[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
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
3
Q
What is Hypoproliferative Anemia?
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Bone marrow does not produce adequate numbers of erythrocytes. May result from bone marrow damage due to medications
4
Q
Hypoproliferative Anemia: Lack of what factors can damage the bone marrow?
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Iron, Vitamin B12 or Folate Deficiency
Decreased Erythropoietin PRoduction or Cancer
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.
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
7
Q
Anemia may also be caused by
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blood loss
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)
9
Q
Types of Hemolytic Anemia
A
Sickle Cell
Thalassemia
Glucose-6 Phsophate Dehydrogenase Defin=ciency
Imune Hemolytic Anemia
Hereditary Hemochromatosis
10
Q
Anemia: Collaborative Problems and Potential Complications
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Heart Failure
Angina
Paresthesias
Confusion
Injury related to falls
Depressed Mood
11
Q
Anemia, Diagnostic Testing: Hemoglobin and Hematocrit Levels
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Will decrease in all anemias
12
Q
Anemia, Diagnostic Testing: RBC Level
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Decrease in all anemias
13
Q
Anemia, Diagnostic Testing: Iron Studies show
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low in iron defiency anemia
14
Q
Anemia, Diagnostic Testing: Folate/Ferritin low in
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iron defieincy anemia
15
Q
Anemia, Diagnostic Testing: Vitamin B12 low in
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pernicious anemia
16
Q
Anemia, Diagnostic Testing: BOne Marrow Aspiration will help determine if
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cause is production within the marrow
17
Q
Anemia: Manifestations include
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Fatigeu, Weakness, Malaise
Pallor or Jaundice
Cardiac and REspraotry Symptoms
Tongue Changes (Red and Beefy)
Nail Changes
Angular Cheilosis
Pica
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
19
Q
Anemia, Diagnoses: What is included here?
A
Fatigue
Altered Nutrition
Altered Tissuse PErfusion
Noncompliance with PRescribed Therapy
20
Q
Anemia: Complcations of severe anemia include
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HF, Paresthesias and Delirium.
21
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Anemia, Complications: Patients with underlying heart disease are far more liekyl to have
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angina or symptoms of heart fialure than those without heart disease
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Q
Anemia, Medical Management: If anemia severe, erythrocytes that are lost or destroyed can be replaced with
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a transfusion of packed RBCs.
23
Q
Anemia, Medical Management: What would be done for a bone marrow issue?
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Immunosuppressive Therapy
24
Q
Anemia, Medical Management: What would be included in a dietary therapy?
A
Increase meat for iron deficiency
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Anemia, Medical Management: What would be included in Iron/Vitamin Supplementation
Iron, Folate, B12
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Anemia, Medical Management: Iron needs to be taken with
Vitamin C, do not take with coffee!
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Anemia, Medical Management: B12 has oto be given by injection because
often patietns hack a lack of IF in their intestine which is n eeded for absorption of B12
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Anemia, Assessment: Common symptoms that are seen
Weakness, fatigue, and general malaise along with palor of the skin and mucous membrane
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Anemia, Medical Management: What symptoms would be present for someone with megaloblastic anemia? (presence of abnormally large, nucleated RBCS)
Jaundice, angular cheilosis and brittle,ridged, concave nails
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Anemia, Assessment: Why would a nutrtional assessment be done?
May indicate deficienties in essential nutrients such as iron, vitamin B12, and folate.
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Anemia, Assessment: Strict vegetarians are at risk for meegloblasteic anemias if they dont do what?
Supplement their diet with B12.
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Anemia, Assessment: Medications should be analyzed because
some medications can depress bone marrow activity, incude hemolysis or interefere with folate metabolism
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Anemia, Assessment: Cardiac Status, when hemoglobin level is low, what does the heart do?
Attempts to compensate by pumping faster and harder in an effort to odeliver more blood to hypoxic tissue.
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Anemia, Assessment: Assessment of GI may disclose complaints of
nausea, vomiting, melena, diarrhea, anorexia and glossitis.
