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Pediatrics Flashcards

1
Q

When to suggest a chromosomal abnormality:

A

◦Facial dysmorphia
◦Intellectual deficiency
◦Delayed motor development
◦Malformation of several organs (CNS, face, fingers, heart)
◦In utero growth retardation

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2
Q

Autosomal aneuploidy can cause

A

Downs syndrome
Patau syndrome
Edwards syndrome

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3
Q

sex chromosome aneuploidy can cause

A

Turner syndrome
Kleinfelder syndrome

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4
Q

structural aberrations can cause

A

Cri-du-chat syndrome
Angelman syndrome
Prader-Willi syndrome
DiGeorge syndrome
Williams syndrome

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5
Q

cause of Down syndrome

A

Trisomy 21 - 47 chromosome instead of normal 46

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6
Q

cause of Patau-syndrome

A

Trisomy 13 - 47 chromosome instead of normal 46

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7
Q

Cause of Edwards syndrome

A

Trisomy 18 - 47 chromosome instead of normal 46

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8
Q

Cause of Turner syndrome

A

Absent X chromosome - 45 chromosomes instead of normal 46
Only viable monosomy

*moisacism is possible !

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9
Q

Cause of Klinefelter syndrome

A

Male with extra X chromosome - 47 chromosome instead of normal 46

XXY

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10
Q

Cause of Cri-du-chat syndrome

A

Terminal deletion of chromosome 5

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11
Q

Cause of Angelman syndrome

A

Deletion + imprinting of chromosome 15 (UBE3A)
Mothers’ gene is silenced

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12
Q

Cause of Prader-Willi syndrome

A

Deletion + imprinting of chromosome 15 (SNRPN)
Mothers’ gene is silenced

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13
Q

Cause of Di George syndrome?

A

Interstitial deletion on chromosome 22

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14
Q

Cause of Williams syndrome?

A

Interstitial deletion on chromosome 7

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15
Q

Cause of respiratory distress syndrome in neonates?

A

Surfactant deficiency - alveolar collapse - loss of lung compliance - increased WOB - hypoxia - IntraPulmonary shunting

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16
Q

Acute neonatal respiratory diseases?

A

Transient tachypnea of the newborn (TTN)
Congenital pneumonia
Meconium aspiration syndrome (MAS)
Milk aspiration

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17
Q

Define newborn

A

< 1 month

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18
Q

Define infant

A

< 1 year

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19
Q

Define toddler

A

< 3 years

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20
Q

Define child

A

> 3 years

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21
Q

Perinatal period

A

week 22 of gestation to 7th day after birth

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22
Q

Define term birth

A

week 37-42

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23
Q

Define early term infant

A

week 37-38

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24
Q

Define full term infant

A

week 39-40

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25
Q

Define late term infant

A

week 41-42

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26
Q

Define preterm infant

A

live birth between seek 20-36

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27
Q

Define postterm birth

A

live birth after week 42 of gestation

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28
Q

tree classifications of birth weight?

A

Appropriate for gestational age
Small for gestational age
Large for gestational age

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29
Q

Define late uterin death

A

after week 24

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30
Q

Define early neonatal deaths

A

within the first week after delivery

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31
Q

most common cause of early neonatal death in developing countries

A

infections

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32
Q

Neonatal mortality rate

A

3/1000 live births before day 28

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33
Q

leading causes of death before the age of 1 year

A
  1. congenital abnormalities
  2. preterm birth and LBW
  3. sudden infant death syndrome
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34
Q

limit between defining stillbirth or abortion?

A

week 20

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35
Q

Apgar score timing?

A

1 and 5 minutes after birth

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36
Q

when to start resuscitation at birth?

A

if onset of respiration has not stared within 20-60 secs

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37
Q

normal weight of newborn?

A

2.7-4 kg

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38
Q

what is the physiological weight loss the first 10 days of life?

A

max 10%

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39
Q

normal weight gain for an newborn?

A

150-250g/week

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40
Q

weight gain at 6 months and 1 year?

A

double bw at 6 months
triple bw at 1 year

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41
Q

normal length of newborn

A

47-53cm

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42
Q

normal increase in length of newborn

A

2cm/month
50% increase at 12 months

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43
Q

Normal head circumference of newborn

A

33-35cm

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44
Q

Normal chest circumference of newborn

A

30-33cm

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45
Q

newborn HR and RF

A

Respiratory rate: 40–60 breaths per minute
Heart rate: 70–190 beats per minute

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46
Q

fontanelle closure

A

posterior 2-3 months
anterior 1.5-2 years

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47
Q

first urine and meconium passage

A

urine within 24h
meconium within 48h

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48
Q

APGAR stands for?

A

really: the doctor that came up with it but also
Appearance
Pulse
Grimace
Activity
Respiration

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49
Q

APGAR scoring numbers

A

7-10 reassuring
4-6 moderately abnormal
0-3 low

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50
Q

Regular medical check-ups (0-3 days (neonatology department)

A

◦Apgar score
◦Major/minor deformities
◦PKU testing & other metabolic diseases: Guthrie test(26 metabolic disease))
◦Audiology screening: BERA test Brain Evoked Response Auditory (for congenital deafness)
◦Ophthalmology screening: red reflex test
◦Physical hip check: Barlow & Ortolani test
◦Cardiology screening: 4 limb pulse oximetry

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51
Q

Regular medical check-ups ( <10 days (1st visit at home)

A

◦Feeding
◦Increased weight
◦Jaundice (—> can cause somnolence —> trouble eating and drinking/thriving)

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52
Q

Regular checkup times?

A

1 , 2 , 3 , 4 , 6 , 9 , 12 ,15 , 18 months, >2 year annually

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53
Q

Normal percentage of newborns?

A

3-97%

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54
Q

Milestones at 2 months

A

Raises head and chest
Recognizes mothers voice
Social smile

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55
Q

Milestones at 4 months

A

Shakes rattle
Holds head
Rolls from front to back
Laughs

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56
Q

Milestones at 6 months

A

Sits without support
Transferes objects from hand to hand
Stranger anxiety
Babbles

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57
Q

Milestones at 9 months

A

Starts crawling
Separation anxiety
Babbles (baba, mama)
Pincer grasp

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58
Q

Milestones at 12 months

A

Starts to walk
Points at objects
Knows 1-2 words
Follows simple commands

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59
Q

ratio of head height and body length

A

Newborn 1:4
Infant 1:6
Adult 1:7

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60
Q

whats bad about formula feeding

A

No AB
Based on cow milk (allergy)
to much Casein

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61
Q

hen to introduce solid foods

A

4-6 months

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62
Q

stomach capacity of newborn

A

◦1 day: 5-7 ml (bead)
◦3 days: 22-27 ml (nut)
◦1 week: 45-60 ml (seed in an apricot)
◦1 month: 80-150 ml (egg)

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63
Q

amount of feeding

A

Newborn: every 3 hours, 8 times daily
‣ 1-3 months: approx. 150 ml/kg
‣ 3-6 months: approx. 120 ml/kg
Above 6 months: 5-6 times daily
‣ 200-250 ml/feeding

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64
Q

feeding of a premature?

A

Not yet developed sucking, breathing and swallowing for feeding so IV or feeding tube is used

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65
Q

mandatory vaccinations

A

‣ 0-4 weeks: BCG (tuberculosis)
‣ 2 months: Pentaxim (DTPa + IPV + Hib) + Prevenar13 (pneumo)
‣ 3 months: Pentaxim (DTPa + IPV + Hib)
‣ 12 months: Prevenar 13 (pneumococcus)
‣ 13 months: Varivax (varicella)
‣ 15 months: MMR (measles, mumps, rubella)
‣ 16 months: Varivax (varicella)
‣ 18 months: Pentaxim (DTPa + IPV + Hib)
‣ 6 years: Tetraxim (DTPa + IPV)
‣ + school vaccinations

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66
Q

vitamin supplementation in newborns

A

Vitamin K orally 2 mg 1/week
Vitamin D from 2w 1 drop/day

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67
Q

pathophysiology of respiratory distress in infants?

A

a) Surfactant deficiency
b) alveolar collapse
c)increased WOB
d) hypoxia

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68
Q

Etiology of respiratory distress in infants?

A

C-section
Hypothermia
Perinatal hypoxia
Meconium aspiration
Congenital pneumonia
Maternal diabetes
Past family history

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69
Q

Physiological Spo2 for neonates

A

Physiologic O2 saturation in neonates is around 90%. A saturation of 100% is considered toxic for neonates!

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70
Q

Treatment of RDS in neonates

A
  1. Nasal CPAP with a PEEP of 3–8 cm H2O
    (If persists, start intubation with mechanical ventilation)
  2. Endotracheal artificial surfactant within 2 hours postpartum
  3. IV fluid replacement; stabilization of blood sugar and electrolytes
  4. AB: if congenital pneumonia
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71
Q

Prevention of RDS in neonates

A

give CS (dexa) to mother 1-7 days before delivery

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72
Q

What can cause acute neonatal respiratory disease?

A
  1. Transient tachypnea of the newborn (TTN)
  2. Congenital pneumonia
  3. Meconium aspiration syndrom (MAS)
  4. Milk Aspiration
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73
Q

Define transient tachypnea of the newborn (TTN)

A

Delayed clearance of lung fluid after birth
(presents within 4h and spontaneously resolves within 24h)

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74
Q

Cause of congenital pneumonia

A

Aspiration of infected AF
(GBS, E.coli, listeria, chlamydia)

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75
Q

Define persistent pulmonary hypertension of newborn (PPHN)

A

closed pulmonary circulation after birth

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76
Q

Pathophysiology of meconium aspiration syndrome

A

a) Hypoxia results in gasping + meconium passage in utero
b) Aspiration of meconium
c) Inhibits surfactant + obstructs respiratory tract
d) Induce pneumonitis

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77
Q

Prevention of meconium aspiration syndrome

A

if AF is meconium-stained then delivery should be induced

if baby apnoic then visualize larynx and suck out meconium.

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78
Q

Cause of milk aspiration induced acute neonatal respiratory disease

A

Swallowing incoordination (neurological, preterm)
Upper airway disorder
Esophageal disorder (GERD/fistula)

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79
Q

what are the routs of acquiring neonatal infections?

A
  1. Transvaginal
  2. Transplacental
  3. During birth- INTRAPARTUM
  4. postnatal from environment
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80
Q

two categorize of neonatal infections

A

early onset infection < 48h postpartum
late onset infection >48h postpartum

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81
Q

Risk factors for early-onset neonatal sepsis:

A

‣ Prolonged rupture of membranes PROM(>18h), especially if preterm
‣ Signs of maternal infection
‣ Vaginal carriage or previous infant with GBS
‣ Preterm labor, fetal distress
‣ Skin and mucosal breaks

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82
Q

Pathogens causing early neonatal infections

A

GBS (usually)
E. Coli
Listeria
Herpes virus
H. Influenza
Candida
Chlamydia trachomatis

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83
Q

Diagnosis og neonatal infections

A
  1. Blood culture
  2. CBC
  3. CSF
  4. Chest x-ray
  5. CRP but diagnostic value of CRP in early neonatal sepsis
    is unclear
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84
Q

Broad spectrum AB?

