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Flashcards in Exam 1 Deck (78)
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1
Q

What are the blood components?

A

1) Plasma
2) Blood
3) Cellular portion

2
Q

What is plasma?

A

90% water

10% Solutes: Albumin, Electrolytes, Proteins

3
Q

What is the cellular portion of blood?

A

1) RBC’s
2) WBCs
3) Platelets (clotting)

4
Q

Function of RBCs

A

Transports hemoglobin which carries oxygen to the cells

5
Q

Function of WBCs

A

Resists/fights infections

  • ANC (Absolute Neutrophil Count: Reflects the bodies ability to handle a bacterial infection.
  • Normal: >2,500
  • Safe: >1,000
  • ANC <500 Protective isolation as patient is at risk for opportunistic infections
  • ANC= Neutrophils + bands (WBC x 10)
6
Q

Elements of blood

A

1) Erythrocytes
2) Monocytes
3) Platelets
4) Eosinophils
5) Lymphocytes
6) Neutrophils
7) Basophils

7
Q

Liquid portion of blood, which has clotting factors that help make bleeding stop

A

Plasma

8
Q

Small parts of cells that help make bleeding stop by forming a clot (or scab) over the hurt area.

A

Platelets.

9
Q

Anemia from decreased RBC production s/s

A
  • Pallor
  • Tachycardia
  • HA
  • Fatigue
  • SOB
  • Muscle weakness
  • Systolic heart murmur
  • Pica (eating clay, paper, paste)
10
Q

Nutritional deficiency anemia

A

1) Iron
2) Folate
3) B12
4) Copper
5) Chronic disease
6) Chronic blood loss

11
Q

Bone marrow failure anemia

A

1) Aplastic anemia
2) Red cell aplasia
3) Malignancy
4) ALL/neuroblastoma
5) Infection (CMV, Parvovirus)

12
Q

Increased RBC loss anemia S/S

A
  • Pallor
  • Fatigue
  • HA
  • Muscle weakness
  • Cool skin
  • Tachycardia
  • Decreased peripheral pulses
  • Low BP (late sign of shock)
13
Q

Reasons for acute blood loss?

A

1) Epistaxis (nose bleed)
2) Hemophilia (blood not able to clot)
3) Hypersplenism (overactive spleen, removing blood cells too early and too quickly)
4) (ITP) Idiopathic thrombocytopenic purpura (ITP): bleeding disorder where the immune system destroys platelets
5) (DIC) Disseminated Intravascular Coagulation: small blood clots develop throughout the bloodstream, blocking small blood vessels. The increased clotting depletes the platelets and clotting factors needed to control bleeding, causing excessive bleeding.

14
Q

Increased RBC destruction anemia s/s

A
  • Icteric sclera/pallor
  • Fatigue
  • HA
  • Tachycardia
  • Dark urine
  • Splenomegaly
  • Hepatomegaly
  • Frontal bossing
15
Q

Intracorpuscular anemia

A

1) Hemoglobinpathies (sickle cell disease, thalassemia)
2) Enzymopathies (G6PD)
3) Membrane defects (hereditary spherocytes)

16
Q

Extracorpuscular anemia

A

1) Immunologic (AIHA, isoimmunization)

2) Drugs/toxic substances (chemo, irradiation infection)

17
Q

Sickle cell anemia pathophysiology

A

RBCs become “sickle” shaped, rather than rounded, potentially causing clumping of the cells. This clumping may lead to thromboses, inadequate tissue perfusion, and damage to organs

18
Q

Sickle cell anemia risk factors

A
  • Autosomal recessive (both parents have to be carriers)

- African descent and Mediterranean descent

19
Q

Sickle cell anemia medical management

A

Prevent sickling or treat actual crisis

20
Q

Sickle cell anemia nursing considerations

A
  • Interventions
  • Support
  • Education
21
Q

Sickle cell anemia interventions

A
  • Rest
  • Hydration (top priority)
  • Electrolyte replacement
  • Analgesics
  • Blood transfusions
  • Antibiotics
  • O2
22
Q

Sickle cell anemia types of crises

A

1) Vaso-occlusive
2) Sequestration
3) Aplastic

23
Q

Vaso-occlusive sickle cell anemia crises

A

Sickle cell RBCs slow or stop flow within blood vessels.. Most often in the legs and arms.

24
Q

Sequestration sickle cell anemia crises

A

Sickle RBCs build up within the spleen and liver resulting in an enlarged spleen (hepatomegaly). Can lead to circulatory collapse and death.

25
Q

Aplastic sickle cell anemia crises

A

Refers to a bone marrow failure condition in which the formed elements of the blood are simultaneously depressed.

26
Q

Vaso-occlusion sickle cell crises may cause?

A
  • Hypoxia
  • Tissue ischemia or infarction resulting in enlarged spleen
  • Altered liver & kidney function
  • Osteoporosis
  • Stroke
  • Cardiomegaly
  • Increased destruction of RBCs
27
Q

Exacerbation for sickle cell anemia

A
  • Dehydration
  • Stress
  • Trauma
  • Infection
  • Cold weather
  • Fluid loss
  • High altitude
28
Q

Sickle cell anemia crisis (inherited RBC disorder): Cell clumping-Obstruction produces vasoocclusive crisis which shows as?

