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6200 Adult /Older Adult II > Hematologic Disorders > Flashcards

Hematologic Disorders Flashcards

1
Q

Causes of Anemia?

A

decreased RBC production, blood loss and increased RBC destruction

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2
Q

Levels of tissue hypoxia and Hgb levels:

1) mild
2) moderate
3) severe

A

1) 10-12 g/dl
2) 6-10 g/dl
3) < 6 g/dl

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3
Q

Anemia Manifestations: Integumentary Changes

A

pallor, jaundice and pruritis (increase in bile salts)

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4
Q

Anemia Manifestataions in older adults?

A

confusion, fatigue, pallor, ataxia and HF

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5
Q

Anemia: Diagnostic Studies

A
  • CBC – Hgb, Hct, MCV, MCH, MCHC, reticulocytes, platelets
  • Iron studies – serum iron, TIBC, serum ferritin
  • Serum B12 level
  • Serum folate
  • Stool guaiac test
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6
Q

Causes of Megaloblastic Anemia?

A
  • Cobalamin (B12) deficiency

- Folic Acid deficiency

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7
Q

At-risk groups for Iron deficiency Anemia?

A

elderly, pregos, premenopausal, low socioeconomic status, and blood loss

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8
Q

Causes of Iron-Deficiency Anemia

A
  • Inadequate dietary intake
    • Iron absorption altered
    • Duodenum
  • Blood loss from GI/GU tract or Hemodialysis
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9
Q

Iron-Deficiency Anemia: Labs

A
  • decreased: H/H, MCV, serum iron

- normal: B12, folate

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10
Q

Oral iron supplement A/E?

A

heartburn, constipation, diarrhea

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11
Q

Indications for parental Iron supplementation?

A

malabsorption of oral iron, oral iron intolerance, need for higher doses, poor compliance with oral iron

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12
Q

What are good dietary sources of iron?

A

Liver and muscle meats, eggs, dried fruit, legumes, dark green leafy vegetables, whole grains, enriched bread, potatoes

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13
Q

Cobalamin (B12) Deficiency: Etiology

A

missing protein needed for absorption

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14
Q

Cobalamin (B12) Deficiency causes?

A
  • Gastric mucosa not secreting
  • GI alterations: surgery, chronic diseases
  • Chronic alcoholics
  • Long-term users of
    • H2-histamine receptor blockers
    • Proton pump inhibitors
  • Strict vegetarians
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15
Q

Gastrointestinal manifestations of Cobalamin (B12) Deficiency?

A

Sore tongue, anorexia, n & v, abdominal pain

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16
Q

Neuromuscular manifestations of Cobalamin (B12) Deficiency?

A

Weakness, paresthesias (feet & hands), ↓ vibratory and position senses, ataxia, muscle weakness, impaired thinking

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17
Q

Treatment of Cobalamin (B12) Deficiency?

A
  • Cobalamin (Parenteral or intranasal)
  • Lifelong if no GI absorption (diet not effective)
  • If long-standing neuromuscular complications, may not reverse
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18
Q

S/S of anemia develop as a result of what issue?

A

slow development, related to tissue hypoxia

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19
Q

Folic Acid Deficiency S/S?

A

similar to cobalamin deficiency, except for neurologic symptoms

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20
Q

Common causes of folic acid deficiency?

A
  • Dietary deficiency/malabsorption syndromes
  • Drugs
  • Increased requirement
  • Alcohol abuse/anorexia
  • Hemodialysis (FA is filtered out)
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21
Q

What is the cause of pernicious anemia?

A

B12 deficiency due to the gastric mucosa not secreting

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22
Q

Megaloblastic Anemia: Nursing & Interprofessional Management?

A
  • Early detection and treatment
    • Family hx of pernicious anemia?
  • Ensure safety
    • Pt haas diminished sensations to heat/pain from neurologic impairment
    • Protect from falls, burns or trauma
  • Frequent medical screening for the potential risk of developing gastric cancers
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23
Q

What differentiates cobalamine (B12) deficiency from folic acid deficiency?

A

both have similar s/s manifestations, the pt with B12 deficiency will have neurologic symptoms which are absent in folic acid deficiency

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24
Q

What are the clinical manifestations or s/s of Sickle Cell Disease?

A
  • Usually asymptomatic except during sickling episodes
  • Pain from tissue hypoxia and damage
  • Pallor of mucous membranes
  • Jaundice from hemolysis
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25
Q

Complications of Sickle Cell Disease?

A
  • Organs affected by hypoxia

- Infection-major cause of morbidity and mortality

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26
Q

SCD Sickling Episodes are triggered by _____ with _____ being the most common precipitator?

A
  • low O2 tension in the blood

- infection

27
Q

Initial sickling in SCD can be reversed with?

A

re-oxygenation

28
Q

S/S of Sickle Cell Crisis?

A
  • Severe, painful, acute exacerbation of sickling → vaso-occlusive crisis
  • Severe capillary hypoxia → tissue necrosis
  • Life-threatening shock: from severe ↓ tissue O2, ↓circulating fluid volume
29
Q

Sickle Cell Disease: Nursing & Interprofessional Management (prevention)?

A

prevent infection (i.e. vaccination) and organ damage with prompt tx

30
Q

Sickle Cell Disease: Nursing & Interprofessional Management (education)

A
  • Avoid high altitudes
  • Keep hydrated
  • Treat infections promptly
  • Importance of prompt medical attention
  • Pain control
31
Q

Tx for hospitalized patients in sickle cell crisis ?