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Anemia, Assessment: Neurologic Assessment performed because Pernicious Anemia can cause
Peripheral Numbness and Paresthesias
Ataxia
Poor Coordination
Confusion
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Anemia,Major Goals: This includes
DEcreased fatigue
Attainment or maintenance of adequate nutrition
Maintenance of adequate tissue perfusion
compliance with prescribed therapy
Absence of complications
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Anemia, Nursing Interventions - Managing Fatigue: Most common syptom and complication of anemia is
Fatigue. Has greatest negative impact on a patietns level.
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Anemia, Nursing Interventions - Managing Fatigue: Nursing Interventions may focus on
Assisting patient to prioritize activities and to establish a balance between acitivity and rest that is acceptable
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Anemia, Nursing Interventions - Maintaining Adequate Nutrition: What is patient told not to have?
Alcohol, because it intereferes with the utilization of essential nnutrients and advice moderation i the intake of alcohol
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Anemia, Nursing Interventions - Promoting Adherence with Prescribed Therapy: Patient education to promote
compliance with medications and nutritions
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Anemia, Nursing Interventions - Monitoring and Managing Potential Complications: Signficiant complcations is
heart failure from chronic diminished blood volume and the hearts compensatory effort to increase CO
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Anemia, Nursing Interventions - Monitoring and Managing Potential Complications: In Megaloblast forms, the significant potential complications are
neurologic
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Anemia, Nursing Interventions - Monitoring and Managing Potential Complications: Monitor what?
VS and Pulse Oximetry; Provide supplemental oxygen as needed
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Hypoproliferative Anemias: Iron DEficiency Anemia: Results from
intake of dietary iron is inadequate for hemoglobin synthesis.
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Hypoproliferative Anemias: Iron DEficiency Anemia: If severe or prolongd, what symptoms may tthey have
smooth, red tongue; brittle and ridged nails and angular cheilosis
Signs subdue after iron replacement
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Hypoproliferative Anemias: Iron DEficiency Anemia: Definitive method for establishing diagnosis is
bone marrow aspiration. Rate stained to detect iron.
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Hypoproliferative Anemias: Iron DEficiency Anemia: A strong correlaiton exisits for what lab values?
Iron Stores and Hemoglobin Levels
Once depleted, hemoglobin levels start to fall
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Hypoproliferative Anemias: Iron DEficiency Anemia: Medical managmenet. Anemia may be a sign of
Curable GI cancer or tumor.
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Hypoproliferative Anemias: Iron DEficiency Anemia: What test should be done?
Stool specimen
Those 50+ should have colonscopy, endoscopy or xray exam.
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Hypoproliferative Anemias: Iron DEficiency Anemia: Primary mode of treating this?
Iron supplements. Must continue taking the iron for as long as 6-12 months
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Hypoproliferative Anemias: Iron DEficiency Anemia: Food sources high in iron include
Organ Meats, Other Meats, Beans, Leafy Green Vegetables, Raisins and Molasses
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Hypoproliferative Anemias: Iron DEficiency Anemia: Eating iron rich food with what enhances the absorption of iron?
Vitamin C but also increases frequency of side effects
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Hypoproliferative Anemias: Iron DEficiency Anemia: Iron is best absorbed on a
empty stomach ; take an hour before meals
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Hypoproliferative Anemias: Iron DEficiency Anemia: What foods shoild not be taken with iron?
antacids or dairy products because they greatly dimish absorption
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Hypoproliferative Anemias: Iron DEficiency Anemia: IV supplementation may be used when
the patients iron stores are completely deploted, the patient cannot tolerate oral iron supplement, or both
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Hypoproliferative Anemias: Anemia of Inflammation: What does this mean?
DElineates the chronic diseases of inflammation, infection, and malignancy as causes for this type of anemia.
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Hypoproliferative Anemias: Anemia of Inflammation: Many chronic inflammatory diseases are associated with
normochronic normocytic anemia (erythrocytes are normal in color and size).
Include RA, Sever Infections, and Many Cancers
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Hypoproliferative Anemias: Anemia of Inflammation: Anemia progression?
