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106 Cards in this Set

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Criteria for cure of cancer
cessation of therapy, continuous freedom from evidence of cancer, no risk of relapse, 2-5 yr remission
Etiology of CA in peds
Genetic theory, peds w/ immune or chromosomal d/o more prone to CA, embryonic/primitive tissue targeted
Cardinal s/s of CA in peds
Mass or swelling, unexplained paleness and loss of energy, sudden tendency to bleed or bruise easily, localized pain or limping, prolonged fever, HA, v, vision changes, and excessive, rapid weight loss
Neuroblastoma s/s, layer, location, prognosis
Arise from cells of sympathetic nervous system, most common tumor located outside cranium (often near adrenal glands). CONGENITAL. Age of onset 22 mos, better prognosis if dx <1 yr (b/c w/ child since fetal devel)
Assessment of neuroblastoma
s/s R/T location, dx during abd. palpation, mass, bladder/bowel dysfunction, fever, anorexia. If pressure on adrenal glands: sweating, flushed face, htn. Mediastinal: dyspnea and neck and facial edema
Bone metastasis: limp, malaise, ptosis and ecchymosis of eyes.
Mgt. of neuroblastoma
Knowledge defecit, pain, altered family processes. Prep for surgery, xrt in advanced cases, chemo.
Nursing intervention w/ XRT
1. Risk for impaired skin integrity
2. Altered oral mucous membrans
3. Risk for infection
*Risk for hemorrhage
*Watch for fungi
Cell-cycle nonspecific drugs
Alkylating drugs, hormones, and antibiotics
Cell cycle specific drugs
Antimetabolites, plant alkaloids, and enzymes, and interferon
Leukemia, etiology
CA of blood forming tissues (marrow and lymph), unrestricted proliferation of IMmature , abnormal WBCs. Most common CA of childhood. Two types: Acute lymphocytic leukemia (ALL-better) and Acute myelogenous leukemia (AML-poor prognosis). Genetic and chromosomal factors, unrestricted immature WBCs , bone marrow infiltration crowds out stem ceslls that normally produce RBCs and plts, can't fight infection
Systemic effects of leukemia
Anemia, neutropenia, and thrombocytopenia. Spleen (overloaded by dead blood cells), liver, and lymph become infiltrated w/ WBCs->fibrose in some cases. Fatigue, clotting and bleeding problems, CNS infiltration(poor prognosis), clinical manifestations r/t area of involvement
Assessment and dx of leukemia
Freq. colds or bleeding, low blood counts, bone marrow aspiration to confirm dx (incr. % of blasts...60-100% compared to <5%), spinal tap to check for CNS involvement, febrile, poor wound healing, infection, pallor, bruises, HA, anorexia, vomiting, weight loss, abd. pain, fatigue, lethargy, tachycardia, and bone and jt. pain
Tx of leukemia
Achieve remission w/ chemo or combined therapy, once achieve <5% blasts, begin 2-3 yrs maintenance therapy of chemo. CNS prophylaxis: XRT to brain and spinal cord or drugs directly into CSF
Nursing care of leukemia pts.
Risk for infection: no flowers, fresh fruit, monitor v.s., esp. temp (usually first sign something wrong), LOC, irritability, weight loss, antiemetics, pain meds, body image issues
Three phases of chemotherapy
1. Induction: 4-6 wks, designed to achieve remission. ALL: Prednisone, oncovin, and Elspar. AML: Daunomycin and cytosine arabinosid
2. Intensification: Further decrease tumor burden, use Elspar and Folex. CNS prophylaxis: intrathecal, methothrexate, cytaranine, and hydrocortisone. XRT for high risk.
3. Maintenance: 2-3 yrs, oral purinethol, weekly IM methotrexate, weekly blood counts for toxicity, reinduction for relapses, bone marrow transplant for ALL after second remission
Bone marrow transplant
Second remission w/ ALL and first remission w/ AML. 25-50% long-term survival rate
Brain tumor
>half in cerebellum and brainstem, rest in cerebrum, benign can be just as fatal as malignant. Cause unknown but XRay and environ. implicated, supporting cells account for many cancers
Assessment of brain tumor
Depend on location of tumor and age of child. Cerebrum: personality changes and seizures, cerebellum and brainstem: ataxia, visual distur., delayed or precocious puberty, and growth failures. Infants may be dx late b/c of open sutures, HA, vomiting, diplopia, dx: MRI, CT, and radiographic studies, biopsy
Wilms' Tumor
Malignant neoplasm of the kidney, most common abdominal tumor, unilateral or bilateral, originates from immature renoblast cells, generally encapsulates early but if later then generally metastasizes to lungs and liver. Usually asymptomatic but may have fever, pain, hematuria, or htn. DON'T PALPATE!
