Exam 3- Neuro, Onc, Msk, Heme Flashcards
1
Q
difference in MSK for children
A
more cartilage, more porous, heal faster, growth plates still growing, stiffness is uncommon, rich vasculature within bones; growth continuous until 18-21
2
Q
assessment of MSK in children
A
observation: signs of deformity, guarding, signs of distress; touch- tender to touch, may radiate, may not show pain but will avoid using it; neurovascularly intact
3
Q
5P’s of compartment syndrome
A
Pain, Paralysis, parasthesia, pulses, pallor
4
Q
compartment syndrome
A
injury that causes an increase in pressure until blood supply is eventually decreased
5
Q
when treating traumatic injuries in children (MSK related)
A
ABCs. bleeding control, call EMS (they may need to reposition or realign if loss of circulation)
6
Q
impact of immobility in children on muscle
A
decreased muscle strength, tone, endurance; decreased cardiac output; decreased metabolism and increased O2 need; decreased exercise tolerance; bone demineralization; muscle atrophy
7
Q
impact of immobilization in children on skeletal
A
bone demineralization: osteoporosis and hypercalcemia
8
Q
impact of immobilization in children on metabolic system
A
decreased metabolic rate; all systems are slower; decreased appetite (treat with small frequent meals); fatigue
9
Q
impact of immobilization on cardiovascular
A
redistribution of body fluids (i.e. edema); heart has to work harder (tachycardia and HTN may be present); venous stasis (pooling blood placed at increased risk of clot); decreased ROM; frequent position changes
10
Q
impact of immobilization on respiratory system
A
decreased chest and lung expansion; decreased respiratory effort (shallow breathing); decreased need for O2, effects of gravity
11
Q
treating respiratory effects from immobilization
A
cough, deep breathing, incentive spirometer; encourage mobility
12
Q
impact of immobilization on elimination/GI GU
A
general muscle weakness and atrophy; inactivity slows peristalsis (decreases motility); urinary stasis (increased risk of UTI); constipation d/t decreased peristalsis and potential pain meds
13
Q
impact of immobilization on integumentary system
A
edema; ulceration of bony prominences; continuous pressure; hard to attend to hygiene; aware of friction moisture and skin tears
14
Q
impact of immobilization on psychological system
A
increased feelings of frustration, helplessness, anxiety, isolation, seen as punishment; depression, anger, aggression; developmental regression such as enuresis, sucking thumb, baby talk, helplessness
15
Q
caring for cast in children
A
assess CSMs (circulation, sensation, movement); assess fit of cast, any apparent swelling skin break down, soiling of cast; may cause itching, tightness, moisture, or heat
16
Q
treatment of MSK injuries
A
traction to realign; external fixation to lengthen and hold still; ambulatory devices such as crutches, walker, walking boot, cane, AFO; surgery
17
Q
Use of AFO
A
used for pt with cerebal palsy to assist in walking
18
Q
developmental dysplasia of the hip
A
aka “clicky hips”; instability of hip in neonate; lax ligament that allow hip to dislocate and relocate spontaneously; caucasian and girls at higher risk can be d/t trauma in utero, decreased movement in utero, IUGR, LGA, twin in womb, oligohydramnios
19
Q
symptoms of developmental dysplasia of hip
A
unequal skin folds; limited abduction; unequal knee height; asymmetrical; ortolani click (if under 4 weeks)
20
Q
diagnosing development dysplasia of the hip
A
ortolani maneuver, barlow maneuver, ultrasound
21
Q
treatment of developmental dysplasia of the hip
A
abduction devices, pavlik harness; if pavlik harness doesnt work by 6 months then other methods take place such as surgery or spica; traction followed by a cast; reduction via surgery then cast
22
Q
nursing considerations of developmental dysplasia of the hip
A
identify, promote normal development, maintain physical mobility, skin care/cast care, proper reducing device use and teaching, family support
23
Q
clubfoot
A
complex deformity of the foot causing forefoot adduction, midfoot supination, hind foot varus and valgus, ankle equinus; 1/2 cases are bilateral; may occur with other abnormalities like CP or spina bifida; males 2x as likely; may lead to hip problems
