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N216 A/B > [216B] Peds > Flashcards

[216B] Peds Flashcards

1
Q

Growth & development are complex interactions between _____ and _____ influences.

A

Genetic & environmental.

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2
Q

List 2 examples of environmental influences.

A

Nutrition

Sensory stimulation

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3
Q

Neurocognitive development is the result of the:

A

myelination of the brain

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4
Q

List the 4 periods of childhood G&D and the ages at which they occur.

A

Infancy (less than 1 y/o)
Preschool/early childhood (1-5)
School-aged (6-12)
Adolescence (12-18)

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5
Q

T/F: normal human growth is linear.

A

False: human growth is pulsatile.

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6
Q

What does it mean when we say human growth is “pulsatile”?

A

Periods of rapid growth (AKA growth spurts) are separated by periods of no measurable growth

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7
Q

What do we consider a “preterm infant”?

A

An infant born before 40 weeks gestation.

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8
Q

How do we calculate the corrected age of a preterm infant?

A

(actual age in weeks) - (weeks preterm) = corrected age

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9
Q

By age 4-6 months, an infant’s weight should be:

A

Double their birth weight

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10
Q

Between ages 1-5, a toddler will gain about __ pounds per year.

A

5

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11
Q

When does the final growth spurt occur?

A

The beginning of puberty (between 9-15)

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12
Q

List the 4 domains of development.

A
  1. Physical
  2. Cognitive
  3. Social & emotional
  4. Language
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13
Q

____ are bands of connective tissue that connect infants’ skull bones

A

Sutures

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14
Q

____ are wide spaces of unossified membranous tissue found at the junction of sutures.

A

Fontanelles

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15
Q

What is the developmental screening schedule for children under 5?

A

Checks at 2/4/6/9/12/18 months, 2 years, then q1year until age 5.

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16
Q

Which 4 growth charts should be used from birth to 24 months?

A
  1. Length-for-age
  2. Weight-for-age
  3. Head circumference (percentile)
  4. Weight for length (percentile)
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17
Q

Which 3 growth charts are used for children 2-19 years old?

A
  1. Height for age
  2. Weight for age
  3. BMI for age
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18
Q

Do we use the WHO or the CDC growth charts in Canada?

A

WHO.

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19
Q

Newborn metabolic screening in Alberta provides blood spot screening for how many treatable conditions?

A

21

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20
Q

[Bilirubin metabolism] What 3 steps occur before bilirubin reaches the liver?

A
  1. Hemoglobin in RBCs breaks down into heme + globin.
  2. Heme + globin become biliverdin.
  3. Biliverdin is converted to free bilirubin, which is protein-bound to albumin for transport to the liver.
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21
Q

[Bilirubin metabolism] What happens when free bilirubin enters the liver?

A

It is absorbed into hepatocytes and conjugated.

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22
Q

[Bilirubin metabolism] Is conjugated bilirubin hydrophilic or lipophilic? Why is this helpful for ADME?

A

Hydrophilic - good for excretion

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23
Q

[Bilirubin metabolism] How does conjugated bilirubin exit the liver? What happens to it after?

A

Secreted with bile.
Goes through small intestine: converted to urobilinogen by intestinal flora, then secreted in feces/reabsorbed to be excreted in urine

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24
Q

What is hyperbilirubinemia? What does it cause s&s wise?

A

Accumulation of bilirubin in the blood (34-50 umol/L)

Causes jaundice

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25
Q

Why do we see jaundice as a result of hyperbilirubinemia?

A

Deposition of unconjugated bilirubin in the skin, conjunctiva & mucous membranes.

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26
Q

Is unconjugated bilirubin hydrophilic or lipophilic? Why is this a concern?

A

Lipophilic - can cross BBB.

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27
Q

Why are more than half of infants susceptible to hyperbilirubinemia?

A

Newborns’ bilirubin metabolism is still in transition from the fetal stage (why it’s more common in preemies)

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28
Q

Describe fetal bilirubin metabolism.

A

Bilirubin is excreted in its lipophilic (unconjugated) form through the placenta.

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29
Q

What are 2 predisposing factors for hyperbilirubinemia in ALL newborns?

A
  1. Immaturity of newborn liver

2. Fetal RBCs have shorter lifespans

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30
Q

When would we expect to see physiologic neonatal jaundice? When would we be concerned that it might be pathologic?

A

Physiologic: typically day 2-3 postpartum

Concerned about pathologic if longer than 1 week or if it presents within the first 24h of birth

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31
Q

List the 3 classifications of pathological neonatal jaundice.

A

Breastfeeding jaundice.
Hemolytic jaundice.
Underlying liver disease.

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32
Q

When will we see breastfeeding jaundice? What is the patho behind it?

A

7th day of life.

Decreased peristalsis d/t poor feeding = inability to excrete bile in feces.

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33
Q

How do we treat breastfeeding jaundice?

A

Continue breastfeeding + formula supplement to help promote bilirubin excretion

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34
Q

What is the patho behind hemolytic jaundice?

