[Exam 1] Chapter 33: Management ofo Patients with Nonmalignant Hematologic Disorders (Page 925-941, 948-949, 951-954) Flashcards

1
Q

What is Anemia?

A

Condition in which the hemoglobin concentration is lower than normal; it reflects the presence of fewer than normal erythrocytes within the circulation. Oxygen delivery is dimished

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2
Q

A physiologic approach to classify anemia is according to whether the erythrocyte deficiency caused by

A

defect in their production or by their destruction

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3
Q

What is Hypoproliferative Anemia?

A

Bone marrow does not produce adequate numbers of erythrocytes. May result from bone marrow damage due to medications

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4
Q

Hypoproliferative Anemia: Lack of what factors can damage the bone marrow?

A

Iron, Vitamin B12 or Folate Deficiency

Decreased Erythropoietin PRoduction or Cancer

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5
Q

Hemolytic Anemia: What is this?

A

Premature destruction of erythrocytes results in the liberation of hemoglobin form the erythrocytes into the plasma. Released hemoglobin is converted in large part to bilirubin.

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6
Q

Hemolytic Anemia: What an Hemolsis result from?

A

Abnormality within the erythrocyt itself., within the plasma, or from direct injury to the erythrocyte within the circulation

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7
Q

Anemia may also be caused by

A

blood loss

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8
Q

Types of Hypoproliferative Anemias?

A

Iron DEficiency Anemia

Anemia in Renal Disease

Anemia of Chronic Disease

Megaloblasic Anemai (Folid Acid/Vitamin B12 Deficiency)

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9
Q

Types of Hemolytic Anemia

A

Sickle Cell

Thalassemia

Glucose-6 Phsophate Dehydrogenase Defin=ciency

Imune Hemolytic Anemia

Hereditary Hemochromatosis

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10
Q

Anemia: Collaborative Problems and Potential Complications

A

Heart Failure

Angina

Paresthesias

Confusion

Injury related to falls

Depressed Mood

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11
Q

Anemia, Diagnostic Testing: Hemoglobin and Hematocrit Levels

A

Will decrease in all anemias

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12
Q

Anemia, Diagnostic Testing: RBC Level

A

Decrease in all anemias

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13
Q

Anemia, Diagnostic Testing: Iron Studies show

A

low in iron defiency anemia

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14
Q

Anemia, Diagnostic Testing: Folate/Ferritin low in

A

iron defieincy anemia

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15
Q

Anemia, Diagnostic Testing: Vitamin B12 low in

A

pernicious anemia

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16
Q

Anemia, Diagnostic Testing: BOne Marrow Aspiration will help determine if

A

cause is production within the marrow

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17
Q

Anemia: Manifestations include

A

Fatigeu, Weakness, Malaise

Pallor or Jaundice

Cardiac and REspraotry Symptoms

Tongue Changes (Red and Beefy)

Nail Changes

Angular Cheilosis

Pica

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18
Q

Anemia, Assessment and Diagnostic Findings: What can be assessed here

A

Health history and physical exam

Lab Data

Presence of symptoms and impact of pt life

Nutritional Assessment

Medications

Cardiac and GI Assessemtn

Blood Loss: Menses, Potential GI loss

Neurologic Assessment

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19
Q

Anemia, Diagnoses: What is included here?

A

Fatigue

Altered Nutrition

Altered Tissuse PErfusion

Noncompliance with PRescribed Therapy

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20
Q

Anemia: Complcations of severe anemia include

A

HF, Paresthesias and Delirium.

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21
Q

Anemia, Complications: Patients with underlying heart disease are far more liekyl to have

A

angina or symptoms of heart fialure than those without heart disease

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22
Q

Anemia, Medical Management: If anemia severe, erythrocytes that are lost or destroyed can be replaced with

A

a transfusion of packed RBCs.

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23
Q

Anemia, Medical Management: What would be done for a bone marrow issue?