24
Q
valgus vs varus
A
valgus is knees more inward; varus is bowed legs
25
causes of club foot
unknown; strong family tendency; multifactorial
26
diagnosing club foot
apparent at birth; check hips
27
treatment of club foot
goal is to straighten the via casting right after birth; surgery if casting does not work
28
nursing considerations for club foot
cast care, post op care, neurovascular checks, follow-up care, parent education, promote normal development
29
scoliosis
abnormal curvature of the spine; most common spinal deformity consisting of curvature and rotation; classified as congenital, infantile, childhood/juvenile, adolescent (increase in incidence during preadolescent growth spurt)
30
symptoms of scoliosis
uneven hips, one scapula more prominent
31
diagnosing scoliosis
consists of physical exam, X-ray, and screening
32
treatment of scoliosis
depends on the degree of curvature, location of malformation, type of malformation, and age of child; consists of observation, wearing a brace, and surgery if warranted
33
surgery for scoliosis
spinal fusion and insertion of rods
34
nursing considerations for scoliosis
body image alteration (most common complications); skin integrity; surgical pre-op and post-op if needed; pt teaching
35
osteomyelitis
infection of the bone; more common in ages less than 10
36
pathophysiology of osteomyelitis
bacteria adheres to bone and causes inflammatory reaction which can rupture through the bone; typically caused by GBS in infants; could be due to otitis media or a respiratory infection
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signs and symptoms of osteomyelitis
severe pain, fever, irritability, crying, tenderness to touch, resist movement, guarding
38
diagnosing osteomyelitis
cultures of joint fluids; labs such as CBC to analyze WBCs; imaging- xray, MRI, bone density scan; biopsy; aspiration of synovial fluid
39
treatment of osteomyelitis
IV antibiotics (usually use multiple different antibx); comfort measures; immobilization; physical therapy; teaching
40
soft tissue injuries
consist of contusions, dislocations, sprains, strains; manage with RICE and ICES; seek further medical attention if unable to use limb, pain persists, or 5Ps arise
41
RICE and ICES
rest ice compression elevation; ice compression elevation support
42
Fractures
usually result from birth trauma, injury, or child abuse; true fractures rarely occur in infancy; most common site in childhood is forearm; children heal faster d/t increased blood supply; can be due to trauma, overuse, or disease
43
healing for children
approximately 1 week/year of age until 10 years old
44
types of fractures
complete or incomplete; spiral, oblique, transverse, comminuted, wedge, impacted/compression, displaced, open/compound
45
symptoms of a fractured bone
swelling, pain, decreased ROM; if 5Ps present then it is medical emergency
46
diagnosing fractures
Xray is most useful but can also detect old fractures (signs of child abuse and need to contact CPS); physical exam; history
47
treatment of fracture
reduction/repairing of fracture; immobilization with traction, brace, casting, splinting; surgery if needed
48
reduction vs traction
reduction is repairing of fracture or dislocation where traction is applying manual pulling
49
complications with fracture
circulatory compromise; nerve compression; compartment syndrome
50
assessing signs of circulatory compromise
vital signs, capillary refill, sin color
51
nerve compression
can occur at injury, during, or after; can cause carpal tunnel or sciatic nerve pain
52
compartment syndrome is
increased pressure within compartment of tissue that increases and causes decrease in circulation to muscle and nerves;
53
treatment of compartment syndrome
remove cast, pressure, or dressing to allow free flow of blood to prevent damage tissue, prevent necrosis, and prevent paralysis; DO NOT ELEVATE; require fasciotomy
54
osteogenesis imperfecta
aka brittle bone disease; genetic disorder that causes bones to break easily; main goal is to prevent fractures
55
