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Study GuideExam 2Remember—a general guide only: Not guaranteed to be all inclusive1. Metabolic/Endocrine: Define terms: thelarche, adrenarche, menarche, Acanthosis Nigricans, Tanner staging, Thelarche: breast budding (tanner staging I-V in females)Adrenarche: axillary & pubic hair (tanner staging I-VI in males & females); refers to the onset of adrenal angrogen production- adrenal hormones lead to the production of acne, axillary and pubic hair and adult body odor Menarche: menses begins (first period); usually occurs as 12.1 years of age in African American girls and 12.6 years of age in Caucasian girlsAcanthosis nigricans: skin rash on neck and skin folds due to elevated insulin levels Precocious pubertyPrecocious puberty: the early development of secondary sexual characteristicsMales= development of pubic hair <9 yearsFemales= breast development or pubic hair <6 yrs for AA & <7 yrs for caucasians Breast budding normally occurs between 9-14 years of ageFinal height will be less if start puberty early, but will appear tall for age when younger; social issues; abuse potentialOther signs of precocious puberty: accelerated growth rate, advanced bone age, acne, adult body odor, behavioral changes Central precocious puberty: premature activation of HPG axis; GnRH released begins puberty too early! Short stature as a result bc early growth spirt & early closure of growth plates. 50% males due to CNS insult or abnormality. 90% girls idiopathic.AKA “true” PP- caused by the premature activation of the HPG axis“primary PP”: is idiopathic & most common type“secondary PP”: caused by CNS tumor, infection, injury, congenital anomaly such as hydrocephalus, ischemia, etc.Peripheral precocious puberty: is gonadotropin-independent; caused by increased secretion of sex hormones (estrogen, androgens): from- gonads (ovarian cyst, tumors), adrenals (tumors, CAH), or primary hypothyroidism & mccune albright syndrome; increased release or exposure to estrogen/androgens puberty begins AKA “pseudo” PP= early puberty resulting from some other hormone stimulation (estrogen or androgens)Premature thelarche (breast budding)Premature adrenarche (development of pubic hair)Premature menarche (beginning of menses)Symptoms can be isolated and not associated with an endocrine problem (idiopathic)Key difference seen between central & peripheral? NO rapid growth spurt in peripheral Nursing considerations r/t precocious pubertyA child should be interacted with according to their mental age, rather than their chronological age or physical appearance Dress and activities should be age-appropriate & developmentally appropriate- not physical appearance-related (consider having to buy clothes for a 6-year old child who has a body that looks like a teenager) At adolescence, the physical differences between peers should resolve Explain to the child and family that the physical changes are normal but occurring at an earlier than usual age. Reassuring the child that their friends will experience the same stages of development eventually Growth Hormone DeficienciesA growth hormone deficiency is caused by a failure of the pituitary to produce enough growth hormone and is called hypopituitarism or growth hormone deficiency. Other acquired causes: tumors of the pituitary or hypothalamus glands, brain trauma, and chemotherapy.By 12 months <3% growth percentile Clinical manifestations: short stature, deteriorating or absent growth rate, delayed bone age, micropenis and small testes in males, delayed sexual maturation, delayed dentition, hypoglycemia- increased insulin sensitivity, youthful facial features, higher pitched voicesTreatment: daily SQ growth hormone injections during childhood an d adolescence to max height potential; very expensive & insurance doesn’t always cover!Refer to endocrinologist Other causes of short statureThere are other causes of short stature besides growth hormone deficiency. Familial short stature, constitutional growth delay which is a late pubertal growth spurt caused by delayed pubertal hormone secretion, hypothyroidism, and genetic disorders such as Turner’s syndrome