A

Immunosuppressive Therapy

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24
Q

Anemia, Medical Management: What would be included in a dietary therapy?

A

Increase meat for iron deficiency

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25
Q

Anemia, Medical Management: What would be included in Iron/Vitamin Supplementation

A

Iron, Folate, B12

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26
Q

Anemia, Medical Management: Iron needs to be taken with

A

Vitamin C, do not take with coffee!

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27
Q

Anemia, Medical Management: B12 has oto be given by injection because

A

often patietns hack a lack of IF in their intestine which is n eeded for absorption of B12

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28
Q

Anemia, Assessment: Common symptoms that are seen

A

Weakness, fatigue, and general malaise along with palor of the skin and mucous membrane

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29
Q

Anemia, Medical Management: What symptoms would be present for someone with megaloblastic anemia? (presence of abnormally large, nucleated RBCS)

A

Jaundice, angular cheilosis and brittle,ridged, concave nails

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30
Q

Anemia, Assessment: Why would a nutrtional assessment be done?

A

May indicate deficienties in essential nutrients such as iron, vitamin B12, and folate.

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31
Q

Anemia, Assessment: Strict vegetarians are at risk for meegloblasteic anemias if they dont do what?

A

Supplement their diet with B12.

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32
Q

Anemia, Assessment: Medications should be analyzed because

A

some medications can depress bone marrow activity, incude hemolysis or interefere with folate metabolism

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33
Q

Anemia, Assessment: Cardiac Status, when hemoglobin level is low, what does the heart do?

A

Attempts to compensate by pumping faster and harder in an effort to odeliver more blood to hypoxic tissue.

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34
Q

Anemia, Assessment: Assessment of GI may disclose complaints of

A

nausea, vomiting, melena, diarrhea, anorexia and glossitis.

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35
Q

Anemia, Assessment: Neurologic Assessment performed because Pernicious Anemia can cause

A

Peripheral Numbness and Paresthesias

Ataxia

Poor Coordination

Confusion

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36
Q

Anemia,Major Goals: This includes

A

DEcreased fatigue

Attainment or maintenance of adequate nutrition

Maintenance of adequate tissue perfusion

compliance with prescribed therapy

Absence of complications

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37
Q

Anemia, Nursing Interventions - Managing Fatigue: Most common syptom and complication of anemia is

A

Fatigue. Has greatest negative impact on a patietns level.

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38
Q

Anemia, Nursing Interventions - Managing Fatigue: Nursing Interventions may focus on

A

Assisting patient to prioritize activities and to establish a balance between acitivity and rest that is acceptable

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39
Q

Anemia, Nursing Interventions - Maintaining Adequate Nutrition: What is patient told not to have?

A

Alcohol, because it intereferes with the utilization of essential nnutrients and advice moderation i the intake of alcohol

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40
Q

Anemia, Nursing Interventions - Promoting Adherence with Prescribed Therapy: Patient education to promote

A

compliance with medications and nutritions

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41
Q

Anemia, Nursing Interventions - Monitoring and Managing Potential Complications: Signficiant complcations is

A

heart failure from chronic diminished blood volume and the hearts compensatory effort to increase CO

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42
Q

Anemia, Nursing Interventions - Monitoring and Managing Potential Complications: In Megaloblast forms, the significant potential complications are

A

neurologic

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43
Q

Anemia, Nursing Interventions - Monitoring and Managing Potential Complications: Monitor what?

A

VS and Pulse Oximetry; Provide supplemental oxygen as needed

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44
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: Results from

A

intake of dietary iron is inadequate for hemoglobin synthesis.

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45
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: If severe or prolongd, what symptoms may tthey have

A

smooth, red tongue; brittle and ridged nails and angular cheilosis

Signs subdue after iron replacement

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46
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: Definitive method for establishing diagnosis is

A

bone marrow aspiration. Rate stained to detect iron.

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47
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: A strong correlaiton exisits for what lab values?