A

Penicillin
Gentamicin
Flucloxacillin
Ampicillin/amoxicillin if Listeria

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85
Q

AB in meningitis

A

Cefotaxime +/- Ampicillin/amoxicillin

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86
Q

Risk factors for late-onset neonatal sepsis

A

‣ Central lines and catheters
‣ Congenital malformations, eg spina bifida
‣ Severe illness, malnutrition, immunodeficiency

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87
Q

Diagnosis of late onset neonatal infection

A
  1. Blood culture
  2. CBC
  3. Uranalysis (clean catch)
  4. urine culture
  5. CSF glucose (low in infection)
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88
Q

what AB to give in coagulase negative staph

A

vancomycin

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89
Q

transplacental congenital infection pathogens?

A

TORCH
Toxoplasmosis
Others (e.g., syphilis, varicella, parvovirus B19 infection, listeriosis, enterovirus, HIV, hepatitis B, rarely bacterial; GBS, N. Gonorrhoeae)
Rubella
Cytomegaly (CMV)
Herpes simplex virus (HSV) infection

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90
Q

Common findings in TORCH infections in neonates

A

Hepatosplenomegaly
Jaundice
Lethargy
Growth retardation
Thrombocytopenia

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91
Q

syphilis treatment

A

Benzylpenicillin

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92
Q

Toxoplasmosis treatment

A

Spiramycin alternating with pyrimethamine + Sulfadiazin

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93
Q

Normal total serum bilirubin level

A

0,1-1,2 mg/dL

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94
Q

two classifications of neonatal jaundice

A
  1. Physiological
  2. Pathological
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95
Q

Type of hyperbilirubinemia in physiological jaundice

A

Always unconjugated

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96
Q

Type of hyperbilirubinemia in pathological jaundice

A

can be both conjugated or unconjugated

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97
Q

Onset of hyperbilirubinemia in pathological vs physiological jaundice

A

Physiological: > 24 hours after birth
Pathological: can present < 24 hours after birth

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98
Q

Peak bilirubin level in hyperbilirubinemia - pathological vs physiological jaundice

A

Physiological < 15 mg/dL
Pathological can rise to > 15 mg/dL

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99
Q

Daily rise in bilirubin levels in hyperbilirubinemia - pathological vs physiological jaundice

A

Physiological < 5 mg/dL/day
Pathological > 5 mg/dL/day

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100
Q

Etiologi of neonatal physiological jaundice

A

Hemolysis of fetal hemoglobin and an immature hepatic metabolism of bilirubin

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101
Q

Etiologi of Pathological hemolytic unconjugated hyperbilirubinemia

A

Hemolytic disease of the newborn ( ABO or Rh incompatibility)
Erythrocyte enzyme defects (G6PD deficiency, PKA deficiency)
Erythrocyte membrane defects (e.g., hereditary spherocytosis)
Hemoglobinopathies (e.g., sickle cell anemia, thalassemias)
Hematomas (vacuum delivery, vitamin K deficiency bleeding)
Infection/sepsis
Polycythemia

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102
Q

Etiologi of Pathological Non-hemolytic unconjugated hyperbilirubinemia

A
  • decreased conjugation of bilirubin:
    Gilbert syndrome
    Crigler-Najjar syndrome
    Deficiency of UDP-glucuronosyltransferase
    Hypothyroidism
  • decreased stool passage ; increased enterohepatic circulation of bilirubin:
    GI obstruction
    Hirshprung disease
    CF
    breastfeeding jaundice
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103
Q

Etiology of pathological conjugated hyperbilirubinemia - intrahepatic

A
  • decreased excretion of bilirubin:

Alagille syndrome [4]
TORCH infections
Dubin-Johnson syndrome [3] ( ABCC2 gene, bile collects in liver)

Sepsis
Idiopathic neonatal hepatitis
Alpha-1-antitrypsin deficiency
Cystic fibrosis
Galactosemia
Hypothyroidism
Medication

  • decreased hepatic uptake of bilirubin:
    Rotor syn (defect in gene encoding transport protein)
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104
Q

Etiology of pathological conjugated hyperbilirubinemia - extrahepatic

A

Biliary atresia
Biliary/choledochal cyst
Tumors/strictures

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105
Q

Treatment of neonatal jaundice

A

Phototherapy (primary treatment)
Exchange transfusion
IV immunoglobulins

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106
Q

Complications of prematurity?

A
  • Bronchopulmonary dysplasia (BPD)
  • Retinopathy of preterm infants (ROP)
  • Necrotizing enterocolitis (NEC)
  • Intraventricular hemorrhage (IVH)
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107
Q

Bronchopulmonary dysplasia (BPD)

A

Pulmonary barotrauma and oxygen toxicity with subsequent inflammation of lung tissue due to
ventilation of the immature lung (ventilation for more than 28 days)

seen in NRDS

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108
Q

Retinopathy of preterm infants (ROP)

A

retinal vascularization may be incomplete in premature infants and therefore continue after birth
—> elevated and fluctuating partial pressures of oxygen
—> pathological extraretinal
neovascularization
—> hemorrhages, formation of fibrovascular membranes, and in severe cases: retinal detachment

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109
Q

Necrotizing enterocolitis (NEC)

A

Dangerous hemorrhagic inflammation of the intestinal wall that
most often affects premature infants

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110
Q

Intraventricular hemorrhage (IVH)

A

Immaturity of basal lamina + lack of astrocytic protein leads to abnormal cerebral autoregulation

alteration in infants BP (eg. during birth)
–> failure of cerebral autoregulation to compensate BP change
–> cause rupture of and bleeding from vessels in the germinal matrix and rupture of ependyma
—> blood flows into ventricles

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111
Q

typical symptoms of intraventricular hemorrhage in children?

A

Most children are asymptomatic
Lethargy .Hypotonia
Irregular respiration
Seizures
Bulging anterior fontanelle (increased ICP)
Cranial nerve abnormalities

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112
Q

countries with highest and lowest rates of SIDS

A

◦Highest rate: New Zealand, US, Argentina
◦Lowest rate: Netherlands, Japan, Sweden

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113
Q

Prevention of SIDS

A

‣ Infant should be placed in supine (on back) for sleeping
‣ Safe sleep environment: firm mattress, no pillows
‣ In first 6 months, co-sleeping without bed-sharing
‣ No second-hand smoking and overheating during sleeping
‣ Breastfeeding until 4-6 months
‣ Tummy time: when playing baby should be in prone position
‣ Immunization in line with the official schedule

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114
Q

SSS in children BLS

A

Safety
Stimulate
Shout for help

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115
Q

Child defibrillation strength?

A

4 J/kg

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116
Q

Children BLS adrenalin dose

A

10 mcg/kg

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117
Q

Children BLS amiodarone dose

A

5 mg/kg
Max 300mg

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118
Q

Meconium ileus?

A

Failure to pass the first stool in neonates (meconium usually passes within the first 24–48 hours after birth)

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119
Q

Clinical findings in meconium Ileus

A

Bilious vomiting
Abdominal distention
No passing of meconium or stool

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120
Q

Meconium ileus treatment

A

Enema with a contrast agent (injection of fluid to empty)
Surgery is required if complications (intestinal perforation, volvulus)

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121
Q

Intestinal atresia

A

Congenital defect that can occur at any point along the GI tract leading to complete (atresia) or incomplete (stenosis) occlusion of the affected lumen

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122
Q

clinical findings in intestinal atresia

A

Intrauterine: polyhydramnios
Postpartum: signs of intestinal obstruction
- Abdominal distention
- Bilious vomiting
- Failed or delayed meconium passage

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123
Q

common types of intestinal atresia

A

Duodenal atresia
Jejunal atresia

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124
Q

what disease is intestinal atresia commonly ass. with?

A

chromosomal anomalies like downs syndrom

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125
Q

X-ray sign of meconium ileus

A

Neuhauser sign: bubble like appearance in distal ileum from mixed meconium and swallowed air
X-ray abdomen (with contrast agent)
* Dilated small bowel loops
* Microcolon: narrow caliber of the colon, as it is still unused (meconium has not been passed through yet)
*because of the viscous consistency of meconium>missing air fluid level)

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126
Q

X-ray sign of intestinal atresia?

A

Double bubble sign (air in stomach and duodenum)

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127
Q

Pyloric stenosis

A

Hypertrophic pyloric stenosis, the most common cause of gastric outlet obstruction in infants, is characterized by hypertrophy and hyperplasia of the pyloric sphincter in the first months of life.

0.5-5/1000
more in boys
due to nicotine, bottle feeding, macrolide

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128
Q

clinical presentation of pyloric stenosis

A

Usually develop between 2nd and 7th week of age
Frequent regurgitation progressing to projectile, nonbilious vomiting immediately after feeding
Enlarged, thick, olive-shaped, nontender pylorus (diameter of 1–2 cm) should be palpable in the epigastrium
A peristaltic wave, moving from left to right, may be evident in the epigastrium
“Hungry vomiter”: demands re-feeding after vomiting

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129
Q

imaging sign in pyloric stenosis

A

Beak sign: distended stomach and narrow pyloric

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130
Q

Congenital diaphragmatic hernias

A

Common developmental defect, resulting from an incomplete fusion of embryonic components of the diaphragm.

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131
Q

Types of diaphragmatic hernias

A

Left-sided postero-lateral diaphragmatic defects (Bochdalek hernias) are the most common.
Anterior defects (Morgagni hernias).
50% of babies with CDH have additional congenital malformations.

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132
Q

clinical presentation of congenital diaphragmatic hernias

A

Depends on degree of pulmonary hypoplasia and HT
Respiratory distress
Barrel-shaped chest, scaphoid abdomen
Auscultation of bowel sounds in the chest
Absent breath sounds on the ipsilateral side
Mediastinal shift: shift of heart sounds to the right side

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133
Q

what is the most common etiology of meconium ileus?

A

cystic fibrosis

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134
Q

Define intussusception?

A

when a proximal part of the bowel invaginates into the distal part causing mechanical obstruction and ischemia

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135
Q

when does intussusception normally happen?

A

2 months to 2 years

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136
Q

Clinical presentation of intussusception

A

Child typically looks healthy.
Acute cyclical colicky abdominal pain
Acute attacks occur approx. every 15–30 min.
Vomiting (initially nonbilious)
Abdominal tenderness
Palpable sausage-shaped mass in the RUQ
High-pitched bowel sounds on auscultation
“Currant jelly” stool: Dark red stool (resembling currant jelly)
Lethargy , pallor or other symptoms of shock may be present

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137
Q

US findings in intussusception

A
  1. Target sign: invaginated part looks like rings on a target
  2. Pseudo- kidney sign: lead point of invagination looks like kidney
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138
Q

What is Hutchinson maneuver in intussusception?