and Dwarfism.Diagnostic tests: serum GH, TSH, T4, MRI pituitary, bone age (looks at skeletal maturation of bones in hand and wrist)Expected height for boys= father’s height (cm) plus mom plus 13 cm/2Girls=father’s height cm plus moms minus 13/2Diabetes Insipidus DI is a disorder of the posterior pituitary gland. Normally fluid balanced is maintained by actions of the hypothalamus, pituitary gland and kidney. When there is inadequate production or secretion of ADH, the tubules do not reabsorb water, leading to polyuria (large volume of urine) and the result is severe dehydration.Central (neurogenic)- ADH deficiency; disorder of the posterior pituitary gland as a result of trauma, tumors or infectionNephrogenic (from the kidneys) when renal tubules are unresponsive to ADH; may develop secondary to drug toxicity or an adverse drug reaction Sx: polyuria (lots of dilute urine), polydipsia (excessive thirst), severe dehydration, hypernatremia seizures, specific gravity <1.005, enuresis (inability to control urination esp. at night), tachycardia, hypotension Diagnosis: Measure plasma arginine vasopressin levels before and during a fluid deprivation test. The specific gravity remains low even after dehydration. Then a dose of vasopressin is given. A response of decreased urine output and increased urine concentration confirms the diagnosis of central DI. No response to vasopressin is diagnostic of nephrogenic DI.Tx- DDAVP for central DI bc this concentrates urine and reduces urine output & diuretics for nephrogenic DI bc this promotes sodium excretion and stimulates the kidneys to reabsorb water plus increasing fluid intake, restricting salt and following a low protein diet Congenital HypothyroidismCongenital hypothyroidism is caused by a spontaneous gene mutation, an autosomal recessive genetic transmission of an enzyme deficiency, hypoplasia of the thyroid gland, iodine deficiency, or failure of the CNS. Mental retardation or cretinism is irreversible if not treated. Clinical manifestations- prolonged neonatal jaundice, hypothermia, enlarged tongue, hypotonia (floppy baby syndrome), feeding problems, decreased mental alertness, bradycardia, large posterior fontanel >1 cm Tx: thyroid replacement- synthroid (closely monitor growth & thyroid labs)Acquired hypothyroidismCauses: Can be idiopathic or secondary to autoimmune response (Hashimoto’s thyroiditis)Antibodies are developed against the thyroid gland > T4 levels decrease and TSH levels increase Late onset of thyroid dysfunctionSecondary to drugs that inhibit thyroid hormone synthesis Lithium Clinical manifestations: dry, cool skin, hair loss, decreased DTR, bradycardia, constipation, abnormal menses, GOITER, weight increase, decreased height, delayed or precocious puberty, delayed bone age, delayed dental ageTx: thyroid replacement with synthroid (life-long treatment)Hyperthyroidism (graves disease) Graves disease is an autoimmune disorder. Hyper-function of the thyroid glandClinical manifestations: GOITER, decreased concentration, fatigue, decreased sleep, exophthalmos (bulging eyes), weight loss, tachycardia, hyperthermia Thyroid storm: tremor, diarrhea, excessive sweating and palpitations that can lead to cardiac failure Rare in kidsTx: antithyroid medication or radioactive iodine therapy; thyroidectomy is definitive cure Congenital Adrenal HyperplasiaResults from a deficiency of an enzyme necessary for the synthesis of cortisol and aldosterone. 95% of the children have 21 hyroxylase deficiency resulting from a defective gene on chromosome 6.Inherited autosomal recessive disorder Increased androgen production results in ambiguous genitalia in newborn girls. Genetic testing will determine the newborns gender. Males will look normal at birth but may have an adult size penis by school age, tall stature, acne and excessive muscle development. If not treated, the overproduction of androgens results in accelerated height as a child, early closure of the growth plates so adult stature is shorter, and premature sexual development with both pubic and axillary hair.75% of cases result in salt losing, due to not enough aldosterone and cortisol produced (hyponatremia, hyperkalemia, acidosis, hypoglycemia) requires aldosterone replacement and extra dietary salt Tx: maternal steroids if diagnosed prenatally, life-long steroid therapy, salt supplements, reconstructive surgery for females Type I DM Impaired carbohydrate, protein, and fat metabolism due to a partial or incomplete deficiency of insulinAutoimmune destruction of insulin-producing pancreatic beta cells in genetically predisposed individuals Peak onset in children 10-15 years Clinical presentation- polyuria, polydipsia, polyphagia, weight lossDiagnosis- FBG >126, random BG >200, 2 hr >200, HgbA1c levels are not recommended for diagnosis of diabetes Tx: insulin therapy, nutrition therapy, exercise program, psychosocial supportHoneymoon phase: period during new-onset diabetes when child has some residual beta cell function which reduces exogenous insulin requirements; child and family may assume this is an indication that the diabetes is all better, however insulin requirement does eventually return (length of this phase varies among individuals)Sx of hypoglycemia: BG <70; rapid onset, irritability, nervousness, tremors, shaky feeling, difficulty concentrating or speaking, behavior change, confusion, repeating something over and over, unconsciousness, seizure, shallow breathing, tachycardia, pallor, sweating, moist mucous membranes, hunger, headache, dizziness, blurred vision, double vision, photophobia, numb lips or mouthSx or hyperglycemia: gradual onset, lethargy, sleepiness, slowed responses, or confusion, deep rapid breathing, flushed skin, dry skin, dry mucous membranes, thirst, hunger, dehydration, weakness, fatigue, headache, abdominal pain, nausea, vomiting, shockDKA- emergency! Medical emergency!!s/sx: polyuria, polydipsia, weight loss, abdominal pain, N/V, dehydration, hypotension, altered LOC, fruity breath, Kussmaul respirations (deep & labored breathing) with metabolic acidosis may progress to electrolyte disturbances, arrhythmias, respiratory distress and eventually diabetic coma nursing care: isotonic fluids, IV insulin, mannitol as needed for cerebral edema, close monitoring of vital signs, resp. & cardiac status, mental status Type 2 DM Due to insulin resistance; increasing amounts of insulin are required to effectively control blood glucoseIncreasing numbers of children due to obesity, sedentary lifestyles, genetic predisposition Pre-diabetes dx: FBG of 100-125, 2 hour of 140-160Type 2 dx: symptoms plus random BG >200, FBG >126, 2 hour >200, c-peptide levels used to differentiate between type 1 and type 2 (normal or elevated in type 2 diabetes)Management: dietary intervention, exercise, weight loss, metformin can be used in older children and adolescents, insulin therapy may be added and is the treatment of choice for children without optimal glycemic control 2. Nutrition, Fluid/Electrolytes Review all slides/notes/readings in textbook: pay attention to bold printBreast milk for the first yearDefine dehydration, edemaDehydration- extracellular fluid volume deficitEdema- extracellular fluid volume excess or interstitial fluid volume excessFactors that predispose infants to dehydration?Greater total body water contentGreater ratio of surface area to massGreater extra-cellular fluid volumeGreater daily body water turnoverHigher metabolic and respiratory rateImmature kidney’s inability to concentrate urine Types of dehydration (isotonic, hypotonic, hypertonic); define; causesIsotonic (H20=NA+)Loss of water and sodium are proportionateSerum Na+ is normal, decreased total blood volumeMost of fluid lost is extracellularAKA fluids loss is from veins Cause: common in infants and children with vomiting and diarrhea Hypotonic (low Na+)Loss of sodium>water Serum Na+ level is below normal levelsFluid shifts from extracellular to intracellular to preserve cell functionAKA fluid moves from veins to compensateCauses: prolonged vomiting and diarrhea, burns, renal disease, administration of IV fluids without electrolytes in dehydrationHypertonic (high Na+)Water loss>sodium lossFluid shifts from intracellular to extracellular to compensateAKA fluid moves into veins to compensateSerum Na+ level is elevatedDecreased