Usually mild to moderate and slow progressive
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Hypoproliferative Anemias Aplastic Anemia: What is this?
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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Hypoproliferative Anemias Aplastic Anemia: Stem cell damage caused by bodys
T Cells mediating an inappropriate attack agains thte bone marrow, resulting in bone marrow aplasi a(markedly reduced hematopoiesis)
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Hypoproliferative Anemias Aplastic Anemia: Most cases happen by what cause?
Idiopathic (without apparent cause)
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Hypoproliferative Anemias Aplastic Anemia: Typical complications are
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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Hypoproliferative Anemias Aplastic Anemia: In many sitations, this occur when what happens?
Medication or chemical is ingestied in toxic amounts . But may be taken after taking recommended dosage
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Hypoproliferative Anemias Aplastic Anemia: A CBc would reveal what?
Pancytopenia (Decrease in all myeloid stem cell-derived cells)
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Hypoproliferative Anemias Aplastic Anemia: Bone Marrow aspirate shows
an extremely hypoplastic or even aplastic (very few to no cells) marrow replace with fat
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Hypoproliferative Anemias Aplastic Anemia, Medical Management: It is presumed that the body does what to stem cells?
T Lymphocytes destroy stem cells and consequently impair the production of erythrocytes, leukocytes and platelets.
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Hypoproliferative Anemias Aplastic Anemia, Medical Management: Treatability?
Can be successfully treated in most people
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Hypoproliferative Anemias Aplastic Anemia, Medical Management: How can disease be managed?
Immunosuppresive therapy, commonly using a combination of antithymocyte globulin and androgens
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Hypoproliferative Anemias Aplastic Anemia, Medical Management: What do Immunosuppresents prevent?
The patients lymphocytes from destroyig the stem cells
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Hypoproliferative Anemias Aplastic Anemia, Medical Management: Corticosteroids are not very useful as immunosuppresive agents because
patients with asplastic anemia are particularly susceptible to the devleopment of bone complications
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Hypoproliferative Anemias Aplastic Anemia, Nursing Management: Patients are vulnerables to problems related to
erythrocyte, leukocyte and platelet insufficiencies
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Hypoproliferative Anemias Aplastic Anemia, Nursing Management: Patietns should be carefully assesed for
signs of infection and bleeding
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Hypoproliferative Anemias, Megaloblastic Anemias: What can cause this?
Deficiencies of Vitamin B12 or Folic Acid which cause identical bone marrow and peripheral blood changes
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Hypoproliferative Anemias, Megaloblastic Anemias: Along with large size of Megaloblast cells, what other cells appear abnormal?
Other cells derived from myeloid stem cells (nonlymphoid leukocytes and platelets)
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Hypoproliferative Anemias, Megaloblastic Anemias: BOne marrow analysis reveals
Hyperplasia (abnormal increase in the number of cells) Many do not leave the marrow however causing Pancytopenia
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Hypoproliferative Anemias, Megaloblastic Anemias: How will this appear in Causadians?
Skin develops a lemon-yellow color resulting from simultaneous pallor and mild jaundice that results from mild hemolysis of red cells
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Hypoproliferative Anemias, Megaloblastic Anemias, Folic Acid DEficiency: Folate found in
green vegetables and liver
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Hypoproliferative Anemias, Megaloblastic Anemias, Folic Acid DEficiency: This occurs in those who rarely eat
uncooked vegetables.
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Hypoproliferative Anemias, Megaloblastic Anemias, Folic Acid DEficiency: What increaases folic acid requirements?
Alcohol consumption and those with liver disease.
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Hypoproliferative Anemias, Megaloblastic Anemias, Vitamin B12 Deficiency: Can devleop how?
Inadequate Diet Rare
Strict Vegans who caonsume no red meat or dairy.
Faulty absorption from GI tract
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Hypoproliferative Anemias, Megaloblastic Anemias, Vitamin B12 Deficiency: Chronic use of what can dimish B12 absorption?