A

surgical intervention with manual proximal compression and reduction of bowel, resection + end to end anastomosis

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139
Q

Define Volvulus

A

twisting of a bowel on its mesentery almost always due to midgut volvulus as a result of intestinal malrotation

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140
Q

Clinical presentation of volvulus

A

Bilious vomiting with abdominal distension in a neonate/infant
Signs of bowel ischemia: hematochezia, hematemesis, hypotension, and tachycardia

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141
Q

Define incarcerated hernia

A

content of hernial sac cannot return back through the abdominal wall

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142
Q

symptoms of mechanical bowel obstruction

A

sudden onset of pain, nausea, vomiting, abdominal distention, constipation or obstipation

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143
Q

labs in appendicitis

A

CPR > 10 mg/L
WBC > 16.000/mL

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144
Q

common causes of obstipation in children

A
  1. Congenital intestinal atresia
  2. Intussusception
  3. Congenital structures like Ladd bands attach cecum to peritoneum and liver in intestinal malrotation
  4. Hirschsprung disease
  5. Meconium ileus
  6. Rectal atresia
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145
Q

Define Hirschsprung disease

A

Defective caudal migration of parasympathetic neuroblasts (precursors of ganglion cells) from the neural crest to the distal colon. This process takes place between the 4th and 7th week of development.

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146
Q

pathophysiology of Hirschsprung disease

A

Inability of the myenteric plexus to control the intestinal wall muscles → uncoordinated peristalsis and slowed motility
Spastic contraction of intestinal muscles → stenosis and functional obstruction
Expansion of the colon segment proximal to the aganglionic section (possible megacolon)

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147
Q

Associated diseases to Hirschsprung disease

A

Downs syndrom
Multiple endocrine neoplasm 2 (MEN2)
Waardenburg syndrome
Neuroblastoma

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148
Q

Extent of Hirschsprung disease

A

Ultra-short segment: limited to distal rectum
Short-segment: limited to the rectosigmoid (80% of cases)
Long-segment: Distal colon up to the splenic flexure (10% of cases)
Total colonic: entire colon (3–8% of cases)

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149
Q

Define testicular torsion

A

Sudden twisting of the spermatic cord within the scrotum

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150
Q

at what age does most commonly testicular torsion happen

A

First 30 days of life
At puberty (10-14 years)

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151
Q

Is testicular torsion a medical emergency?

A

yes due to risk of ischemia and possible infarction of testis

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152
Q

When is testicular torsion a irreversible damage?

A

6-12h after torsion

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153
Q

Clinical feauters of testicular torsion

A

Abrupt onset of testicular pain and/or pain in the lower abdomen
Typically swollen/tender testis and/or lower abdominal tenderness
Nausea and vomiting
Negative Prehn sign
In neonates: possible absent testis

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154
Q

What is Prehn sign?

A

Elevation of the scrotum relives testicular pain
This sign is negative in testicular torsion and positive in epididymitis

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155
Q

Diagnosis of testicular torsion

A

Duplex US of the scrotum

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156
Q

Define ovarian torsion

A

Sudden twisting of ovary around the adnexal ligaments

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157
Q

when does ovarian torsion normally happen?

A

women of childbearing age

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158
Q

is ovarian torsion an medical emergency?

A

yes, due to risk of ischemia and ovarian necrosis

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159
Q

Define cryptorchidism

A

Failure of one or both testicles to descend to their natural position in the scrotum

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160
Q

Risk factor of cryptorchidism

A

Prematurity
Low birth weight

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161
Q

clinical features of cryptorchidism

A

Clinical features
Palpable (80% of cases): testicle cannot be manually manipulated into the scrotum
Non-palpable: may be intra-abdominal or absent

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162
Q

Treatment of cryptorchidism?

A

Typically resolves on its own
Surgery: Orchidoplexy

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163
Q

Classification of hemostasis and bleeding disorders

A

Primary hemostasis (when caused by a platelet abnormality), Secondary hemostasis (when caused by defects in the extrinsic and/or intrinsic pathway of the coagulation cascade)
Hyperfibrinolysis (when there is increased clot degradation)

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164
Q

What are coagulopathies, name diseases

A

Disorders of secondary homeostasis
Von Willebrand disease
Hemophilia
Vitamin K deficiency

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165
Q

Name primary homeostasis disorders

A

Thrombocytopenia

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166
Q

Von Willebrand disease types?

A

Type 1 AD decreased level (most common)
Type 2 AD decrease in function
Type 3 AR causing complete absence

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167
Q

Define hemophilia

A

Hereditary blood-clotting disorder (XR)

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168
Q

Types of hemophilia

A

Hemophilia A: low levels of clotting factor 8
Hemophilia B: low levels of clotting factor 9

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169
Q

Clinical features of Von Willebrand

A

Frequent nose bleeds
Easy brusing
Bleeding gums
Menorrhagia (>7 days)

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170
Q

Clinical features of Hemophilia

A

Large cephalohematoma
Easy brusing, swelling
Heavy bleedingfrom cuts and surgery
hemarthosis

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171
Q

what deficiency does lack of Vit K lead to?

A

Factors 2, 7, 9, 10

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172
Q

define thrombocytopenia with numbers

A

Thrombocytes < 150 GL

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173
Q

Types of anemia

A

Microcytic hypochromic anemia
Normocytic normochromic anemia
Macrocytic anemia

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174
Q

Hemoglobin levels in certain ages
anemic levels

A

Newborn 180-200 g/l (like a professional athlete)
3 months < 100 g/l
6 months - 5 years < 110 g/l
6-14 years < 120 g/l
Adult women <120 g/l
Adult men < 140 g/l

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175
Q

Microcytic hypochromic anemia
value

A

MCV < 75 fL
MCH < 25pg

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176
Q

Normocytic normochromic anemia

A

MCV 75-90 fL
MCH < 27 pg

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177
Q

Macrocytic anemia

A

> 90 fL

178
Q

Neonatal sepsis definition?

A

Sepsis occur < 28 days
Early onset < 7 days after delivery
Late onset > 7 days after delivery

179
Q

pathogenesis of early onset neonatal sepsis

A

Vertical transmission (vaginal flora, chorioamnionitis)

180
Q

pathogenesis of late onset neonatal sepsis

A

Horizontal transmission (environment)

181
Q

pathogens most commonly causing neonatal sepsis

A

GBS
E. Coli
Listeria
Herpes virus
Enterovirus
Candida albicans

182
Q

clinical features of neonatal sepsis

A

Apgar < 6 points
Meconium-stained liquor (amniotic fluid)
Fever, irritability, seizures
Tachycardia, poor peripheral perfusion, hypotension, cyanosis
Dyspnea
PPHN (persistent pulmonary hypertension
Lethargy, poor feeding, vomiting
Jaundice, hepatomegaly,
abdominal distension, diarrhea

183
Q

AB in meningitis

A

Ampicillin
Cefotaxime
Ceftriaxone
Meropenem (if multidrug resistant)

184
Q

AB in pneumonia

mild vs severe
< 5 yr
> 5 yrs

A

MILD
<5yrs : amoxicillin , erythromycin, azithromycin, clarithromycin

> 5yrs : macrolides (usually atypical)

severe:
0-6m> cefotaxime + ampicillin

> 6m : 2,3 gen cephalosporin: cefuroxime, cefotaxime +macrolide

185
Q

AB in skin, soft tissue, bone infection

A

Vancomycin

186
Q

AB in catheter related infections

A

Vancomycin
Gentamycin

187
Q

8 subtypes of herpes virus

A

HHV-1: Herpes simplex virus 1 (HSV-1)
HHV 2: Herpes simplex virus 2 (HSV2)
HHV 3: Varicella zoster virus (VZV)
HHV 4: Epstein-Barr virus (EBV)
HHV 5: Cytomegalovirus (CMV)
HHV 6 + HHV 7: (roseolae)
HHV 8: Kaposi’s sarcoma associated virus (KSHV)

188
Q

HHV 1 disease and treatment

A

Herpes labialis (cold sores)
◦Treatment: antivirals (acyclovir

189
Q

HHV 2 disease and treatment

A

Genital herpes,
viral meningitis,
neonatal herpes simplex

◦Treatment: antivirals (acyclovir)

190
Q

HHV 3 disease and treatment

A

Primary infection —> chickenpox (varicella)
Secondary infection —> shingles (zoster)
◦Treatment: vaccinations

191
Q

HHV 4 disease and treatment

A

Infectious mononucleosis
‣ Highly contagious acute condition w/ lymphocyte proliferation
‣ Presents as fever, malaise, fatigue —> later develop
acute pharyngitis, tonsillitis, lymphadenopathy, splenomegaly

◦Treatment:
symptomatic
avoid physical activity that may trigger splenic rupture (eg contact sports) for at least 3 weeks

192
Q

HHV 5 disease and treatment

A

◦Cytomegalovirus infection
‣ Typically asymptomatic in immunocompetent patients, but can cause mononucleosis-like symptoms

‣ In immunocompromised patients it can cause localized disease (rhinitis, colitis, encephalitis) and severe systemic disease
◦Treatment: antivirals (ganciclovir, foscarnet, fomivirsen)

193
Q

HHV 6 and 7 disease and treatment

A

◦Roseola infantum
‣ Viral exanthematous infection that mainly affects babies
‣ Characterized by high fever, followed by sudden appearance of
maculopapular rash on trunk that sometimes spreads to face
nd extremities, fading within two days
◦Treatment: self-limiting

194
Q

HHV 8 disease and treatment

A

Kaposi sarcoma
‣ Malignant spindle cell tumor that originates from endothelial cells, mostly in immunocompromised
‣ Cause solitary or multiple nodular purplish/blue-violet/ reddish-brown submucosal, skinless plaques
◦Treatment: treat immunocompromised state (eg antiretrovirals in HIV patients)

195
Q

Define measles

A

Measles (Rubeola) is a highly infectious disease that is caused by the measles virus.

196
Q

measles transmission

A

direct contact or inhalation of virus

197
Q

Phases of measles disease?

A
  1. Catarrhal/prodromal stage:
    fever
    conjunctivitis
    coryza (rhinitis)
    cough
    pathognomonic Koplik spots on buccal mucosa
  2. Exanthem stage:
    high fever, malaise,
    exanthem (erythematous maculopapular rash) that originates behind ears and spreads to rest of body
198
Q

Measles treatment

A

Symptomatic treatment
Vitamin A supplementation reduces morbidity and mortality (especially in malnourished children).
PEP in patients without prior vaccination (post-exposure prophylaxis) immunoglobin or vaccine (within 72 hr)

199
Q

what does a measles biopsy show?

A

Lymph Nodes show paracortical hyperplasia and warthin-Finkeldey cells (Multinucleated giant cells)

200
Q

Transmission of Rubella

A

Respiratory droplets
Transplacental

201
Q

Phases of rubella

A

A) Prodromal stage:
post-auricular + suboccipital lymohadenopathy,
low-grade fever,
mild sore throat,
conjunctivitis,
headache, aching joints, dermatological findings on soft palate

B. Exanthem stage:
fine + nonconfluent + pink maculopapular rash (originates behind ears and extends to trunk and extremities,
sparing palms and soles), polyarthritis

202
Q

Scarlet fever

A

Scarlet fever is a syndrome caused by infection with toxin-producing group A β‑hemolytic streptococci (Streptococcus pyogenes, GAS)
and primarily affects children between the ages of 5 and 15.