A

-Pain: Abdominal & long bones in the hands and feet, syndrome, and joint pain

29
Q

Complications for sickle cell anemia crisis?

A
  • Infections
  • Stroke
  • URI’s
  • Leg ulcers
  • Splenomegaly
30
Q

Treatment for sickle cell anemia crisis

A

HOP
Hydration
Oxygenation
Pain management/relief

31
Q

Prognosis of sickle cell anemia

A
  • No cure
  • Possible bone marrow transplant
  • Supportive care/prevention of sickling episodes
  • Frequent bacterial infections because of immunocompromise
  • Bacterial infection: leading cause of death in young children with sickle cell disease
  • Usual life span: into the fifth decade
32
Q

Pooling of large amounts of blood (hepatomegaly, splenomegaly, circulatory collapse)

A

Sequestration Crisis

33
Q

What is B-Thalassemia?

A
  • Inherited blood disorder resulting in less hemoglobin and fewer RBCs than normal
  • More common in Mediterranean areas, also seen in Southern China, India, & Southeast Asia
34
Q

What are the types of B-Thalassemia?

A

1) Minor

2) Major

35
Q

Minor B-Thalassemia

A
  • Asymptomatic, silent
  • Carrier state
  • Pallor
  • Splenomegaly
  • Mild anemia
  • Normal life span expected
36
Q

Major B-Thalassemia

A
  • Cooley anemia
  • Severe anemia
  • Pallor
  • Failure to thrive (FTT)
  • Chronic hypoxia
  • Iron overload
  • Usually shorter life span
37
Q

Nursing interventions for B-Thalassemia

A
  • Blood transfusion protocols
  • Education
  • Emotional support

*Blood transfusions every 3-5 weeks, can lead to too much iron from disease and transfusions

38
Q

Medical Management for B-Thalassemia

A
  • Exchange transfusions
  • Iron chelation therapy (remove excess iron, binds iron and gets rid of it. Too much iron causes damage to heart, liver, endocrine system)
  • Removal of spleen
  • Bone marrow transplant (BMT)
39
Q

What happens if children with B-Thalassemia are not treated?

A

They will have low O2, fatigue, jaundice, their forehead will show bossing (sticks out), facial deformities, and an enlarged head

40
Q

Aplastic anemia. What is it?

A
  • Hypoplasia of all cell lines (no real structure)
  • May be congenital or acquired (through radiation therapy)
  • Anticonvulsant medication
  • Autoimmune disease
  • Usually has an insidious onset
41
Q

Diagnosis of aplastic anemia

A
  • Past medical history, physical exam
  • Bone marrow studies
  • S/S bleeding, history of bleeding
  • Common to have purpura (purple spots) in mouth and petechia (red dots)
42
Q

Nursing Interventions for aplastic anemia

A
  • Blood transfusion protocols

- Education

43
Q

Medical management for aplastic anemia

A
  • Transfusions
  • Immunosuppressive therapy
  • Bone marrow transplant (BMT) (more susceptible to infections)
44
Q

Patient teaching for iron supplementation

A
  • Diet rich in vit C (citrus fruits, tomatoes, melons, strawberries) and heme iron (meats) increases iron supplementation absorption: include these in diet
  • Bran, tea, coffee, milk, oxalates (spinach & swiss chard), and egg yolk decrease iron absorption. Avoid consuming at same time of iron supplementation
  • iron absorbed best if taken when stomach is empty; take between meals with beverage other than tea, coffee, or milk
  • can take at bedtime if abdominal discomfort occurs when it is taken between meals
  • if iron dose is missed, take it as soon as remembered if within 13 hours of scheduled dose. Do not double up on dose
  • keep in childproof container and out of reach of children
  • iron may cause stools to be black or dark green
  • Constipation is common so a diet high in fiber with adequate fluid intake recommended
45
Q

Types of hemophilia

A

1) Hemophilia A
2) Hemophilia B
3) Von Willebrand disease

46
Q

Hemophilia A

A
  • Classic hemophilia

- Deficiency of factor VIII

47
Q

Hemophilia b

A
  • Christmas disease

- Deficiency of factor IX

48
Q

Von Willebrand disease

A

Deficiency of von willebrand factor and factor VIII

49
Q

Hemophilia, what is it?