signs and symptoms of osteogenesis imperfecta
frequent bone fractures (most common); looseness in ligament; bone deformity and pain; bruising easily; curved spine; small stature; blue sclerae
56
detecting osteogenesis imperfecta
genetic testing; blood testing to check for gene mutations; bone density scans
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treating osteogenesis imperfecta
increase bone strength; occupational therapy for fine motor skills; physical therapy to increase strength and flexibility and ROM; calcium and vitamin D, decrease pain, increase growth, bisphosphonate as ordered
58
anemia
reduction of RBC volume and/or Hgb concentration to levels below normal range for age
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causes of anemia
excessive RBC loss; increased destruction of RBCs; impaired or decreased rate of RBC production d/t bone marrow failure or deficiency of essential nutrient
60
clinical manifestations of anemia
all symptoms related to decrease in O2 carrying capacity; muscle weakness, fatigue, inability to concentrate, palpitations, tachycardia, dyspnea on exertion, pallor, PICA, dry brittle nails, concave/spoon shaped nails, CNS manifestations, growth retardations
61
CNS manifestations in anemia
headache, dizziness, lightheadedness, irritability, slowed though processes, decreased attention span, apathy, depression
62
diagnosing anemia
screening and checking Hgb/Hct during infancy/early childhood/late childhood/adolescence; history and physical; Labs such as CBC, iron studies, reticulocytes, bone marrow aspiration
63
normal Hgb by age
1-3 days: 14.5-22.5 g/dL; 2 mos: 9-14 g/dL; 6-12 yrs: 11.5-15.5 g/dL; 12-18 male yrs: 13-16 g/dL; 12-18 female yrs: 12-16 g/dL
64
treatment of anemia
prepare child for lab tests; treat underlying causes by replacing blood or nutrient; decrease oxygen tissue needs; prevent complications
65
iron deficiency anemia
caused by inadequate supply of iron essential for normal RBC production; iron is required to produce hemoglobin (decreased iron = decreased hemoglobin); prominent in age groups with rapid growth (9mo-2yrs)
66
causes of iron deficient anemia
low iron stores at birth, maternal iron stores in newborn become depleted, inadequate dietary intake of iron
67
clinical manifestations of iron deficiency anemia
s/s of classic anemia; "milk baby" appearance, glossitis (tongue), angular stomatitis (inflammation and small cracks in one or both corners of mouth), koilonychia (soft concave or "spoon" fingernails), impaired neurocognitive function
68
managing iron deficient anemia- prevention
screening, only breast milk or formula during first 12 mo., iron supps as prescribed, limit milk intake, iron-rich foods
69
managing iron deficiency anemia- meds
ferrous sulfate 2 or 3 divided doses daily; between meals if tolerated
70
parent education for iron deficiency anemia
take with vitamin C to enhance absorption, brush teeth to minimize staining; watch for side effects such as vomiting, constipation, dark green or black stools, tooth discoloration, consult diet
71
blood transfusions
take vitals before admin., take vitals 15 min after admin., then take vitals hourly while infusing, then take final set after infusion; check ID of pt and blood type of pt compared to donor; admin first 50mL or initial 20% (whatever is smaller) slowly and stay with child; admin normal saline PB; admin through filter; use blood within 30 minutes or return to blood bank; infuse unit within 4 hours
72
if blood transfusion reaction is suspected
stop transfusion, take vitals, keep vein open with NS and new tubing, notify provider, do not restart until child has been medically evaluated
73
signs of transfusion reaction
sudden severe headache, chills, shaking, fever, pain at needle site or along vein, N/V, sensation of tightness in chest, red or black urine, flank pain, hives, wheezing
74
sickle cell anemia
hereditatry disorder where presence of abnormal hemoglobin S; autosoma recessive
75
patho of sickle cell
states of dehydration, acidosis, hypoxia, or extreme temps cause abnormal hemoglobin to sickle and causes obstruction and increased RBC destruction
76
sickle cell causes...