A

Hastened breakdown of RBCs (ex: d/t Rh mismatch)

35
Q

Why would underlying liver disease cause hyperbilirubinemia/jaundice?

A

Inability to conjugate bilirubin = hyperbilirubinemia

36
Q

Why is cephalhematoma a risk factor for neonatal hyperbilirubinemia?

A

Bruising at the scalp = RBC breakdown = increased demand for bilirubin metabolism (transitioning infant cannot keep up)

37
Q

How does colostrum promote bilirubin excretion?

A

Enhances GI motility

38
Q

Besides breastfeeding + formula supplements, list 3 other txs for neonatal hyperbilirubinemia.

A
  1. Phototherapy
  2. Exchange blood transfusion
  3. Tx causes of underlying liver disease/hemolytic disease (ex: liver transplant)
39
Q

What is phototherapy? Why is it effective in tx of hyperbilirubinemia?

A

Use of visible light to penetrate skin
Bilirubin absorbs energy > undergoes photoisomerization > forms non-toxic isomers that can be excreted without liver conjugation (hydrophilic)

40
Q

What is the wavelength range for effective phototherapy?

A

400-500 nm

41
Q

What is kernicterus?

A

Brain damage d/t hyperbilirubinemia (>425 umol/L)

42
Q

Describe hemolytic disease of the newborn.

A

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).

43
Q

How do we prevent hemolytic disease of the newborn?

A

2 doses of RhoGAM (Rh immunoglobulin) IM/IV
Once during pregnancy (26-28 weeks)
Once within 72h of delivery

44
Q

Where does bilirubin accumulate in the brain in kernicterus (2)? What do these areas control?

A

Brainstem: HR, breathing, hearing, balance, coordination, reflexes
Basal ganglia: motor control, behaviours, emotions, movement execution

45
Q

List 7 consequences of chronic, severe hyperbilirubinemia.

A
  1. Cerebral palsy (difficulty with movement/coordination)
  2. Oculomotor disturbances in gaze (especially upwards)
  3. Sensory hearing loss
  4. Learning difficulties
  5. Seizures
  6. Coma
  7. Death
46
Q

Define FTT in children.

A

Below expected standards of growth

47
Q

How can we treat organic FTT in infants?

A

Increasing caloric density of formula to >20 kcal/oz or parenteral nutrition

48
Q

Describe the 2 types of hemolytic anemia in children.

A
  1. Intrinsic: inherited; RBCs destroyed d/t a flaw in the RBCs
  2. Extrinsic: RBC destruction is d/t a cause outside of cells
49
Q

List 5 causes of extrinsic hemolytic anemia.

A
  1. Bacteria/viral infection
  2. Meds: abx (ex: penicillin, sulfonamides), malaria meds
  3. Cancers: leukemia, lymphoma, etc.
  4. Autoimmune disorders: lupus (SLE - systemic lupus erythematous), RA (rheumatoid arthritis)
  5. Hypersplenism: spleen destroys more RBCs than normal
50
Q

How does an RBC in sickle cell anemia (Hgb S) differ from a healthy RBC?

A

Hgb S break apart easily & have trouble moving through small capillaries = clots.
Usually die in 10-20 days = anemia.

51
Q

How does the body attempt to adapt to sickle cell disease (SCD)?

A

Increased erythropoiesis (RBC production) + chronic inflammatory state > endothelial activation + enhanced RBC/leukocyte adhesion

52
Q

List 9 s&s of SCD.

A
  1. Pain crises (major symptom)
  2. High risk for stroke, seizures & organ damage
  3. Bacterial infections
  4. Abd pain d/t enlarged spleen
  5. Sensitive to cold d/t increased nociceptor sensitivity from pain crises
  6. Delayed puberty
  7. Swelling of joints
  8. Vision abnormalities
  9. Anemia
53
Q

Explain why we would see pain crises, high risk for stroke/seizures/organ damage and bacterial infections with SCD.

A

Pain crises: when RBCs block blood flow to capillaries

Others: ^ + thromboembolism

54
Q

List 7 treatments for SCD.

A
  1. Hydroxyurea (antineoplastic - cancer drug)
  2. L-glutamine (amino acid)
  3. Pain meds for crises (NSAIDs, opioids)
  4. Bone marrow transplant - helps produce healthy RBCs
  5. Abx (daily prophylactic penicillin)
  6. Regular immunization
  7. Blood transfusions during aplastic crisis
55
Q

Why is hydroxyurea helpful in SCD tx (3)?

A
  • 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
56
Q

Why is L-glutamine helpful for SCD tx (2)

A
  • Reduces disease severity

- Decreases RBC adherence to endothelium (prevent vessel blockage)

57
Q

Why is regular immunization so important for pts with SCD?

A

Prevents bacterial sepsis since their spleen is enlarged and dysfunctional

58
Q

Down syndrome is the presence of an extra chromosome ___ (_____)

A

21 (trisomy)

59
Q

Why do pts with down syndrome require life-long, multidisciplinary care? (7)

A
  1. Hearing loss & vision abnormalities
  2. Obstructive sleep apnea (d/t tongue)
  3. Ear infections d/t shorter ear canal
  4. Eye diseases
  5. Heart defects present at birth (VSDs, AVSDs, pulmonary HTN)
  6. Thyroid abnormalities
  7. GERD & other
60
Q

List the 3 tx for GERD in a down syndrome pt.

