[216B] Peds Flashcards
Growth & development are complex interactions between _____ and _____ influences.
Genetic & environmental.
List 2 examples of environmental influences.
Nutrition
Sensory stimulation
Neurocognitive development is the result of the:
myelination of the brain
List the 4 periods of childhood G&D and the ages at which they occur.
Infancy (less than 1 y/o)
Preschool/early childhood (1-5)
School-aged (6-12)
Adolescence (12-18)
T/F: normal human growth is linear.
False: human growth is pulsatile.
What does it mean when we say human growth is “pulsatile”?
Periods of rapid growth (AKA growth spurts) are separated by periods of no measurable growth
What do we consider a “preterm infant”?
An infant born before 40 weeks gestation.
How do we calculate the corrected age of a preterm infant?
(actual age in weeks) - (weeks preterm) = corrected age
By age 4-6 months, an infant’s weight should be:
Double their birth weight
Between ages 1-5, a toddler will gain about __ pounds per year.
5
When does the final growth spurt occur?
The beginning of puberty (between 9-15)
List the 4 domains of development.
- Physical
- Cognitive
- Social & emotional
- Language
____ are bands of connective tissue that connect infants’ skull bones
Sutures
____ are wide spaces of unossified membranous tissue found at the junction of sutures.
Fontanelles
What is the developmental screening schedule for children under 5?
Checks at 2/4/6/9/12/18 months, 2 years, then q1year until age 5.
Which 4 growth charts should be used from birth to 24 months?
- Length-for-age
- Weight-for-age
- Head circumference (percentile)
- Weight for length (percentile)
Which 3 growth charts are used for children 2-19 years old?
- Height for age
- Weight for age
- BMI for age
Do we use the WHO or the CDC growth charts in Canada?
WHO.
Newborn metabolic screening in Alberta provides blood spot screening for how many treatable conditions?
21
[Bilirubin metabolism] What 3 steps occur before bilirubin reaches the liver?
- Hemoglobin in RBCs breaks down into heme + globin.
- Heme + globin become biliverdin.
- Biliverdin is converted to free bilirubin, which is protein-bound to albumin for transport to the liver.
[Bilirubin metabolism] What happens when free bilirubin enters the liver?
It is absorbed into hepatocytes and conjugated.
[Bilirubin metabolism] Is conjugated bilirubin hydrophilic or lipophilic? Why is this helpful for ADME?
Hydrophilic - good for excretion
[Bilirubin metabolism] How does conjugated bilirubin exit the liver? What happens to it after?
Secreted with bile.
Goes through small intestine: converted to urobilinogen by intestinal flora, then secreted in feces/reabsorbed to be excreted in urine
What is hyperbilirubinemia? What does it cause s&s wise?
Accumulation of bilirubin in the blood (34-50 umol/L)
Causes jaundice
Why do we see jaundice as a result of hyperbilirubinemia?
Deposition of unconjugated bilirubin in the skin, conjunctiva & mucous membranes.
Is unconjugated bilirubin hydrophilic or lipophilic? Why is this a concern?
Lipophilic - can cross BBB.
Why are more than half of infants susceptible to hyperbilirubinemia?
Newborns’ bilirubin metabolism is still in transition from the fetal stage (why it’s more common in preemies)
Describe fetal bilirubin metabolism.
Bilirubin is excreted in its lipophilic (unconjugated) form through the placenta.
What are 2 predisposing factors for hyperbilirubinemia in ALL newborns?
- Immaturity of newborn liver
2. Fetal RBCs have shorter lifespans
When would we expect to see physiologic neonatal jaundice? When would we be concerned that it might be pathologic?
Physiologic: typically day 2-3 postpartum
Concerned about pathologic if longer than 1 week or if it presents within the first 24h of birth
List the 3 classifications of pathological neonatal jaundice.
Breastfeeding jaundice.
Hemolytic jaundice.
Underlying liver disease.
When will we see breastfeeding jaundice? What is the patho behind it?
7th day of life.
Decreased peristalsis d/t poor feeding = inability to excrete bile in feces.
How do we treat breastfeeding jaundice?
Continue breastfeeding + formula supplement to help promote bilirubin excretion
What is the patho behind hemolytic jaundice?
Hastened breakdown of RBCs (ex: d/t Rh mismatch)
Why would underlying liver disease cause hyperbilirubinemia/jaundice?
Inability to conjugate bilirubin = hyperbilirubinemia
Why is cephalhematoma a risk factor for neonatal hyperbilirubinemia?