RBCs clump causing thrombosis, arterial obstruction, and increased viscoscity; can lead to entanglement of cells, hemolysis, intermittent vascular occlusion, tissue ischemia causing organ dysfunction)
77
in order for a pt to have sickle cell anemia
both parents must carry the trait
78
clinical manifestations of sickle cell anemia
possible growth retarrdation, chronic anemia (Hgb 6-9), infection/sepsis susceptibility; spleen enlargement; liver failure and necrosis; kidney impairment leads to hematuria, inability to concentrate urine, enuresis, occasional nephrotic syndrome; retinopathy of eyes; bone changes due to hyperplasia of bone marrow, osteomyelitis susceptibility; stroke or CVA; chronic stress on heart from anemia, cardiomegaly, murmur
79
types of sickle cell disease crises
vaso-occlusive (VOC), Acute splenic sequestration, Acute chest syndrome
80
vaso-occlusive crisis (VOC)
ischemia causes pain, significant pain in areas involved, dactylitis, severe abdominal pain resembling surgical conditions
81
acute splenic sequestration
pooling of blood can cause decreased blood volume and shock, may require splenectomy to avoid splenic sequestration
82
treatment of sickle cell
aim to prevent sickling; treat crisis with pain relief, hydration, improve O2 utilization by decreasing activity, transfusions, antibiotics to treat infections, O2 therapy; prevent infections with prophylactic PCN and vaccines
83
causes of sickle cell crises
high altitudes, cold weather, swimming in cold water, physical labor
84
hemostasis
process required to stop bleeding when blood vessel is injured via vascular influence (vasoconstriction and von willebrand), platelet plug formation, clotting cascade (fibrinogen converted to fibrin to strengthen clot)
85
hemophilia
group of inherited bleeding disorders caused by deficiency of certain coagulation factors; X linked recessive; ~60% have family history of disease (rest is spontaneous mutation of gene)
86
hemophilia A
aka classic hemophilia; deficiency of factor VIII; occurence is 1:5000; accounts for 80% of hemophilia cases
87
hemophilia B
aka christmas disease; deficiency of IX factor; occurrence is 1:20000-30000
88
clinical manifestations of hemophilia
prolonged bleeding anywhere, hemoarthrosis (bleeding into joints), ecchymosis, spontaneous hematuria, epistaxis, hemorrhage anywhere in body, severe hemophilia need IV factor VIII
89
diagnostic testing for hemophilia
generally dx based on bleeding episode history, X linked inheritance patter, lab findings
90
lab findings for hemophilia
platelet, PT, and fibrinogen are normal; low factor VIII or IX levels; prolonged PTT
91
management of hemphilia
replacing missing clotting factors via transfusions of XIII or IV; DDAVP for mild hemophilia A; pain management with acetaminophen (aspirin and ibuprofen can limit platelet activity); regular exercise and play; encourage full ROM
92
hemophilia nursing interventions
recognize and control bleeding immediately, prevent bleeding, prevent crippling effects of bleeding, family support
93
Neuro assesment
compare baseline to current assessment and if no baseline known then compare to normal developmental; assessment includes- LOC, pupil response, cranial nerves, reflexes, motor function, posturing, overall physical exam
94
assessing LOC
full consciousness, confusion, disorientation, lethargy, obtundation, stupor, coma, persistent vegetative state
95
GCS
assesses visual response, verbal, and motor; scored 3-15; 8 is considered coma
96
eye opening GCS
spontaneous, verbal stimuli, pain response, no response; 1-4
97
verbal response GCS
coos or babbles, irritable cries, cries to pain, moans to pain, no response; 1-5
98
motor response GCS
spontaneous movement/purposefully, withdraws to touch, withdraws to pain, decorticate posturing, decerebrate posturing to pain, no response; 1-6
99
diagnosing increased ICP
testing of spinal fluid via LP, EEG to test electrical changes, xray for fx or dislocations, CT for density, MRI for target structures and tissue discrimination
100
nursing role to help kids prepare for neuros testing
parent and pt teaching, take fear away via explaining and allowing kid to become familiar, monitor vitals, be truthful
101
manifestations of increased ICP
early- irritability, fatigue, personality changes; late- decreased motor response, decreased sensory response to pain, change in pupils (decreased reactivity and size), decreased LOC, decorticate or decerebrate posturing
102
symptoms of increased ICP in infants/young children
tense bulging fontanelle, high pitched cry, increased head circumference, "setting-sun" sign, irritability, restlessness, feeding changes