A
  1. Losec (Omeprazole) + high dose Prevacid (Lansoprazole) - PPI
  2. Pepcid (Famotidine), Zantac (Ranitidine) - H2 blocker
  3. Antacids
    * Compound meds d/t difficulties swallowing.
61
Q

List 2 tx for pulmonary HTN in down syndrome pts.

A
  1. Sildenafil (Viagra) - PDE5 (phosphodiesterase type 5) inhib
  2. Dilation of pulmonary arteries
62
Q

Define eczema.

A

Itchy, inflamed skin disorder

63
Q

Describe the s&s of eczema in the acute and chronic stages.

A

Poorly defined erythema with edema, vesicles and weeping in the acute stage.
Lichenification (thickened, pebbly skin d/t trauma) chronically.

64
Q

What type of sensitivity reaction is eczema? Which immunoglobulin mediates it?

A

Type I hypersensitivity - IgE

65
Q

What happens when antibodies are released in the presence of an allergen?

A

Mast cell degranulation + histamine/other inflammatory mediator release

66
Q

List 5 possible manifestations of eczema.

A
  1. Nasal allergic reactions.
  2. Ocular allergic reactions.
  3. Erythema.
  4. Asthma.
  5. Peripheral vasodilation.
67
Q

Eczema tx targets these 4 underlying abnormalities:

A
  1. Dryness
  2. Pruritus
  3. Infection
  4. Inflammation
68
Q

List 5 tx for eczema.

A
  1. Emollients (ex: Glaxal base) - tx dry skin.
  2. Topical corticosteroids (ex: hydrocortisone cream/ointment - 0.5-1% only) - tx skin inflammation.
  3. Bronchodilators (beta agonists ex: albuterol) via inhaler - tx bronchospasm.
  4. Antihistamines PO (H1 - diphenhydramine; H2 - famotidine/ranitidine) - adjunct tx for hives/pruritis.
  5. Desensitization therapy
69
Q

Why shouldn’t you scratch areas affected by eczema (2)?

A
  1. Causes scarring of the dermis layer.

2. Can introduce Staph aureus infection.

70
Q

What is the tx for Staph aureus infections with eczema (2)?

A
  1. Bleach baths

2. Intranasal mupirocin ointment

71
Q

When does childhood iron deficiency anemia (IDA) peak in prevalence? Why?

A

Toddler years (1-3 y/o) d/t nutritional factors (ex: picky eating, not eating foods with highly bioavailable iron)

72
Q

Why are children younger than 2 at particularly high risk for IDA?

A

Rapid growth + inadequate dietary iron

73
Q

List 3 s&s of childhood IDA.

A
  1. Irritability.
  2. Poor appetite.
  3. Pallor: conjunctiva, tongue, palms, nailbeds.
74
Q

If a child’s IDA is severe, their s&s may resemble the s&s of:

A

CHF: fatigue, tachypnea, hepatomegaly, edema.

75
Q

Which 3 neurotransmitters are impacted by decreased brain iron stores in IDA? Why?

A
  1. Dopamine.
  2. Serotonin.
  3. NE.
    They all require iron-dependent enzymes to be synthesized.
76
Q

List 6 recommendations to prevent childhood IDA.

A
  1. Bottles should be discontinued by 12-15 months or earlier.
  2. Infants should not be put to sleep with a bottle.
  3. Introduce iron-rich/fortified foods into the diet (ex: meat/meat alternatives, iron-fortified cereal).
  4. Provide iron supplements.
  5. Limit cow’s milk consumption (500-750 mL/day).
  6. Blood transfusions (severe cases).
77
Q

Where is Vitamin D3 (cholecalciferol) found (2)?

A
  1. Made in the skin.

2. In oily fish, egg yolks & fortified food.

78
Q

Where is Vitamin D2 (ergocalciferol) found?

A

Fortified foods, salmon, mushrooms & egg yolks.

79
Q

Which 2 organs (in order) contribute to the metabolism of VitD?

A

Liver first, then kidneys.

80
Q

Vit D helps the body absorb and retain _____ and _____, which are critical for building ___.

A

Calcium & phosphorus.

Bone.

81
Q

List 3 outcomes of chronic/severe pediatric Vit D deficiency.

A
  1. Irritability.
  2. Developmental delays.
  3. Nutritional rickets: pain, softening & fractures of bone d/t inadequate mineralization.
82
Q

How much Vit D do peds need to be supplemented throughout the year?

A

Summer months: 400 I.U.

Winter months: 800 I.U.

83
Q

Vit D toxicity results in _________, which would have the following 6 s&s:

A

Hypercalcemia.

  1. Kidney stones.
  2. Renal insufficiency.
  3. GI upset.
  4. Headaches.
  5. Arrhythmias.
  6. Muscle pain.

N216 A/B (26 decks)

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