose if malabsorption.

38
Q

What is a risk associated with excess FA?

A

Clotting

39
Q

What is thalassemia?

A

Microcytic, pale cell anemia.

RBCs are malformed (more square) due to absent or reduced globulin protein.

40
Q

Why is thalassemia linked to reduced RBC production?

A

Malformed RBCs due to absent / reduced globulin protein –> Inadequate production of normal Hgb leads to decreased RBC production.

41
Q

What is the difference between Thalassemia minor and Thalassemia major?

A

Thalassemia minor - mild form (1 gene of pair): not all RBCs are malformed, mild signs + symptoms
Thalassemia major: severe (both genes of pair –> leads to bone deformities, CHF, and splenomegaly (delayed physical and mental growth due to chronic hypoxia).

42
Q

Describe the assessment findings in a client w thalassemia minor

A
  • patient frequently asymptomatic

- mild-moderate anemia w microcytosis and hypochromia

43
Q

Describe the assessment findings in a client w thalassemia major

A
  • delayed physical and mental growth due to chronic hypoxia
  • splenomegaly as the spleen tries to remove damaged RBCs
  • hepatomegaly from iron deposition
  • thickening of cranium and maxillary cavity
  • jaundice
  • fatigue
44
Q

Which ethnic groups are at an increased risk of thalassemia?

A

Mediterranean, South East Asia, Middle East, China, African Descent

45
Q

At which age does thalassemia typically present?

A

Most noticed in infants, symptoms develop by 2y.

46
Q

What Hgb level should be achieved when treating thalassemia?

A

100 mmol / L to foster the patient’s own erythropoesis w/o enlarging the spleen.

47
Q

what is erythropoiesis?

A

Production of Red Blood Cells.

48
Q

Is diet therapy used to treat thalassemia? Should iron be given?

A

Zinc and vit C supplements can be given

FA may be given, iron should not be given.

49
Q

Why is there no drug therapy used to treat thalassemia?

A

Because thalassemia is a genetic condition.

50
Q

Why are iron-chelating agents given when treating thalassemia?

A

To reduce the risk of iron overload (which can lead to hepatomegaly).

51
Q

Why would vit C be given with iron chelatin therapy when it is known to increase the absorption of iron in the body?

A

Because it also increases iron excretion.

52
Q

How does hematopoietic stem cell transplant cure thalassemia?

A

restores the body’s ability to make healthy blood ells by giving healthy stem cells to the patient.

53
Q

Why does thalassemia major cause jaundice?

A

Liver damage which leads to increased serum bilirubin in the blood.

54
Q

Which chronic diseases are associated w anemia? (ACD)

A

Many causes

  • chronic inflammation
  • malignancy
  • chronic kidney disease
  • infections or autoimmune diseases
  • cancer, AIDS, cirrhosis, HIV
55
Q

Chronic anemias are often described as normochromic, normocytic, and hypo-proliferative. What do these terms mean?

A
  • Normochromic = normal in colour
  • Normocytic = normal in size
  • Hypo-proliferative - low numbers
56
Q

What factors contribute to the hypo-proliferative state of RBCs in Anemia of Chronic Disease?

A
  • reduced iron absorption
  • shorter RBC survival bc the body marks the RBCs for destruction
  • decreased response to circulating erythropoeitin
57
Q

What is aplastic anemia?

A

Disease in which the patient has peripheral blood pancytopenia and hypocellular bone marrow. This leads to:

  • impaired bone marrow function and a decrease of all blood cell types.
  • Inability to replace regular loss of RBCs
  • increased yellow bone marrow (fatty tissue).
58
Q

Is the cause of aplastic anemia known?

A

idiopathic - unknown

59
Q

In aplastic anemia are the cells normochromic or hypochromic? Microcytic, normocytic, or macrocytic?

A

Normochromic and normocytic.

60
Q

What is secondary aplastic anemia? What causes it?

A

secondary aplastic - damage to bone marrow. Caused by cancers, radiation, chemotherapy, industrial chemicals, drugs, viral infections

61
Q

A client is described as having pancytopenia. What would the nurse find on an assessment of a client?