neurological signs may appear with signs of dehydrationCauses: administration of IV fluids or tube feedings with high electrolyte levelsConditions that can cause fluid imbalance (phototherapy, fever, etc.)PhototherapyIncreased respiratory rateFeverVomiting & diarrheaDrainage tubesRenal diseaseIllnesses: jaundice, RSV, burns, viral gastroenteritis, sepsisDehydration accounts for 9% of pediatric hospitalizations How to calculate severity of dehydration; Calculate % wt. loss; % dehydrationTo calculate % of weight lossSubtract the child’s present weight from the original weight to find the lossDivide the loss by the child’s original weightChild weighed 12 kg prior to V/D. Present weight is 11 kg. 12-11=1 kg. 1kg/12 kg=8.3% (moderate dehydration)Define & identify signs/symptoms of Mild/Moderate/Severe Dehydration Mild- up to 5% loss of body weightModerate- 6-9% lossSevere- >10% lossId s/sx of dehydration in an infantSunken fontanelleSunken eyes and cheeksDecreased skin turgorFew or no tearsDry mouth or tongueSunken abdomen Know the parameter that is the MOST significant clinical assessment when assessing for dehydration (% weight loss). Other—Cap refill >2 secs; decreased uop (<4 wet/day) (SG >1.030), >RR, decreased skin elasticity (skin turgor)Labs r/t dehydration & expectations- elevated bun & low serum bicarb; elevated creatinine; elevated glucose, elevated specific gravity; acid-base balance CMP- complete metabolic panel or serum electrolyte panelTX- rehydration- po or IV depending upon severity; reintro of nutrition; Mild-Oral Rehydration Solution amt? (initially 50 ml/kg over 4 hours then 100 ml/kg/24 hours); Mod- IV; Severe-Hospitalization IFV with bolus; *When can you add K to IVF? After voiding (D5W with Na+ and K+); What fluid is usual initial bolus? Lactated ringers or NS bolus (isotonic)Recipe for Oral Rehydrating Solution for parents to make at home?8 tsp sugar + 1 tsp salt + 1 liter water Infant nutrition (6-12 months): When to introduce solid food & why?Human milk or iron fortified infant formula should be primary source of nutrition during first yearIntroduce fruits and vegetables slowlyFinger foods (pincer grasp by 8-9 months of age)Rice cereal is usually offered first at 6 monthsWhen introducing fruits and vegetables, offer a new one every 3 days and watch for an allergic reaction (yellow veggies first, most hypoallergenic)Mashed boiled fresh vegetables are bestGo through all the vegetables first, then the fruits are offered because they are sweetestBy 8 months introduce the proteins such as meats, cooked beans and cheeseFoods to avoid:Cereal shouldn’t be added to bottle unless GERD or an ex-premie (prescribed by a primary care provider)No honey until 1 year= botulism sporesNo eggs until 2 years= allergyNo strawberries, wheat, corn or fish products until 3 years= allergyNo hard candy, gum, popcorn until 5 years= chokingAvoid bottle propping; babies should be help to promote bonding between baby and parents; parents are not to let the baby go to sleep with a bottle because it promotes tooth decay and otitis media Signs and symptoms of food allergies. Peanut allergies place child at high risk for anaphylaxisEczema Why is cow’s milk avoided in children <1 year old?Human milk is tolerated and absorbed best by the infant’s gastrointestinal tractBreastfeeding informationContraindicationsMaternal chemo-antimetabolites and certain neoplastic drugsActive TB not under treatment in motherHIV in motherGalactosemia in infantMaternal HSV lesion on breastMaternal substance abuseHuman T-cell leukemia virus type IReceiving diagnostic or radioactive isotope or exposure to radioactive materials The American Academy of Pediatrics recommends breastfeeding for the first year. In situations where breastfeeding does not occur, the child should receive iron-fortified formula for the first year. If an infant is not getting enough calories through breastfeeding, supplementing with formula would be appropriate. Human milk fortifier should only be used in premature infants less than 37 weeks’ gestation.Physiological benefits of breastfeedingFor babies- decreases incidence of otitis media, respiratory