Osteogenic sarcoma vs. Ewings sarcoma
Osteogenic:arises from bone cell, most common in femur, pain, swelling, taller child, freq. mestastasizes to lungs. AMPUTATE w/ chemo
Ewing's: malignant, small, round cell infolving the shaft portion of long bones, pain, soft tissue mass, freq. metastasizes, NO amputation, XRT and chemo
Diff. in children (GU)
Not fully developed til one year, body more fluid, kidneys less efficient in regul. f/e(<2 yr), <2, can't control bladder->innervation occurs around 2, short urethra, don't have fat padding to protect kidneys/gut so more traumatic
Diff. in children (GI)
Absorption and exretion don't begin until after birth and continues to mature until 6, voluntary control over swallowing after 6 wks, easily lose fluids, difficulty digesting protein, relaxed cardiac sphincter, deficient amylase, lipase, and trypsin, liver immature
Assessment guidlines for GI/GU in peds
Look for pain, changes in diet, g and d, diarrhea, thirst, food intolerances, age
S/S of something wrong in GI
Anorexia, poor feeding, n/v, diarrhea, constipation, abd pain, recent weight loss or gain, blood in stool. Stool exam for ova and parasites, esophageal pH monitoring for GERD
S/S something wrong w/ GU
freq. voiding, crying on voiding, persistent diaper rash/foul smelling urine, dehydration, flank pain
UTIs in peds
More common in girls (2-6 yrs), E. coli or urinary stasis (more often in paralysis pts)
Cleft lip
Incomplete fusion of the embryonic structures surrounding the primitive oral cavity, can be unilateral or bilateral, dentition often affected, often assoc. w/ abnormal devel. of external nose and nasal cartilage->otitis media
Cleft palate
Palatine plates fail to fuse during enbryonic devel, in severe cases, nasal and oral cavities communicate, problems w/ aspiration and resp.
Etiology of CL and CP
Teratogens, genetics, Folic acid deficiency
ESSR feeding technique
for CL and CP, enlarged nipple to stimulate sucking. Let them suck, watch them swallow, takes a long time
Preop instructions to repair CL and CP
Instruct parents about postop routine: avoid prone position (on side w/ HOB elevated), arm restraints, initiate post-op feeding technique, demonstrate surgical wound care
Postop care for CL
airway patency, vs, protect op site, Logan's Bow (lip protector), elbow restraints, pain, clear liquids, position upright (supine, infant seat, propped on side), mist tent
Postop care for CP
May lie prone, soft-tipped spoon, position w/ support to promote breathing, elbow restraints, pain, encourage child to talk, avoid hard foods
EA
esophageal atresia, failure of teh esophagus to develop a continuous passage. When alone, unable to tolerate feeding, regurgitation->aspiration
TEF
Tracheoesophageal fistula, only sign may be cyanosis, choking
EA w/ TEF
Most common malformation. Proximal end terminates in blind pouch, distal end attaches to trachea
Pre-op for EA and TEF
Maintain patent airway, prevent pneumonia, NPO if EA and TEF, continuous low suction and elevate HOB, antibiotic therapy, maintain f/e, stabilize
Postop care for EA and TEF
Radiant warmer, parenteral nutrition, gastrostomy tube to gravity 5-7 days, then advance feedings, chest tube, prevent skin breakdown, pacifier for non-nutritive sucking, oral training, careful suctioning w/ premeasured catheter
Pyloric stenosis
Full term males w/ no other problems, narrowing of pyloric sphincter, obstruction of the gastric outlet->distension, dilation, and hypertrophy, projectile vomit. Initial hunger, then irritability, lethargy, dehydration, and malnourishment
Tx of pyloric stenosis
Rehydration, correct metabolic alkalosis, NG tube to decompress stomach, usually NPO, but if feeding, small quantities in high fowler's, pyloromyotomy, small amt. of clear liquid 4-6 hrs postop. MSo4 for 24h, then tylenol
Assoc. conditions w/ GERD
prematurity, BPD, TEF or EA repair, neurological do, scoliosis, asthma, CF, CP,
BPD
Bronchopulmonary dysplasia, iatrogenic condition that occurs w/ PEEP. A chronic lung dz in premature infants
Clinical manif. of GERD
Passive regurgitation or emesis, poor weight gain, heme-positive emesis or stools, anemia, irritability, heartburn, gagging or choking w/ feeding, apnea, recurrent pneumonias/Resp tract infections
Rotavirus
Most common viral infection in young children causing diarrhea
ELISA
Enxyme linked immunosorbent assay used to confirm rotavirus
Reintroduction of food after acute gastroenteritis (what not to give)
No BRAT: bananas, rice, apples, tea, or toast. Give clear liquids, high carb, low electrolyte, high osmolality, if breast feeding-continue!