A

bruising, bleeding from nose, gums, vagina, and GI tract
poor healing akin and mucosal sores
immunosuppression and susceptibility to infection

62
Q

Which anemias are related to RBC destruction?

A

Intrinsic + extrinsic hemolytic anemias

63
Q

What is sickle cell anemia?

A

Intrinsic hemolytic anemia.

Recessive genetic disorder resulting in abnormal Hgb protein. Which causes RBCs to elongate + become rigid.

64
Q

Why does the shape of the RBCs change in sickle cell anemia?

A

The Hgb is deoxygenated which causes the shape of the cell to become sickled in response to low oxygen levels in the blood.

65
Q

A client is experiencing a sickle cell crisis. What is it? What are the clinical manifestations of this condition?

A
  • premature hemolysis of RBCs. Cells live ~20 days.
  • Very, very painful (tissue ischemia).
  • hyperbilirubinemia due to RBC destruction and jaundice
  • cells are elongated and rigid, obstruct small blood vessels, and predispose patient to thrombus and multiple infarctions.
  • Significant damage and loss of function can occur to many organ systems due to lack of O2.
66
Q

What is hemolytic anemia? What are the clinical manifestations of hemolytic anemia?

A
caused by premature hemolysis of RBCs
mild to life threatening
can result in:
- decreased Hct, Hgb
- increased reticulocyte count
- increased bilirubin (jaundice)
- can potentially cause acute renal failure, injury w/in nephrons + impaired kidney function
67
Q

What are some potential causes of hemolytic anemia?

A
  • transfusion rxns
  • hemolytic disease of the neborn
  • infections
  • autoimmune destruction of erythrocytes
  • genetic disorders (sickle cell anamia, thalassemia)
  • mechanical (heart valve disease, dialysis)
  • osmotic lysis from hypotonic infusion
68
Q

Why does serum iron rise w hemolytic anemia?

A

Hemolysis leads to decreased iron stores and increased levels of iron in the blood.

69
Q

Why would a heart valve disease and dialysis cause hemolytic anemia?

A
  • bc they are traumatic events that cause disruption of the RBC membrane.
  • physical destruction of RBCs results from the exertion of extreme force on the cells
70
Q

What is the difference between acute + chronic blood loss?

A

Acute blood loss occurs as a result of sudden hemorrhage (trauma, compications of surgery, conditions / diseases that disrupt vascular integrity)

chronic blood loss causes are similar to those of iron-deficiency anemia (bleeding ulcer, hemorrhoids, menstrual and postmenopausal blood loss). Effects of chronic blood lossd are usually related to the depletion of iron stores.

71
Q

How would a client’s vital signs change if they were experiencing acute bleeding?

A
  • decreased BP
  • increased HR
  • Low RBC, Hgb, and Hct levels
72
Q

What are 13 signs of bleeding in the body?

A
  • bruising, ecchymoses, petechiae
  • bleeding gums
  • epistaxis (nose bleed)
  • hematuria (blood in urine)
  • melena (blood in bowel)
  • positive fecal occult blood test
  • vomiting blood
  • stiff or painful abdomen
  • cullen’s sign (blueish hue around umbilicus)
  • retroperitoneal tenderness
  • low BP, high or low HR, low oxygen saturation
  • decreased LOC, confusion
  • fatigue
73
Q

Why does the admininstration of IV fluids sometimes cause Hgb / Hct levels to rise slowly in cases of acute bleeding?

A

Once volume replacement is established from IV fluid, the body needs 2-5 days to produce more RBCs in reponse to erythropoietin found in the IV fluid

74
Q

What is polycythemia?

A

Increased RBC mass, leads to impaired circulation as a result of hyperviscosity and hypervolemia.

75
Q

What are the clinical manifestations of polycythemia?

A
  • Hypertension
  • Vessel distension
  • Impaired blood flow
  • Circulatory stasis
  • Thrombosis
  • Tissue hypoxia
  • Headache, dizziness, tinnitus, visual disturbances
  • Pruritis
  • Painful burning and redness of hands and feet caused by paroxysmal peripheral dilation.
  • plethora (ruddy complexion)
  • angina, HF, intermitten claudication (cramping)
  • thrombo-phlebitis (clot in legs)
  • embolism
76
Q

What is the difference between primary and secondary polycythemia?

