Exam 2: Hematological Alterations Flashcards

1
Q

What organs keep your blood in balance?

A

Spleen: destroys cells and platelet storage

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2
Q

What stimulates RBC production?

A
  • Stimulated by decreased oxygen

- Kidney then produces erythropoietin

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3
Q

How long do RBC’s live?

A

90-120 days

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4
Q

RBC Labs: Size (Cytic)

A
MCV:
Normal 80-94
Small: microcytic
Normal: normocytic 
Large: macrocytic
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5
Q

RBC Labs: Hemoglobin (Chromic)

A

MCH:
Normal 26-24
Normal: normochromic
<26: hypochromic

*Look at these values. Especially for iron deficiency anemia.

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6
Q

WBC: Lymphocytes

A
  • Found in bone marrow, spleen, lymph glands

- Responsible for immunity

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7
Q

WBC: Neutrophils

A
  • Attack bacteria/viruses

- Elevated in acute inflammation

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8
Q

WBC: Monocytes

A
  • Macrophages

- Increased in chronic inflammation

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9
Q

WBC: Eosinophils

A
  • Kills parasites

- Increased in allergies

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10
Q

WBC: Basophils

A

-Elevated during healing

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11
Q

Platelets

A
  • Promote hemostasis
  • Produced in bone marrow
  • Stored in the spleen
  • Live 8-10 days
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12
Q

Iron Deficiency Anemia

A
  • Most common cause of anemia in infancy, childhood and adolescence.
  • Depleted Fe stores -> decreased supply of Fe needed to make hgb for RBC
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13
Q

What are risk factors for iron deficiency anemia?

A
  • Decreased iron intake
  • Increased iron or blood loss
  • Periods of increased growth
  • Fastest growth periods: 6-24 months and Adolescence
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14
Q

What are the causes of iron deficiency anemia?

A
  1. Decreased iron intake
  2. Inadequate iron stores: premature, multiple birth, anemic mother
  3. Decreased absorption: never give iron w/ milk; vitamin C enhances absorption
  4. Blood loss: hemorrhage, parasites
  5. Excessive demands: premature, pregnancy
  6. Inability to form Hgb: Lack of B12 and folic acid
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15
Q

Iron Deficiency Anemia: Decreased iron intake

A

Rare before 6 months: maternal iron stores still present

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16
Q

Increasing iron intake

A
  • Cow’s milk: whole milk after 1 year; formula/breast milk until 1 year
  • After four months: cereal/veg/fruits/meats
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17
Q

What are clinical manifestations of iron deficiency anemia?

A
  • Pallor with porcelain-like skin
  • Pale mucous membranes
  • Pale conjunctiva
  • Tachycardia
  • Tachypnea
  • Lethargy
  • Fatigue
  • Irritability
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18
Q

Children with lead poisoning often have associated

A

Iron-deficiency anemia

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19
Q

Diagnostics: Iron Deficiency Anemia

A
  1. History: emphasis on nutrition
  2. CBC:
    - Low hgb
    - Decreased MCV
    - Decreased MCH
    - Increased TIBC (total iron binding capacity)
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20
Q

Iron Deficiency Anemia: Management

A
  • Increase dietary intake

- Iron supplementation

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21
Q

Iron Deficiency Anemia Management: Increased Dietary Intake

A
  • Iron fortified
  • Limit cow’s milk to 24 oz/day or less
  • Iron rich foods
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22
Q

Iron Deficiency Anemia Management: Iron Supplementation

A
  • Daily oral preparation
  • Give with a multivitamin or fruit juice: Vitamin C increases absorption
  • Don’t give with milk or antacids: decreases absorption
  • 2 divided doses between meals
  • Can stain teeth (take through a straw and brush teeth after)
  • Causes black, tarry stools
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23
Q

Iron Rich Foods include

A
  • Carbs: bread, cereal, whole grains
  • Proteins: egg yolk, meats/liver, shellfish, tofu
  • Veggies/fruits: dark leafy greens, potatoes, dried fruits, raisins and prune juice
  • Other: kidney beans, legumes, nuts and seeds
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24
Q

Sickle Cell Disease

A
  • Inherited
  • Autosomal recessive condition
  • Primarily affects individuals from African decent
25
Q

Sickle Cell Disease is characterized by

A
  • Production of sickle hemoglobin
  • Chronic Hemolytic Anemia
  • Ischemic tissue injury
26
Q

Sickle Cell Disease Manifestations are a result of

A
  • Obstruction caused by the sickled RBC’s and increased destruction of RBC’s.
  • Infants do not produce HgS until about 4 months of age (d/t maternal stores)
27
Q

What are clinical manifestations of sickle cell disease?

