quiz 2 Flashcards
complementary feeding; Introduction of Solid Foods in Infants
Complementary foods: At 6 months
-6mo- cereal -> fruit/veg -> meat
- Meats are an important source of iron and zinc (inadequate to meet an infant’s needs in human milk by 6 months)
Peanut protein:
- If severe eczema or egg allergy: introduce at 4–6 months as puree (~6–7g/week) to reduce peanut allergy risk
12 months:
- whole milk: Before that, risk of iron deficiency and protein overload
- honey: risk of botulism
juice: not necessary, give in a cup (not a bottle), < 4 oz/day
vitamin deficiencies: vitamin A
-Basic constituent of vitamin A group is retinol
-Ingested plant carotene or animal tissue retinol esters release retinol after hydrolysis by pancreatic and intestinal enzymes
-Eye: Retinol is metabolized to form rhodopsin
-Action of light on rhodopsin is the first step of the visual process
-Deficiency appears as a group of ocular signs termed xerophthalmia
-Night blindness, followed by xerosis of conjunctiva and cornea
-Clinical/subclinical signs: Immunodeficiency (measles)
niacin (B3) deficiency
-Involved in fat synthesis, intracellular respiratory metabolism, and glycolysis
-Content of tryptophan must be considered (converted to niacin)
-Pellagra (niacin deficiency): Weakness, lassitude, dermatitis, photosensitivity, inflammation of mucous membranes, V/D, dysphagia, dementia (severe cases)
vitamin C deficiency
-Principal forms are ascorbic acid and dehydroascorbic acid
-Scurvy: Irritability, bone tenderness/swelling, pseudoparalysis of legs
-Progression: Subperiosteal hemorrhage, bleeding gums/petechiae, hyperkeratosis of hair follicles, mental changes, anemia, decreased iron absorption, abnormal folate metabolism
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vitamin D deficiency
-Cholecalciferol (D3) and ergocalciferol (D2) require further activation to become active
-Clothing, lack of sunlight, and skin pigmentation decrease generation of vitamin D in epidermis and dermis
-Vitamin D deficiency appears as rickets in children and as osteomalacia in postpubertal adolescents
-RICKETS:
-Failure of mineralization -> soft zones of bone -> compression/lateral bulging or flaring of ends of bones
-Sx- MC < 2yo
-Craniotabes: Thinning of outer table of skull (when compressed > feels like ping-pong ball)
-Enlargement of costochondral junction (rachitic rosary) and thickening of wrists and ankles
-Enlarged anterior fontanelle
-Scoliosis, exaggerated lordosis, bow-legs/knock knees, greenstick fractures
-DX: Based on hX and poor intake of vitamin D/little UV exposure
-Serum calcium low-normal, phosphorus reduced, alkaline phosphatase activity increased
-Best measure is level of 25(OH)D
-Radiographic changes:
-Distal ulna/radius: Widening, concave cupping, frayed/poorly demarcated ends
vitamin k deficiency
BLEEDING (especially in newborns without prophylaxis)
- Easy bruising
- Bleeding and signs of blood loss (e.g., pale skin)
- Hematuria, hematochezia
pyloric stenosis def
-Postnatal pyloric muscular hypertrophy with gastric outlet obstruction
-Incidence of 1-8/1000 births with 4:1 male predominance
-Projectile postprandial vomiting between 2 and 4 weeks of age (as late as 12 weeks)
-Vomitus rarely bilious, but may be blood-streaked
-Infants usually hungry and nurse avidly
-Upper abdomen may be distended after feedings, and prominent gastric peristaltic waves from L to R may be seen
-Oval mass, 5-15 mm in longest dimension palpable in the RUQ of abdomen (only present in 13.6% of patients)
pyloric stenosis dx and tx
-Labs:
-Hypochloremic alkalosis with potassium depletion
-Dehydration: Elevated hemoglobin/hematocrit
-Imaging:
-US shows a hypoechoic muscle ring > 4 mm thickness with hyperdense center and pyloric channel length > 15 mm
-Barium upper GI series: Retention of contrast in stomach and a long narrow pyloric channel with a double track of barium
