Exam 1 Flashcards
(78 cards)
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
Aplastic sickle cell anemia crises
Refers to a bone marrow failure condition in which the formed elements of the blood are simultaneously depressed.
26
Vaso-occlusion sickle cell crises may cause?
- Hypoxia
- Tissue ischemia or infarction resulting in enlarged spleen
- Altered liver & kidney function
- Osteoporosis
- Stroke
- Cardiomegaly
- Increased destruction of RBCs
27
Exacerbation for sickle cell anemia
- Dehydration
- Stress
- Trauma
- Infection
- Cold weather
- Fluid loss
- High altitude
28
Sickle cell anemia crisis (inherited RBC disorder): Cell clumping-Obstruction produces vasoocclusive crisis which shows as?
-Pain: Abdominal & long bones in the hands and feet, syndrome, and joint pain
29
Complications for sickle cell anemia crisis?
- Infections
- Stroke
- URI's
- Leg ulcers
- Splenomegaly
30
Treatment for sickle cell anemia crisis
HOP
Hydration
Oxygenation
Pain management/relief
31
Prognosis of sickle cell anemia
- 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
Pooling of large amounts of blood (hepatomegaly, splenomegaly, circulatory collapse)
Sequestration Crisis
33
What is B-Thalassemia?
- 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
What are the types of B-Thalassemia?
1) Minor
| 2) Major
35
Minor B-Thalassemia
- Asymptomatic, silent
- Carrier state
- Pallor
- Splenomegaly
- Mild anemia
- Normal life span expected
36
Major B-Thalassemia
- Cooley anemia
- Severe anemia
- Pallor
- Failure to thrive (FTT)
- Chronic hypoxia
- Iron overload
- Usually shorter life span
37
Nursing interventions for B-Thalassemia
- Blood transfusion protocols
- Education
- Emotional support
*Blood transfusions every 3-5 weeks, can lead to too much iron from disease and transfusions
38
Medical Management for B-Thalassemia
- 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
What happens if children with B-Thalassemia are not treated?
They will have low O2, fatigue, jaundice, their forehead will show bossing (sticks out), facial deformities, and an enlarged head
40
Aplastic anemia. What is it?
- 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
Diagnosis of aplastic anemia
- 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
Nursing Interventions for aplastic anemia
- Blood transfusion protocols
| - Education
43
Medical management for aplastic anemia
- Transfusions
- Immunosuppressive therapy
- Bone marrow transplant (BMT) (more susceptible to infections)
44
Patient teaching for iron supplementation
- 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
Types of hemophilia
1) Hemophilia A
2) Hemophilia B
3) Von Willebrand disease
46
Hemophilia A
- Classic hemophilia
| - Deficiency of factor VIII
47
Hemophilia b
- Christmas disease
| - Deficiency of factor IX
48
Von Willebrand disease
Deficiency of von willebrand factor and factor VIII
49
Hemophilia, what is it?
- 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
Hemophilia S/S
- 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
Hemophilia Medical Management
- 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
Nursing intervention/considerations for hemophilia
- 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
Inherited blood disorder: Factor VII, Classic, or Type A
Hemophilia
54
hemophilia main points
- 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
Von Willebrand Disease: What is it?
Deficiency or defect called von willebrand factor
- herediatary
- autosomal dominant inheritance
56
Von Willebrand disease S/S
- Mild, moderate, or severe bleeding (usually only requires intervention for dental or surgical procedures)
- Increased tendency of bleeding in mucous membranes
57
Medical Management for Von Willebrand Disease
- DDVAP
| - Special clotting factor-Humate-P
58
Nursing Interventions/Considerations for Von Willebrand disease
- Educate parents
- ID Symptoms
- Patient teaching for procedures
59
Leukemia
- Most common form on childhood cancer
| - unrestricted proliferation of immature WBCs in the blood-forming tissues of the body
60
Two forms of leukemia
1) Acute lymphoid leukemia (ALL)
| 2) Acute nonlymphoid leukemia (ANLL or AML)
61
Nursing considerations for leukemia
- 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
Symptoms of leukemia
ANT
Anemia-decrease hemoglobin
Neutropenia-Risk of infection
Thrombocytopenia-bleeding
63
Hodgkin lymphoma
- 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
Non-Hodgkin lymphoma
- Usually diffuse, not nodular
- Dissemination occurs early, fast
- Mediastinal and meninges commonly affected areas
- Common tx: chemo
65
where are lymph nodes?
Around heart, abdomen, neck, armpits, groin, spleen
66
Characteristics of burns: First degree
Superficial
67
Characteristics of burns: Second degree
Partial thickness
68
Characteristics of burns: Third degree
Full thickness
69
Characteristics of burns: Fourth degree
Full thickness and underlying tissue
70
Characteristics of burns: rule of nines
Body is divided by 9%. There are different charts used to determine how much of the body is burned
71
Burns charts for assessment
1) Lund and Browder Chart
| 2) Wallace rule of nines
72
Lund and Browder Chart
Most accurate measurement as it allows for consideration of body shape with age
73
Wallace rule of nines
Used to calculate burn percentages for adults (divided into “9%” areas of the body), however it is not accurate for assessing children.
74
Complications of burn injuriess
- Immediate threat of airway compromise
- Profound shock
- Infection (local and systemic sepsis)
- Inhalation injuries, aspiration, pulmonary edema, pulmonary embolus
75
Therapeutic management of burn injuries: Emergency care priorities
- Stop burning process
- Assess child's condition
- Cover burn to prevent contamination
- Transport child to appropriate level of care
- Provide reassurance
76
Therapeutic Management of Burn Injuries
- First priority: airway maintenance
- Fluid replacement therapy: critical in first 24 hours
- Nutrition: enhanced metabolic demands
- Medication: antibiotics, analgesics, anesthetics for procedural pain
77
Care of minor burns
- Wound cleansing
- Débridement
* Removal of blisters (controversial)
- Dressings
* Covering wound with antimicrobial ointment or use of occlusive dressings (controversial)
78
Burns: Long term care
- 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