A

Iron Stores and Hemoglobin Levels

Once depleted, hemoglobin levels start to fall

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48
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: Medical managmenet. Anemia may be a sign of

A

Curable GI cancer or tumor.

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49
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: What test should be done?

A

Stool specimen

Those 50+ should have colonscopy, endoscopy or xray exam.

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50
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: Primary mode of treating this?

A

Iron supplements. Must continue taking the iron for as long as 6-12 months

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51
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: Food sources high in iron include

A

Organ Meats, Other Meats, Beans, Leafy Green Vegetables, Raisins and Molasses

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52
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: Eating iron rich food with what enhances the absorption of iron?

A

Vitamin C but also increases frequency of side effects

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53
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: Iron is best absorbed on a

A

empty stomach ; take an hour before meals

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54
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: What foods shoild not be taken with iron?

A

antacids or dairy products because they greatly dimish absorption

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55
Q

Hypoproliferative Anemias: Iron DEficiency Anemia: IV supplementation may be used when

A

the patients iron stores are completely deploted, the patient cannot tolerate oral iron supplement, or both

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56
Q

Hypoproliferative Anemias: Anemia of Inflammation: What does this mean?

A

DElineates the chronic diseases of inflammation, infection, and malignancy as causes for this type of anemia.

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57
Q

Hypoproliferative Anemias: Anemia of Inflammation: Many chronic inflammatory diseases are associated with

A

normochronic normocytic anemia (erythrocytes are normal in color and size).

Include RA, Sever Infections, and Many Cancers

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58
Q

Hypoproliferative Anemias: Anemia of Inflammation: Anemia progression?

A

Usually mild to moderate and slow progressive

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59
Q

Hypoproliferative Anemias Aplastic Anemia: What is this?

A

Rare disease caused by a decrease in or damange to marrow stem cells, damage to microenviorment within the marrow, and replacement of the marrow with fat

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60
Q

Hypoproliferative Anemias Aplastic Anemia: Stem cell damage caused by bodys

A

T Cells mediating an inappropriate attack agains thte bone marrow, resulting in bone marrow aplasi a(markedly reduced hematopoiesis)

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61
Q

Hypoproliferative Anemias Aplastic Anemia: Most cases happen by what cause?

A

Idiopathic (without apparent cause)

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62
Q

Hypoproliferative Anemias Aplastic Anemia: Typical complications are

A

infection and symptoms of anemia (fatigue, pallor, dyspnea).

Purpura (brusing) may occur later and should trigger a CBC and hematologic eval.

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63
Q

Hypoproliferative Anemias Aplastic Anemia: In many sitations, this occur when what happens?

A

Medication or chemical is ingestied in toxic amounts . But may be taken after taking recommended dosage

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64
Q

Hypoproliferative Anemias Aplastic Anemia: A CBc would reveal what?

A

Pancytopenia (Decrease in all myeloid stem cell-derived cells)

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65
Q

Hypoproliferative Anemias Aplastic Anemia: Bone Marrow aspirate shows

A

an extremely hypoplastic or even aplastic (very few to no cells) marrow replace with fat

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66
Q

Hypoproliferative Anemias Aplastic Anemia, Medical Management: It is presumed that the body does what to stem cells?

A

T Lymphocytes destroy stem cells and consequently impair the production of erythrocytes, leukocytes and platelets.

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67
Q

Hypoproliferative Anemias Aplastic Anemia, Medical Management: Treatability?

A

Can be successfully treated in most people

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68
Q

Hypoproliferative Anemias Aplastic Anemia, Medical Management: How can disease be managed?

A

Immunosuppresive therapy, commonly using a combination of antithymocyte globulin and androgens

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69
Q

Hypoproliferative Anemias Aplastic Anemia, Medical Management: What do Immunosuppresents prevent?