Congenital hematologic problems
Hemophilia (x-linked recessive trait), sickle cell dz, thalassemia (do of hgb synthesis)
Hgb in Sickle cell trait pts
HgbS constitutes only 35-45% of hgb, not enough to cause problems unless in high stress, low O2 conditions->splenomegaly, shock
Life span of RBCs
Normal: 120 days
Sickl cells: less->anemia
Factors that cause a SC crisis
Dehydration, acidosis, hypoxia, or fever->sickling->reversible procedure
Fetal hgb and SC
Fetal hgb protects the sickle cell pt, converts to HgbA after first year of life. Give hydroxyurea to increase fetal hgb.
Effect of SCD on spleen
splenomegaly r/t sickle cells->infarction->formation of fibrotic tissue->by 5, have functional asplenia->more prone to infection r/t inability to filter bacteria or release phagocytes in lg. numbers
Splenic Sequestrations
Pooling of large quantities of blood in spleen, results in drop in BP and shock, may result in death, profound anemia, pallor
Tx: w/ plasma expanders, removal of spleen
Aplastic Crisis
Aplastic crisis: diminished RBCs production and incr. destruction of RBCs, r/t viral infection (parvovirus). TRANSFUSE w/ packed RBCs if CHF occurs.
Prevention of crisis
Prophylactic pcn at 2mos. to 6 yrs, childhood immunizations PLUS pneumococcal vaccine, folate, lots of water, avoid extreme temp., avoid over-exertion or stress, sleep, regular check-ups
Desferal
Deferoxamine-antidote for Fe from multiple transfusions
Primitive reflexes
Usually disappear w/in one year, if not, a sign of cortical defects
Myelination complete at...
2 years
Neural tube defects
More common in Caucasian, females, may be folic acid deficiency, maternal heat exposure, or valproic acid
Anencephaly
Absence of both cerebral hemispheres, brain stem intact-can maintain vital functions for a few hours to several days, death due to resp. failure. Organs transplanted
Spina bifida occulta
Incomplete fusion of the neural arch w/o protrusion of intraspinal contents. May have one or more:dimple, hair over malformed vertebrae, portwine nevi, soft cutaneous lipomas, slight neuromuscular disturb.
Spina bifida cystica: meningocele
Visible sac protrudes through the spina bifida, worry about rupturing the sac->infection->meningitis->hydrocephalus->neurodamage.
Spina bifida cystica: myelomeningocele
Occurs during first month of pregnancy, visible sac contains CSF, meninges, spinal cord, and/or nerve tracts. Symptoms depend on location, hydrocephalus occurs in 90-95% of cases, sac is shiny (if not ruptured), LTCS if know about SB
Levels and amount of mobility
L2 or above: wheelchair
L2-5: strong hip flexors, crutches or braces
L3-4: Imbalance b/w sensory and motor nerve, hip dislocation common.
Sacral: able to walk, may require ankle braces.

Physical therapy ESSENTIAL
Clinical manifestations of myelomeningocele
Visible defect, loss of bowel and bladder control (look for constant dribbling), no mov't in BLE, sensory disturb. paralell motor involvement
Nursing care of SB
prevent injury, less damage means less risk of nerve damage, prone prior to surgery, Dsg: sterile, non-adherant, head circumference and ant. fontanel tension, sensory and motor changes, number and character of voiding, response tofeedings and bathing, spontaneous mov't, skin care, ROM
Mgt. of GU function in myelomeningocele
90% have voiding dysfunction. Diaper up to 2 years, then teach parents to straight cath, then at 5-6, teach pt. Clean intermittent cath (CIC).
Bowel function in myelomeningocele
Diet control, regular toilet habit w/ laxatives, enemas, and suppositories.
Hydrocephalus
Congenital: maldevelopment or intrauterine infection
Acquired: infection, neoplasm, or hemorrhage.
Communicating: impaired absorption of CSF w/in the subarachnoid space
Non-communicating: obstruction of the flow of CSF through the ventricular system
Clinical manifestations of hydrocephalus in infancy
Enlarged skull, brow protrusion, ant. fontanel bulging, scalp vein dilation, skull bones thin, depressed eyes (setting-sun sign), irritable, lethargic, poor feeder
Clinical manifestations of hydrocephalus in childhood
HA, behavioral change, personality change, ataxia (coordination problems), visual changes, s/s r/t increased ICP
VP shunt
If inserted b/c of neural tube defect, permanent. Meningitis related: temporary
Craniosynostosis
premature closure of sutures, associated w/ inherited syndromes, surgically correct if found early enough
Meningitis
Acute inflammation of the meninges and CSF. Bacterial, viral, and TB
Viral meningitis in infants and older children clinical presentation
Acute onset w/ fever, irritability, and lethargy in infants. Older: frontal HA, photophobia, abd. pain, diarrhea, vomiting, fever.