Histmaine blockers, Antacids, OR PPI to reduce gastric acid production can inhibit this
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Hypoproliferative Anemias, Megaloblastic Anemias, Vitamin B12 Deficiency: Resultant anemia is called
Pernicious Anemia.
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Hypoproliferative Anemias, Megaloblastic Anemias, Vitamin B12 Deficiency: B12 has to be paried with what to be absorbed to the ileum?
Intrinsic Factor
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Hypoproliferative Anemias, Megaloblastic Anemias, Vitamin B12 Deficiency: Those with Pernicious Anemia develop a
smooth, sore, red tongue and mild diarrhea.
Extremely pale particularly in the mucous membranes
Become confused more often and presthesias in the extremities
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Hypoproliferative Anemias, Megaloblastic Anemias, Assessment: Serum levels in both vitamins can be
measured. Small amounts of folate increase the folate level
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Hypoproliferative Anemias, Megaloblastic Anemias, Assessment: You should measure folate in the
RBC
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Hypoproliferative Anemias, Megaloblastic Anemias, Assessment: Useful test to test for B12 would be
IF Antibody test. Positive test indicates presence of antibodies that bind to VitaminB12
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Hypoproliferative Anemias, Megaloblastic Anemias, Medical Management: Folate deficiency treated by
increasing amount of folic acid in the diet and administering 1 mg of folic acid daily
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Hypoproliferative Anemias, Megaloblastic Anemias, Medical Management: Folic acid is given how?
Intramuscularly only to people with absopriton issues
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Hypoproliferative Anemias, Megaloblastic Anemias, Medical Management: B12 deficiency is treated bby
B12 replacement. Vegans can treat with oral supplements with vitamins and fortified soy milk
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Hypoproliferative Anemias, Megaloblastic Anemias, Nursing Management: Assessment inludes
inspection of the skin, mucous membranes and tongue.
Mild jaundice may be present
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Hypoproliferative Anemias, Megaloblastic Anemias, Nursing Management: Neurologic assessments includes
testing of positions, virbation sense, and cognitive function
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Hemolytic Anemias: What happens here?
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
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Hemolytic Anemias: All types of hemolytic anemia share what lab values?
Reticulocyte count elevated,
Fraction of indirect bilirubin increased.
Supply of Hapotoglobin (binding protein for free hemoglobin) is depleted.
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Hemolytic Anemias, Sickle Cell Disease: Can cause severe
hemolytic anemia that results from inheritance of the sickle hemoglobin gene(HbS) which causes it to be defective
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Hemolytic Anemias, Sickle Cell Disease: Hemoglobin of RBC akes on what appearance?
Sickle or "s" shape and then cannot pass through vessels. This can cause clotting , pain, sickle cell crisis
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Hemolytic Anemias, Sickle Cell Disease: What can cause this to happen?
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.
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Hemolytic Anemias, Sickle Cell Disease: What can aggravte the sickling process?/
Cold because vasoconstriction slows the blood flow.
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Hemolytic Anemias, Sickle Cell Disease: HbS gene inhereited in people of
African desent and peole form Middle east, Mediterranean and aboriginal tribes in India.
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Hemolytic Anemias, Sickle Cell Disease, Clinical Manifestations: Symptoms of SCD vary and are somewhat based on
amount of HbS
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Hemolytic Anemias, Sickle Cell Disease, Clinical Manifestations: Symptoms and complications result from
chronic hemolysis or thrombosis
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Hemolytic Anemias, Sickle Cell Disease, Clinical Manifestations: Chronic Anemia is associated with
tachycardia, cardiac murmurs and often an enlarged heart. Dysrhythmias and heart failure may occur
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Hemolytic Anemias, Sickle Cell Disease, Clinical Manifestations: Patients with SCD are usualyl susceptible to
infection, particularly pneumonia and osteomyelitis.
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Hemolytic Anemias, Sickle Cell Disease, Clinical Manifestations: COmplcations include
Infection
Stroke
Kidney Injury
Impotence
HF
Pulmonary HYpertension
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Hemolytic Anemias, Sickle Cell Disease, Acute Vaso-Occlusive: What is this?