Bruising at the scalp = RBC breakdown = increased demand for bilirubin metabolism (transitioning infant cannot keep up)
How does colostrum promote bilirubin excretion?
Enhances GI motility
Besides breastfeeding + formula supplements, list 3 other txs for neonatal hyperbilirubinemia.
- Phototherapy
- Exchange blood transfusion
- Tx causes of underlying liver disease/hemolytic disease (ex: liver transplant)
What is phototherapy? Why is it effective in tx of hyperbilirubinemia?
Use of visible light to penetrate skin
Bilirubin absorbs energy > undergoes photoisomerization > forms non-toxic isomers that can be excreted without liver conjugation (hydrophilic)
What is the wavelength range for effective phototherapy?
400-500 nm
What is kernicterus?
Brain damage d/t hyperbilirubinemia (>425 umol/L)
Describe hemolytic disease of the newborn.
Rh- mother’s first pregnancy is with an Rh+ fetus, creating anti-Rh antibodies.
Antibodies attack fetal RBCs causing severe anemia and jaundice (appears within the first 24h).
How do we prevent hemolytic disease of the newborn?
2 doses of RhoGAM (Rh immunoglobulin) IM/IV
Once during pregnancy (26-28 weeks)
Once within 72h of delivery
Where does bilirubin accumulate in the brain in kernicterus (2)? What do these areas control?
Brainstem: HR, breathing, hearing, balance, coordination, reflexes
Basal ganglia: motor control, behaviours, emotions, movement execution
List 7 consequences of chronic, severe hyperbilirubinemia.
- Cerebral palsy (difficulty with movement/coordination)
- Oculomotor disturbances in gaze (especially upwards)
- Sensory hearing loss
- Learning difficulties
- Seizures
- Coma
- Death
Define FTT in children.
Below expected standards of growth
How can we treat organic FTT in infants?
Increasing caloric density of formula to >20 kcal/oz or parenteral nutrition
Describe the 2 types of hemolytic anemia in children.
- Intrinsic: inherited; RBCs destroyed d/t a flaw in the RBCs
- Extrinsic: RBC destruction is d/t a cause outside of cells
List 5 causes of extrinsic hemolytic anemia.
- Bacteria/viral infection
- Meds: abx (ex: penicillin, sulfonamides), malaria meds
- Cancers: leukemia, lymphoma, etc.
- Autoimmune disorders: lupus (SLE - systemic lupus erythematous), RA (rheumatoid arthritis)
- Hypersplenism: spleen destroys more RBCs than normal
How does an RBC in sickle cell anemia (Hgb S) differ from a healthy RBC?
Hgb S break apart easily & have trouble moving through small capillaries = clots.
Usually die in 10-20 days = anemia.
How does the body attempt to adapt to sickle cell disease (SCD)?
Increased erythropoiesis (RBC production) + chronic inflammatory state > endothelial activation + enhanced RBC/leukocyte adhesion
List 9 s&s of SCD.
- Pain crises (major symptom)
- High risk for stroke, seizures & organ damage
- Bacterial infections
- Abd pain d/t enlarged spleen
- Sensitive to cold d/t increased nociceptor sensitivity from pain crises
- Delayed puberty
- Swelling of joints
- Vision abnormalities
- Anemia
Explain why we would see pain crises, high risk for stroke/seizures/organ damage and bacterial infections with SCD.
Pain crises: when RBCs block blood flow to capillaries
Others: ^ + thromboembolism
List 7 treatments for SCD.
- Hydroxyurea (antineoplastic - cancer drug)
- L-glutamine (amino acid)
- Pain meds for crises (NSAIDs, opioids)
- Bone marrow transplant - helps produce healthy RBCs
- Abx (daily prophylactic penicillin)
- Regular immunization
- Blood transfusions during aplastic crisis
Why is hydroxyurea helpful in SCD tx (3)?
- Decreases production of Hgb S cells
- Promotes production of larger, more flexible RBCs to prevent vessel blockage
- Produces Hgb F (fetal Hgb) & mean corpuscular volume (size) of Hgb A
Why is L-glutamine helpful for SCD tx (2)
- Reduces disease severity
- Decreases RBC adherence to endothelium (prevent vessel blockage)
Why is regular immunization so important for pts with SCD?
