Ob-Peds Final

Front 1

Criteria for cure of cancer

Back 1

cessation of therapy, continuous freedom from evidence of cancer, no risk of relapse, 2-5 yr remission

Front 2

Etiology of CA in peds

Back 2

Genetic theory, peds w/ immune or chromosomal d/o more prone to CA, embryonic/primitive tissue targeted

Front 3

Cardinal s/s of CA in peds

Back 3

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

Front 4

Neuroblastoma s/s, layer, location, prognosis

Back 4

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)

Front 5

Assessment of neuroblastoma

Back 5

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.

Front 6

Mgt. of neuroblastoma

Back 6

Knowledge defecit, pain, altered family processes. Prep for surgery, xrt in advanced cases, chemo.

Front 7

Nursing intervention w/ XRT

Back 7

1. Risk for impaired skin integrity
2. Altered oral mucous membrans
3. Risk for infection
*Risk for hemorrhage
*Watch for fungi

Front 8

Cell-cycle nonspecific drugs

Back 8

Alkylating drugs, hormones, and antibiotics

Front 9

Cell cycle specific drugs

Back 9

Antimetabolites, plant alkaloids, and enzymes, and interferon

Front 10

Leukemia, etiology

Back 10

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

Front 11

Systemic effects of leukemia

Back 11

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

Front 12

Assessment and dx of leukemia

Back 12

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

Front 13

Tx of leukemia

Back 13

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

Front 14

Nursing care of leukemia pts.

Back 14

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

Front 15

Three phases of chemotherapy

Back 15

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

Front 16

Bone marrow transplant

Back 16

Second remission w/ ALL and first remission w/ AML. 25-50% long-term survival rate

Front 17

Brain tumor

Back 17

>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

Front 18

Assessment of brain tumor

Back 18

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

Front 19

Wilms' Tumor

Back 19

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!

Front 20

Osteogenic sarcoma vs. Ewings sarcoma

Back 20

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

Front 21

Diff. in children (GU)

Back 21

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

Front 22

Diff. in children (GI)

Back 22

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

Front 23

Assessment guidlines for GI/GU in peds

Back 23

Look for pain, changes in diet, g and d, diarrhea, thirst, food intolerances, age

Front 24

S/S of something wrong in GI

Back 24

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

Front 25

S/S something wrong w/ GU

Back 25

freq. voiding, crying on voiding, persistent diaper rash/foul smelling urine, dehydration, flank pain

Front 26

UTIs in peds

Back 26

More common in girls (2-6 yrs), E. coli or urinary stasis (more often in paralysis pts)

Front 27

Cleft lip

Back 27

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

Front 28

Cleft palate

Back 28

Palatine plates fail to fuse during enbryonic devel, in severe cases, nasal and oral cavities communicate, problems w/ aspiration and resp.

Front 29

Etiology of CL and CP

Back 29

Teratogens, genetics, Folic acid deficiency

Front 30

ESSR feeding technique

Back 30

for CL and CP, enlarged nipple to stimulate sucking. Let them suck, watch them swallow, takes a long time

Front 31

Preop instructions to repair CL and CP

Back 31

Instruct parents about postop routine: avoid prone position (on side w/ HOB elevated), arm restraints, initiate post-op feeding technique, demonstrate surgical wound care

Front 32

Postop care for CL

Back 32

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

Front 33

Postop care for CP

Back 33

May lie prone, soft-tipped spoon, position w/ support to promote breathing, elbow restraints, pain, encourage child to talk, avoid hard foods

Front 34

EA

Back 34

esophageal atresia, failure of teh esophagus to develop a continuous passage. When alone, unable to tolerate feeding, regurgitation->aspiration

Front 35

TEF

Back 35

Tracheoesophageal fistula, only sign may be cyanosis, choking

Front 36

EA w/ TEF

Back 36

Most common malformation. Proximal end terminates in blind pouch, distal end attaches to trachea

Front 37

Pre-op for EA and TEF

Back 37

Maintain patent airway, prevent pneumonia, NPO if EA and TEF, continuous low suction and elevate HOB, antibiotic therapy, maintain f/e, stabilize