A

The patients lymphocytes from destroyig the stem cells

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70
Q

Hypoproliferative Anemias Aplastic Anemia, Medical Management: Corticosteroids are not very useful as immunosuppresive agents because

A

patients with asplastic anemia are particularly susceptible to the devleopment of bone complications

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71
Q

Hypoproliferative Anemias Aplastic Anemia, Nursing Management: Patients are vulnerables to problems related to

A

erythrocyte, leukocyte and platelet insufficiencies

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72
Q

Hypoproliferative Anemias Aplastic Anemia, Nursing Management: Patietns should be carefully assesed for

A

signs of infection and bleeding

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73
Q

Hypoproliferative Anemias, Megaloblastic Anemias: What can cause this?

A

Deficiencies of Vitamin B12 or Folic Acid which cause identical bone marrow and peripheral blood changes

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74
Q

Hypoproliferative Anemias, Megaloblastic Anemias: Along with large size of Megaloblast cells, what other cells appear abnormal?

A

Other cells derived from myeloid stem cells (nonlymphoid leukocytes and platelets)

75
Q

Hypoproliferative Anemias, Megaloblastic Anemias: BOne marrow analysis reveals

A

Hyperplasia (abnormal increase in the number of cells) Many do not leave the marrow however causing Pancytopenia

76
Q

Hypoproliferative Anemias, Megaloblastic Anemias: How will this appear in Causadians?

A

Skin develops a lemon-yellow color resulting from simultaneous pallor and mild jaundice that results from mild hemolysis of red cells

77
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Folic Acid DEficiency: Folate found in

A

green vegetables and liver

78
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Folic Acid DEficiency: This occurs in those who rarely eat

A

uncooked vegetables.

79
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Folic Acid DEficiency: What increaases folic acid requirements?

A

Alcohol consumption and those with liver disease.

80
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Vitamin B12 Deficiency: Can devleop how?

A

Inadequate Diet Rare

Strict Vegans who caonsume no red meat or dairy.

Faulty absorption from GI tract

81
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Vitamin B12 Deficiency: Chronic use of what can dimish B12 absorption?

A

Histmaine blockers, Antacids, OR PPI to reduce gastric acid production can inhibit this

82
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Vitamin B12 Deficiency: Resultant anemia is called

A

Pernicious Anemia.

83
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Vitamin B12 Deficiency: B12 has to be paried with what to be absorbed to the ileum?

A

Intrinsic Factor

84
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Vitamin B12 Deficiency: Those with Pernicious Anemia develop a

A

smooth, sore, red tongue and mild diarrhea.

Extremely pale particularly in the mucous membranes

Become confused more often and presthesias in the extremities

85
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Assessment: Serum levels in both vitamins can be

A

measured. Small amounts of folate increase the folate level

86
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Assessment: You should measure folate in the

A

RBC

87
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Assessment: Useful test to test for B12 would be

A

IF Antibody test. Positive test indicates presence of antibodies that bind to VitaminB12

88
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Medical Management: Folate deficiency treated by

A

increasing amount of folic acid in the diet and administering 1 mg of folic acid daily

89
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Medical Management: Folic acid is given how?

A

Intramuscularly only to people with absopriton issues

90
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Medical Management: B12 deficiency is treated bby

A

B12 replacement. Vegans can treat with oral supplements with vitamins and fortified soy milk

91
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Nursing Management: Assessment inludes

A

inspection of the skin, mucous membranes and tongue.

Mild jaundice may be present

92
Q

Hypoproliferative Anemias, Megaloblastic Anemias, Nursing Management: Neurologic assessments includes

A

testing of positions, virbation sense, and cognitive function

93
Q

Hemolytic Anemias: What happens here?

A

Erythrocytes have a shortened life span thus their number is circulatoin is reduced. Erythropoietin released from kidney which stimulates the bone marrow to compensate by producing new erythrocytes and releasing some into cirulation prematurely.

If continued to be broken down, majority of heme converted to bilirubin

94
Q

Hemolytic Anemias: All types of hemolytic anemia share what lab values?

A

Reticulocyte count elevated,

Fraction of indirect bilirubin increased.