203
Q

Phases of scarlet fever

A

Initial stage/acute tonsillitis

Exanthem stage (12-48 hrs after fever onset) maculopapular exanthem

Tonsillopharyngitis : strawberry tongue

Desquamation phase (7-10 days after resolution of rash)

204
Q

Systemic autoimmune diseases

A

Pediatrics Rheumatology
Juvenile Idiopathic Arthritis
Systemic lupus Erythematosus
Scleroderma

205
Q

Types of juvenile idiopathic arthritis? (JIA)

A

Oligoarticular JIA
Seronegative polyarticular JIA
Seropositive polyarticular JIA
Systemic JIA
Psoriatic JIA
Enthesitis JIA

206
Q

Pathophysiology of JIA

A

a) Autoimmune and/or autoinflammatory disease
b) Chronic synovial inflammation with infiltration of plasma cells, B cells, T cells
c) Joint capsule hyperplasia
d) Growth of fibrovascular connective tissue (pannus)
e) Invasion of the articular surface
f) Loss of joint function/movement

207
Q

allergy skin symptom

A

urticaria, angioedema

208
Q

Allergy respiratory symptoms

A

Acute respiratory obstruction with laryngeal edema
Bronchospasms

209
Q

Type of shock in anaphylaxis

A

Distributive shock (Warm)

210
Q

Epinephrin dose children

A

0,01 ml/kg
Max 0,5 mL
repeat every 15 min if needed

211
Q

types of otitis media

A

OM with effusion
OM acute purulent

212
Q

surgical treatment og OME

A

Incision of the tympanic membrane (myringotomy)

213
Q

Etiology of acute purulent otitis media

A

Acute bacterial infection in the middle ear with pus. often following a URTI

214
Q

Diagnosis of OME

A

‣ History
‣ Otoscopy: TM appears irregular, opaque, thickened, bulging outward, air bubbles, cloudy —> no longer smooth and reflective! color: pale, reddish, yellowish or bluish depending on
the effusion
‣ Pneumoscopy: ↓ or absent mobility of tympanic membrane
‣ Tympanogram: Flat type B- curve or type C-curve in mild and acute cases
‣ Hearing tests: PTA, Weber, Rinne (conductive hearing loss)
‣ Imaging: CT, MRI to rule out complications

215
Q

Diagnosis of AOM

A

History
‣ Otoscopy, pneumoscopy
‣ Hearing tests: PTA, Weber, Rinne (hearing loss)
‣ Tympanogram: Type B-curve
‣ Imaging: plain X- ray, CT for complications
‣ Laboratory test: culture and sensitivity testing

216
Q

Sudden infant death syndrome (SIDS)?

A

unexplained death of an infant (under 1 year old). Diagnosis requires that a forensic examination reveals no other cause of death.

217
Q

viral bronchiolitis cause?

A

RSV
Influenza

218
Q

Viral bronchiolitis symptoms

A

Starts with rhinorrhea, low fever, dry cough
Followed by
wheezing dyspnea signs,
end-inspiratory crackles

219
Q

Forign body aspiration symptomes?

A

SUDDEN dry cough,
generalized wheezing,
choking,
stridor,
dyspnea, tachypnea

220
Q

Tracheomalasia?

A

congenital disease where trachea collapses
symptoms manifest at 4-8 weeks

221
Q

Most common chronic disease in childhod?

A

broncheal asthma

222
Q

trigger of asthma

A

Cold activity
Atopy
Infections
Allergens
Air pollution

223
Q

x-ray sign in croup?

A

steeple sign due to narrowing

224
Q

what is encephalopathy

A

A diffuse disruption of brain function and/or structure

225
Q

pathophysiology of encephalopathy

A

Diffuse cortical injury
Supratentorial mass lesion
Brainstem lesion

Leading to disturbed consciousness

226
Q

Etiology of Encephalopathy

A

Trauma
Neuro infection
Vascular/hematological disorder
Hypoxic/ischemia lesions
Tumor
Acute ventricular obstruction
Intoxication
Fluid/electrolyte disturbance
Acid/base disturbance
Endocrine disorders
Renal insufficiency
Hepatic insufficiency
Reyes syndrome
Congenital metabolic disorder
Chronic Neurological Diseases

227
Q

Extrapyramidal symptoms

A

ADAPT:
Acute Dystonia (involuntary contraction)
Akathisia (inability to remain physically stil)
Parkinsonism
Tardive dyskinesia (uncontrollable, abnormal, and repetitive movements of the face, torso, and/or other body parts)

228
Q

contraindications of lumbar puncture

A
  • Increased intracranial pressure (risk of cerebral herniation)
  • Thrombocytopenia, bleeding disorder, or ongoing anticoagulation
  • Epidural abscess
  • Severe respiratory compromise
229
Q

where do we do a lumbar puncture?

A

L3-L4

230
Q

What is the Cushing’s triad in increased ICP

A
  1. Bradycardia
  2. Irregular respiration
  3. Increased blood pressure
231
Q

Signs + symptoms of increased intracranial pressure all ages

A

◦Vomiting
◦Bradycardia
◦Increased respiratory rate
◦Lethargy
◦Seizures
◦Disturbed vital functions
◦Herniation signs
◦Papillary edema

232
Q

Signs + symptoms of increased intracranial pressure infants

A

◦Loss of appetite
◦Irritability
◦Bulging fontanelle
◦Setting-sun eyes

233
Q

Meningitis symptoms older children

A

◦Fever
◦Loss of appetite
◦Joint and muscle pain
◦Altered mental state
◦Increased ICP
◦Positive meningeal signs (nuchal rigidity, brudzinski sign, kernig sign)

234
Q

Meningitis sign in infants

A

◦Fever/hypothermia
◦Projectile vomiting
◦Irritability
◦Bulging fontanelle

235
Q

meningitis sign in all ages

A

◦Petechiae (meningococcemia)
◦Photophobia
◦Fever
◦Seizures

236
Q

What are some disorders of the nervous system?

A

Trauma
Infections
Degeneration
Structural defects
Tumors
Blood flow disruption
Autoimmune disorders

237
Q

Reyes phenomenon

A

Viruses alter the metabolism of salicylates → accumulation of salicylate metabolites in the liver → mitochondrial injury and reversible inhibition of enzymes required for fatty acid oxidation → failure of hepatic ATP production → acute hepatic failure → hyperammonemia, metabolic acidosis, and hepatic steatosis → acute encephalopathy
Hyperammonemia → cerebral edema → ↑ ICP

238
Q

meningitis types

A

◦Bacterial/septic: CSF cell count >1000, proteins↑↑, glucose↓↓
◦Aseptic: CSF cell count <1000, proteins↑, glucose: normal
◦Chronic granulomatous (TBC): CSF cell count <1000, proteins↑↑, glucose↓↓

239
Q

what is the place of inflammation in meningitis?

A

Subarachnoid space

240
Q

most common cause of meningitis in < 3 month olds

A

GBS
E. coli
Listeria

gram -
s.pneumonia
Niesseria, H.influenza

241
Q

AB in meningitis if trauma/neurosurgery

A

meropenem
vancomycin

242
Q

what is also always given in meningitis with AB

A

corticosteroids to avoid waterhouse Friderichsen syndrome

-HiB (Dexamethasone) decrease CNS complication
-Meningococcaemia: hydrocortisone

243
Q

what is waterhouse friderichsen syndrome

A

acute primary insufficiency of the adrenal gland

244
Q

name a immune related cause of encephalitis?

A

ADEM
acute disseminated encephalomyelitis (demyelination fisease in kids)

245
Q

name a autoimmune related cause of encephalitis

A

NMDAe
Autoantibodies against NMDA receptors causing inflammation

246
Q

Symptomes of encephalitis

A

Fever
Headache
Vomiting
Light sensitivity
Change in consciousness, hallucination, delirium
Focal signs depend on affected area
Seizures

247
Q

treatment in NMDAe (Anti-NMDA receptor encephalitis ) and ADEM (Acute disseminated encephalomyelitis ) encephalitis?

A

high dose CS (methylprednisolone)
IVIG
Plasmapheresis

248
Q

Etiology of peripheral facial nerve palsy

A
  • Trauma (e.g., temporal bone fracture)
  • Infection
    *EBV
    *Bells palsy
    *Borreliosis (Lyme disease)
    *Herpes zoster (Ramsay Hunt syndrome)
    *HSV reactivation
    *HIV
  • Malignant otitis media (choleosteatoma, rarely tumor)
  • Tumors (parotid gland tumors, acoustic neuroma)
  • Pregnancy
  • Diabetes mellitus
  • Guillain-Barré syndrome
  • Sarcoidosis (Heerfordt syndrome)
  • Amyloidosis
  • Stroke
249
Q

how to test the parasympathetic innervation of the fascial nerve?

A

Schirmer’s test:
Gaustometry:

250
Q

Schirmer’s test in facial nerve palsy

A

◦Strips of filter paper in the lower eyelid and comparing the sides
◦A 30% reduction in lacrimal secretion relative to the opposite side is considered abnormal

251
Q

Gaustometry test in facial nerve palsy

A

◦Evaluation of taste on anterior 2/3

252
Q

what can happen durin ga tonic-clonic seizure

A

vocal cord: screaming
Eyes: looking up/blinking
Jaw muscles: biting tongue
Oropharyngeal muscles respiratory secretion spool in mouth
Urinary and stool: incontinence

253
Q

phases of seizures

A

*Prodromal.
*Early ictal (the “aura”)
*Ictal.
*Postictal

254
Q

post ictal phase of tonic clonic seizure

A

Unresponsiveness
Confusion
Amnesia of the event
Aphasia- language disorder
Fatigue
Muscular flaccidity and muscle pain
Headache
Hypersalivation with or without airway obstruction

255
Q

Clinical presentation of abcent seizure

A

Interrupted motion or activity, blank stare, unresponsiveness
Can occur several 100/day and usually lasts < 10 seconds
Subtle automatisms (often go unnoticed): lip-smacking, eye fluttering, or head nodding are common.
Sudden onset and stop
Triggers: hyperventilation, flashing lights

256
Q

causes of seizures

A

VITAMINE
FEVER (2/3 causes <3yrs)

Vascular
Infection
Trauma/Toxins
Autoimmune
Metabolic , electrolyte (hypogylcemia)
Idiopathic (10-20% in all ages)
Neoplasms
S is for Psychogenic or syncope

257
Q

status epilepticus?

A

seizure for more than 5 minutes OR multiple sezures without regaining mental status

258
Q

Managment of seizures 5-10 min

A

First line is midezolam, diazepam, Lorazepam

259
Q

Managment of seizures 10-20 min

A

< 1 year: Levetiracetam, Valproic acid
> 1 year: Levetiracetam, Valproic acid, Phenobarbitol

260
Q

Managment of seizures after 15 min

A

ICU treatment
Potent antiepileptic agents Ketamines, propofol

muscle paralytics

261
Q

Complications of seizures

A

◦Hypoventilation —> hypoxia, hypercapnia
◦Rhabdomyolysis —> organ damage (kidney failure)
◦Increased lactic acid —> metabolic acidosis
◦Abnormal blood sugar levels
◦Super-refractory (lasting > 24hrs) seizures —>
‣ Brain edema
‣ CNS injury
‣ High mortality

262
Q

what is a febrile seizure?