infections, gastrointestinal infections, asthma, eczema, allergies, cardiovascular disease, type 2 diabetes, obesity, SIDSFor moms- Less likely to develop osteoporosisLower risk of breast cancer, uterine cancer, and ovarian cancerLoose weight fasterBonding with infantEasier (no bottles, no expense)Baby’s BM are smaller & less odiferous When to add free water/juice to diet?No free water until 6 monthsNo juice until 6 monthsIntroduce sipee cup by 9 monthsWean from bottle at 12 monthsWhole milk from 12-24 months Role of pacifiers: non-nutritive suckingInfants have a need to suckNon-nutritive sucking: fingers, thumb, pacifierNo harm to teeth before 4 years of ageRecent research indicates some benefit of night time pacifier use and relationship to decreased SIDSPacifiers are avoided until breastmilk is established at 3 weeks of age in breastfed infants Dental Care recommendationsClean first teeth with a soft clothFirst tooth appears around 6 monthsAvoid excessive juice (sugar!)No bottles in bed!First dental visit 1-3 years of ageNo fluoride toothpaste until around 18 months of age (when kids learn to spit)Toddler, preschool, school age, and adolescent nutritionToddlers (1-3 years):Growth rate slows, appetite declinesMost of nutrition should come from solid foodsOffered in chair at table3 meals & 2 snacks1 tbsp each food per year3 cups whole milk/day until 2 years then 2% milk? cup pasteurized juice/dayavoid all carbonated drinks with high fructose corn syrup and caffeine normal physiological anorexia- around 18 months do not need to eat as much because growth has slowed downavoid battles over eating can start sitting with family around 1 year and eating what family eats as long as it is mushed up and doesn’t have peels Preschoolers:Eating becomes a social eventFood jags are commonOnly eating a few foods for several days Assess food intake over 1-2 weeks rather than at each meal to obtain a more accurate impression of total intake A good time to introduce table mannersQuality of diet depends on nutritionShould have 5 servings of fruits and vegetables a dayBegin brushing teeth on their own twice a day School age:Dietary preferences are influenced by peersFirst tooth lost at around 6 yearsBegin flossingSchool lunches Go and eat lunch with your school age and see what they choose to eat in the cafeteriaAdolescents:At risk for nutritional deficiencies, anemia3000 calories/day bc increased caloric intake during growth spurtsmost rapid growth spurt since first 6 months of lifealso at risk for nutritional deficiencies bc fast food is low in nutrients, vitamins, and fibereating disorders:anorexia nervosabulimia peak at 12 to 13 years of age and again at 17 to 18 yearscultural emphasis on thinness may contribute to over concern with dieting, body image and fear of becoming fat that is experienced by many adolescentsoften a significant life stress, loss or change precedes the onset of anorexia and when parents are over controlling and perfectionist. The adolescents eating behaviors may be an attempt to exercise independence and control and resolve internal psychological conflicts Obesity: risks associated with this/causes of obesity14-20% of children and adolescents >/= 95% on growth charts obesity is directly related to increase in childhood type 2 diabetes, stroke, gallbladder disease, arthritis, cardiovascular disease, hypertension, depression, acanthosis nigricans, high cholesterol, certain cancers, and sleep apnea acanthosis: external sign of increased insulin production and insulin resistance seen on necks, axilla, antecubital areas and other “skin folds”; precursor to T2Dcauses of obesity: less exercise due to screen time, high fat diet, effects of media on food choices, eating junk foods with watching TV, fast foods, sodas with high fructose corn syrup, decrease in human milk during the first year of life Common dietary deficiencies/food allergiesIronFetal iron stores decrease at 4-6 monthsIron fortified rice cereal is a good source of iron at 6 months Menstruating females become anemicCalcium- increased need during adolescence since 40% of adult bone mass is accumulated in adolescence (increase in soda drinking which