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
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Hemolytic Anemias, Sickle Cell Disease, Acute Vaso-Occlusive: What cacn further happen here?
Endothelium of the vessel becomes dysfunctional and vasculopathy develops
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Hemolytic Anemias, Sickle Cell Disease, Aplastic Crisis: What is this?
Results from infection with the human parvovirus. Hemoglobin level falls rapidly and marrow cannot compensate
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Hemolytic Anemias, Sickle Cell Disease, Sequestration Crisis: What is this?
Results when other organs pool the sickled cells. Normally pools in spleen but by age 10, hchildren have splenic infarction
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Hemolytic Anemias, Sickle Cell Disease, Sequestration Crisis: In adults, common organs involved include
liver and more seriously, the lungs
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Hemolytic Anemias, Sickle Cell Disease, Acute Chest Syndrome: Manifested by
fever, respiratory disstres and new infiltrates seen on the chest x-ray.
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Hemolytic Anemias, Sickle Cell Disease, Acute Chest Syndrome: Causes include
Bacteria infection, pulmonary fat embolism, pulmonary infarction, pulmonary thromboembolism and bone marrow embolism
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Hemolytic Anemias, Sickle Cell Disease, Acute Chest Syndrome: Medical Management includes
Red Cell Transfusion, Antimicrobial Therapy,,Bronchodilators, Inhaled Nitric Oxide Therapy.
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Hemolytic Anemias, Sickle Cell Disease, Acute Chest Syndrome: Risk of Acute chest syndrome can be reducecd by use of
incentive spirometry during episodes of vaso-occlusive crisis and cred cell transfursion preoperatively.
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Hemolytic Anemias, Sickle Cell Disease, Pulmonary Hypertension: Diagnosing is dificult because
clinical symptoms rarely occur until damage is irreversible.
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Hemolytic Anemias, Sickle Cell Disease, Pulmonary Hypertension: Patients may complain of
Fatigue, Dyspnea on Exertion, Dizziness, Chest Pain or Syncope
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Hemolytic Anemias, Sickle Cell Disease, Pulmonary Hypertension: Screening patients with Doppler Echocardiography may be useful in identifying those with
elevated pulmnary artery pressures
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Hemolytic Anemias, Sickle Cell Disease, Stroke: What strokes are common in children and then in adults?
Ischemic strokes most common, in young children and older adults
Hemorrhagic stroke more common in younger adults
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Hemolytic Anemias, Sickle Cell Disease, Stroke: Stroke often results from
decreased cerebral blood flow due to anemia, hemolysis and increased hypoxic stress
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Hemolytic Anemias, Sickle Cell Disease, Stroke: Medical management includes
REd Cell TRansfusion to reduce level of hemoglobin S to less than 30%, reducing cerebral edema
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Hemolytic Anemias, Sickle Cell Disease, Reproductive Problems: WHat can occur in men symptoms wise
Low testerone levels, low libido, erecticle dysfunction and infertility
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Hemolytic Anemias, Sickle Cell Disease, Assessment and Diagnostic Findings: Patient with Sickle cell trait has normal
hemoglobin
Hematocrit
Blodo smear
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Hemolytic Anemias, Sickle Cell Disease, Assessment and Diagnostic Findings: Those with SCD have what lab values?
Low Hematocrit and sickled cells.
WBC and Platelet count often higher than normal
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Hemolytic Anemias, Sickle Cell Disease, Prognosis: Usually diagnosed at what age?
Childhood because they become anemic in infancy and begin to have sickle cell crises at 1-2 years old
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Hemolytic Anemias, Sickle Cell Disease, Medical Management: Hematopoietic Stem Cell TRansplant may cure
SCD. Only available to small amoutn of pts, either due to lack of compatible donor or due to severe organ damage
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and Pharmacologic Therapy: What is Hydroxyurea?