A

Febrile seizures are seizures that are associated with fever (mainly temperatures exceeding 38°C (100.4°F)) in the absence of CNS infection, metabolic abnormalities, or a history of afebrile seizures.

263
Q

what is the most common seizure type < 5 years of age?

A

febrile seizures

264
Q

pathomechanism of febrile seizure

A

Pathomechanism: (not exactly known) increase body temp —> increased cytokine release —> neuronal
hyperexcitability

265
Q

pathophysiology of DM1

A

autoimmune destruction of beta cells in the pancreas —> absolute insulin deficiency

266
Q

DM1 symptoms in children

A

polyuria, enuresis (inability to control urination), polydipsia, weight loss, blurred vision
Polyphagia= excessive hunger

267
Q

DM1 symptoms in infants

A

Vomiting
Dehydration
Toxicosis
Coma

268
Q

diagnosis of DM1

A

fasting glucose > 7 mmol/l
ramdom glucose > 11.1 mmol/l

269
Q

can you measure long terms blood glucose?

A

Hemoglobin A1C (HbA1c or A1C): glycated hemoglobin, which reflects the average blood glucose levels of the prior 8–12 weeks. if above ≥ 6.5% them DM

270
Q

C-peptide in DM

A

C-peptide: can help differentiate between types of diabetes
↑levels may indicate insulin resistance+ hyperinsulinemia: T2DM
↓ C-peptide levels indicate an absolute insulin deficiency: T1DM

271
Q

Urin analysis in DM

A

Urinalysis
Glucosuria: if the renal threshold for glucose is reached

Ketone bodies: positive in acute metabolic decompensation

Microalbuminuria: early sign of diabetic nephropathy

272
Q

kidney treshold of glucose

A

It is generally accepted that when blood glucose concentrations exceed ~180 mg/dL, urinary glucose excretion occurs

273
Q

autoantibody in DM1?

A

Antiglutamic acid decarboxylase antibodies (Anti-GAD)
An antibody against the enzyme glutamic acid decarboxylase, which is responsible for the conversion of glutamic acid to GABA

274
Q

differential diagnosis of DM

A

Glucagonoma
Somatostatinoma

275
Q

Insulin treatment - Starting dose calculation

A

Exogenous insulin dose will depend on the residual insulin.
Total daily dose (TDD) of insulin: usually ∼ 0.4–1.0 units/kg/day, divided into 50% basal and 50% prandial insulin.
Consider initiating treatment with 0.5 units/kg per day.

276
Q

Fast acting insulin:
Normal acting:
Long acting insulin:

A

Fast acting insulin: Aspart, Lispro, Glusin
Normal acting: Regular insulin NPH
Long acting insulin: Glargin, Detemir

277
Q

patophysiology of ketoacidosis

A
  1. Insulin deficiency → hyperglycemia → hyperosmolality → osmotic diuresis and loss of electrolytes → hypovolemia
  2. Insulin deficiency → ↑ lipolysis → ↑ free fatty acids → hepatic ketogenesis → ketosis → bicarbonate consumption (as a buffer) → anion gap metabolic acidosis
  3. Insulin deficiency → hyperosmolality → K+ shift out of cells + lack of insulin to promote K+ uptake → intracellular K+depleted → total body K+ deficit despite normal or even elevated serum K+
278
Q

Managment of kedoacidosis

A

Treatment* :
A. ABCDE
B. Fluids
*Balanced crystalloids
*Calculate for 48h + add suspected fluid losses (5-10% depending on clinical situation)
*Administer slowly, unless patient is in shock —> fluid bolus: 10 ml/kg
*Complication of too fast fluid administration: cerebral edema

C. Insulin
*Fast-acting insulin IV (only switch to subcutaneous when patient has normal pH and is stabilized)
*0,05 U/kg/h

D. Insulin + glucose
*When glucose < 15 mmol/l —> change crystalloid solution to 5% glucose solution (10% is necessary if drop in glucose is too fast)

E. Electrolyte resuscitation
*Monitor K+ carefully for any decrease (insulin pushes K+ intracellularly) —> K+ < 5 mmol/l or
when child produce urine —> administer K+
*Monitor Na+ carefully (but have to calculate with corrected Na+ according to glucose levels) b.
—> administer Na+ if too low

Insulin therapy: short-acting insulin once potassium > 3.3 mEq/L
IV NaHCO3 only for severe refractory metabolic acidosis

  1. Identify and treat precipitating causes (e.g., sepsis).
  2. Consider endocrine consult and admission to the ICU.
279
Q

complication of to fast fluid res. in DKA

A

Cerebral edema

280
Q

Fluid therapy in kids

A

< 10kg - 4ml/kg/h
>10 kg 40ml/kg/h +2 ml/kg for every kg over 10

281
Q

Congenital adrenal hyperplasia (CAH)

A

Congenital adrenal hyperplasia (CAH) encompasses a group of autosomal recessive defects in the enzymes that are responsible for cortisol, aldosterone, and, in very rare cases, androgen synthesis

282
Q

3 subtypes of CAH

A

21β-hydroxylase (∼ 95% of CAH) (high androgens)
11β-hydroxylase (∼ 5% of CAH) (high androgens)
17α-hydroxylase (rare) (low androgens)

283
Q

female with 21β-hydroxylase deficiency or
11β-hydroxylase deficiency

A

Clitoromegaly and/or male external genitalia along with a uterus and ovaries
Precocious puberty
Virilization, irregular menstrual cycles, infertility

21β-hydroxylase defect ◦
Hypotension (↓aldosterone + DOC)

284
Q

male with 21β-hydroxylase or 11β-hydroxylase deficiency

A

Normal male external genitalia at birth
Precocious puberty

285
Q

female with 17α-hydroxylase defect deficiency

A

normal female external genitalia at birth,
delayed puberty,
sexual infantilism (ovaries ‣
cannot produce estrogen)

286
Q

Male with 17α-hydroxylase defect (rare) deficiency

A

male pseudohermaphroditism (female external genitalia),
delayed puberty
sexual infantilism

287
Q

General symptomes of CAH

A

Hypoglycemia
Adrenal crisis → vomiting and diarrhea → dehydration
Failure to thrive
Hyperpigmentation in areas that are not exposed to sunlight (e.g., palm creases, mucous membranes of the oral cavity, genitalia) is a common feature in all forms of CAH.

288
Q

what can happen to a infants with 21β-hydroxylase deficiency

A

Can present with shock within the first few weeks of life because of severe dehydration due to an adrenal crisis and salt-wasting due to hypoaldosteronism.

only form which causes hypotension!!!

289
Q

Treatment of CAH

A

Therapy aims to replace deficient hormones and reduce excess androgen production.
Glucocorticoid replacement therapy is indicated in all forms of CAH
hydrocortisone

21β-hydroxylase defect —> fludrocortisone (aldosterone substitution), salt supplements

11β-hydroxylase defect —> spironolactone (block mineralocorticoid receptor), reduced salt intake

17α-hydroxylase defect —> spironolactone, estrogen replacement therapy (XX), reduced salt intake

290
Q

obstructive bronchitis etiologies

A
  • Common cold
  • Acute asthma exacerbation
  • Viral bronchiolitis
    Start with rhinorrhea, low-grade fever, dry cough
    —> followed by wheezing, fine end-inspiratory ‣
    crackles, tachypnea, nasal flaring, intercostal retractions
    RSV, influenza
  • Foreign body aspiration (FBA)
    Sudden onset of dry cough/generalized wheezing/choking, stridor, dyspnea, tachypnea, crepitus
  • Acute bronchitis
    Start with rhinorrhea, sore throat, headache, malaise, myalgia —> followed by cough with/ ‣
    without sputum and chest pain, rhonci, wheezing, fine crackles, mild dyspnea
  • Croup
  • Tracheomalacia
    Congenital disease with abnormal collapse of tracheal walls —> symptoms usually manifest at ‣
    4-8 weeks
    Ineffective croup-like cough (due to tracheal collapse), inspiratory stridor, wheezing, recurrent ‣
    respiratory illnesses
    Obstruction goes away if child is crying —> increased pressure pushes tracheal walls open ‣
    (make child cry)
  • Cystic fibrosis
291
Q

asthma bronchiale pathophysiology

A

respiratory hyperreactivity
—> increased capillary permeability and histamine release *
due to inflammation
—> increased gland secretion and proliferation + inflamed mucosa + smooth muscle spasm
—> decreased airflow due to airway narrowing + hyperinflated and collapsed alveoli
—> insufficient ventilation

292
Q

Chronic asthma management

A

1st line: anti-inflammatory drugs ‣
Inhaled corticosteroids (Budesonide, Fluticasone) *
Alternative: leukotriene antagonists (Montelukast, Zileuton)

2nd line: bronchodilatory drugs ‣
Long-acting beta agonists (Formoterol, Salmeterol) *
Used less frequently in children ◦
Additional treatment to anti-inflammatory drugs

293
Q

Acute asthma management

A

Bronchodilatory drugs ‣
Short-acting beta agonists (Salbutamol, fenoterol, Terbutaline) or short-acting antimuscarinics *
(ipratropium)

294
Q

Acute subglottic laryngitis

A

= Croup
Pseudocroup (since real croup is caused by Diphteria)

Inflammation of tissues in subglottic space +/- tracheobronchial tree —> obstruction
Affects children 1-7 years old *
Appear in upper respiratory tract infections

295
Q

Acute subglottic laryngitis pathogens

A

Parainfluenza virus, RSV

296
Q

Acute subglottic laryngitis symtpoms

A

commonly start at night, appears and resolves suddenly

Hoarseness, barking cough, inspiratory stridor (extrathoracic obstruction)

Late signs: restlessness, tachycardia, tachypnea, perioral pallor, cyanosis

297
Q

Acute subglottic laryngitis treatment

A

mild —> cold humidified air, fluid intake, rectal steroids (can be treated at home)

Moderate —> hospital admission, epinephrine inhalation, systemic glucocorticoids

Severe —> same as moderate + ICU transfer

298
Q

Fluid therapy in kids

A

< 10kg - 4ml/kg/h
>10 kg 40ml/kg/h +2 ml/kg for every kg over 10

299
Q

Neonatal features of hypothyroidism

A

Abdominal distention
Delayed passage of meconium
Umbilical hernia
Prolonged neonatal jaundice
Hypotonia
Decreased activity, poor feeding, and adipsia
Hoarse cry, macroglossia
Hypothermia
Failure to thrive (length affected more than weight)

300
Q

Etiology of congenital hypothyroidism

A

Primary: most common (ectopic thyroid gland, aplasia

Secondary: pituitary aplasia, cerebral midline defects

Transient: temporary deficiency

301
Q

What causes transient hypothyroidism

A

Maternal autoimmune thyroiditis
Maternal drug use (thyrostatics, amiodarone)
Maternal iodine deficiency,
Preterm baby (immature hypothalamic-pituitary axis)

302
Q

how is the onset of symptoms in congenital hypothyroidism

A

Usually little to no features are present at birth as maternal T4 can cross the placenta.
Features can develop over weeks to months if screening is not performed.
Features can be apparent at birth in fetal iodine deficiency syndrome.