Supply of Hapotoglobin (binding protein for free hemoglobin) is depleted.

95
Q

Hemolytic Anemias, Sickle Cell Disease: Can cause severe

A

hemolytic anemia that results from inheritance of the sickle hemoglobin gene(HbS) which causes it to be defective

96
Q

Hemolytic Anemias, Sickle Cell Disease: Hemoglobin of RBC akes on what appearance?

A

Sickle or “s” shape and then cannot pass through vessels. This can cause clotting , pain, sickle cell crisis

97
Q

Hemolytic Anemias, Sickle Cell Disease: What can cause this to happen?

A

When venous level in the blood is low enough. If exposed to adequate oxygen before membrane becomes too rigid, it will revert to nromal shape.

98
Q

Hemolytic Anemias, Sickle Cell Disease: What can aggravte the sickling process?/

A

Cold because vasoconstriction slows the blood flow.

99
Q

Hemolytic Anemias, Sickle Cell Disease: HbS gene inhereited in people of

A

African desent and peole form Middle east, Mediterranean and aboriginal tribes in India.

100
Q

Hemolytic Anemias, Sickle Cell Disease, Clinical Manifestations: Symptoms of SCD vary and are somewhat based on

A

amount of HbS

101
Q

Hemolytic Anemias, Sickle Cell Disease, Clinical Manifestations: Symptoms and complications result from

A

chronic hemolysis or thrombosis

102
Q

Hemolytic Anemias, Sickle Cell Disease, Clinical Manifestations: Chronic Anemia is associated with

A

tachycardia, cardiac murmurs and often an enlarged heart. Dysrhythmias and heart failure may occur

103
Q

Hemolytic Anemias, Sickle Cell Disease, Clinical Manifestations: Patients with SCD are usualyl susceptible to

A

infection, particularly pneumonia and osteomyelitis.

104
Q

Hemolytic Anemias, Sickle Cell Disease, Clinical Manifestations: COmplcations include

A
Infection
Stroke 
Kidney Injury
Impotence
HF
Pulmonary HYpertension
105
Q

Hemolytic Anemias, Sickle Cell Disease, Acute Vaso-Occlusive: What is this?

A

Type of sickle cell crisis. Results from entrapment of erythrocytes and leukocytes in the microcirculation, causing itssue hypoxia, inflammation and necrosis due to inadequate blood flow to a specific region

106
Q

Hemolytic Anemias, Sickle Cell Disease, Acute Vaso-Occlusive: What cacn further happen here?

A

Endothelium of the vessel becomes dysfunctional and vasculopathy develops

107
Q

Hemolytic Anemias, Sickle Cell Disease, Aplastic Crisis: What is this?

A

Results from infection with the human parvovirus. Hemoglobin level falls rapidly and marrow cannot compensate

108
Q

Hemolytic Anemias, Sickle Cell Disease, Sequestration Crisis: What is this?

A

Results when other organs pool the sickled cells. Normally pools in spleen but by age 10, hchildren have splenic infarction

109
Q

Hemolytic Anemias, Sickle Cell Disease, Sequestration Crisis: In adults, common organs involved include

A

liver and more seriously, the lungs

110
Q

Hemolytic Anemias, Sickle Cell Disease, Acute Chest Syndrome: Manifested by

A

fever, respiratory disstres and new infiltrates seen on the chest x-ray.

111
Q

Hemolytic Anemias, Sickle Cell Disease, Acute Chest Syndrome: Causes include

A

Bacteria infection, pulmonary fat embolism, pulmonary infarction, pulmonary thromboembolism and bone marrow embolism

112
Q

Hemolytic Anemias, Sickle Cell Disease, Acute Chest Syndrome: Medical Management includes

A

Red Cell Transfusion, Antimicrobial Therapy,,Bronchodilators, Inhaled Nitric Oxide Therapy.

