quiz 2 final 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
`
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
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
short stature - normal variants vs pathologic
-Important to distinguish normal variants of growth (familial short stature and constitutional growth delay) from pathologic conditions
-Endocrine: Maintenance or increase in BMI percentiles
-Pathologic: Low growth velocity, significantly short for their family
-Chronic illness, nutritional deficiencies: Poor linear growth, inadequate weight gain and low BMI
normal short stature: familial short stature (test)
-takes on average of mom and dad (they are both short)
-Normal birth weight and length
-Linear growth velocity decelerates until nearing genetically determined percentile
-Once target percentile reached, child resumes normal linear growth parallel to growth curve
-Skeletal maturation and timing of puberty consistent with chronologic age
-Child grows along own growth percentile and final height is short, but appropriate for family
-growth curve is normal (decelerates briefly) then goes back to normal but just lower than average
-Ba(bone age) = Ca (chronological age) > Ha (height age)
normal short stature: constitutional growth delay (test)
-late bloomers
-born normal ht and wt
-Decline in linear growth velocity, followed by maintenance of normal growth velocity prior to puberty
-Follow growth percentile below what is expected based on parental heights, delayed skeletal maturation compared to chronologic age, delayed onset of puberty
-Late puberty: Exaggerated short stature
-Growth continues beyond the time the average child stops growing, final height appropriate for target height
-17-18yo growth spirt
-Ba = Ha < Ca
short stature: growth hormone deficiency
-Decreased growth velocity and delayed skeletal maturation in absence of other explanations
-May be isolated or coexist with other pituitary hormone deficiencies
-May be congenital, genetic, or acquired
-Idiopathic GHD is MC form
-Infantile GHD: Normal birthweight and slightly reduced length, hypoglycemia (with adrenal insufficiency), micropenis (with gonadotropin deficiency), and conjugated hyperbilirubinemia
-Diagnosis typically combination of clinical and laboratory evidence
-Labs: Serum IGF-1 gives reasonable estimations of GH secretion and action in adequately nourished child
-All patients diagnosed with GHD should have MRI of hypothalamus/pituitary gland to evaluate for tumor
disproportionate short stature: achondroplasia (dwarfisim)
-dwarfism
-MC form of short-limbed dwarfism
-Autosomal dominant transmission, mutation in fibroblast growth factor receptior-3 gene (80% of time random mutation)
-Upper arms and thighs are proportionately shorter than forearms/legs
-Skeletal dysplasia suspected based on abnormal stature, disproportion, dysmorphism, or deformity
-Height measurements for screening
-Bowing of extremities, waddling gait, limitation of motion of major joints, relaxation of ligaments, short stubby fingers, frontal bossing, midface hypoplasia, otolaryngeal dysfunction, moderate hydrocephalus, depressed nasal bridge, lumbar lordosis
-Imaging:
-Short, thick, tubular bones and irregular epiphyseal plates
-Ends of bones are thick, with broadening and cupping
-Delayed epiphyseal ossification
-Narrowed spinal canal (diminished growth of pedicles)
-Tx: Growth hormone
short stature: SGA/IUGR
-SGA (birth weight and/or length below 3rd percentile for population’s birth weight-gestational age relationship) infants include constitutionally small infants and infants with IUGR
-Most with mild SGA/IUGR exhibit catch-up growth during first 3 years of life
-Have skeletal maturation that corresponds to chronologic age
Short Stature Associated with Syndromes
Turner, Down, Noonan, and Prader-Willi
Psychosocial Short Stature
-Growth impairment associated with emotional deprivation
-Change in environment results in improved growth and improvement of GH secretion, personality, and eating behaviors
short stature work up
-guided by H&P:
