Hematology in depth Flashcards

1
Q

Go look at slide 1/45

A

types of anemia (morphology, examples, lab values expected)

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2
Q

Classification of anemia: hypoproliferative

A

iron
vit b12 deficiency
cancer/inflammation

results from the inability of bone marrow to produce adequate numbers of red blood cells

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3
Q

Classification of anemia: bleeding

A

GI, trauma, genitourinary, epistaxis

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4
Q

Classification of anemia: hemolytic

A
Altered erythropoiesis
Hypersplenism
Drug-induced anemia 
Autoimmune anemia 
Mech health valve

Red blood cells are destroyed faster than they can be replaced

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5
Q

Describe iron deficiency anemia:

A

Body’s iron stores are depleted an no iron available for hemoglobin synthesis.

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6
Q

Describe microlytic anemia

A

transferrin saturation is below 20% and ferritin is below 30

happens when your red blood cells are smaller than usual because they don’t have enough hemoglobi

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7
Q

What are general manifestations of anemia?

A
tachycardia
SOB
dyspnea
chest pain
muscle pain or cramping
pallor
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8
Q

What labs are evaluated when determining is someone has anemia?

A
Hbg/Hct
Retiulocyte count
RBC
Iron studies – TIBC, % saturation, ferritin
Vitamin B12
Folate
Haptogloin – if hemolysis is suspected)
Erythropoietin
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9
Q

What are factors that can influence the development of anemia-associated symptoms?

A
  1. The rapididy with which anemia has developed
  2. The duration of the anemia
  3. The metabolic requirements of the patient
  4. Other concurrent disorders or disabilities (i.e., cardiopulmonary dx)
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10
Q

Anemia assessment: general

A

Weakness, fatigue
Dizziness
Pica (craving unusual items including - ice, starch, or dirt)

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11
Q

Anemia assessment: neurological

A

Numbness and tingling (paresthesias), irritability
Weakness
Headache
Poor coordination, confusion
Gait disturbances
Reflex abnormalities
Loss of position (proprioception) and vibration sense
Spasticity
Roaring, rushing, ringing, or pounding sensation in the ears

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12
Q

Anemia assessment: respiratory

A

Dyspnea
Orthopnea
Tachypnea

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13
Q

Anemia assessment: GI

A
Anorexia, nausea, vomiting
Dysphagia
Abdominal pain
Flatulence
Diarrhea
Hepatomegaly
Splenomegaly
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14
Q

Anemia assessment: musculoskeletal

A

Muscle pain (claudication)

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15
Q

Anemia assessment: integumentary

A

Pallor of the skin and mucous membranes
Jaundice (hemolytic anemia)
Brittle, ridged, concave nails
Impaired wound healing
Loss of elasticity
Early thinning and graying of hair
Dry skin
Painful mouth sores
Beefy red, sore tongue (megaloblastic anemia)
Smooth and red tongue (iron deficiency anemia)
Ulcerated corners of the mouth (angular cheilitis)

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16
Q

Anemia assessment: cardiovascular

A
Palpitations
Chest pain
Tachycardia
Hypotension
Peripheral edema
Murmurs
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17
Q

Medical and nursing management for anemia

A
  1. Correct or control cause
  2. manage fatigue
  3. maintain adequate nutrition
  4. maintain adequate perfusion
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18
Q

What can decrease the severity of fatigue in patients with anemia?

A

short periods of daily exercise can decrease the severity of fatigue

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19
Q

What should clients with anemia keep in mind about their nutrition?

A

Iron, vitamin b12, folic acid are essential

  • avoid alc
  • culturally centered food and food preferences
  • dietary supplements may be needed
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20
Q

Iron deficiency anemia: causes

A

Blood low
Low iron in diet
Heavy menstruation

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21
Q

Iron deficiency anemia: s/s

A
SOB
Fatigue
Increased workload of the heart
Tachycardia 
Dizziness
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22
Q

Iron deficiency anemia: dx

A

MCV < 90fL
Stool for occult blood
Colonoscopy

mean corpuscular volume. An MCV blood test measures the average size of your red blood cells

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23
Q

Iron deficiency anemia: tx

A

Iron

Transfussion

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24
Q

What are things to keep in mind about iron transfusions?

A

Hemoglobin rise after 1 week – full 1-2g/dL 4-8 weeks

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25
Q

What are sfx of iron?