113
Q

Hemolytic Anemias, Sickle Cell Disease, Acute Chest Syndrome: Risk of Acute chest syndrome can be reducecd by use of

A

incentive spirometry during episodes of vaso-occlusive crisis and cred cell transfursion preoperatively.

114
Q

Hemolytic Anemias, Sickle Cell Disease, Pulmonary Hypertension: Diagnosing is dificult because

A

clinical symptoms rarely occur until damage is irreversible.

115
Q

Hemolytic Anemias, Sickle Cell Disease, Pulmonary Hypertension: Patients may complain of

A

Fatigue, Dyspnea on Exertion, Dizziness, Chest Pain or Syncope

116
Q

Hemolytic Anemias, Sickle Cell Disease, Pulmonary Hypertension: Screening patients with Doppler Echocardiography may be useful in identifying those with

A

elevated pulmnary artery pressures

117
Q

Hemolytic Anemias, Sickle Cell Disease, Stroke: What strokes are common in children and then in adults?

A

Ischemic strokes most common, in young children and older adults

Hemorrhagic stroke more common in younger adults

118
Q

Hemolytic Anemias, Sickle Cell Disease, Stroke: Stroke often results from

A

decreased cerebral blood flow due to anemia, hemolysis and increased hypoxic stress

119
Q

Hemolytic Anemias, Sickle Cell Disease, Stroke: Medical management includes

A

REd Cell TRansfusion to reduce level of hemoglobin S to less than 30%, reducing cerebral edema

120
Q

Hemolytic Anemias, Sickle Cell Disease, Reproductive Problems: WHat can occur in men symptoms wise

A

Low testerone levels, low libido, erecticle dysfunction and infertility

121
Q

Hemolytic Anemias, Sickle Cell Disease, Assessment and Diagnostic Findings: Patient with Sickle cell trait has normal

A

hemoglobin
Hematocrit
Blodo smear

122
Q

Hemolytic Anemias, Sickle Cell Disease, Assessment and Diagnostic Findings: Those with SCD have what lab values?

A

Low Hematocrit and sickled cells.

WBC and Platelet count often higher than normal

123
Q

Hemolytic Anemias, Sickle Cell Disease, Prognosis: Usually diagnosed at what age?

A

Childhood because they become anemic in infancy and begin to have sickle cell crises at 1-2 years old

124
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management: Hematopoietic Stem Cell TRansplant may cure

A

SCD. Only available to small amoutn of pts, either due to lack of compatible donor or due to severe organ damage

125
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and Pharmacologic Therapy: What is Hydroxyurea?

A

Chemotherapy agent that is effective in increasing fetal hemoglobin, therefore decreasing the formaiton of sickled cells

126
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and Pharmacologic Therapy: SE of Hydroxura include

A

Chronic suppression of leukocyte formation

Teratogensis

Potential for later development of malignancy

127
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and Pharmacologic Therapy: Patients with SCD may require daily

A

folic acid replacement to maintain the supply required for increased erythropoiesis from hemolysis

128
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and Pharmacologic Therapy: Acute Chest Syndrome managed by prompt

A

initiation of antibiotic therapy. Incentive spirometry also decrease incidence of pulmonary complications

129
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and TRansfusion Therapy: RBC transfusions have been shown to be highly effective in what situations

A

An Acute exacerbation of enamia

Prevention of severe complciations from anesthesia an dsurgery

Improving response to infection

130
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and TRansfusion Therapy: Complcations may include

A

Poor Venous Access

Delayed Hemolytic TRansfuins REactions

Infections

Iron Overload

131
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and TRansfusion Therapy: Iron overload is likely, with majority of iron deposition occuring in

A

the liver

132
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and TRansfusion Therapy: What is Alloimmunization?

A

When pateitns develop multiple antibodies to other blood antigens, making cross matching difficult

133
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and TRansfusion Therapy: Alloimmunization can develop from

A

disparity in blood group antigens irrespective of ABO antigens been the donor

134
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and Supportive Therapy: Acute pain is typically caused by

A

vaso-occlusive crisis

135
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and Supportive Therapy: What med is useful for fimishing mild to moderate pain??