-Radiographs of left hand/wrist (bone age)
-Bloodwork: Serum electrolytes (Ca/P - renal tubular ds/metabolic bone disease), CBC (chronic anemia, leukocyte markers of infection), TFTs (T4 and TSH), BUN/Cr, ESR, IGF-1 and/or IGFBP-3 (children younger than 4 years/malnourished)
-Urinalysis
-Stool exam for fat/TTG (malabsorption or celiac disease)
-Karyotyping/Noonan syndrome testing
short stature tx
-Growth Hormone Therapy
-FDA-approved for children with GHD, growth restriction associated with CRF, Turner/Prader-Willi/Noonan syndromes, SGA without catch-up growth by age 2, SHOX gene mutations, those with idiopathic short stature whose current height is 2.25 SDs below normal for age
-Subcutaneous, 6-7 days/week with total weekly dose of 0.15-0.47 mg/kg (dont know)
precocious puberty in girls (know this)
-onset of secondary sexual characteristics before 8yo in Caucasian girls
-7 years for African American and Hispanic girls
-Central PP: Idiopathic or 2ndary to a CNS abnormality that disrupts prepubertal restraint on the GnRH pulse generator
-Abnormalities include hypothalamic hamartomas, CNS tumors, cranial irradiation, hydrocephalus, and trauma
-Peripheral PP (GnRH-independent): Ovarian/adrenal tumors, ovarian cysts, late-onset congenital adrenal hyperplasia, McCune-Albright syndrome, or exposure to exogenous estrogen
-starts with breast development, followed by pubic hair growth and menarche
-PPP:
-!Ovarian cysts/tumors usually with signs of estrogen excess: Breast development, vaginal discharge, vaginal bleeding
-!Adrenal tumors and CAH with signs of androgen excess: Pubic hair, axillary hair, acne, and increased body odor
-know the difference
-Accelerated growth/maturation; skeletal maturation quicker than linear growth = compromised adult stature
precocious puberty in girls dx
-Labs:
-CPP: Random FSH and LH concentrations may confirm diagnosis
-PPP: LH response to GnRH is suppressed by autonomously secreted gonadal steroids
-Estradiol levels, androgen levels (testosterone, androstenedione, dehydroepiandosterone sulfate), and 17-hydroxyprogesterone should be measured
-Imaging:
-Bone age (radiographs of L hand and wrist)
-CPP: MRI of brain for CNS lesions
-PPP: Imaging of ovaries and/or adrenal gland
delayed puberty in girls overview
-No pubertal signs by age 13 or menarche by 16 years
-MCC is constitutional growth delay
-Primary hypogonadism: Primary abnormality of the ovaries
-MCC is Turner syndrome
-Other causes: Gonadal dysgenesis, galactosemia, autoimmune ovarian failure, radiation, and CTX
-Central hypogonadism: Hypothalamic or pituitary deficiency of GnRH or FSH/LH
-Functional (reversible): Stress, undernutrition, prolactinemia, excessive exercise, or chronic illness
-Permanent: Congenital hypopituitarism, CNS tumors, or cranial irradiation
delayed puberty in girls: clinical eval
-H&P, BONE AGE:
-Low bone age (< 12 years):
-Short stature, normal growth velocity > constitutional growth delay
-Growth rate abnormal > evaluation for causes of growth delay warranted
-Bone age > 12 years:
-FSH/LH distinguishes between primary ovarian failure (elevated FSH/LH) and central hypogonadism (low FSH/LH)
-Karyotyping for elevated gonadotropins
-Cranial MRI for central
-GIRLS W/ ADEQUATE BREAST DEVELOPMENT AND AMENORRHEA:
-Progesterone challenge to determine if sufficient estrogen is being produced and to evaluate for anatomical defects
-Producing estrogen: Withdrawal bleeding 5-10 days of PO progesterone -> MCC of amenorrhea in this case is PCOS
-Estrogen-deficient/anatomical defect: No bleeding
precocious puberty in boys
-2ndary sexual characteristics before 9yo; also either central or peripheral
-Pubic hair > penile enlargement > scrotal maturation, axillary hair, voice deepening, increased growth velocity
-CPP: Testes enlarge
-PPP: Testes remain much smaller than expected for degree of virilization
-Labs:
-Elevated testosterone levels
-CPP: High LH/FSH
-PPP: Low LH/FSH -> CAH: Adrenal androgens and 17-hydroxyprogesterone will be elevated
-Imaging:
-Bone age
-CPP: Brain MRI
-PPP: Rule out hepatic, adrenal, and testicular tumors