A

nausea, epigastric discomfort can take with meals but then decrease absorption

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26
Q

Iron supplement education

A

Take iron on empty stomach (1 hour before, or 2 hours after a meal) - absorption is reduced with food, especially diary products and antacids

To prevent gastrointestinal distress, the following schedule may work better if more than one tablet a day is prescribed: Start with only one tablet per day for a few days, then increase to two tablets per day, and then three tablets per day. This method permits the body to adjust gradually to the iron.

Increase the intake of vitamin C, to enhance iron absorption.

Eat foods high in fiber to minimize problems with constipation.

Remember that stools will become dark in color.

To prevent staining the teeth with a liquid preparation, use a straw or place a spoon at the back of the mouth to take the supplement. Rinse the mouth thoroughly afterward.

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27
Q

What foods are high in vitamin C?

A

citrus fruits and juices, strawberries, tomatoes, broccoli

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28
Q

Anemia and kidney disease

A

Creatinine level > 3
Decreased production of erythropoietin
Can cause HTN d/t rapid production

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29
Q

What are s/s of having anemia with kidney disease?

A

Fatigue, decreased activity tolerance

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30
Q

Anemia with chronic disease

A

Rheumatoid arthritis

Cancers

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31
Q

What deficiencies are present with megoblastic anemia?

A

Folic acid and vitamin b12

a type of anemia characterized by very large red blood cells.

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32
Q

Megoblastic anemia: cause

A

Autoimmune condition

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33
Q

Megaloblastic anemia: s/s

A
Fatigue
Mood changes
Memory difficulty
Weakness
Vitiligo (patchy loss of skin pigmentation)
Premature graying of hair
Tongue is smooth, red, and sore
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34
Q

Megaloblastic anemia: dx

A

MCV < 90 fL

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35
Q

Megaloblastic anemia: tx

A

IM injections of b12 or folic acid orally

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36
Q

Where is folate found?

A

green leafy vegetables, legumes, egg yolks, fortified foods like cereal, and liver

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37
Q

Why are folic acid and vb12 needed?

A

To have DNA maturation and RBC

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38
Q

Someone with newly diagnosed megaloblastic anemia will need what?

A

endoscopy

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39
Q

B12 deficiency comes from what?

A

absorption - examples include Crohns, gastric bypass or gastrectomy

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40
Q

What is happening in hemolytic anemias?

A

The erythrocytes have a shortened lifespan; thus, their number in circulation is reduced.

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41
Q

What happens when there are too few erythrocytes with hemolytic anemia?

A

result in decreased available oxygen, causing hypoxia, which, in turn, stimulates an increase in erythropoietin release from the kidney. The erythropoietin stimulates the bone marrow to compensate by producing new erythrocytes and releasing some of them into the circulation somewhat prematurely as reticulocytes

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42
Q

What are the 2 types of hemolytic anemias that we talked about in class?

A

Thalassemia

Autoimmune hemolytic anemia (AIHA)

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43
Q

Thalassemia: cause

A

hereditary

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44
Q

Thalassemia: highest population

A

Mediterranean, African, and Southeast Asian ancestry

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45
Q

Thalassemia: alpha

A

occurs without s/s

milder than beta

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46
Q

Thalassemia: beta

A

fatal within the 1st few years of life

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47
Q

Thalassemia: tx

A

Tranfusion of PRBC

– can develop anti-RBC antibodies, transfusion-associated infections and iron overload

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48
Q

What are treatments of iron overload?

A

Deferoxamine, Deferasirox, and deferiprone

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49
Q

Deferoxamine, Deferasirox, and deferiprone: side effects

A

Bone marrow suppression, liver function abnormalities, annual eye and hearing exams, n/v, diarrhea, abdominal pain

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50
Q

Deferoxamine, Deferasirox, and deferiprone: issues

A

adherence

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51
Q

Autoimmune Hemolytic Anemia (AIHA): patho

A

own immune system hemolyzes RBCs

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52
Q

Autoimmune Hemolytic Anemia (AIHA): causes

A

unknown 50%, chronic lymphocytic leukemia, lupus, or infections

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53
Q

Autoimmune Hemolytic Anemia (AIHA): tx for mild

A

Monitoring
corticosteroids
try other immunosuppressive agents

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54
Q

Autoimmune Hemolytic Anemia (AIHA): tx for severe

A

blood transfussions

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55
Q

Autoimmune Hemolytic Anemia (AIHA): nursing considerations

A

If splenectomy - get vaccinations

Corticosteroids - monitor BP and BG

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56
Q

Jaundice is a s/s of hemolytic anemia; what are nursing considerations and/or teaching points about this?