Front 38

Postop care for EA and TEF

Back 38

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

Front 39

Pyloric stenosis

Back 39

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

Front 40

Tx of pyloric stenosis

Back 40

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

Front 41

Assoc. conditions w/ GERD

Back 41

prematurity, BPD, TEF or EA repair, neurological do, scoliosis, asthma, CF, CP,

Front 42

BPD

Back 42

Bronchopulmonary dysplasia, iatrogenic condition that occurs w/ PEEP. A chronic lung dz in premature infants

Front 43

Clinical manif. of GERD

Back 43

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

Front 44

Rotavirus

Back 44

Most common viral infection in young children causing diarrhea

Front 45

ELISA

Back 45

Enxyme linked immunosorbent assay used to confirm rotavirus

Front 46

Reintroduction of food after acute gastroenteritis (what not to give)

Back 46

No BRAT: bananas, rice, apples, tea, or toast. Give clear liquids, high carb, low electrolyte, high osmolality, if breast feeding-continue!

Front 47

Congenital hematologic problems

Back 47

Hemophilia (x-linked recessive trait), sickle cell dz, thalassemia (do of hgb synthesis)

Front 48

Hgb in Sickle cell trait pts

Back 48

HgbS constitutes only 35-45% of hgb, not enough to cause problems unless in high stress, low O2 conditions->splenomegaly, shock

Front 49

Life span of RBCs

Back 49

Normal: 120 days
Sickl cells: less->anemia

Front 50

Factors that cause a SC crisis

Back 50

Dehydration, acidosis, hypoxia, or fever->sickling->reversible procedure

Front 51

Fetal hgb and SC

Back 51

Fetal hgb protects the sickle cell pt, converts to HgbA after first year of life. Give hydroxyurea to increase fetal hgb.

Front 52

Effect of SCD on spleen

Back 52

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

Front 53

Splenic Sequestrations

Back 53

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

Front 54

Aplastic Crisis

Back 54

Aplastic crisis: diminished RBCs production and incr. destruction of RBCs, r/t viral infection (parvovirus). TRANSFUSE w/ packed RBCs if CHF occurs.

Front 55

Prevention of crisis

Back 55

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

Front 56

Desferal

Back 56

Deferoxamine-antidote for Fe from multiple transfusions

Front 57

Primitive reflexes

Back 57

Usually disappear w/in one year, if not, a sign of cortical defects

Front 58

Myelination complete at...

Back 58

2 years

Front 59

Neural tube defects

Back 59

More common in Caucasian, females, may be folic acid deficiency, maternal heat exposure, or valproic acid

Front 60

Anencephaly

Back 60

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

Front 61

Spina bifida occulta

Back 61

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.

Front 62

Spina bifida cystica: meningocele

Back 62

Visible sac protrudes through the spina bifida, worry about rupturing the sac->infection->meningitis->hydrocephalus->neurodamage.

Front 63

Spina bifida cystica: myelomeningocele

Back 63

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

Front 64

Levels and amount of mobility

Back 64

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

Front 65

Clinical manifestations of myelomeningocele

Back 65

Visible defect, loss of bowel and bladder control (look for constant dribbling), no mov't in BLE, sensory disturb. paralell motor involvement

Front 66

Nursing care of SB

Back 66

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

Front 67

Mgt. of GU function in myelomeningocele

Back 67

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).

Front 68

Bowel function in myelomeningocele

Back 68

Diet control, regular toilet habit w/ laxatives, enemas, and suppositories.

Front 69

Hydrocephalus

Back 69

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

Front 70

Clinical manifestations of hydrocephalus in infancy

Back 70

Enlarged skull, brow protrusion, ant. fontanel bulging, scalp vein dilation, skull bones thin, depressed eyes (setting-sun sign), irritable, lethargic, poor feeder

Front 71

Clinical manifestations of hydrocephalus in childhood

Back 71

HA, behavioral change, personality change, ataxia (coordination problems), visual changes, s/s r/t increased ICP

Front 72

VP shunt

Back 72

If inserted b/c of neural tube defect, permanent. Meningitis related: temporary

Front 73

Craniosynostosis

Back 73

premature closure of sutures, associated w/ inherited syndromes, surgically correct if found early enough

Front 74

Meningitis

Back 74

Acute inflammation of the meninges and CSF. Bacterial, viral, and TB

Front 75

Viral meningitis in infants and older children clinical presentation

Back 75

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

Front 76

Bacterial meningitis

Back 76

Acute inflammation, extends to ventricles-obstruction of CSF flow, posturing. HIB vaccine prevents 95% of cases.