A
  • O2 for hypoxia and to control sickling
  • Vigilance for respiratory failure
  • Rest
  • DVT prophylaxis
  • Administration of fluids and electrolytes
  • Transfusion therapy
  • Chelation therapy with repeat exacerbations
32
Q

Sickle Cell Disease: Nursing & Interprofessional Management (pain management)?

A
  • Often pain medication tolerant
  • Require continuous & breakthrough analgesia with morphine & hydromorphone
  • Multimodal & interdisciplinary approach involving emotional & adjunctive measures
33
Q

Sickle Cell Disease: Nursing & Interprofessional Management (other)

A
  • Administer folic acid
  • Hydrea - only antisickling agent shown to be clinically beneficial
  • Hematopoietic stem cell transplantation (HSCT)-only available cure
34
Q

Thrombocytopenia

A

Condition where platelets levels are < 150K

35
Q

Thrombocytopenia: Clinical Manifestations?

A
  • Patients are often asymptomatic
  • Most common symptom is mucosal or cutaneous bleeding
  • ↓ Platelet count
36
Q

Prolonged bleeding with routine procedures occur with a platelet count of?

A

< 50k

37
Q

Patients are at increased risk of hemorrhage with a platelet level of?

A

< 20k

38
Q

What is the most common symptom of thrombocytopenia?

A

mucosal or cutaneous bleeding

39
Q

What is the most common type of acquired thrombocytopenia?

A

Immune Thrombocytopenic Purpura (ITP)

40
Q

What is Immune Thrombocytopenic Purpura (ITP)?

A
  • Syndrome of abnormal destruction of circulating platelets

- Primarily an autoimmune disease

41
Q

ITP Interprofessional Care?

A
  • Corticosteroids

- Splenectomy if patients do not respond to other treatments

42
Q

When are platelet transfusions done?

A
  • <10k or if actively bleeding or prophylactically for planned procedure
43
Q

Acute Intervention for Thrombocytopenia: Nursing Management?

A
  • Evaluate and treat bleeding
  • Avoid SQ/IM injections-apply pressure or ice packs
  • Monitor labs: platelet count, coagulation studies, Hgb, Hct
44
Q

Health Promotion/Teaching

for Thrombocytopenia: Nursing Management

A
  • Teach self-care measures to reduce risks for bleeding
  • Prompt treatment for symptoms of bleeding
  • Awareness of medication risks: cancer chemotherapy drugs, heparin, OTC meds that can cause acquired thrombocytopenia
45
Q

A group of malignant disorders affecting the blood and blood-forming tissues

A

Leukemia

46
Q

Leukemia can affect what tissues?

A
  • Bone marrow
  • Lymph system
  • Spleen
47
Q

Acute versus Chronic Leukemia?

A
  • Acute: Immature hematopoietic cells proliferate, abrupt onset
  • Chronic: Mature forms of WBC, onset is more gradual
48
Q

Leukemia: Classification?

A
  • Acute myelogenous leukemia (AML)
  • Acute lymphocytic leukemia (ALL)
  • Chronic myelogenous leukemia (CML)
  • Chronic lymphocytic leukemia (CLL)
49
Q

Acute Myelogenous Leukemia (AML)

A

– myeloblast proliferation

- S/S-infection/abnormal bleeding, hyperplasia of bone marrow and spleen

50
Q

Acute Lymphocytic Leukemia (ALL)

A
  • small, immature lymphocytes
  • S/S:
    • abrupt onset fever,
    • bleeding
    • Insidious onset of progressive weakness, fatigue, pain, bleeding tendencies
    • CNS manifestations are common (e.g. meningitis)
51
Q

What is the most common type of leukemia in children?

A

ALL

52
Q

What is the most common type of leukemia in adults?

A

CLL

53
Q

Excessive mature neoplastic granulocytes in bone marrow?

A

Chronic Myelogenous Leukemia (CML)

54
Q

Why is folic acid given to treat Sickle Cell Disease?

A

to increase RBC’s

55
Q

Which genetic marker is present in > 90% of AML patients?

A

Philadelphia chromosome

56
Q

Course of CML?

A

can be stable for years then have an aggressive (blastic) phase the may not respond well to treatment

57
Q

Chronic Lymphocytic Leukemia (CLL)

A

Proliferation of functionally inactive but long-lived, mature-appearing lymphocytes

58
Q

Complications from early-stage CLL?

A
  • are rare
  • May develop as the disease advances
  • Lymph nodes enlarge-pain, paralysis from pressure
59
Q

Tx for CLL?

A

may not be needed

60
Q

Leukemia: Clinical Manifestations r/t bone marrow failure?

A
  • Anemia
  • Thrombocytopenia
  • ↓ number and function of WBCs
61
Q

Leukemia: Clinical Manifestations r/t infiltration?

A
  • Splenomegaly
  • Hepatomegaly
  • Lymphadenopathy
  • Bone pain
  • Meningeal irritation
  • Oral lesions
62
Q

Leukemia: Diagnostic Studies

A
  • Blood counts, Bone marrow biopsy

- Look for leukemic cells outside of the blood/bone marrow with a Lumbar puncture or CT scan

63
Q

Phases of chemotherapy?

A
  • Induction
  • Postinduction/postremission
  • Maintenance
64
Q

Tx for Leukemia?

A
  • Chemotherapy
  • Corticosteroids
  • Radiation therapy-targeted or total body
  • Hematopoietic stem cell transplant
  • Biologic and targeted therapy

6200 Adult /Older Adult II (17 decks)

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