Prevents bacterial sepsis since their spleen is enlarged and dysfunctional
Down syndrome is the presence of an extra chromosome ___ (_____)
21 (trisomy)
Why do pts with down syndrome require life-long, multidisciplinary care? (7)
- Hearing loss & vision abnormalities
- Obstructive sleep apnea (d/t tongue)
- Ear infections d/t shorter ear canal
- Eye diseases
- Heart defects present at birth (VSDs, AVSDs, pulmonary HTN)
- Thyroid abnormalities
- GERD & other
List the 3 tx for GERD in a down syndrome pt.
- Losec (Omeprazole) + high dose Prevacid (Lansoprazole) - PPI
- Pepcid (Famotidine), Zantac (Ranitidine) - H2 blocker
- Antacids
* Compound meds d/t difficulties swallowing.
List 2 tx for pulmonary HTN in down syndrome pts.
- Sildenafil (Viagra) - PDE5 (phosphodiesterase type 5) inhib
- Dilation of pulmonary arteries
Define eczema.
Itchy, inflamed skin disorder
Describe the s&s of eczema in the acute and chronic stages.
Poorly defined erythema with edema, vesicles and weeping in the acute stage.
Lichenification (thickened, pebbly skin d/t trauma) chronically.
What type of sensitivity reaction is eczema? Which immunoglobulin mediates it?
Type I hypersensitivity - IgE
What happens when antibodies are released in the presence of an allergen?
Mast cell degranulation + histamine/other inflammatory mediator release
List 5 possible manifestations of eczema.
- Nasal allergic reactions.
- Ocular allergic reactions.
- Erythema.
- Asthma.
- Peripheral vasodilation.
Eczema tx targets these 4 underlying abnormalities:
- Dryness
- Pruritus
- Infection
- Inflammation
List 5 tx for eczema.
- Emollients (ex: Glaxal base) - tx dry skin.
- Topical corticosteroids (ex: hydrocortisone cream/ointment - 0.5-1% only) - tx skin inflammation.
- Bronchodilators (beta agonists ex: albuterol) via inhaler - tx bronchospasm.
- Antihistamines PO (H1 - diphenhydramine; H2 - famotidine/ranitidine) - adjunct tx for hives/pruritis.
- Desensitization therapy
Why shouldn’t you scratch areas affected by eczema (2)?
- Causes scarring of the dermis layer.
2. Can introduce Staph aureus infection.
What is the tx for Staph aureus infections with eczema (2)?
- Bleach baths
2. Intranasal mupirocin ointment
When does childhood iron deficiency anemia (IDA) peak in prevalence? Why?
Toddler years (1-3 y/o) d/t nutritional factors (ex: picky eating, not eating foods with highly bioavailable iron)
Why are children younger than 2 at particularly high risk for IDA?
Rapid growth + inadequate dietary iron
List 3 s&s of childhood IDA.
- Irritability.
- Poor appetite.
- Pallor: conjunctiva, tongue, palms, nailbeds.
If a child’s IDA is severe, their s&s may resemble the s&s of:
CHF: fatigue, tachypnea, hepatomegaly, edema.
Which 3 neurotransmitters are impacted by decreased brain iron stores in IDA? Why?
- Dopamine.
- Serotonin.
- NE.
They all require iron-dependent enzymes to be synthesized.
List 6 recommendations to prevent childhood IDA.
- Bottles should be discontinued by 12-15 months or earlier.
- Infants should not be put to sleep with a bottle.
- Introduce iron-rich/fortified foods into the diet (ex: meat/meat alternatives, iron-fortified cereal).
- Provide iron supplements.
- Limit cow’s milk consumption (500-750 mL/day).
- Blood transfusions (severe cases).
Where is Vitamin D3 (cholecalciferol) found (2)?
- Made in the skin.
2. In oily fish, egg yolks & fortified food.
Where is Vitamin D2 (ergocalciferol) found?
Fortified foods, salmon, mushrooms & egg yolks.
Which 2 organs (in order) contribute to the metabolism of VitD?
Liver first, then kidneys.
Vit D helps the body absorb and retain _____ and _____, which are critical for building ___.
Calcium & phosphorus.
Bone.
List 3 outcomes of chronic/severe pediatric Vit D deficiency.
- Irritability.
- Developmental delays.
- Nutritional rickets: pain, softening & fractures of bone d/t inadequate mineralization.
How much Vit D do peds need to be supplemented throughout the year?
Summer months: 400 I.U.
Winter months: 800 I.U.
Vit D toxicity results in _________, which would have the following 6 s&s:
Hypercalcemia.
- Kidney stones.
- Renal insufficiency.
- GI upset.
- Headaches.
- Arrhythmias.
- Muscle pain.