-Tx:
Pyloromyotomy – Incision down the mucosa along the pyloric length
Treatment of dehydration/electrolyte imbalance prior
duodenal obstruction/atresia
-Obstruction is either intrinsic or extrinsic
-Extrinsic: Congenital peritoneal bands associated with intestinal malrotation, annular pancreas, or duodenal duplication
-Intrinsic: Congenital atresia, stenosis, mucosal webs
-Imaging:
-Prenatal ultrasound versus postnatal abdominal plain films: Presence of a “double-bubble” – distention of the stomach and proximal duodenum
-Absence of distal intestinal gas suggests atresia
-Barium enema may be usual in determining atresia
-Duodenal Atresia:
-Maternal polyhydramnios
-Bilious emesis and epigastric distention within several hours of birth
-Pre-term birth and Down syndrome associations
-Tx:
Surgical intervention – Duodenoduodenostomy to bypass atresia
Good prognosis, mortality risk due to associated anomalies other than duodenal obstruction
intestinal malrotation
-Bowel from ligament of Treitz to mid-transverse colon rotates around narrow mesenteric root (from incomplete rotation during development) and occludes the SMA (volvulus)
-Malrotation with volvulus accounts for 10% of neonatal intestinal obstructions
-First 3 weeks of life: Bilious emesis or overt SBO
-Later signs: Intermittent intestinal obstruction, malabsorption, protein-losing enteropathy, or diarrhea
-Older children: Chronic GI symptoms of N/V/D, abdominal pain, dyspepsia, bloating, and early satiety
-Imaging:
-Upper GI series is gold standard: Duodenojejunal junction and the jejunum on the R side of the spine; “corkscrew sign” from twisted configuration of proximal small bowel loops
-Barium enema: Mobile cecum in midline, RUQ, or left abdomen
-US/CT scan: “Whirlpool sign” denoting midgut volvulus
-Tx:
-Surgical intervention – Ladd procedure: Duodenum mobilized, short mesenteric root extended, and bowel fixed in a more normal distribution
-Midgut volvulus is a surgical emergency (bowel necrosis from occlusion of the SMA)
-Guarded prognosis if perforation, peritonitis, or extensive intestinal necrosis is present
intussusception
-one segment of intestine telescopes into another
-Can occur anywhere along the small and large bowel and usually starts proximal to the ileocecal valve and extends for varying distances into the colon
-MCC of intestinal obstruction in 1st 2 years of life and 3x more common in males
-Sx related to obstruction and ischemia are due to swelling, hemorrhage, vascular compromise, and necrosis of intussuscepted ileum
-Primary causes include SB polyp, Meckel diverticulum, omphalomesenteric remnant, duplication, lymphoma, lipoma, parasites, FB, and viral enteritis with hypertrophy of Peyer patches (MC)
-In children > 6yo, lymphoma is the MCC
-Previously healthy 3-12mo develops recurring paroxysms of abdominal pain with screaming and drawing up of knees
-Vomiting and diarrhea occur (90% of cases)
-Bloody bowel movements with mucus (“currant jelly stools”) appear within first 12 hours
-May be febrile, lethargic between episodes
-Abdomen tender/distended
Sausage-shaped mass may be palpated, upper mid abdomen
-Dx/Tx
-Abdominal US is 98-100% sensitive for diagnosis – “Target sign”
-Barium enema and air enema are diagnostic and therapeutic
-Not if ischemic damage to intestine is suspected > perforation
-Surgery for identifying lead point
inguinal hernia
-Occur at any age, MC indirect, more frequent in boys (9:1)
-Painless inguinal swelling
-Partial obstruction > severe pain
-Rarely, bowel becomes trapped in the hernia and complete intestinal obstruction occurs
-Gangrene of hernia contents or testis may occur
-In girls, hernia may prolapse into the hernia sac presenting as a mass below the inguinal ligament
-History of inguinal fullness associated with coughing or long periods of standing, or presence of firm, globular, and tender swelling sometimes associated with vomiting and abdominal distention