303
Q

complication of hypothyroidism in children

A

Cretinism
—> from untreated hypothyroidism that leads to impaired development of the brain and skeleton

—> skeletal abnormalities + permanent intellectual disabilities

304
Q

Cause of neonatal hyperthyroidism

A

Occurs in ∼ 5% of babies born to mothers with Graves disease
Etiology:
transplacental passage of maternal TRAbs

(TSH receptor autoantibodies)

305
Q

clinical features of hyperthyroidism in neonates

A

Irritability
Restlessness
Tachycardia
Diaphoresis (sweating)
Hyperphagia (extreme hunger)
Poor weight gain
Diffuse goiter (can cause tracheal compression),
microcephaly (due to craniosynostosis) birth defect in which the bones in a baby’s skull join together too early

306
Q

treatment of congenital hyperthyroidism

A

Resolves on its own after 1-3 months
If symptomes : Methamizole (decrease synthesis) inhibits thyroid peroxidase
Propanolol (decrease heartrate)

307
Q

most common cause of hyperthyroidism in children?

A

Graves disease

308
Q

treatment of Graves disease

A

‣ Antithyroid medications: 1st line) Methamizole
‣ Symptom control: beta-blockers (atenolol, propanolol)
‣ Radioactive iodine ablation: potential first line treatment in patients >10 years or second line if relapse after long-term therapy
‣ Surgery (near-total thyroidectomy): in children <5 years who do not improve with antithyroid drugs or if have large goiters

309
Q

what is osteomalacia and rickets?

A

Osteomalacia is a disorder of impaired mineralization of the osteoid
Rickets is a disorder of impaired mineralization of cartilaginous growth plates.

310
Q

clinical features of osteomalacia

A

Occurs in adults and children
Bone pain and tenderness
Pathologic fractures
Waddling gait and difficulty walking
Myopathy
Muscle weakness
Spasms
Cramps
Bone deformity only in very severe cases of osteomalacia

311
Q

clinical features of rickets

A

Only occurs in children (growth plates have not fused)

Bone deformities
Bending of primarily the long bones
Distention of the bone-cartilage junctions
Marfan sign
Impression of a double medial malleolus on inspection and palpation of the ankle

Craniotabes: softening of the skull
Deformities of the knee, especially genu varum

Increased risk of fracture

Harrison groove: depression of the thoracic outlet due to muscle pulling along the costal insertion of the diaphragm
Late closing of fontanelles
Impaired growth

312
Q

Cause of both osteomalacia and rickets

A

Vitamin D deficiency resulting from
inadequate intake
, malabsorption,
or lack of exposure to sunlight.

313
Q

pathophysiologyy of vitamin D deficiency (consequence)

A

Hypocalcemia → defective bone matrix mineralization (osteomalacia) or cartilaginous growth plate mineralization (rickets).
Hypocalcemia → ↑ PTH levels → ↓ phosphate levels → impaired mineralization.

314
Q

Diagnosis of osteomalacia and rickets

A

Laboratory tests
↓ Calcium and ↓ phosphate
↑ Alkaline phosphatase and ↑ PTH
Vitamin D-dependent rickets type 1: ↓ calcitriol concentration
Vitamin D-dependent rickets type 2: ↑ calcitriol concentration

315
Q

treatment of osteomalacia and rickets

A

VItamin D

316
Q

What is IgA vasculitis
(Henoch-Schonlein purpura, Anaphylactoid purpura)

A

IgA vasculitis (IgAV), formerly known as Henoch-Schonlein purpura (HSP), is an acute immune complex-mediated small vessel vasculitis that most commonly occurs in children.

317
Q

etiology of Henoch-Schonlein purpura

A

Preceding infection
Up to 90% of cases preceded by viral or bacterial infection 1–3 weeks prior
Most commonly an URTI caused by group A Streptococcus
GI infections also possible
IgA nephropathy
Drugs (especially β-lactam antibiotics and antiarrhythmics) Vaccines (Yellow fever)

318
Q

pathophysiology of Henoch-Schonlein purpura

A

(hypothesis):
exposure to allergen/antigen (eg infection, drugs)
—> stimulation of IgA production

–>Deposition of IgA immune complexes in vascular walls (in the skin, GI tract, joints, kidneys)
→ activation of complement
→ vascular inflammation and damage

319
Q

Symptome onset in Henoch-Schonlein purpura

A

Symptom onset often 1–3 weeks after an infection, typically affecting the upper respiratory tract

320
Q

clinical manifestation of Henoch-Schonlein purpura

typical triad

A

PAPAH:

Typical tetrad:
1) palpable purpura (most commonly on lower extremities, buttocks)
2) arthritis/ arthralgia (most commonly ankles, knees)
3) abdominal pain
4) renal disease (hematuria)

intussusception,
bloody stool/melena,
nausea/vomiting,
scrotal swelling/pain/tenderness,
headaches, seizures, focal neurological deficits, ataxia,
intracerebral hemorrhage,
mild interstitial pulmonary changes,
pulmonary hemorrhage,
keratitis/uveitis

321
Q

treatment of Henoch-Schonlein purpura

A

Most are self-limiting and only require supportive care (NSAIDs for pain, rest, adequate hydration)

Severe disease —>
*systemic glucocorticoids for severe abdominal pain
*IV fluids for hydration

*for severe renal disease:
methylprednisolone pulse therapy
acute dialysis
antihypertensives
renal transplantation

322
Q

Define kawasaki syndrome

A

Kawasaki disease is an acute, necrotizing vasculitis of unknown etiology.
Primarily affects children, under age of 5, more common in Asian population

323
Q

Clinical diagnosis of Kawasaki

A
  1. Requires fever for at least 5 days + either:
    > 4 specific symptomes
    < 4 specific symtpmes but coronary artery involvement
324
Q

Kawasaki specific symptoms

A

Erythema + edema of hands and feet (first week)
‣ Desquamation of fingertips and toes (2-3 week)
‣ Polymorphous rash originating from trunk
‣ Conjunctivitis without exudate
‣ Oropharyngeal mucositis: strawberry tongue or cracked red lips
‣ Cervical lymphadenopathy

325
Q

lab findings in Kawasaki

A

Laboratory findings
↑ ESR and CRP
Leukocytosis (wbc in urine)
Thrombocytosis
↑ AST, ALT

326
Q

treatment in Kawasaki

A

IV immunoglobulin (IVIG)
High single-dose to reduce the risk of coronary artery aneurysms
Most effective if given within the first 10 days following disease

High-dose oral aspirin

IV glucocorticoids: may be considered in addition to standard treatment, esp. in cases of treatment-refractory disease, as they lower the risk of coronary involvement

327
Q

what is MISC

A

Multisystem inflammatory syndrome in children

MISC-C is a complication of COVID-19 in children that manifests with
hyperinflammation,
severe illness, and
involvement of multiple organ systems.

328
Q

clinical features of MISC

A

Fever

Gastrointestinal symptoms

Mucocutaneous symptoms (rash and/or mucositis, including erythema, morbilliform, retiform purpura, targetoid and urticarial)

Shock

329
Q

Diagnostic criteria: of MISC

A

All of the following must be met
Age < 21 years
Fever (documented fever ≥ 38°C (100.4°F) OR report of subjective fever lasting ≥ 24 hours
Laboratory evidence of inflammation (e.g., ↑ CRP, ↑ ESR, ↑ neutrophils)
Involvement of ≥ 2 organ systems (including the hematological system)
Severe illness requiring hospitalization
Confirmed current or recent SARS-CoV-2 infection OR exposure to an individual with COVID-19 < 4 weeks prior to symptom onset
No other plausible diagnosis

330
Q

treatment of MISC

A

Initial treatment: intravenous IG
PLUS methylprednisolone

Antithrombotic therapy (unless contraindicated

331
Q

Cause of UTI in children

A

Escherichia coli (in up to 90% of cases)
Klebsiella pneumoniae
Proteus mirabilis [2]
Enterococcus faecalis
Enterobacter species
Rarely: Pseudomonas aeruginosa, group B Streptococcus, Staphylococcus aureus

332
Q

special about UTI not due to E. coli?

A

UTIs caused by a pathogen other than E. coli are considered atypical pediatric UTIs.

333
Q

risk factors of UTI in pediatrics

A

All ages
- Female sex
- Personal or family history of CAKUT
- Bowel and bladder dysfunction (e.g., chronic constipation)
-Vesico-ureteral reflux
-Bladder catheterisation
- Instrumentation of the urinary tract

Children ≤ 2 years of age
- Uncircumcised boys
- Age < 1 year

Children > 2 years of age and adolescents
- Kidney stones
- Diabetes
- Sexual activity

334
Q

symptoms of UTI

A

Urinary frequency
Dysuria
Suprapubic pain
Flank pain
Fever

335
Q

Classification of UTI

A

Classification: depending on level of infection
◦Upper urinary tract infection: pyelonephritis
◦Lower urinary tract infection: cystitis
◦Uncomplicated: limited to the lower tract, age >2, no underlying medical problems or anatomical malformations, caused by typical microorganism
◦Complicated: if any of above is false

336
Q

diagnosis of UTI

A

Dipstick
Urine culture
Microscopic evaluation

337
Q

Diagnosis of UTI in children not potty trained?

A

catherization, suprapubic aspiration, (sterile collection
bag - not recommended)

338
Q

UTI treatment

A

Start empiric antibiotics for pediatric UTI (e.g., cephalosporins) while awaiting urine culture results.

Adjust treatment when culture results become available.

Provide supportive treatment, e.g., antipyretics, analgesia.

If fever persists for > 72 hours, consider urgent imaging for pediatric UTI to rule out renal abscess.

339
Q

Admission criteria for pediatric UTI

A

IV antibiotics required
Consider admitting patients with any of the following:
Age 1–2 months
Significant renal tract anomalies
Barriers to follow-up

340
Q

Considerations in neonates with UTI:

A

◦Blood culture should also be obtained for diagnosis (but relative high risk of an urosepsis)

◦US is recommended to identify structural abnormalities

◦Empiric treatment:
ampicillin + gentamicin 10-14 days,
then amoxicillin until radiologic evaluation is done

341
Q

VACTERL syndrom in babies

A

Vertebral anomalies
Anal atresia
Cardiovascular anomalies
Tracheoesophageal fistula
Esophageal atresia
Renal anomalies
Limb defects

342
Q

Kidney malformations

A

Renal agenesis (failure to develop)
Renal hypoplasia (smaller in size)
Horseshoe kidney
Kidney dysplasia (abnormal histology)
Multicystic dysplastic kidney
Ectopic kidney (no migration)
Hydronephrosis
Duplex kidney

343
Q

if the child has horsechoes kidney what is important to look for?