103
symptoms of increased ICP in older children
headache, vomiting, cognitive or personality changes, diplopia/blurred vision, anorexia, nausea, weight loss, seizures
104
nursing care/management of increased ICP
assess for early changes, admin prescribed meds, keep head and neck at neutral, monitor hydrations status closely, promote normal bowel regimen, prevent weight loss and admin feeds as ordered, prevent skin breakdown, monitor for SIADH or DI caused by hypothalamic dysfunction
105
concussion
bruising of brain from bouncing off inside of skull; usually no alteration of mental status; mild
106
skull fracture
be aware for potential if child has fall more than 2x their height, signs are battle signs behind the ears and racoon eyes; can be linear fracture, depressed fracture, diastatic fracture, or basilar fracture
107
hydrocephalus
increased CSF in ventricles and subarachnoid spaces of brain; caused by impaired absorption, excessive production, obstructed circulation of CSF; communicating (impaired absorption) vs. non-communication (obstruction)
108
manifestations of hydrocepha;us
newborn/infant- bulging fontanelle, increased head circumference, sun set eyes, irritability, high pitched cat-like cry, visible scalp veins; chilcusdren- headache, visual disturbance, N/V, pupils are sluggish, decrease in consciousness, seizures, cushings triad
109
cushings tirad
HTN (widened pulse pressure), bradycardia, irregular respirations
110
management of hydocephalus
ventriculoperitoneal (VP) shunt to drain excess CSF (can cause infection and malfunction)
111
parent education for VP shunt
watch for signs of increased CSF at home, changes can be subtle like school performance headache or behavior changes, participate in normal activities, contact sports are prohibited, frequent developmental screenings and medical check ups, may need to revise shunt as child grows
112
epilepsy
seizure; uncontrolled electrical activity in brain that may produce convulsion, minor physical signs, though disturbances, or combo of symptoms
113
patho of epilepsy
abnormal electrical discharge occurring in cerebral cortex; seizure occurs when sudden imbalance between excitatory and inhibitory forces
114
types of seizures
focal (partial)- symptoms confined to one are of brain, EEG localized to one spot; without impaired awareness (simple)- may be motor, sensory, autonomic primarily; with impaired awareness (complex)- impaired consciousness with associated aura and psychomotor manifestations; generalized- involves both hemispheres (usually no aura, tonic clonic; absence seizures- day dreaming'; status epilecticus- longer then 5 minutes without regaining consciousness
115
when seizure occurs, monitor for...
when it started, was there aura, characteristics of seizure, how long it lasted; ABCs are priority
116
febrile seizure
seizure associated with febrile illness in absence of CNS infection in children older then 1 month without prior seizure activity; simple partial is most common; common ages 6mo-5yrs; treatment to decrease temp with tylenol/motrin, increase fluids, luke warm tub; fever up to 104 is still ok; 105+ is an issue and indicative of bacterial infection
117
risk factors for febrile seizure
family hx, temp > 101.8 F, preceded UTI or GI illness
118
treating seizure disorders
assess the seizure for time, characteristics, aura, post-ictal; pad crib, stay with child, do not interrupt, promote patent airway, record activity, admin seizure meds, admin diastat as needed; treat with meds, ketogenic diet, vagus nerve stimuli, surgery; as nurse need to educate
119
neural tube defects
group of related defects of CNS involving cranium or spinal cord that vary from mild to severely disabling; 50% associated with folic acid deficiency and rest are multifactorial
120
patho of neural tube defects
3rd-4th week gestation the neural plat closes to form neural tube that eventually forms brain and spinal cord; inappropriate closure of neural tubes
121
spina bifida
part of group of neural tube defects consisting of failure of osseous spine to close; spina bifida occulta, spina bifida cystica
122
spina bifida occulta
not visible externally; does not affect spinal cord but may have external signs like dimpling of skin, nevi, or hair tufts; may go undetected d/t most have no neuro effects; if neuro effects then usually motor or sensory deficit of lower extrem and urinary output
123
spina bifida cystica
visible defect with external saclike protrusion; can be menigocele or myelomeningocele
124
meningocele spina bifida cystica
sac contains meninges and spinal fluid but no neural elements; no neuro deficits