A

Aspirin.

136
Q

Hemolytic Anemias, Sickle Cell Disease, Medical Management and Supportive Therapy: NSAIDS useful for

A

Moderate pain or in combinaion with opiod analgesics

137
Q

Nursing Process: Patient with Sickle Cell Anemia - Assessment: What is included here?

A

Health history and physical xam

Pain Assessment

Lab Data (S-Shaped Hemo)

Presence of symptoms like swelling , fever, pain

Sickle Cell Crisis Assessment

Blodo Loss (Menses, Potential GI loss)

Cardiovascular and Neurologic Assessment

138
Q

Nursing Process: Patient with Sickle Cell Anemia - Assessment: Potential Complications?

A

Hypoxia, Ischemia, Infection

Dehydration

CVA

Anemia

Acute and chronic renal failure

Heart Failure

139
Q

Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions: What is included here?

A
Pain Management
Fluid
Manage Fatigue
Infection Prevention
Promote Coping
Education of disease process
Monitor for complications
140
Q

Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Managing Pain: Whats helpful for some patients?

A

RElaxation technique, breathing exercises, and distraction.

After episoe, PT, whirlpool baths and transcutaneous electrical nerve stimulation should be done

141
Q

Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Managing Fatigue: Assist the patient to find

A

Appropriate balance between exercise and rest

142
Q

Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Managing Fatigue: Patient should maximize

A

Nutritoin, Hydration, Healthy Sleep Cycles and Diminishing Tissue Hypoxia

143
Q

Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Preventing and Managing Infection: What should be initiated promptly?

A

Prescribed antibiotics and patient should be assessed for signs of dehydration

144
Q

Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Promoting Coping Skills: What can enhance effective coping skills?

A

Focusing on patients strengths rather than deficits

145
Q

Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Managing Deficient Knowledge: If Hydroxyurea is prescribed for a women of childbearing age, she should be informed that

A

drug can cause congenital harm to unborn child

146
Q

Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Priapism Leading to Impotenece: Patient is taught to do what?

A

Empty his bladder at the onset of the attack, exercise, and take a warm bath. If longer than 3 hours, medical attention required.

147
Q

Thrombocytopenia: Results from various factors like

A

Decreased production of platelets within the bone marrow

Increased destruction of platelets

Increased consumption of platelets

148
Q

Thrombocytopenia, CM: When can petechiae appear?

A

When level is less than 20,000. This can appear along wiht nasal and gingival bleeding, excessive menstural bleeding and excessing bleeding after surgery

149
Q

Thrombocytopenia : What is this?

A

Low Platelet level below 50,000

150
Q

Thrombocytopenia, CM: What happens when level less than 5,000?

A

Spotaneous potentially fatal central nervous system or GI hemorrhad can occur

151
Q

Thrombocytopenia, Assessment and Diagnostic Findings: Platelet deficiency that results from decreased production can usually be diagnosed by

A

examining the bone marrow via aspiration and biopsy

152
Q

Thrombocytopenia, Assessment and Diagnostic Findings: Genetic causes paired to this include

A

Autosomal DOminant

Autosomal Recessive

X-Linked Mutations

153
Q

Thrombocytopenia, Assessment and Diagnostic Findings: If platlet destruction is the cause, the marrow shows

A

increased magakarocytes and normal or even icnreased platelet production as the body attempts to compensate for hte decreased platelets in circulation

154
Q

Thrombocytopenia, Assessment and Diagnostic Findings: What happens if EDTA is present during a CBC collection?

A

Platelets aggregate and clumb in the presence of this anticoagulant that is int he tube

155
Q

Thrombocytopenia, Medical Management: Most common cause of platelet destruction is

A

immune thrombocytopenic purpura (ITP)

156
Q

What is Polycythemia?

A

Increased volume of RBCs

157
Q

What is secondary polycythemia?