A

Males: Gonadal dysgenesis
Female: Turner syndrom

344
Q

Progression of polycystic kidney disease

A

cysts and their size increases with age

345
Q

types of polycystic kidney disease

A

ARPKD (less common)
ADPKD (more common)

346
Q

Mutation in ARPKD

A

PKHD 1 gene mutation

347
Q

Types of polycystic kidney disease

A

ADPKD (most common)
ARPKD (less common)

348
Q

Mutation in ADPKD

A

PKD1 mutation

349
Q

Mutation in ARPKD

A

PKHD1 mutation

350
Q

Clinical presentation of ARPKD

A

Symptoms manifest in infancy or childhood.
Intrauterine oligohydramnios (low amniotic fluid)
pulmonary hypoplasia - neonatal resp distress
Early HTN
Urinary sepsis
End stage kidney failure by 18

351
Q

Clinical presentation of ADPKD

A

Symptoms usually occur after 30 years of age
Gross hematuria
Flank or abdominal pain
Recurrent urinary tract infections
Nephrolithiasis
Kidneys might be palpable and enlarged
Multiple benign hepatic cysts (prevalence increases with age)
Cysts may also occur in the pancreas, spleen, ovary, and testicles.
Berry aneurisms

352
Q

Ureter development disorders

A

Pyelouretral junction (PUJ) stenosis
Ureter-vesicular junction (UVJ) stenosis
Ureterocele
Vesico-ureteral reflux (VUR)

353
Q

types of bladder abnormalities

A

Bladder Extrophy
Bladder diverticulum
Urachus persistence

354
Q

Bladder extrophy

A

◦Complex, severe developmental disorder
◦Abdominal wall defect in lower abdominal region —>
bladder is herniating outside of skin
◦Diagnosis: after birth
◦Treatment: surgery

355
Q

Bladder diverticulum

A

◦Bladder mucosa protrudes btw DETRUSOR muscle fibers
◦Can be caused by subvesicular obstruction
◦Symptoms: UTI, obstruction, VUR, stones
◦Diagnosis: US, MCU(Micturating Cysto-Urethrogram) , exclusion of primary cause (obstruction)
◦Treatment: resection, treat primary cause

356
Q

Urachus persistens

A

◦The embryonic passage connecting the tip of the bladder to
the navel is not absorbed/closed —> remnant structure
◦Caused by subvesicular obstruction with high pressure in
the bladder
◦Symptoms: moist navel (urine), soft tissue inflammation
◦Diagnosis: US, fistulography, MCU(Micturating Cysto-Urethrogram)
◦Treatment: surgery

357
Q

Urethra anomalies

A

PosteriorUrethral valve
Hypospadius
Epispadius

358
Q

Glomerulonephritis definition

A

A condition in which the tissues in the kidney become inflamed and have problems filtering waste from the blood.

359
Q

Glomerulonephritis clinical symptoms

A

◦Hematuria
◦Oliguria
◦Edema
◦Hypertension
◦Variable proteinuria

360
Q

Glomerulonephritis etiology

A

Post-infectious: most common
MPGN (membranoproliferative glomerulonephritis)
IgA nephropathy
Systemic lupus erythematosus
Subacute bacterial endocarditis
Shunt nephritis

361
Q

Post infectious Glomerulonephritis etiology

A

‣ Bacterial: streptococci (most common), staphylococci, mycoplasma, salmonella
‣ Viral: herpesvirus (EBV, varicella, CMV)
‣ Fungi: candida, aspergillus
‣ Parasites: toxoplasma, malaria, schistosomiasis

362
Q

what NOT to use in renal disease

A

ACEI

363
Q

Nephrotic syndrom

A

Nephrotic syndrome is a collection of signs and symptoms indicating damage to the glomerular filtration barrier. Characterized by:
1. Massive proteinuria (> 3.5 g/24 hours)
2. Hypoalbuminemia
3. Edema

364
Q

Define presentations in Nephrotic syndrome

A

◦Proteinuria (urinary protein to creatinine ratio >200 mg/mmol)
◦Hypoalbuminemia (albumin <25 g/l)
◦Edema
◦Hyperlipidemia

365
Q

nephrotic range of proteinuria

A

proteinuria > 3.5 g/24 hours

366
Q

Etiology of nephrotic syndrom

A

Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Membranoproliferative glomerulonephritis
Diabetic nephropathy
Amyloid nephropathy
Lupus nephritis

367
Q

Diagnosis of nephrotic syndrom

A

◦Urinalysis: protein +++
◦Microscopy: hematuria/casts (suggests other than MCD)
◦Culture
◦Protein:creatinine ratio
◦Serum albumin
◦C3/C4 (if decreased not MCD)
◦Lipids
◦Immunoglobulins
◦Renal biopsy if steroids are not helping

368
Q

Nephrotic syndrom hypoalbuminemia value

A

hypoalbuminemia (less than 30 g/L)

369
Q

Cyanotic congenital heart defects

A

Right-to-left shunt:
*Tetralogy of Fallot

Separate circulations:
*Transposition of the great arteries

Complete mixing:
*Tricuspid atresia
*Truncus arteriosus
*Hypoplastic left heart syndrome
*TAPVR (Total anomalous pulmonary venous return)

370
Q

Tetrad of fallot

A

right to left shunt
Characterized by four particular abnormalities:
Right ventricular outflow obstruction due to pulmonary stenosis
Right ventricular hypertrophy
Ventricular septal defect (VSD)
Overriding aorta (above the VSD) misplaced aorta

371
Q

tetrad o fallot clinical symptoms

A

◦Boot-shaped heart on x-ray
◦Patients learn to squat in response to cyanosis —> increase systemic resistance —> more blood
flow through stenotic pulmonary arteries to lungs

372
Q

Transposition of the great vessels

associated with what
treatment

A
  • Characterized by pulmonary a. arising from LV + aorta arising from RV
  • Associated with maternal diabetes
  • Clinical features:
    ◦Early cyanosis —> pulmonary + systemic circuits do not mix
    PGE1 is given to maintane PDA until surgery
373
Q

tricuspid atresia

A

Absent or rudimentary tricuspid valve resulting in no blood flow between RA and RV

374
Q

truncus arteriosus

A

Underdevelopment of aorticopulmonary septum —> failure of truncus arteriosus to divide into the aorta
and pulmonary trunk —> instead a single trunk that receives output from both ventricles

375
Q

hypoplastic left heart syndrom

ass with what diseases

A

Spectrum of disease consisting of severe hypoplasia of left ventricle with possible and/or atresia of the
mitral valve, aortic valve, or aortic arch

ass. with patau, edward, turner sy

376
Q

Total anomalous pulmonary venous return (TAPVR)

A

All four pulmonary veins drain into systemic venous circulation instead of left ventricle —> oxygenated
blood returns back to right atrium —> pulmonary edema

377
Q

Non-cyanotic heart defects

A

Left to right shunt:
Arial septal defect
Ventricular septal defect
Atrioventricular septal defect
Patent ductus arteriosus

obstructive:
AS
PS
Coarctation of aorta

378
Q

what is Eisenmenger syndrom

A

when a ventricular septal defect shunting L-V changes to R-L due to RV hypertrophy

379
Q

infection ass with patent ductus arteriosus

A

congenital Rubella

380
Q

pharma to close PDA

A

Indomethacin decreases PDE causing closure of PDA

381
Q

Calori need for children

A

< 10kg : 100kcal/kg
> 10kg: 1000kcal/day + 50kcal per kg over 10
> 20kg: 1500kcal/day + 20kcal per kg over 20

382
Q

Vit D dose for infants

A

one drop (450-500 U)

383
Q

Malabsorption classification

A

Impaired intraluminal digestion
Intestinal malabsorption
Malabsorption due to fermentation (maldigestion of carbohydrates)

384
Q

celiac disease

A

Definition: autoimmune disorder characterized by an intestinal hypersensitivity to gluten, a grain protein
Synonyms: celiac sprue; gluten-sensitive enteropathy

385
Q

Celiac disease etiology

A

Asociation to HLA antigens
- HLA-DQ2 in 90–95% of patients
- HLA-DQ8 in 5–10% of patients
Consuming gliadin from grains such as wheat, rye, and barley leads to an autoimmune reaction within the small intestinal wall.

386
Q

Celiac disease pathophysiology

A
  1. Consumption of food containing gluten
  2. Tissue transglutaminase is released → modifies gliadin from gluten 3. Pathogenic T cells react to and are activated by modified gliadin
  3. Mediate chronic intestinal inflammation
  4. Epithelial damage resulting in villous atrophy, crypt hyperplasia, and loss of brush border
  5. Impaired resorption of nutrients in the small intestine (especially in the distal duodenum and proximal jejunum)
  6. Malabsorption symptoms
387
Q

GI symptoms in celiac disease

A

Chronic or recurring diarrhea: steatorrhea
Flatulence, abdominal bloating, and pain
Nausea/vomiting
Lack of appetite
Constipation (rarely)

iron deficiency anemia
delayed puberty, ammenorrhea,
osteoporosis, osteopenia
failure to thrive

388
Q

Extraintestinal symptoms in children
celiac disease

A

◦Chronic abdominal pain, distension
◦Chronic fatigue
◦Failure to thrive, weight loss, stunted growth
◦Iron-deficiency anemia
◦Dermatitis herpetiformis rash (Duhring disease)
◦Diarrhea, obstipation
◦Delayed puberty, amenorrhea
◦Nausea, vomiting
◦Recurrent aphthosus stomatitis
◦Abnormal live biochemistry
◦Osteoporosis, osteopenia

389
Q

Diagnosis of celiac disease

A
  1. Clinical suspicion of CD or risk group for CD? yes —>
  2. Measure transglutaminase ab (TGA-IgA) & total IgA? positive —>
    (If negative —> esophagogastroduodenoscopy biopsies distal duod)
  3. Test for endomysial antibodies (EMA-IgA), positive —>
    (If negative —> esophagogastroduodenoscopy biopsies distal duod)
390
Q

duodenal biopsy in celiac disease

A

Taken from distal duodenum (min 4x) and duodenal bulb (min 1x)
not done in children unless absolutley needed

391
Q

Gluten free diet is

A

Not allowed: wheat, barley, bulgur, cuscus, malt, normal beer, cans, instant coffee

392
Q

what is normally secreted in the bile

A

bile acids
bilirubin
cholesterol

393
Q

etiology of cholestasis

A

◦Biliary atresia
◦Alagille syndrome
◦Alpha-1 antitrypsin deficiency

394
Q

biliary atresia

A

◦Uncommon disease in infants
◦Closed/discontinuous biliary tracts
◦Destructive, obliterative cholangiopathy that affects both intra- and extrahepatic bile ducts

395
Q

Allagile syndrome

A

Uncommon genetic condition characterized by intrahepatic biliary duct aplasia or hypoplasia
◦Autosomal dominant inheritance of mutation in the JAG1 gene

396
Q

Diagnosing allagile syndrom

A

5 major criteria: 3 is needed (interlobular bile duct atresia + 2)
* Interlobular bile duct absence/cholestasis
* Cardiac malformation/insufficiency
* Spine deformity: butterfly vertebra
* Characteristic face : triangular
* Ocular abnormality: post. embryotoxon