-Tx:
-Incarceration of inguinal hernia: Manual reduction
-CI if present > 12 hours or if blood stools noted
-Surgery if hernia has incarcerated in past
umbilical hernia
-Occur MC in full-term, African American infants
-Most regress spontaneously if fascial defect has a diameter of < 1 cm
-Asymptomatic UHs are managed expectantly with no intervention until 4-5 years, after which they are usually treated surgically
meckel diverticulum
-MC form of omphalomesenteric duct remnant
-Complications 3x more common in males and 50% occur in first 2 years of life
-40-60% of pts have painless episodes of maroon or melanotic rectal bleeding
-Bleeding due to ileal ulcers adjacent to the diverticulum caused by acid secreted by heterotopic gastric tissue (may cause shock and anemia)
-Intestinal obstruction in 25% of symptomatic patients -> Ileocolonic intussusception
-Imaging:
-Dx is made with a Meckel scan
-Technetium-99m-pertechnetate take up by heterotopic gastric mucosa in the diverticulum and outlines diverticulum on a nuclear scan
-Tx: Surgical with good prognosis
acute appendicitis
-MC indication for emergency abdominal surgery in childhood
-Frequency increases with age and peaks between 15 and 30 years
-Obstruction of appendix by fecalith (25%) is a common predisposing factor
-Incidence of perforation is high in childhood (40%) – pain poorly localized and nonspecific
-Low grade fever and periumbilical abdominal discomfort, becoming localized to RLQ with signs of peritoneal irritation
-Anorexia, vomiting, constipation, and diarrhea can also occur
-Serial examinations are important
-Labs:
-WBCs seldom > 15K/uL
-Pyuria, fecal leukocytes, guaiac + stool sometimes present
-Combo of elevated CRP and leukocytosis has been reported to have PPV of 92%
-Imaging:
-Radio-opaque fecalith in 2/3 of cases of ruptured appendix
-US: Noncompressible, thickened appendix in 93% of cases
-Abdominal CT after rectal instillation of contrast may be dx
-Tx:
-Exploratory laparotomy or laparoscopy when diagnosis cannot be ruled out
-Post-operative antibiotics for patients with gangrenous or perforated appendix
-< 1 % mortality rate during childhood, despite high rate of perforation
congenital aganglionic megacolon/hirschsprung ds overview
-1 in 5,000 live births, 4x greater in males
-MC chromosomal abnormality associated is Down syndrome
-Results from an absence of ganglion cells in the mucosal and muscular layers of the colon
-Absence of ganglion cells results in failure of the colon muscle to relax
-Aganglionic segments have normal or slightly narrowed caliber with dilation of the normal colon proximally
-Mucosa of the dilated colonic segment may become thin and inflamed > diarrhea, bleeding, and protein loss
congenital aganglionic megacolon/hirschsprung ds presentation
-Failure of newborn to pass meconium (within first 24 hours of life), followed by vomiting, abdominal distention, and reluctance to feeds
-Enterocolitis manifested by fever, dehydration, and explosive diarrhea in 50% of affected newborns
-May lead to inflammatory and ischemic changes in the colon, with perforation and sepsis
-Later infancy: Alternating obstipation and diarrhea predominate
-Older children: Constipation alone
-Other symptoms may include foul-smelling or ribbon-like stools, distended abdomen, intermittent bouts of abdominal obstruction, hypoproteinemia, and FTT
-DRE: Anal canal/rectum devoid of fecal material despite obvious retained stool on abdominal examination/radiograph
Congenital Aganglionic Megacolon/Hirschsprung Disease
lab and imaging
Laboratory findings
- Rectal suction bx: Ganglion cells are absent in both the submucosal and muscular layers of involved bowel
Imaging
Plain abdominal radiographs:
- Dilated proximal colon and absence of gas in the pelvic colon