A

caused by a build-up of bilirubin in the body. This causes severe itching, but the client should avoid scratching because this can worsen the condition and cause breaks in the skin. The client should not use soap when bathing and bathe in tepid water to avoid pruritis

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57
Q

What is the primary cause of death of AIHA?

A

iron overload

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58
Q

Thrombocytopenia: what is it?

A

Low platelet count.

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59
Q

Thrombocytopenia: causes

A

Malignancy, infections, medications, autoimmunity (ITP), and DIC

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60
Q

Thrombocytopenia: clinical manifestations

A

Less than 50,000/mm3 - bleed occurs following surgery or trauma

Less than 20,000/mm3, – petechiae, spontaneous nasal and gingival bleeding, menstrual bleeding, bleeding after dental procedures

Less than 10,000/mm3 – fatal CNS or GI hemorrhage can occur

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61
Q

Thrombocytopenia: medical management

A

Medications associated with the cause (abx., cardio meds, etc)
Platelet transfusion

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62
Q

Chemo patients must maintain their platelets above what

A

10,000

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63
Q

What is normal platelet count?

A

150,000-450,000 (150-450)

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64
Q

Thrombocytopenia: nursing management / education

A

caution with activity d/t increased bleeding risk

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65
Q

Heparin induced Thrombocytopenia (HIT)

A

Formation of antibodies against the heparin-platelet complex.

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66
Q

HIT risk factors:

A
Type of heparin used
Duration of heparin therapy (>4 days) 
Surgery (esp. if required cardiopulmonary bypass)
Women
Dose (SQ/IV) is not risk factor
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67
Q

HIT characteristics

A

Decline in platelet count (5-10 days after heparin therapy)
Drop 50% below baseline over 1-3 days
Risk for thrombosis (DVT, CVA, ACS, ischemic damage to extremity)

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68
Q

HIT: tx

A

Stop heparin
use alternative means of anticoagulations
If thrombosis occurs, 3-6 months of anticoagulation therapy will be needed

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69
Q

What is the alternative anticoagulation therapy is someone gets HIT?

A

argatroban - thrombin inhibitor

NOT COUMADIN – promotes thrombosis in the microvasculature by depleting protein C

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70
Q

HIT nursing interventions

A

Discuss the need to not have Heparin for 3-4 months

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71
Q

Immune Thrombocytopenia Purpura (ITP): what is it?

A

Platelet count is decreased by destruction and impaired production
Low amounts of thrombopoietin

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72
Q

Immune Thrombocytopenia Purpura (ITP): s/s

A

incidental finding
bruising vs bleeding from mucous membrances
less than 10,000 platelets

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73
Q

Immune thrombocytopenia purpura (ITP): risk factors

A

uncontrolled HTN and peptic ulcer disease

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74
Q

Immune Thrombocytopenia Purpura (ITP): medical management

A

need to keep safe platelet levels (30-50,000)
lifestyle (caution with activities)
transfusons are not common
less than 5,000 –> high dose IVIG and corticosteroids

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75
Q

Immune Thrombocytopenia Purpura (ITP): nursing management

A

lifestyle
report HA or visual disturbances - could show intracranial bleeding
avoid IM and rectal meds - stimulate bleeding
avoid constipation
electric razors
soft bristled toothbrush
no intercourse until greater than 50,000

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76
Q

Immune Thrombocytopenia Purpura (ITP): Incidence in children

A

acute - children 1-6 weeks after a viral illness

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77
Q

Platelet defects: functional platelet disorder cause

A

induced by aspirin

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78
Q

Functional Platelet Disorder: clinical manifesations

A

Ecchymoses

Risk for bleeding with trauma or surgery

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79
Q

Functional Platelet Disorder: medical management

A

stop medication prior to surgery - typically days prior

80
Q

Functional Platelet Disorder: nursing management

A

caution with OTC meds

81
Q

Von-Willebrand disease

A

Inherited bleeding disorder.