A

Primary: called polycythemia vera

  • low / normal erythropoietin
  • pathological
  • splenomegaly and hepatomegaly are common

Secondary:

  • erythropoietin is high
  • can either be hypoxia driven or hypoxia independent
  • hypoxia independent
  • physiological response
77
Q

How does a lack of oxygen in the body contribute to polycythemia?

A

Hypoxia stimulates EPO production in the kidney, which in turn stimulates RBC production.

78
Q

Outline the laboratory values associated w polycythemia:

  • Hgb
  • Hct
  • Platelets
  • MCV
  • MCHC
A
  • Hgb: HIGH
  • Hct: HIGH
  • Platelets: HIGH or normal
  • MCV: NORMAL
  • MCHC: NORMAL
79
Q

What are PRBCs (packed red blood cells)?

A

RBCs collected and stored for future use in blood transfusions.

80
Q

What are platelets?

A

common name for thrombocytes.

small, colourless disk-shaped cell fragments w/o a nucleus

81
Q

What are 4 blood products used in blood transfusions?

A
  1. PRBCs
  2. Platelets
  3. Fresh Frozen Plasma (FFP)
  4. Albumin (protein)
82
Q

What is the desired effect when administering Fresh Frozen Plasma (FFP)?

A

Decreased prothrombin time.

83
Q

What questions would you ask when completing a PAST health history interview for a client with an RBC disorder?

A
  • Have you had any previous problems w anemia, bleeding disorders, recent bleeding, blood diseases or cancers such as leukemia, any other cancers? GI disorders? Gastritis, Crohn’s)
  • Have you ever had a blood transfusion?
  • Do you have a history of kidney disease?
  • Family history of the same?
  • Have you ever had an occupational exposure to a hazardous substance or radiation?
  • Do you drink alcohol?
  • Have you ever had a gastrectomy or small bowel resection?
  • What medications do you take (vit / iron supplements, NSAIDs or anticoagulants, erythropoeitin, heparin, etc).
84
Q

Complete a ROS assessment for a client with an RBC disorder

  • cns
  • eyes
  • nose
  • skin, hair, nails
  • CV
  • respiratory
  • GI
  • GU
A
CNS (neurological)
• B12 - sensory or motor deificiencies 
• activity intolerance or lack of energy (fatigue sign of all anemias)
• lethargy, apathy
• lightheadedness, fainting
• headache (anemia or thrombocytopenia)
• depression, impaired thoughts (anemia)
• sensitivity to cold
• fever (immune origin)
Eyes
• jaundiced scleva, conjunctival pallor
• visual changes
Nose
• epistaxis
Skin, hair, nails
• pallor in skin, nail neds, conjuctiva (anemia)
• cyanosis
• transient skin flushing or painful redness in hands and feet (polycythemia)
• jaundice
• cheilitis, atrophic glossitis, smooth tongue, stomatitis (anemia, iron deficiency)
• gingival bleeding (anemia, thrombocytopenia)
• purpura, petechiae, eccymoses)
• hematoma
• spoon-shaped nails 
CV
• tachycardia
• palpitations
• hyper / hypotension 
• orthostatic hypotension
• angina
• intermittent claudication
• DVT (deep vein thrombosis)
• hypervolemia
Respiratory 
• tachypnea
• orthopnea
• dyspnea 
• increased WOB
• low oxygen saturation
• chronic lung disease

GI
• diet - vegetarian
• activie gastritis or disorders of small bowel
• anorexia, weight loss
• GI bleeding (hematemesis, melena)
• hepatomegaly
• splenomegaly (hemolytic anemia, thrombocytopenia)

Genitourinary
• decreased urinary output
• chronic kidney disease
• menorrhagia (increased volume / length of periods
• metorrhagioa (irregular menstrual bleeding)
• pregnancy or recent pregnancy
• acute renal failure due to products of RBC destruction