decreases absorption due to phosphorus)Vitamin D- deficiency can cause rickets (increase in US partially due to decrease in sun exposure with inside activities)Folic acid- females of child bearing age should take folic acid to prevent spina bifida and cleft lip and palate since 50% of pregnancies in the US are unplanned Food intoleranceAbnormal physiological response that is not IgE mediatedIndigestion, flatulence, rhinitis, urticarialFood allergyIgE mediated- most common cause of anaphylaxisRapid onset, can be fatalRAST testing- radioimmunoassay is used to measure IgE antibodies to allergensWhat is Failure to Thrive (FTT)?Inadequate growth resulting from an inability to obtain and/or use calories required for growthWeight <3-5% for the child’s ageA persistent deviation from the established growth curveWeight falls more than 2 major percentiles (ie., from >75% to <25%)FTT accounts for 1-5% of hospitalizations in children under 1 year of ageOrganic vs Non organic causes of FTT ?Organic FTTThere is a physical cause of the child’s inability to meet their nutritional needsCHD (congenital heart disease)GERDHIVCystic fibrosisInborn errors of metabolism Non organic FTT (feeding disorder of infancy)Impaired parent-child interactionPovertyInadequate nutrition knowledgeFamily stressFeeding resistanceInsufficient breast milkNeglectPreterm infantsNot associated with any medical condition Idiopathic FTTUnknown causeProbably a combination of organic and non-organic FTTClinical manifestationsEvidence of growth failureLoss of subcutaneous fatReduced muscle massApathy and listlessness Long term consequencesChronic weight loss may lead to delayed linear growth as wellDevelopmental delaysImmune dysfunction Diagnosis of FTTVery specific history and ROS, with specific focus on feeding and GIRule out organic causeDietary interventions to provide nutrients and nurturingIf infant/child gains expected amount of weight in hospital, diagnosis of NFTT is made Child is hospitalized initially and evaluated for potential organic causes while staff members feed the child Nutrition goalsCorrect nutritional deficienciesAllow for catch-up growthRestore optimum body compositionEducate parents re: nutrition & feeding techniques How does environment affect Non-Organic FTT?Impaired parent-child interaction, poverty, inadequate nutrition knowledge, family stress, feeding resistance, insufficient breast milk, neglect, preterm infants 3. Alterations in Nutrition & GI System—See voice-over pptGastroenteritis Inflammation of the stomach and intestinesClinical manifestations: vomiting/diarrhea, may be accompanied by feverEtiology: viral (rotavirus), bacterial, parasiticRotavirus vaccine available at 2,4 monthsMost common complications are dehydration and electrolyte imbalance Assessment: clinical s/sx, amt of weight loss, degree of electrolyte imbalance determines severity of dehydrationLabs: stool for culture, hemoccult, electrolytes (CMP), UATreatment depends upon severity of fluid/electrolyte imbalance- fluids, antiemetics, antimicrobials if bacterial or parasiticBRAT diet- bananas, rice, applesauce, toast (plain & simple)Avoid carbonated beverages high in sugar GER Gastroesophageal reflux is the passive upward movement of stomach contents into the esophagus due to relaxation of lower esophageal sphincter “happy spitter”Normal phenomenon that nearly all infants experience Peaks at 1-4 months; resolves by 9-12 monthsMales more commonly affected GERDGERD is very different and is manifested by poor weight gain, recurrent vomiting, crying more than 3 hours a day, arching with feeding, refusal to feed, and sometimes coughing and wheezingAt risk for aspiration & apneaDiagnostic tests: CBC to rule out anemia or infection, electrolyte imbalancesEsophageal pH monitoringUpper GITest for cow milk protein allergypH probe monitoring- insertion of a small catheter into the esophagus through the nose that is left in place for 24 hours to measure pH and thus determine the number of reflux episodes Treatment: small, frequent feedings, frequent burping every 1-2 oz, positioning after feeds (elevate on shoulder for 20-30 mins post feeds or elevate the head of