125
myelomeningocele spina bifida cystocele
sac contains meninges, spinal fluid, and nerves (more severe); can occur anywhere along spinal column; varying degrees of neuro deficit- usually involves urinary or bladder, can be associated with club feet and congenital dislocation of hips
126
nursing assessment/care of spina bifida
assess defect, assess neuro and associated anomalies, monitor for hydrocephalus meningitis and spinal cord dysfunction
127
pre-op and post-op nursing care for spina bifida
pre-op: prevent infection and protect sac, position and associated difficulties, early closure within 12-72 hours after birth; post-op: monitor for ongoing complications, monitor bowel and bladder, monitor neuro status; C-section birth to avoid birth canal
128
cerebral palsy
non-progressive neuromuscular disorder of varying degrees resulting from damage or developmental defects in part of the brain that controls motor function; manifests differently in each child; most common permanent physical disability in childhood
129
clinical manifestations of cerebral palsy
delayed gross motor development, abnormal motor performance, alterations of muscle tone, abnormal postures, reflex abnormalities, associated disabilities
130
spastic cerebral palsy
most common type (80%); cortex area of brain is affected; can be hemiplegia, diplegia, quadriplegia, quadriplegia; characterized by stiffness and difficulty moving
131
other signs of spastic cerebral palsy
persistence of primitive reflexes, hypertonicity with poor control of posture balance and coordinated, impairment of fine and gross motor skills, tendency to have contractures, weakness of affected limbs
132
therapeutic management of cerebral palsy
mobilizing devices, surgical interventions, pharmacologic treatments such as baclofen diazepam (valium) botox AEDs if seizures, technical aids, manage associated problems
133
therapies and education for CP
physical therapy, occupational therapy, speech therapy, hearing aids, education, recreation
134
muscular dystrophy
group of inherited sidorders with progressive degeneration of symmetric muscle groups causing progressive muscle weakness and wasting; body does not break down protein in muscle; all have increasing disability and deformity with loss of strength
135
duschennes muscular dystrophy (DMD)
most severe and ost common type; x-linked recessive (only affects males); mutation in gene that codes of dystrophin; onset between 3-5yrs
136
dystrophin
protein that strengthens muscle fibers and prevents them from injury as they contract; found primarily in skeletal muscle or voluntary muscle that controls movement; fat and connective tissue replace degenerated nerve fibers
137
clinical manifestations of DMD
normal development early in life; first seen in extremities and trunk; progressive generalized weakness starting around 3-5 yrs; progressive muscular weakness, wasting, and contractures; gowers sign
138
gowers sign
child stands up by using hands to walk themselves to standing position
139
complications with DMD
contractures and joint deformity, scoliosis, atrophy from disuse, infections, obesity, cardia complications, respiratory complications
140
diagnosing DMD
dx based on clinical manifestations, serum levels of dystrophin, muscle biopsy, prenatal diagnosis
141
interventions for DMD
no effective cure or treatment; treatment is symptomatic; glucocorticoids can help with muscle strength, multidisciplinary approach; surgery for lengthing muscles for contractures; respiratory devices
142
nursing interventions for DMD
immobility, skin breakdown, CSMs with devices, helping prevent complications, coping, decision making, child development
143
meningitis
can be bacterial (worse) or viral; invasion of meninges; droplet infection through nasopharyngeal secretions; caused by type B influenzae, neisseria, strep pneumonia
144
symptoms of meningitis
nuchal rigidity, headache, high fever, kernigs sign (difficulty extending leg), brudzinski sign (knee and neck), petechiae
145
treatment and management of meningitis
LP, labs and cultures, IV antibiotics, isolation, neuro assessment, treat pain, treat fever, vaccine education, family support
146
encephalitis
inflammation of CNS that causes altered function of various portions of brain and spinal cord
147
lymphoma
malignant solid tumor of the immune systems constitutional cells; these lymphoid cells multiply uncontrollably and form tumors; infiltrate mediastinum, spleen, liver, bone marrow, CNS, skin
148
non-hodgkins lymphoma
malignant disease from lymphocytic lineage; typically arise in lymph nodes and spleen; more common in children under 10non-ho
149