A

Excessive production of erythropoietin fom reduced amounts fof oxygem , cyanotic heart disease, and nonpathologic conditions or neoplasms

158
Q

MEdical Management for Polycythemia?

A

Treatment not needed if condiiton mild

Treat underlying cause

Therapeutic Phlebotomy

159
Q

Hemophilia: What is this?

A

Two inhereited bleeding disorders distinguished by laboratory tests.

160
Q

Hemophilia: Hemophilia A is caused by

A

Genetic defect that results in deficient or defective factor VII

161
Q

Hemophilia: Hemophilia B stems from

A

genetic defect that causes deficient or defective factor IX

162
Q

Hemophilia: WHich hemophilia is more common?

A

A, five times more common than B

163
Q

Hemophilia: Both types are inherited as X-Linked traits, meaning most affected people are

A

Males.

164
Q

Hemophilia: This is passed by

A

mothers to sons. Women are only carriers.

165
Q

Hemophilia, CM: MAnifestated by

A

hemorrhages into various parts of the body. Can be severe even after minimal trauma

166
Q

Hemophilia, CM: Patients with mild factor VIII deficiency rarely develop hemorrhage spontaneously, hemorrhage tends to occur

A

secondary to trauma

167
Q

Hemophilia, CM: Spontaneous hemorrhages can frequently occur in patients with severe

A

Factor VIII deficiency

168
Q

Hemophilia, CM: About 75% of all bleeding occurs in

A

joints

169
Q

Hemophilia, CM: Most commonly affected bleeding joints are

A

knees, elbows, ankles, shoulders, wrists

170
Q

Hemophilia, CM: With Severe factor VII deficiency, hematomas can occur wihtout

A

known traum and progressively extend in all directions

171
Q

Hemophilia, CM: What happens when hematomas occur in muscles?

A

Peripheral nerves can be compressed. Over time, this leads to decreased sensation, weakness, or atrophy

172
Q

Hemophilia, CM: Bleeding is commonly associated with

A

dental extraction.

173
Q

Hemophilia, CM: Most dangeous site for hemorrhage is

A

the head . Any head trauma requires prompt evaluation and treatment

174
Q

Hemophilia, Medical Management: PAtients are given what when they are bleeding?

A

REcombinant forms of Factor VIII and X, crucial to initiate treatment as soon as possible

175
Q

Hemophilia, Medical Management: Children typically recieve factor administration prophylactically how often?

A

3-4 times a week, which markedly reduced the incidence and severity of joint complications

176
Q

Hemophilia, Medical Management: Mainstay of inhibitor management is

A

inducing immune tolerance. Special formaultions of factor replaement products are given on a daily basis.

177
Q

Hemophilia, Medical Management: Patients with severe factor deficiency should be screened for

A

antibodies, particularly before major surgery so that apropriate therapy can be initiated and major bleedingcomplciations from surgery averted

178
Q

Hemophilia is a failure of

A

hemostatic mecnanisms

179
Q

Hemophilia: What can cause a bleeding disorder?

A

Trauma
Platelet Abnormality
Coagulation Factor Abnormality

180
Q

Hemophilia, Medical Management for bleeding disorders?

A

Specific blood products, Vitamin K

181
Q

Hemophilia, Nursing Management: Patients an family are instructed how to administer the

A

factor concentrate at home at first sign of bleeding so bleeding is minimized.

182
Q

Hemophilia, Nursing Management: Use of Prophylactic factor replacement cna be very efective in dimihsing

A

the morbidity associated with repeated bleeding. However requires administration 2-3 times a week

183
Q

Hemophilia, Nursing Management: Patients areinstructed to avoid agents that interefere wth platelet aggregration such as

A

aspirin, NSAIDs, and some herbal/nutritional supplements and alcohol

184
Q

Hemophilia, Nursing Management: What is commonly required to alleviate the pain associated with hematomas?

A

Analgesic agents