Necessary for factor VIII and platelet adhesion at site of vascular injury

82
Q

Von-Willebrand disease: diagnostic

A

Question after procedures (dental), nosebleeds and large bruises, heavy menses
Lab – normal platelet but prolonged bleeding time (PTT)

83
Q

Von Willebrand Disease (vWD): management

A

Minimize postprocedural bleeding (vasopressin)

Avoid Aspirin and other NSAIDs

84
Q

What are sfx of vasopressin?

A

HA, Facial flushing, tachycardia, hyponatremia, rarely –seizures

85
Q

Why might women be encouraged to get on birth control with vWB disease?

A

increases the # of vWB factors they have in their blood

86
Q

Acquired Coagulation Disorders: Liver disease (cirrhosis, tumor or hepatitis)

A

Coagulation factors are synthesized in liver
Significant bleeding risk
Transfusion of FFP
Esophageal varices or peptic ulcers

87
Q

Acquired Coagulation Disorders: Vitamin K deficiency

A

occurs in malnourished patients

88
Q

Acquired Coagulation Disorders: complications of antocoagulant therapy

A

Antidote to heparin = protamin sulfate

antidote to warfarin = VK

89
Q

Acquired Coagulation Disorders: Disseminated Intravascular Coagulation (DIC) – what is it triggered by

A

sepsis, trauma, cancer, shock, allergic reaction

90
Q

DIC: s/s

A

bleeding from mm., venipuncture sites and GI/urinary tract

91
Q

DIC: tx

A
Treat underlying cause 
Improve o2
replace fluids
correct electrolyes imbalances
vasopressor meds
92
Q

Who is the most common patient at risk for developing DIC?

A

Sepsis and acute promyelocytic leukemia

93
Q

DIC can lead to what organs to fail

A

kidney, lung, brain, skin

94
Q

What are examples of Malignant Hematologic Condictions

A

Polycythemia Vera
Essential Thrombocytopenia
Chronic Myeloid Leukemia (CML)

they are myeloproliferative neoplasms

95
Q

Polycythemia Vera: what is it?

A

Myeloid stem cells are too high in number

– elevated erythrocyte, leukocyte and platelet counts

96
Q

Polycythemia Vera: s/s

A

Hallmark signs: splenomegaly, severe and painful itching triggered by water

Ruddy complexion
LUQ pain
blood volume complaints (HA, dizzy, fatigue, blurred vision)
increase blood viscosity
increase uric acid (potential kidney stones)
pruritus d/t increased basophils

97
Q

What is essential thrombocytopenia

A

Result of elevated platelet on CBC
Can cause vaso-occlusion in the microvasculature

Asymptomatic

98
Q

What is Chronic Myeloid Leukemia

A

Over production of myeloid WBC; platelets can also be elevated

99
Q

Chronic myeloid leukemia: s/s

A

Bone Pain, enlargement of liver and spleen
Fatigue, night sweats, abd pain, early satiety and weight loss
High WBC – confusion, vision changes, SOB, chest pain

100
Q

Chronic myeloid leukemia: nursing considerations

A

Durg interactions, fluid retention, GI sfx

101
Q

How to decrease pruritus

A

bathing in cool water with mild soap

102
Q

What is the therapeutic management of polycythemia vera?

A

therapeutic phlebotomy

103
Q

What is secondary polycythemia?

A

excessive production of erythropoietin

104
Q

Secondary polycythemia: cause

A

smoking, OSA, COPD, cyanotic heart disease, living at high altitude

105
Q

Secondary Thrombocytosis: causes

A

infection, chronic inflammatory disease, acute hemorrhage, and splenectomy
— Increased production of platelets, but not over 1 million/mm3

106
Q

Secondary Thrombocytosis: tx

A

should return to normal

107
Q

What are examples of bone marrow failure syndromes

A
Aplastic anemia (AA)
Myelodysplastic syndromes (MDSS)
108
Q

What is aplastic anemia

A

Damage to bone marrow stem cells

109
Q

Aplastic anemia: cause

A

acquired or congential - idiopathic

– insideous manifestions

110
Q

Aplastic anemia: s/s

A

show similar as anemia

111
Q

Aplastic anemia: tx

A

if severe – Treat quickly (transfusion of blood and platelets) or anx with fever

or

stem cell transplant

112
Q

Nursing considerations with Aplastic anemia:

A

monitor for decrease RBC, WBC, platelet

113
Q

What is the end result of Aplastic anemia:

A

cytopenias (reduction in # RBC)

114
Q

Aplastic anemia - death is often caused by what?