Chemotherapy agent that is effective in increasing fetal hemoglobin, therefore decreasing the formaiton of sickled cells
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and Pharmacologic Therapy: SE of Hydroxura include
Chronic suppression of leukocyte formation
Teratogensis
Potential for later development of malignancy
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and Pharmacologic Therapy: Patients with SCD may require daily
folic acid replacement to maintain the supply required for increased erythropoiesis from hemolysis
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and Pharmacologic Therapy: Acute Chest Syndrome managed by prompt
initiation of antibiotic therapy. Incentive spirometry also decrease incidence of pulmonary complications
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and TRansfusion Therapy: RBC transfusions have been shown to be highly effective in what situations
An Acute exacerbation of enamia
Prevention of severe complciations from anesthesia an dsurgery
Improving response to infection
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and TRansfusion Therapy: Complcations may include
Poor Venous Access
Delayed Hemolytic TRansfuins REactions
Infections
Iron Overload
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and TRansfusion Therapy: Iron overload is likely, with majority of iron deposition occuring in
the liver
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and TRansfusion Therapy: What is Alloimmunization?
When pateitns develop multiple antibodies to other blood antigens, making cross matching difficult
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and TRansfusion Therapy: Alloimmunization can develop from
disparity in blood group antigens irrespective of ABO antigens been the donor
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and Supportive Therapy: Acute pain is typically caused by
vaso-occlusive crisis
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and Supportive Therapy: What med is useful for fimishing mild to moderate pain??
Aspirin.
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Hemolytic Anemias, Sickle Cell Disease, Medical Management and Supportive Therapy: NSAIDS useful for
Moderate pain or in combinaion with opiod analgesics
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Nursing Process: Patient with Sickle Cell Anemia - Assessment: What is included here?
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
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Nursing Process: Patient with Sickle Cell Anemia - Assessment: Potential Complications?
Hypoxia, Ischemia, Infection
Dehydration
CVA
Anemia
Acute and chronic renal failure
Heart Failure
139
Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions: What is included here?
Pain Management
Fluid
Manage Fatigue
Infection Prevention
Promote Coping
Education of disease process
Monitor for complications
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Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Managing Pain: Whats helpful for some patients?
RElaxation technique, breathing exercises, and distraction.
After episoe, PT, whirlpool baths and transcutaneous electrical nerve stimulation should be done
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Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Managing Fatigue: Assist the patient to find
Appropriate balance between exercise and rest
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Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Managing Fatigue: Patient should maximize
Nutritoin, Hydration, Healthy Sleep Cycles and Diminishing Tissue Hypoxia
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Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Preventing and Managing Infection: What should be initiated promptly?
Prescribed antibiotics and patient should be assessed for signs of dehydration
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Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Promoting Coping Skills: What can enhance effective coping skills?
Focusing on patients strengths rather than deficits
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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
drug can cause congenital harm to unborn child
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Nursing Process: Patient with Sickle Cell Anemia - Nursing Interventions, Priapism Leading to Impotenece: Patient is taught to do what?
Empty his bladder at the onset of the attack, exercise, and take a warm bath. If longer than 3 hours, medical attention required.
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Thrombocytopenia: Results from various factors like
Decreased production of platelets within the bone marrow
Increased destruction of platelets
Increased consumption of platelets
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Thrombocytopenia, CM: When can petechiae appear?
When level is less than 20,000. This can appear along wiht nasal and gingival bleeding, excessive menstural bleeding and excessing bleeding after surgery
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Thrombocytopenia : What is this?
Low Platelet level below 50,000
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Thrombocytopenia, CM: What happens when level less than 5,000?
Spotaneous potentially fatal central nervous system or GI hemorrhad can occur
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Thrombocytopenia, Assessment and Diagnostic Findings: Platelet deficiency that results from decreased production can usually be diagnosed by
examining the bone marrow via aspiration and biopsy
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Thrombocytopenia, Assessment and Diagnostic Findings: Genetic causes paired to this include
Autosomal DOminant
Autosomal Recessive
X-Linked Mutations
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Thrombocytopenia, Assessment and Diagnostic Findings: If platlet destruction is the cause, the marrow shows
increased magakarocytes and normal or even icnreased platelet production as the body attempts to compensate for hte decreased platelets in circulation
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Thrombocytopenia, Assessment and Diagnostic Findings: What happens if EDTA is present during a CBC collection?