Spinal fluid: protein and glu normal, gram stain negative, clear or slightly cloudy. Give antipyretic, pain meds, acyclovir. May have slight LD
Bacterial meningitis
Acute inflammation, extends to ventricles-obstruction of CSF flow, posturing. HIB vaccine prevents 95% of cases.
S/s of bacterial meningitis
Fever, high-pitched cry, bulging fontanels, poor muscle tone, jaundice, hyperactive reflexes, positive gram stain, low glu, increased protein in a cloudy, turbid CSF,
Complications of bacterial meningitis:
obstructive hydrocephalus, brain abscess, sepsis, mental retardation, CP, ADHD, hearing loss, seizures, death
Encephalitis
Inflammatory process of CNS caused mainly by viruses. Majority from MMR and varicella. Can lead to Reye syndrome: fever, impaired consciousness, disordered hepatic function
Assessment of Down's Syndrome pt.
IQ 45-50, small skull, protruding tongue, other congential anomalies such as heart defects, poor lung functioning, GI do, visual and hearing, leukemia 10x more freq.
Early infant stimulation program
For Down's pts, drastically improves functional development
CP
Non-progressive do, characterized by early onset of impaired mov't and posture, may be accompanied by perceptual problems, language deficits, and intellectual involvement. Cause unknown in 24%, some due to existing prenatal brain abnormalities or postnatal injury
Possible signs of CP
poor head control after 3 mos, stiff or rigid arms or legs, pushing away or arching back, floppy or limp body posture, can't sit up w/o support by 8 mos, irritable, no smile by 3 mos, feeding difficulties
Therapeutic mgt of CP
AFO's (ankle foot orthosis/braces), kto prevent deformity, use of mobility devices such as go car or skateboard
Surgical mgt of CP
Spastic type: tendon lengthening procedures, release of spastic wrist flexor muscles, or correction of hip and adductor muscle spacticity of contractures for improved locomotion.
Meds for CP
Antiepileptic drugs, anxiolytics, short term muscle relaxants for older children and adolescents, botox to paralyze certain muscles
Cardinal s/s of musculoskeletl d/o
Delayed walking, pain or stiffness, physical limitations, limited ROM, maternal infections, use of substances/meds, position in utero, or fetal hypoxia
Osteogenesis imperfecta
Four types of heterogeneous ingerited d/o involving connective tissue and bone defects. Decrease collagen->lax joints and weak muscles->increase in fractures whenever stress is placed on bones->deformities
Clinical manifestations of OI
freq. fractures, thin skin, hyperextensible ligaments, easy bruising, blue sclerae, opalescent teeth, hearing loss, excess diaphoresis, multiple callous formations at fracture sites.
Mgt. of OI
Continuous assessment for fractures or other injuries, handle carefully, home teaching, support and encouragement, biophophanate therapy
Developmental dysplasia of hip
DDH: group of congenital anomalies of hip joints inclides subluxation, dislocation, and preluxation. Often seen w/ neural tube defects, left hip in 60%, usually white female, can lead to permanent disability if not corrected by 6 years
Etiology and pathology of DDH
Maternal hormones, breech, twins, LGA, family hx, Rx in first 2 mos, best chance.
Preluxation
apparent delay in acetabular development but femoral head remains in the acetabulum
Subluxation
incomplete dislocation; femoral head remains in contact w/ acetabulum but ligaments are torn
Dislocation
femoral head loses contact w/ acetabulum and displaced
Clinical manifestations of DDH
Asymmetry of gluteal and thigh folds, limited hib abduction, shortening of the femur, ortolani click, pos. trendelenberg sign
Talipes equinovarus
(TEV) congenital clubfoot, bone deformity and soft tissue contracture, fixed by series of casts w/ gradual changes. Almost half don't require surgery.
5 P's
Pain, pallor, pulselessness, paresthesia, paralysis
Five stages of bone healing
Hematoma formation, cellular proliferation, callus formation, ossification, consolidation and remodeling
Upper extremity traction
Dunlop traction
Lower extremity traction
Bryant, Buck extension, 90-90 degree, balance suspension
Cervical traction
Skin and Crutchfield tong
Boston Brace
AKA thoracolumbosacral orthosis (TLSO) custom molded jacket to be worn 16-23 hours/day to correct scoliosis. encourage exercises and skin care.
Surgery for scoliosis
only if >40 degrees. Realignment and straightening w/ internal fixation and instrumentation combined w/ bony fusion. Monitor motor, sensory, and neurological status`
Autism
More common in males, more severe in females. Inability to have eye contact, social defecits, nothing to do w/ parents, solitary play, ritualistic patterns or behavior, Early recognition key. If speech began and doesn't come back by 6, not a good prognosis. Genetic.
Treating an autistic child in the hospital
Have parents stay in hospital, private room, decr. stimulation, encourage to bring familiar objects, do NOT hold or touch child, sedate for invasive procedures