A

hemorrhage or infection

115
Q

Myelodysplastic syndrome (MDSS) - what

A

ineffective hematopoiesis

116
Q

Myelodysplastic syndrome (MDSS) - risk factor of what

A

leukemia

117
Q

Myelodysplastic syndrome (MDSS): s/s

A

Fatigue, dyspnea, activity intolerance, unexplained bruising or bleeding or recurrent infections

118
Q

Myelodysplastic syndrome (MDSS) - what should nurse monitor patient for

A

report s/s of anemia, thrombocytopenia and infection

119
Q

What is acute myeloid leukemia

A

result of genetic mutations that occur during hematopoiesis and ultimately reflect the type, quality and quantity of cells produced.

The bone marrow becomes packed with abnormal cells and ultimately begins to release these cells into the circulation prematurely

120
Q

What is the stongest risk factors for acute myeloid leukemia?

A

The strongest risk factors for resistant disease, early relapse, and decreased survival include advanced age, poor functional status, and complex cytogenetic abnormalities

121
Q

Acute Myeloid Leukemia: onset

A

Abrupt - 1 week to a month

122
Q

What is a sign of acute myeloid leukemia?

A

fever and infection

123
Q

Acute myeloid leukemia: what happens to blood cells

A

Decrease in erythrocytes and platelets, leukocyte count can be low, normal or high, decreased neutrophil count

124
Q

Acute Myeloid Leukemia: thrombocytopenia

A

increased risk of bleeding

125
Q

Acute Myeloid Leukemia: medical management

A

stem cell transplant

126
Q

Acute myeloid leukemia: nursing management

A

prevent infection and bleeding, promote comfort and patient education

127
Q

What are other types of malignant hematologic disorders?

A
Acute Promyelocytic Leukemia (subtype of acute myeloid leukemia)
Acute lymphocytic leukemia 
Hodgkin lymphoma 
Non-Hodgkin Lymphoma 
Chronic Lymphocytic Leukemia (CKK)
Multiple myeloma
128
Q

Who is at risk for developing chronic lymphocytic leukemia?

A

vietnam war veterans

129
Q

Acute lymphocytic leukemia: what is it?

A

controlled proliferation of immature lymphoid cells – decreased leukocytes, erythrocyte, and platelets

130
Q

Acute lymphocytic leukemia: signs and symptoms

A

Testes and CNS – s/s testicular swelling, HA, visual changes, vomiting, and neurologic deficits

131
Q

How are malignant hematologic disorders typically treated?

A

All of these will typically be treated with some type of chemo, no raw veggies or fruits, no plants, no flowers, avoid crowds, private room

132
Q

Why would someone need a splenectomy?

A
  1. Emergency removal d/t trauma or rupture
  2. Elective - treating selected hematologic disorder
  3. severe hemorrhage
133
Q

What is Sickle Cell Disease?

A

Inheritance of HgS (sickle hemaglobin) gene

134
Q

Sickle Cell Disease: patho

A

Hgb forms sickle shape when exposed to low oxygen levels

Hgb loses its round, pliable, biconcave disc shape and becomes dehydrated, rigid, and sickle shaped

Rigid RBCs can adhere to vessel walls, predisposing for clot formation

If HgS is exposed to enough oxygen before becoming too rigid, it can revert back to normal shape

135
Q

What can trigger HgS to sickle?

A

Normal o2 levels in venous blood

136
Q

What are the types of sickle cell crises?