Front 77

S/s of bacterial meningitis

Back 77

Fever, high-pitched cry, bulging fontanels, poor muscle tone, jaundice, hyperactive reflexes, positive gram stain, low glu, increased protein in a cloudy, turbid CSF,

Front 78

Complications of bacterial meningitis:

Back 78

obstructive hydrocephalus, brain abscess, sepsis, mental retardation, CP, ADHD, hearing loss, seizures, death

Front 79

Encephalitis

Back 79

Inflammatory process of CNS caused mainly by viruses. Majority from MMR and varicella. Can lead to Reye syndrome: fever, impaired consciousness, disordered hepatic function

Front 80

Assessment of Down's Syndrome pt.

Back 80

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.

Front 81

Early infant stimulation program

Back 81

For Down's pts, drastically improves functional development

Front 82

CP

Back 82

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

Front 83

Possible signs of CP

Back 83

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

Front 84

Therapeutic mgt of CP

Back 84

AFO's (ankle foot orthosis/braces), kto prevent deformity, use of mobility devices such as go car or skateboard

Front 85

Surgical mgt of CP

Back 85

Spastic type: tendon lengthening procedures, release of spastic wrist flexor muscles, or correction of hip and adductor muscle spacticity of contractures for improved locomotion.

Front 86

Meds for CP

Back 86

Antiepileptic drugs, anxiolytics, short term muscle relaxants for older children and adolescents, botox to paralyze certain muscles

Front 87

Cardinal s/s of musculoskeletl d/o

Back 87

Delayed walking, pain or stiffness, physical limitations, limited ROM, maternal infections, use of substances/meds, position in utero, or fetal hypoxia

Front 88

Osteogenesis imperfecta

Back 88

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

Front 89

Clinical manifestations of OI

Back 89

freq. fractures, thin skin, hyperextensible ligaments, easy bruising, blue sclerae, opalescent teeth, hearing loss, excess diaphoresis, multiple callous formations at fracture sites.

Front 90

Mgt. of OI

Back 90

Continuous assessment for fractures or other injuries, handle carefully, home teaching, support and encouragement, biophophanate therapy

Front 91

Developmental dysplasia of hip

Back 91

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

Front 92

Etiology and pathology of DDH

Back 92

Maternal hormones, breech, twins, LGA, family hx, Rx in first 2 mos, best chance.

Front 93

Preluxation

Back 93

apparent delay in acetabular development but femoral head remains in the acetabulum

Front 94

Subluxation

Back 94

incomplete dislocation; femoral head remains in contact w/ acetabulum but ligaments are torn

Front 95

Dislocation

Back 95

femoral head loses contact w/ acetabulum and displaced

Front 96

Clinical manifestations of DDH

Back 96

Asymmetry of gluteal and thigh folds, limited hib abduction, shortening of the femur, ortolani click, pos. trendelenberg sign

Front 97

Talipes equinovarus

Back 97

(TEV) congenital clubfoot, bone deformity and soft tissue contracture, fixed by series of casts w/ gradual changes. Almost half don't require surgery.

Front 98

5 P's

Back 98

Pain, pallor, pulselessness, paresthesia, paralysis

Front 99

Five stages of bone healing

Back 99

Hematoma formation, cellular proliferation, callus formation, ossification, consolidation and remodeling

Front 100

Upper extremity traction

Back 100

Dunlop traction

Front 101

Lower extremity traction

Back 101

Bryant, Buck extension, 90-90 degree, balance suspension

Front 102

Cervical traction

Back 102

Skin and Crutchfield tong

Front 103

Boston Brace

Back 103

AKA thoracolumbosacral orthosis (TLSO) custom molded jacket to be worn 16-23 hours/day to correct scoliosis. encourage exercises and skin care.

Front 104

Surgery for scoliosis

Back 104

only if >40 degrees. Realignment and straightening w/ internal fixation and instrumentation combined w/ bony fusion. Monitor motor, sensory, and neurological status`

Front 105

Autism

Back 105

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.

Front 106

Treating an autistic child in the hospital

Back 106

Have parents stay in hospital, private room, decr. stimulation, encourage to bring familiar objects, do NOT hold or touch child, sedate for invasive procedures