bed), thickened feeds, meds- H2 blockers like Pepcid or zantac or PPIs like prilosec or prevacid for MINOR GERD, SEVERE GERDsurgery- nissen fundification @ 9-12 months to close esophageal sphincterNursing care- observe, educateColic/Purple CryingRecurrent crying and inability to be consoled in infants <3 months of ageUsually begins in first few weeks of life; peaks at about 6 weeks of ageUsually resolves by 3-4 months of ageRule of 3: 3 hours per day in afternoon or eve, >3 days per week, lasts for >3 weeksAffects 5-30% of infantsHigher incidence in households with smokersMust rule out other sources of irritability such as pain, infection, GI dysfunction, or lactose sensitivity PURPLE- peak of crying, unexpected, resists soothing, pain-like face, long lasting, evening Possible causes- rapid feeding, overeating, food (milk) allergy, fruit juices, swallowing excessive air, improper feeding techniques, emotional stress between parent and child Possible solutions- avoidance of overfeeding, music, rhythmic movement, swaddling, tummy massage, warm bath, reduce environmental stimuliSupport parents and encourage respite from family and friends (reassure parent’s they are not the blame for infant’s condition) Esophageal Atresia & Tracheoesophageal Fistula EA= incomplete formation of the esophagus so it ends before the stomachTEF= a fistula (small opening) between the trachea and the esophagus Can occur alone or can have boths/sx: excessive mucous drooling from mouth, intermittent cyanosis cleared with suctioning, 3 C’s of TEF (coughing, choking, cyanosis)aspiration places the infant at risk for pneumoniaDx: identify defect quickly with ng tube or x-rayIf ng tube meets resistance EAPrevent complications (aspiration) by identifying early & surgery ASAPNursing care: maintain patent airway by removing excessive mucous & positioning upright, maintain hydration w/ IV fluids, moist environment, assess for respiratory difficulty, maintain nutrition- IV fluids gastrostomy feedings oral feedings Cleft lip/PalateCongenital defect that can be a dimple in the lip or extend to the floor of the nose, may be unilateral or bilateral, may just involve the palate and not the nose and not be as obvious Etiology: genetic and environmental- lack of folic acid, tobacco use, anticonvulsants, steroid use during pregnancy Clefting occurs during the 6th week of gestation More common in males Feeding is a major concern, otitis media, hearing loss, dental issues/anomalies co-exist, speech problems, cosmetic issuesTx: surgical repairsOT- feeding assistance, special bottles/nipples to assist latching onNursing care: post op positioning (prone position is avoided), protect operative site, elbow restraints may be used to prevent flexion of arms, older infant may need a restraint jacket to keep from rolling over, distraction and pain management are used to prevent prolonged crying, soft diet until suture line heals, may resume feedings once fully awake Umbilical herniaReducible hernia can be pushed back inStrangulated hernia is when part of intestine or other tissue becomes tightly trapped and blood supply is cut offStrangulated requires treatment or if still present by the time the child turns 4Constipation in pedsCaused by psychological factors, diet or underlying diseaseMost common in school aged males bc of unfamiliar bathroom, limited time for toileting, or diet lacking fiber Rare in infants Diagnosed w/ digital rectal exam, KUB (kidney, ureter, bladder xray), or labs (thyroid function, CMP, CBC & UA)Tx: relaxation of bathroom privileges at school, get up earlier to allow time for toileting, sit on toilet after meals, removing constipating foods, increase high fiber foods, glycerin suppository, miralaxPyloric stenosisHypertrophied pyloric sphincter causes outlet obstruction from the stomach Develops within the first few weeks of lifeFirst borns and males more commonly affectedFamilial tendencyClinical manifestations:Regurgitation and non-projectile vomiting at firstVomiting occurs within 30-60 min. post feedingProgresses to projectile (up to 3 ft) vomitingEmesis frequently contains curdled milkInfant remains hungry post-emesis; will