397
Q

Alpha-1 antitrypsin deficiency

A

Genetic disorder characterized by the accumulation of defective alpha-1 antitrypsin enzyme
◦Caused by mutation in the SERPINA1 gene

398
Q

Alpha-1 antitrypsin deficiency effect on liver and lungs

A

Effect on liver: accumulation of faulty AAT in hepatocellular endoplasmic reticulum —> hepatocyte destruction —> hepatitis and liver cirrhosis

Effect on lungs: deficient AAT —> uninhibited protease activity —> destruction of pulmonary parenchyma —> panacinar emphysema (differ from centrilobular emphysema from smoking)

399
Q

Viral Hepatitis transmission

A

◦Hepatitis A —> fecal-oral transmission
◦Hepatitis B —> blood/sexual transmission
◦Hepatitis C —> blood/sexual transmission

400
Q

Hepatitis symptoms

A

Fever, fatigue, malaise, anorexia, nausea, arthralgia, RUQ pain, jaundice +/- hepatomegaly, splenomegaly, adenoma they, urticaria

401
Q

hepatitis diagnosis

A

◦Increased liver enzymes: ↑ALT, ↑AST, ↑GGT, ↑ALP
◦Viral serology (IgM antibodies),
viral PCR,
blood culture

402
Q

NAFLD in childhood

A

One of the most common causes of chronic liver disease in young people in the developed world

7% general pop
34% in obese children

403
Q

NAFLD in childhood pathophysiology

A

Increased insulin resistance —>
◦↑Hepatic uptake of fatty acids
◦↑Triglyceride synthesis
◦↑Peripheral lipolysis

404
Q

treatent of NAFLD

A

Treatment: few efficient ones in pediatrics
◦Insulin sensitisers (not recommended)
◦Statins (only in adults)
◦Vitamin E (conflicting results)
◦Docosahexaenoic acid (DHA) (encouraging results)
◦Probiotics (potential effect)

405
Q

Autoimmune hepatitis types

A

Type 1 (80%): characteristic ANAs, ASMAs, anti-soluble liver antigen Abs
Type 2: characteristic anti-liver-kidney Abs, anti-liver cytosol Abs
◦Seronegative autoimmune hepatitis/ hepatitis associated aplastic anemia (HAA)
◦Giant cell hepatitis with autoimmune hemolytic anemia
◦De novo -alloimmune- hepatitis post liver transplantation

406
Q

treatment of autoimmune hepatitis

A

Immunosuppressive medications
-induction (prednisone +- azathioprine) (mycophenolate, cyclosporine, tacrolimus)
- maintenence : low dose prednisone/azathioprine

Transplant

407
Q

Most common infectious enteritises

A

Bacterial enteritis
Viral gastroenteritis

408
Q

◦Common pathogens in viral enteritis

A

‣ Fall-winter: Rotavirus (6 months-2 years), Astrovirus (<4 years)
‣ All around the year: Norovirus (all ages, highly contagious), Sapovirus

409
Q

clinical presentation of viral enteritis

A

non-bloody diarrhea, vomiting, fever, abdominal pain, anorexia, headache,
myalgia

410
Q

Bacterial enteritis symptoms

A

high fever,
tenesmus,
severe abdominal pain,
gross blood or mucus in the stool

411
Q

◦Common pathogens in bacterial enteritis

A

Shiga-toxin producing E. Coli (STEC),
Salmonella,
Shigella,
Clostridium difficile,
Campylobacter Jejuni,
Yersinia enterocolitica

412
Q

treatment in bacterial enteritis

A

Azithromycin

EXCEPT in STEC AB not recommended

413
Q

Inflammatory bowel disease (IBD)?

A
  • Ulcerative colitis (UC) or Crohn’s disease (CD)
414
Q

risk factor of IBD

A

◦Antibiotic administration,
smoking,
lack of breastfeeding,
familial IBD (2-8x higher risk if parent has IBD)
◦Breast milk reduces incidence of CD by 33% and UC by 23%

415
Q

Chron’s disease appearance

A

◦Wall involvement: transmural, with knife-like fissures
◦Location: anywhere from mouth —> anus with skip lesions, terminal ileum is the most common
◦Symptoms: right lower quadrant pain (ileum) with non-bloody diarrhea, weight loss, appetite loss
◦Inflammation: lymphoid aggregates with granulomas

416
Q

Ulcerative colitis (UC) appearance

A

◦Wall involvement: mucosal + submucosal
◦Location: ONLY colon, begins in rectum —> spreads proximal up to cecum (continuous/segmental)
‣ 1st: proctitis —> 2nd: proctosigmoiditis (“left-side colitis”) —> 3rd: extensive colitis —> 4th:
pancolitis
◦Symptoms: left lower quadrant pain (rectum), bloody diarrhea, increased number of stool, mucus in
stool, urgency, fecal incontinence, 25% experience obstipation, tenesmus (feeling of fecal residue)
◦Inflammation: crypt abscesses with neutrophils
◦Gross appearance: psedupolyps

417
Q

Extraintestinal manifestations of IBD

A

◦Eye symptoms: uveitis, episcleritis, keratopathy
◦Skin symptoms: erythema nodosum, pyoderma gangrenosum, metastatic Crohn’s disease (skin lesions in areas not connected to GI tract)
◦Joint symptoms: arthritis, sacroileitis
◦Other: fever, growth retardation, delayed puberty, hepatitis, pancreatitis

418
Q

Endoscopic findings in IBD

A

‣ CD: granuloma
‣ UC: crypt abscesses

419
Q

indicates acute severe ulcerative colitis

A

≥ 6 bowel movements daily
≥ 1 sign of systemic toxicity (e.g., tachycardia, fever, hemoglobin < 10.5 g/dL, ESR > 30 mm/hour)

420
Q

chrons treatment

A

CD:
1. induction :
exclusive enteral nutrition (EEN) : nasogastric tube insertion and strict formula-based (no solid-food 6-8w)
Better then steroids

  1. maintenance : PEN”partial” , AZT/MTX
  2. Relapse: EEN
  3. rescue therapy: TNFa-I (Adalimumab,Infliximab),
    Integrin inhibitor: vedolizuman
    Anti-IL13/23 : ustekinumab
    JAK-I tofacitinib

or surgery (ileocecal resection w/diversion stoma)

421
Q

UC treatment

A
  1. induction:
    anti-inflammatory (5-ASA: aminosalicylate), steroids
  2. maintenence: 5-ASA, immunomod(MTX, AZT)
  3. relapse: steroid
  4. biological (ustekinumab(Anti-IL 12/23), infliximab, adalimumab= TNF-a inhibitor)
  5. surgery
422
Q

UC treatment

A
  1. INDUCTION:
    Mesalasin (5-ASA)
    and steroids
  2. maintence:
    5-AS , AZT/MTX
  3. RELAPSE:
    STEROID
  4. rescue therapy: TNFa-I (Adalimumab,Infliximab),
    Integrin inhibitor: vedolizuman
    Anti-IL13/23 : ustekinumab
    JAK-I tofacitinib

or surgery (total colectomy w/ pouch prep)

423
Q

classification of UC

A

Ulcerative proctitis (E1) - Limited to the rectum
Left-sided ulcerative colitis (E2) - Limited colon distal to the splenic flexure
Extensive ulcerative colitis (E3) - Extends proximal to the splenic flexure

424
Q

Enuresis?

A

Repeated involuntary elimination of urine that is inappropriate for developmental age (bed-wetting)

425
Q

Diagnostic criteria: Enuresis

A

1) occurs 2x/week > 3 months
2) patients developmental age must be 5 or more
3) symptoms not caused by medication/other medical condition

426
Q

types of Enuresis

A

Nocturnal (mostly boys) or diurnal (mostly girls)
Primary (patient never achieved continence)
Secondary (after patient achieved continence)

427
Q

Enuresis treatment

A

First line:
fluid restriction at night,
behavioral training,
timed voiding,
parent management training, psychoeducation

Second line: desmopressin, behavioral training with an enuresis alarm

428
Q

Define Polyuria and polydipsia

A
  • Polyuria: excessive urinary output
  • Polydipsia: excessive thirst/drinking
429
Q

etiology of Polyuria and polydipsia

A

Primary polydipsia
Diabetes insipidus
Diabetes mellitus

430
Q

Polyuria and polydipsia in DM why

A

Chronic hyperglycemia cause excess excretion of glucose —> osmotically active glucose particles draws water with them —>↑urination —>↑fluid loss —>↑thirst

431
Q

Polyuria and polydipsia in Diabetes insipidus

A

Kidneys are not able to concentrate urine —>↑urination —>↑fluid loss —>↑thirst

432
Q

Polyuria and polydipsia in primary polydipsia

A

Excessive oral intake of fluid in the absence of physiological stimulus to drink —>↑fluid volume —>↑urination —>↑fluid loss —>↑thirst
‣ May include psychogenic polydipsia secondary to psychoses or other mental disorders

433
Q

Classification of edema

A

◦Peripheral (edema of extremities)
◦Central (edema in organs and body cavities)
◦Pitting edema ( indentation left by pressure on the site of the swelling)
◦Non-pitting edema (no residual indentation left by pressure on the site of swelling)

434
Q

Anion gap

A

[Na + K] - [Cl + HCO3], normally 10-15 mmol/l

435
Q

anemia definition

A

Hb
Htc
or RBC is under the normal range.
Red cell indices vary considerably with age

436
Q

changes in Hb and Htc with age

A

fetal Hb is high in 1-2 weeks because fetal in hypoxia so makes more
increases binding capacity of Hb to mother O2-bound Hb

437
Q

microcytic hypochromatic anemia causes

A
  • iron deficiency
  • thalassaemias (decreased globulin for Hb pro)
  • chronic disease (produce AcutePhaseProtein lock Fe in storage site)
  • Sideroblastic anaemia (decreased protoporphyrin needed to produce heme)
  • Copper deficiency
  • Lead poisoning (glass with lead paint with vitc, air pollution)
438
Q

causes of normocytic normochromic anemia

A
  • hemolytic anemia (in early phase, when it’s still compensated)
  • chronic inflammations
  • malignancy
  • acute blood loss
  • bone marrow deficiency
  • chronic kidney disease
439
Q

macrocytic anemia causes

A
  • megaloblastic anemia (b12, folate)
  • liver disease
  • mds (methotrexate, zidovudine, azathioprine, antiretroviral agents, valproic acid, and phenytoin )
  • aplastic, hypoplastic anemias
  • gestation
  • hypothyrosis
440
Q

Actual iron defiency

A

enhanced bone marrow hence we have thrombocytosis

-rbc↓ , Hb↓ decreased
-Htc ↓↓ decreased

441
Q

Most common pathogens causing pneumonia by age

A
  • Newborn:
    -GBS
    -Staph aureus
  • 1-3 month:
    -RSV
    -strep pneumonia
    -chlamydia trachomatis
  • 3m-5y:
    -RSV
    -Streptoccocus pneumonia
  • > 5yrs: Mycoplasma pneumonia, chlamydia pneumonia

Parm (15 decks)

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