Platelets aggregate and clumb in the presence of this anticoagulant that is int he tube
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Thrombocytopenia, Medical Management: Most common cause of platelet destruction is
immune thrombocytopenic purpura (ITP)
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What is Polycythemia?
Increased volume of RBCs
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What is secondary polycythemia?
Excessive production of erythropoietin fom reduced amounts fof oxygem , cyanotic heart disease, and nonpathologic conditions or neoplasms
158
MEdical Management for Polycythemia?
Treatment not needed if condiiton mild
Treat underlying cause
Therapeutic Phlebotomy
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Hemophilia: What is this?
Two inhereited bleeding disorders distinguished by laboratory tests.
160
Hemophilia: Hemophilia A is caused by
Genetic defect that results in deficient or defective factor VII
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Hemophilia: Hemophilia B stems from
genetic defect that causes deficient or defective factor IX
162
Hemophilia: WHich hemophilia is more common?
A, five times more common than B
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Hemophilia: Both types are inherited as X-Linked traits, meaning most affected people are
Males.
164
Hemophilia: This is passed by
mothers to sons. Women are only carriers.
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Hemophilia, CM: MAnifestated by
hemorrhages into various parts of the body. Can be severe even after minimal trauma
166
Hemophilia, CM: Patients with mild factor VIII deficiency rarely develop hemorrhage spontaneously, hemorrhage tends to occur
secondary to trauma
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Hemophilia, CM: Spontaneous hemorrhages can frequently occur in patients with severe
Factor VIII deficiency
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Hemophilia, CM: About 75% of all bleeding occurs in
joints
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Hemophilia, CM: Most commonly affected bleeding joints are
knees, elbows, ankles, shoulders, wrists
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Hemophilia, CM: With Severe factor VII deficiency, hematomas can occur wihtout
known traum and progressively extend in all directions
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Hemophilia, CM: What happens when hematomas occur in muscles?
Peripheral nerves can be compressed. Over time, this leads to decreased sensation, weakness, or atrophy
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Hemophilia, CM: Bleeding is commonly associated with
dental extraction.
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Hemophilia, CM: Most dangeous site for hemorrhage is
the head . Any head trauma requires prompt evaluation and treatment
174
Hemophilia, Medical Management: PAtients are given what when they are bleeding?
REcombinant forms of Factor VIII and X, crucial to initiate treatment as soon as possible
175
Hemophilia, Medical Management: Children typically recieve factor administration prophylactically how often?
3-4 times a week, which markedly reduced the incidence and severity of joint complications
176
Hemophilia, Medical Management: Mainstay of inhibitor management is
inducing immune tolerance. Special formaultions of factor replaement products are given on a daily basis.
177
Hemophilia, Medical Management: Patients with severe factor deficiency should be screened for
antibodies, particularly before major surgery so that apropriate therapy can be initiated and major bleedingcomplciations from surgery averted
178
Hemophilia is a failure of
hemostatic mecnanisms
179
Hemophilia: What can cause a bleeding disorder?
Trauma
Platelet Abnormality
Coagulation Factor Abnormality
180
Hemophilia, Medical Management for bleeding disorders?
Specific blood products, Vitamin K
181
Hemophilia, Nursing Management: Patients an family are instructed how to administer the
factor concentrate at home at first sign of bleeding so bleeding is minimized.
182
Hemophilia, Nursing Management: Use of Prophylactic factor replacement cna be very efective in dimihsing
the morbidity associated with repeated bleeding. However requires administration 2-3 times a week
183
Hemophilia, Nursing Management: Patients areinstructed to avoid agents that interefere wth platelet aggregration such as
aspirin, NSAIDs, and some herbal/nutritional supplements and alcohol
184
Hemophilia, Nursing Management: What is commonly required to alleviate the pain associated with hematomas?
Analgesic agents