usually vigorously refeedMay have an olive-like mass in the epigastric area- just to the right of the umbilicusVisible peristaltic waves across abdomenWeight lossDehydrationConstipation Diagnosed by ultrasound. Upper GI reveals a string sign (elongated pyloric canal)Tx: IVF, pyloromyotomy, introduction of feedings post-op w/ NG tube for gastric decompression, may be discharged as soon as 24 hours post opInfant is usually taking fluids within a few hours and discharged on full strength human milk or formula within 24 hours IntussusceptionTelescoping of the intestine into adjacent intestine Most common site is ileocecal valveMost common cause of bowel obstruction between 3 months and 3 years Is most common in children with CFCommonly follows viral GI infectionSudden onset of colicky abdominal pain with drawing up of legs, intermittent periods of inconsolable crying, yellow-green bile emesis, “current jelly” (blood + mucus) stools- sometimesSausage shaped mass in RUQ or mid upper abdomen may be palpable Dx: made on basis of history and confirmed by xrays and ultrasound of the abdomen Barium enema will reveal obstruction w/ US or xray and is often therapeutic and will relieve obstruction (non-surgical hydrostatic reduction in 70-90% of cases)Hirschprung Disease AKA congenital aganglionic megacolon (genetic condition)Absence of parasympathetic nerve (ganglion) cells in a segment of the colon that prevents transmission of peristaltic waves that propel feces and gas through the colon. Because stool cannot move forward normally, the intestine can become partially or completely obstructed (blocked), and begins to expand to a larger than normal size. Results in accumulation of intestinal contents and abdominal distention. In most cases, the area lacking ganglion cells is limited to the rectosigmoid region of the colon.In newborns, the symptoms include failure to pass meconium stool in the first 48 hours, abdominal distention and bilious vomiting. Constipation occurs in older children. If not treated, can lead to bloody diarrhea, abdominal distention and enterocolitis.Dx- history, x-ray of abdomen, barium enema, rectal or large intestine biopsy to confirm absence of ganglionic cells Tx- surgical removal of section of aganglionic bowel, may need a temporary colostomy, reanastomosis is performed between 2-6 months of ageNursing care- teaching for colostomy and colostomy careIBD- Chrons & UCCrohn’s Disease: chronic inflammatory process with fistulas & deep ulcers in wall of mucosa throughout GI tract (affects segments) w/ no rectal bleeding; affects mostly Caucasian, adolescents & young adults Ulcerative Colitis: chronic, recurrent disease of the superficial mucosa and can be continuous throughout entire bowel w/ rectal bleeding; varying degrees of inflammation, ulceration, hemorrhage & edema, emotional and psychological factors; peak onset is 12 years Normal growth & development, cope w/ episodes of GI pain, monitor side effects of meds (steroids cause delayed sexual maturity & growth retardation, delayed immunizations, decreased ability to fight infection with central line)Appendicitis Anorexia and nausea with or without vomiting, diarrhea, pain beginning as periumbilical and shifting 4-6 hours later to RLQ, increased HR, BP, guarding, rebound tenderness, maximal pain at McBurney’s pointOnce perforation occurs (24-48 hours after symptoms begin), pain may decrease initially then increase Peak at 10-19 yearsBiliary AtresiaCongenital absence or obstruction of bile ducts outside of the liver that prevents flow of bile from the liver to the intestines leads to cirrhosis, end stage liver disease death (fatal!!!)Most common reason for liver transplant in children Cause unknownClinical manifestations: asymptomatic at birth, prolonged duration or late onset (2-3 weeks) of jaundice, abdominal distention, dark (tea colored) urine, gray stools, hepatosplenomegaly, failure to thrive, bruises easily with prolonged bleeding time and intense itching Dx- biopsy of liver, liver labsTx- Kasai procedure (palliative only), liver transplantOne year survival rate is 85% ................
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