non-hodgkin lymphoma clinical manifestations
swollen glands, SOB, cough, abdominal pain, changes in bowel patterns
150
treatment of non-hodgkin lymphoma
chemotherapy is primary treatment, radiation therapy, targeted therapy with monoclonal antibodies
151
hodgkin lymphoma
lymphatic system malignancy characterized by reed-sternberg cells
152
hodgkin lymphoma clinical presentation
painless lymphadenopathy, mediastinal mass, pruritis, hepatosmplenomegaly, systemic B symptoms like unexplained fever >38C for 3 days and drenching night sweats and weight loss >10% in 6 months
153
leukemia
malignancy of blood-forming cells (bone marrow cells) causing uncontrolled proliferation of blasts, decreased production of normal cells, accumulation of blasts in body organs/tissues
154
manifestation of leukemia
fatigue, pallor, anorexia, bruising, bleeding, fever, infection, bone/joint pain, abdominal pain, headache, vomiting, visual disturbances, tachycardia
155
acute lymphoblastic leukemia (ALL)
chemotherapy for 2-3 years; goal is to eradicate more than 99% of leukemia cells and restore normal hematopoiesis; CNS directed therapy; intensification/consolidation
156
acute myelogenous leukemia
principles of treatment include intensive chemotherapy required to achieve remission and attain cure; lengthy hospitalizations expected throughout treatment; intensive supportive care; challenging to treat
157
osteosarcoma
malignant tumor of the bone derived from bone-forming mesenchyme (connective tissues); most common sites are long bones like distal femur, proximal tibia, proximal humerus
158
peak incidence of osteosarcoma
2nd decade of life, associated with adolescent growth spurt; male to female ratio 1.5:1
159
manifestation of osteosarcoma
pain and tenderness at affected area; may have soft tissue mass
160
treatment for osteosarcoma
initial is surgical biopsy, then adjuvant combination chemotherapy, then surgery to amputate or limb salvage or rotationplasty
161
prognosis for osteosarcoma
overall survival rate is 65-70%; metastatic is 20-30%
162
wilms tumor
most common primary malignant renal tumor; it is rapidly growing and vascular; incidence higher in females (slightly), peak age 2-3yrs,
163
presentation of wilms tumor (nephroblastoma)
nontender firm flank mass that does not dross midline in healthy appearing child; may be asymptomatic or have pain, vomiting, gross hematuria, anemia, HTN
164
wilms tumor treatment
surgery consisting of unilateral complete nephrectomy, bilateral nephrectomy of more involved kidney and partial nephrectomy of other kidney, chemotherapy, radiation
165
neuroblastoma clinical manifestations
often widespread metastatic disease at diagnosis, fevers, irritability, excess sweating, HTN, anemia/fatigue, anorexia, weight loss, diarrhea, limp/refusal to walk, blueberry muffin spots, orbital ecchymosis
166
neuroblastoma treatment
based on stage of disease; intense high dose chemotherapy, surgery, radiation therapy, stem cell rescue, antibody therapy
167
central nervous system tumors or brain tumors
4500 new tumors diagnosed in children annually (gliomas 25%), most common cause of pediatric cancer and cancer-related deaths, more common in males then females
168
CNS tumor locations
2/3 occur in posterior fossa or infratentorial; 1/3 in supratentorial
169
infratentoral tumors
located in the brainstem and cerebellum area
170
supratentorial tumors
located in areas like the cerebrum or ventricles; the upper part of the brain
171
CNS/brain tumor manifestations
headaches, change in mental status, restlessness, anxiety, confusion, increased intracranial pressure, N/V, nerve palsies, ataxia, aphasia, hemiparesis, visual problems
172
treatment for CNS/brain tumors
surgery, XRT>3 years, chemotherapy, immune/biotherapy, stem cell therapy
173
side effects of radiation
dependent on location, dose, age of pt, adjunctive chemotherapy; N/V, fatigue, cognitive defects, short stature, cataracts, acute pericarditis, dyspnea, pleuritic chest pain, dry cough, increased RR ad effort, diarrhea, cramping, malabsorption
174
side effects of chemotherapy
indiscriminately kills rapidly dividing cells; malignant cells can repair themselves when injured; normal cells are more successful at repairing self; the cells that are most affected by chemo are bone marrow, hair follicles, GI tract (oral mucosa in particular)
175
neuroblastoma is...
type of cancer that develops in nerve cells called neuroblasts; most common extracranial tumor in children; can start in adrenal glands but can develop in head, neck, chest, abdomen, or spine; most often found in an embryo or fetus
176
enteral iron supplementation