A

Vaso-occlusive crisis
Aplastic crisis
Sequestration crisi

137
Q

Sickle cell crisis: Vaso-occlusive crisis

A

Very painful

Results in entrapment of RBCs and WBCs in microcirculation, leading to tissue hypoxia

Oxidative damage to vessel causes dysfunction in vessel wall causing vasculopathy

138
Q

Sickle cell crisis: Aplastic crisis

A

Develops from human parvovirus infection

Hgb levels fall rapidly, bone marrow can’t compensate, no reticulocytes produced

139
Q

Sickle cell crisis: Sequestration crisis

A

Pooling of sickled cells in various organs

Spleen most common in children

Liver and lungs most common in adults

140
Q

Acute Chest Syndrome:

A

Type of vaso-occlusive crisis

most common cause of death in young adults with sickle cell disease

141
Q

Acute Chest Syndrome: what triggers it

A

Often triggered by infection
Fat embolism
PE
pulmonary infarction

142
Q

Acute Chest Syndrome: s/s

A

fever, respiratory distress, new infiltrates in CXR ``

143
Q

Acute Chest Syndrome: tx

A

RBC transfusion, abx, brochodilators, nitric oxide

144
Q

Acute Chest Syndrome: how can someone decrease their risk?

A

use of incentive spirometer & RBC transfusions during vaso-occlusive crisis

145
Q

What is a common sequelae of SCD?

A

pulmonary htn

146
Q

Why can pulmonary HTN be hard to diagnose until late stages?

A

due to little or no s/s in early stages

147
Q

pulmonary HTN s/s

A

Fatigue, dyspnea on exertion, dizziness, chest pain

SpO2 remains normal, BSCTA (?)

148
Q

What type of strokes are common in children and older adults vs young adults who have sickle cell disease

A

Ischemic strokes: children and older adults

Hemorrhagic strokes: young adults

149
Q

What do strokes result from with sickle cell disease?

A

decrease cerebral perfusion d/t anemia, hemolysis or increase hypoxic stress

150
Q

What are reproductive complications that men can experience with SCD?

A

25% men develop hypogonadism

Low testosterone levels, low libido, erectile dysfunction, infertility

Frequent episodes of priapism can contribute to significant pain, decreased libido, and impotence

151
Q

What are reproductive complications that women can suffer from if they have SCD?

A

Menarche can be delayed

Pain episodes may increase during menstruation

Need for reliable birth control when treated with hydroxyurea d/t teratogenic defects

152
Q

Treatment for SCD?

A
Hydroxyurea 
Folic acid replacements
Incenitive spiro
abx
corticosteroids 
hydration
PRBC transfucion
PFT
153
Q

What does hydroxyurea do for SCD tx?

A

increases fetal hemoglobin (high affinity for o2)

154
Q

What are sfx of hydroyurea?

A

chronic suppression of leukocyte formation, teratogenic, potential for development of cancer

155
Q

Why might someone with SCD require daily folic acid replacements?

A

to maintain the supply requires for increased erythropoiesis from hemolysis

156
Q

Why might someone need abx if they have SCD?

A

for acute chest syndrome

157
Q

What is important about hydration with someone who has SCD?

A

fluid overload can develop quickly

158
Q

Why might someone benefit from PRBC transfusions if they have SCD

A

treats hypoxia

159
Q

Why might someone need PFTs regularily if they have SCD?

A

to detect early pulmonary HTN

160
Q

What are adequate pharm therapies, especially during vaso-occlusive crises?

A

Aspring for mild pain - decreases inflammation and reduced risk of thrombosis

NSAIDs - may have ceiling effect, watch for renal disease/damage

IV opioids and PCA for pain crisis

161
Q

what are non-pharm therapies to decrease the pain someone has with SCD?

A

Treatment for neuropathic pain
adequate hydration
supplemental o2

162
Q

What is hemophilia A

A

Deficient Factor VIII

163
Q

What is hemophilia B

A

deficient or defective factor IX

164
Q

What happens with hemophila?

A

Increased propensity to bleed, hemorrhage even from minor trauma

165
Q

Hemophila: what does the extent of the hemorrhage depend on

A

level of factor deficiency and force of trauma

166
Q

Hemophilia: where does 75% of bleeding occur?

A

joints - can cause permanent joint damage with recurrent bleeds of same joint

167
Q

Hemophila: bleeding into muscles can do what

A

compress nerves

168
Q

Hemophilia: tx

A

Factor VIII and X concentrates
Less ofte, FFT
Children can receive factor prophylactically 3-4 times per week

Can develop neutralizing antibodies (inhibitors) to factor concentrates, decreasing effectiveness

Desmopressin - transient increase in Factor VII, mechanism not fully understood

169
Q

Hemophilia: nursing considerations

A

Education on necessary physical restrictions, when to seek care

Coping with disease-related restrictions on lifestyle

Fall prevention– especially with older adults

Home administration of factor at first sign of bleeding

Education on importance of compliance with prophylactic treatments

Education on medications and foods that interfere with platelet aggregation– aspirin, NSAIDs, alcohol