- Barium enema: Narrow distal segment with sharp transition to proximal/dilated (normal) colon
vomiting
-Presenting sign of many pediatric conditions
-MCC in childhood is viral gastroenteritis
-Others: Obstruction, acute/chronic inflammation of GI tract; CNS inflammation, increased ICP, or mass effect; metabolic derangements associated with inborn errors of metabolism, sepsis, drug intoxication
-Tx:
-Control of vomiting with medication is rarely necessary in acute gastroenteritis, but may relieve N/V and decrease need for IV fluids and/or hospitalization
-Antihistamines/anticholinergics for motion sickness
-5-HT3-receptor antagonists (ondansetron, granisetron)
-Benzodiazepines, corticosteroids, and substituted benzamides: CTX
-Butyrophenones (droperidol, haloperidol): Intractable vomiting in acute gastritis, CTX, post-op
acute diarrhea
-Viruses MCC in developing and developed countries
-Rotavirus (developing) and Norovirus (developed) are MC, followed by enteric adenovirus, and Astrovirus
-Affects small intestine, causing voluminous, watery diarrhea without leukocytes or blood
-!Norovirus: Mainly vomiting (also diarrhea) with short duration of symptoms (1-2 days)
acute diarrhea: rotavirus
-In U.S., primary affects infants between 3 and 15 months of age, peaks in winter, transmitted via fecal-oral route and survives for hours and hands/days on environmental surfaces
-Incubation period of 1-3 days
-Vomiting is first symptom (80-90%), followed by low-grade fever and watery diarrhea within 24 hours (diarrhea lasts x 4-8 days)
-Detected in feces using EIA or latex agglutination
-Other lab findings: Normal WBC count, electrolyte abnormalities with dehydration, metabolic acidosis (bicarbonate loss), ketosis, lactic acidosis (severe cases)
-Treatment is supportive
-Replacement of fluid and electrolyte deficits/ongoing losses via ORT/IVT
-ORT solutions appropriate in most cases (not clear liquids or dilute formulas > 48 hours)
-Intestinal lactase levels may be decreased (short course of lactose-free diet)
-Reduced fat intake may decrease N/V
-No anti-diarrheal medications indicated
dehydration - whats tx for mild vs mod vs severe
- MCC in kids is vomiting/diarrhea
-Children at greater risk of hypovolemia
-Higher frequencies of gastroenteritis
-Higher surface area to volume ratio/insensible volume losses
-Unable to communicate fluid needs
-Classified by % of total body water lost (mild, moderate, severe)
-Vitals (including orthostatic BP)
-Urinalysis: Elevated SG, ketonuria; BMP (electrolyte abnormalities); serum bicarbonate (metabolic acidosis); BUN (elevated with hypovolemia)
-Tx:
-Mild-Moderate: ORT (Pedialyte/Gatorade), BRAT diet (diarrhea)
-Typically, 1 mL/kg every 5-10 minutes or 0.5 ounces every 5-10 minutes (higher aliquots for dehydration may be used)
-Ondansetron if needed to tolerate ORT (for vomiting)
-Severe: IV fluids
-Initial bolus of 20 mL/kg normal saline over 20-30 minutes
-½ fluid deficit over first 8 hours, second ½ over next 16 hours
-FD = % dehydration x weight (kg)
normal variants of growth: Familial short stature vs Constitutional growth
Familial short stature - parents are short
- Short parents = short child, nothing wrong.
Constitutional growth - late bloomer
- Delayed puberty and bone age
disturbances of growth
-Disturbances of growth and development are the most common problems evaluated by a pediatric endocrinologist
-Height velocity is most critical parameter in evaluation of growth
-Persistent increase or decrease in height percentiles between 2 years of age and onset of puberty indicates abnormal growth and always warrants evaluation
-Substantial deviations from target height (midparental) may indicate underlying endocrine/skeletal disorders
-Height potential is determined largely by genetic factors
-Target height = Mean parental height (+ 6.5 cm for boys, - 6.5 cm for girls)
-Skeletal maturation/bone age