A
  • Chronic hemolytic anemia
  • Pallor
  • Jaundice
  • Fatigue
  • Cholelithiasis
  • Delayed growth and puberty
  • Avascular necrosis of the hips and shoulders
  • Renal dysfunction
  • Retinopathy
28
Q

Sickle Cell Crisis includes

A
  1. Vaso-Occlusive Crisis
  2. Acute Sequestration Crisis
  3. Apastic Crisis
29
Q

Vaso-Occlusive Crisis: Painful Episode

A
  • Most common
  • Painful episode
  • Precipitated by infection, cold, stress, acidosis and hypoxia
30
Q

Vaso-Occlusive Crisis includes

A
  • Painful episode
  • Acute Chest Syndrome: can be confused with pneumonia
  • Hand-and-foot syndrome
  • Priapism
  • CVS
31
Q

Treatment for Vaso-Occlusive Crisis: Pain Episode

A
  • IVF
  • Opioids
  • NSAIDs
  • O2
32
Q

Acute Chest Syndrome

A

33
Q

Treatment for Acute Chest Syndrome

A
  • IVF
  • O2
  • Transfusion
34
Q

Acute Sequestration Crisis

A
  • Blood volume pooling in the spleen

- Life-threatening condition

35
Q

Acute Sequestration Crisis Treatment

A
  • IVF
  • Blood Transfusion
  • Possible splenectomy
36
Q

Apastic Crisis

A
  • Profound anemia caused by diminished erythropoiesis

- Treat with transfusion

37
Q

Evaluation of Sickle Cell Disease

A
  • CBC: Elevated reticulocyte count
  • Hemoglobin electrophoresis
  • Universal screening for newborns
  • Prenatal diagnosis: chronic villi sampling at 8-10 weeks gestation; amniocentesis at 15 weeks gestation
38
Q

Treatment of Sickle Cell Disease

A
  • Vaccinations: pneumococcal and meningococcal; influenza
  • Spleenectomy
  • Prophylactic ABT: PCN V
  • O2 and blood transfusion: To reduce the number of circulating sickle cells
  • Analgesia
39
Q

Management of Sickle Cell Disease: Monitoring

A
  • Monitor for stroke

- Monitor for infection

40
Q

Management of Sickle Cell Disease: Interventions

A
  • Maintain adequate hydration and blood flow
  • Extend extremities to promote venous return
  • HOB no more than 30 degrees
  • Diet: high calorie, protein w/ folic acid.
41
Q

Hemophilia

A
  • Hereditary bleeding disorder: dysfunction or absence of specific coagulation proteins
  • X-linked autosomal recessive disorder
  • No cure
42
Q

Hemophilia A (Classic)

A

Deficiency of coagulation factor VIII.

Most common.

43
Q

Hemophilia B (Christmas)

A

Deficiency of factor IX

44
Q

Hemophilia Manifestations

A
  • Bruise easily
  • Epistaxis
  • Hematuria
45
Q

Hemophilia: Bleeding with

A
  • Loss of deciduous teeth
  • Injections
  • Minor lacerations
46
Q

Hemophilia: It is common to develop

A

Bleeding in muscles and joints

47
Q

Hemophilia: Labs

A
  • PT
  • PTT
  • Fibrinogen level
  • Platelet count
  • Factor assays
48
Q

Hemophilia Management

A
  • Individual and depends on severity
  • Prevent excessive bleeding and tissue damage.
  • Supply the body with missing or ineffective factor: regularly scheduled, beginning in early childhood
  • Avoid aspirin and NSAIDs: will increase bleeding
49
Q

How is bleeding treated in hemophilia?

A

RICE: Rest, Ice, Compression, Elevation

50
Q

Treatment for Hemophilia

A
  • Replacement of missing clotting factors
  • Additional meds: pain relievers and corticosteroids
  • Desmopressin acetate (DDAVP): vasoconstrictor action to stop bleeding
51
Q

What are major risks associated with factor replacement therapy?

A
  • Hepatitis
  • HIV
  • Joint Problems (prophylactic therapy to prevent)
52
Q

Immune Thromboycytopenia

A
  • Acquired hemorrhagic disorder

- Evolution of antibodies against multiple platelet antigens: usually follows a viral illness; an autoimmune process

53
Q

Immune Thrombocytopenia: Characterized by

A
  • Thrombocytopenia: platelet count <20,000**
  • Purpuric rash
  • Normal bone marrow
54
Q

What are clinical manifestations of immune thrombocytopenic purpura?

A
  • Sudden onset of bruising and petechiae

- Bleeding that involves the mucous membranes and gums

55
Q

Immune Thrombocytopenic Purpura Evaluation

A
  • History
  • Physical Exam
  • CBC
  • Peripheral Blood Smear
56
Q

Immune Thrombocytopenic Purpura Management

A
  • Frequent neurological assessment
  • Restore platelet count to >20,000
  • Anti-D antibody administration
  • IV or oral steroids: blocks the autoimmune destruction of platelets
  • IVIG
  • Splenectomy
  • Platelet transfusion: only if active, uncontrolled bleeding.
57
Q

Immune Thrombocytopenic Purpura Interventions

A
  • Extra-soft bristle tooth brushes

- If splenectomy performed, administer prophylactic penicillin daily

58
Q

What should be avoided in patients with immune thrombocytopenic purpura?

A
  • Avoid aspirin and NSAID’s
  • No contact sports
  • Delay administration of live virus vaccines
  • Avoid IM injections