Avoid heat during acute bleeding episodes

170
Q

Why would someone receive blood

A

low blood d/t surgery, trauma, anemia (low production), renal failure, cancer

171
Q

What is the importance of RBC

A
Body can’t function well without them
Carries hemoglobin (delivers O2 and removes CO2)
172
Q

s/s that someone is low on RBC

A

fatigue; SOB; increased HR

173
Q

What are examples of blood products

A
Whole Blood
Packed Red Blood Cells (PRBC)
Platelets
Fresh Frozen Plasma (FFP)
Albumin
174
Q

What must be set in place in order to prevent transfusion reactions

A

Facility protocol

RN to transfuse the blood

175
Q

blood transfusion: client safety

A

Patient needs to be typed and cross matched

labeling, blood brand

176
Q

know ABO compatability and Rh factor

A

book and slide 38 ppt

177
Q

What should a nurse obtain along with informed consent

A

allergies
previous transfusions
- pre-medicate (benedryl, tylenol)

178
Q

Blood transfusions - what do you need in regard to IV access

A

18g or larger because RBC can lyse

2 IV access because you can not transfuse anything with blood, and the patient may need other medications hung

179
Q

How long does blood transfusion take on avg

A

2 hr

180
Q

Where is blood stored

A

blood bank in fridge

181
Q

how many units of blood can be given at a time

A

1 unit

182
Q

When should the nurse start the blood transfusion

A

Start within 30 minutes of receiving blood and needs to be done within 24 hours

  • needs to be IN BODY to reduce risk of bacteria growth
183
Q

What do you verify with a blood transfusion

A
Order
Pt. identifications
Blood bank info
Blood type and donor type, RH factor
Expiration date
Look at blood and make sure no
184
Q

What do you monitor during blood transfusion

A

baseline vitals

185
Q

What supplies will you need for a blood transfusion

A
Alcohol pads
Gloves
Biohazard bag
Blood tubing “Y tubing with filter”
Blood product
500 mL bag of 0.9% NS—NOTHING ELSE!
10 mL flush
186
Q

Blood transfusion rate

A

TRANSFUSE SLOWLY!

Approx. 2mL/min for first 15 minutes

187
Q

What does the nurse do for the first 15 min of blood trans

A

Stay with patient

minimize amount of blood to patient incase of trans rx

188
Q

When do most transfusion rx occur

A

1st 15 min

189
Q

When does the nurse get vitals after the start of the infusion

A

after 5 min

190
Q

when do the second set of vital get taken after the 1st 5 min

A

15 minutes, another vital set and then you can increase the IV rate

191
Q

What are s/s of blood trans rx

A
Hemolytic
Febrile 
Allergic
Circulatory overload
Rash (hives)
Aching (back, head, chest)
Chills
Tachycardia
Increased RR
Oliguric (low UOP)
Nausea
192
Q

The blood trans procedure

A

Assure patency of IV line

Hang normal saline flush bag

Spike normal saline bag and prime tubing (including the filling blood tubing filter completely)

Close saline roller clamp BEFORE proceeding to next step.
– Keep line clamped. Will open when flushing blood through line after blood bag is empty.

Spike blood bag and prime tubing
– Be sure to prime entire line

Connect tubing to IV access
– 20g or larger should be used
Set pump

Monitor for adverse reactions & STAY with patient!
Measure vital signs after 5 minutes & 15 minutes
Increase infusion rate after 15 minutes per order/policy
Measure vitals during & after infusion complete

193
Q

What should nurse do if the patient has a rx to the blood trans

A

STOP transfusion!! *note the time

Disconnect blood tubing and replace with new tubing primed with 0.9% NS

Notify the doctor and blood bank

STAY WITH PATIENT

Monitor VS every 5 minutes

Send tubing, blood to blood bank
DOCUMENT!

194
Q

Medications for blood trans rx:

A

corticosteroids, fluids, antihistamines, antipyretics, vasopressors, diuretics (dependent on reaction type and patient)

195
Q

Labs to obtain when pt has blood trans rx

A

clotting? DIC? Electrolytes, blood levels, Urine- free hemoglobin