A
  • Bleeding disorder resulting from chromosome deficiency
  • 2 specific coagulation patterns which lead to a clotting factor deficiency
  • X-lined recessive
  • Males more affected
  • Usually have unaffected parents
  • Bleeding in the SQ, IM areas most common for hemorrhage
50
Q

Hemophilia S/S

A
  • S/S of internal bleeding
  • S/S of bleeding into the joint cavity (knees, elbows, ankles); warmth, redness, severe pain, tingling, bubbling sensation, unusual limb position
  • hematuria
  • other bleeding into mouth, nose
  • Minor injuries which won’t clot
  • Bleeding with circumcisions
  • Abnormal coagulation studies: PT/PTT/INR
51
Q

Hemophilia Medical Management

A
  • Factor replacement: 2-3 times/week for prophylaxis, also for invasive procedures
  • No NSAIDS
  • DDVAP- stimulates rise in factor
  • Antifibrolytic agents (Amicar)
  • RICE: Rest, ice, elevation, compression
  • First aid measures for bleeding pressure control, elevation
52
Q

Nursing intervention/considerations for hemophilia

A
  • Educate parents and patient what do they need to do with surgery, dental work, trauma, accidents
  • Support groups
  • Psychosocial issues: guilt, control
  • Finances- counseling
  • Multidisciplinary approach
53
Q

Inherited blood disorder: Factor VII, Classic, or Type A

A

Hemophilia

54
Q

hemophilia main points

A
  • No cure
  • Avoid injury and meds that promote bleeding
  • Good nutrition
  • Good dental hygiene
  • IV Administration of deficient clotting factor
  • Intracranial hemorrhage
  • Prolonged nosebleeds
  • Bruising easily
  • Warm, painful, swollen joints with decreased movement
  • GI Hemorrhage
  • Tarry stools
  • Cola colored urine
  • Coffee ground emesis
55
Q

Von Willebrand Disease: What is it?

A

Deficiency or defect called von willebrand factor

  • herediatary
  • autosomal dominant inheritance
56
Q

Von Willebrand disease S/S

A
  • Mild, moderate, or severe bleeding (usually only requires intervention for dental or surgical procedures)
  • Increased tendency of bleeding in mucous membranes
57
Q

Medical Management for Von Willebrand Disease

A
  • DDVAP

- Special clotting factor-Humate-P

58
Q

Nursing Interventions/Considerations for Von Willebrand disease

A
  • Educate parents
  • ID Symptoms
  • Patient teaching for procedures
59
Q

Leukemia

A
  • Most common form on childhood cancer

- unrestricted proliferation of immature WBCs in the blood-forming tissues of the body

60
Q

Two forms of leukemia

A

1) Acute lymphoid leukemia (ALL)

2) Acute nonlymphoid leukemia (ANLL or AML)

61
Q

Nursing considerations for leukemia

A
  • Pain control
  • No live vaccines until immune system is capable of responding appropriately to vaccine
  • Prevent infection (educate prior to discharge): Nutrition, handwashing by all visitors, staff
  • Prevent injury, especially when platelet count in low
  • Use proper caution with use of chemotherapeutic drugs
62
Q

Symptoms of leukemia

A

ANT
Anemia-decrease hemoglobin
Neutropenia-Risk of infection
Thrombocytopenia-bleeding

63
Q

Hodgkin lymphoma

A
  • Originates in lymphoid system
  • primarily metastasizes to spleen, liver, bone marrow, lungs
  • most common presenation: non-tender, enlarged cervical or supraclavicular lymph nodes
  • Most common Tx: radiation and/or chemo
64
Q

Non-Hodgkin lymphoma

A
  • Usually diffuse, not nodular
  • Dissemination occurs early, fast
  • Mediastinal and meninges commonly affected areas
  • Common tx: chemo
65
Q

where are lymph nodes?

A

Around heart, abdomen, neck, armpits, groin, spleen

66
Q

Characteristics of burns: First degree

A

Superficial

67
Q

Characteristics of burns: Second degree

A

Partial thickness

68
Q

Characteristics of burns: Third degree

A

Full thickness

69
Q

Characteristics of burns: Fourth degree

A

Full thickness and underlying tissue

70
Q

Characteristics of burns: rule of nines

A

Body is divided by 9%. There are different charts used to determine how much of the body is burned

71
Q

Burns charts for assessment

A

1) Lund and Browder Chart

2) Wallace rule of nines

72
Q

Lund and Browder Chart

A

Most accurate measurement as it allows for consideration of body shape with age

73
Q

Wallace rule of nines

A

Used to calculate burn percentages for adults (divided into “9%” areas of the body), however it is not accurate for assessing children.

74
Q

Complications of burn injuriess

A
  • Immediate threat of airway compromise
  • Profound shock
  • Infection (local and systemic sepsis)
  • Inhalation injuries, aspiration, pulmonary edema, pulmonary embolus
75
Q

Therapeutic management of burn injuries: Emergency care priorities

A
  • Stop burning process
  • Assess child’s condition
  • Cover burn to prevent contamination
  • Transport child to appropriate level of care
  • Provide reassurance
76
Q

Therapeutic Management of Burn Injuries

A
  • First priority: airway maintenance
  • Fluid replacement therapy: critical in first 24 hours
  • Nutrition: enhanced metabolic demands
  • Medication: antibiotics, analgesics, anesthetics for procedural pain
77
Q

Care of minor burns

A
  • Wound cleansing
  • Débridement
    • Removal of blisters (controversial)
  • Dressings
    • Covering wound with antimicrobial ointment or use of occlusive dressings (controversial)
78
Q

Burns: Long term care

A
  • Begins once wound coverage has been achieved
  • Prevention/management of contractures
  • Physical/occupational therapy
  • Multidisciplinary team
  • Facilitate adaptation of child and family
  • Prevention of burn injuries