Paeds Flashcards

(451 cards)

1
Q
Normal resp rate for:
Term-3 mo
4-12mo
1-4yrs
5-12yrs
12yrs+
A
Term-3 mo: 30-60
4-12mo: 30-40
1-4yrs: 20
5-12yr: 16
12yrs+: 16
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2
Q
HR MET criteria for: 
Term-3 mo
4-12mo
1-4yrs
5-12yrs
12yrs+
A
Term-3 mo: <100 >180
4-12mo: <100 >180
1-4yrs: <90 >160
5-12yrs: <80 >140
12yrs+: <60 >130
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3
Q

Normal signs of respiration in young children (4)

A

Chest in-drawing
Periodic respiration (not constant rate) BUT NO APNOEA
Incr rates of resp

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4
Q

Definition of apnoea in newborns

A

No respiratory effort for greater than 20 seconds.
No respiratory effort for shorter periods of time may also be classified as apnoea if accompanied by cyanosis or bradycardia

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5
Q

Causes of the following types of tachypnoea:
• Expiratory wheeze (lower airway obstruction with asthma, bronchiolitis)
• Exhaling with a closed glottis (pneumonia)
• Stridor (upper airway obstruction)
• Effortless (DKA)

other

A
  • Expiratory wheeze (lower airway obstruction with asthma, bronchiolitis)
  • Exhaling with a closed glottis (pneumonia)
  • Stridor (upper airway obstruction)
  • Effortless (DKA)

Other: anaemia, fever, cardiac failure, CNS pathology

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6
Q

Most common causes of bradycardia

A

Hypoxia MOST COMMON
Bradyarrhythmia
Drugs

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7
Q

Causes tachycardia

A
Fever
Pain, Anxiety
Hypoxia, hypercarbia, Hypovolaemia
Anaemia
Arrhythmia, cardiac failure
Seizures
Drugs
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8
Q

Causes of hypotension with

  1. Wide PP
  2. Narrow PP
A
  1. Wide PP (120/20)
    - PDA
    - AR
    - Thyrotoxicosis
    - Anaemia
    - Sepsis
  2. Narrow PP (70/50, weak thready pulse)
    - Hypovolaemia
    - Haemmhoragic shock
    - Severe dehydration
    - AS, coarctation of aorta
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9
Q

24 hours of fever, lethargy and vomiting in child.

- primary diagnosis and management

A

Bacterial sepsis until proven otherwise!

  • A: Protect airway (sit up/safety position;; NG tube; yankee sucker)
  • B: Give O2 >5L/min
  • C: Give Hartmann’s or saline
  • BSLs
  • Reassess
  • ORder: Blood cultures, blood gas
  • Prophylactic antibiotics
  • Call reg and PET service
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10
Q

Lump in children - what are the 3 main differential categories?

A
  1. Congenital
  2. Inflammatory
  3. Cancer
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11
Q

What is exomphalos?

What about this kills babies?

A

Exomphalosis a weakness of the baby’s abdominal wall where the umbilical cord joins it. This weakness allows the abdominal contents, mainly the bowel and the liver to protrude outside the abdominal cavity where they are contained in a loose sac that surrounds the umbilical cord.

It is the evaporative heat loss leading to hypothermia that kills babies

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12
Q

What is the most common DDX for a lump on the eyebrow at birth
Treatment

A

Exoid dermoid cyst (developmental remnant)

Treatment is surgical excision

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13
Q

How do you treat strawberry naevi

A

Propranolol accelerates their complete regression (would go away on their own by ~5 years)

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14
Q

What are the signs of hydrocephalous in infants?

A

Macrocephaly
Sun setting eyes (can only see upper half of iris)
Bulging fontanelle
Seizures

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15
Q

Causes of hydrocephalous in infants - what is the most common?

A

Congenital

Acquired

  • Most common is medullary blastoma in 4th ventricle
  • intraventricular haemmhorage
  • SA haemmhorage
  • meningitis
  • SC lesion/tumour
  • Traumatic head injury
  • premature birth
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16
Q

What are you worried about when you see an absent anal cleft?

A

Sacrococcygeal teratoma -> tumor on coccyx that eventually grows to fill out the anal cleft and can grow larger than the baby. Turns malignant peri-natally

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17
Q

What is the functional consequence of cleft palate in babies?

A

Swallowing and sucking difficulties (can usually swallow but not suck)

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18
Q

What is the significance of an enlarged Virchow’s node in children? What does it drain?
What differentials you think of ?

A

Virchow’s node only enlarged with cancers, not inflame conditions. Drains the thoracic duct.

Hodgkins (10-15 year olds) or Neuroblastoma (very young children)

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19
Q

What is the most common anorectal malformation in females?

Symptoms

A

REctovestibular fistula. Abnormal connection between vagina and the rectum.

Symptoms: Gas, faeces, pus passing through vagina

  • Vulvar irritation, inflammation
  • Gross smelling vaginal discharge
  • Frequent UTIs
  • Pain during sex if older
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20
Q

Clinical features of malrotation

A

Early signs

  • Bilious vomiting (flour green)
  • Poor feeding

Late signs include: PR bleeding, abdominal distention and tenderness

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21
Q

What causes malrotation?

A

Anatomical variation where base of mesentery is narrow which means DJ flexure and Ileocaecal flexure are next to each other, in RUQ which results in SHORT BASE OF MESENTERY and predisposes the mesentery to volvulus

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22
Q

With malrotation, at what point does venous and arterial supply become compromised and when is best to intervene?

A
  • If mesentery twists 360deg, venous and lymphatic supply are compromised resulting in bile-stained vomiting. Surgical intervention here has good outcome.
  • If gut rotates further, arterial supply can become compromised -> intestinal ischaemia and infarction
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23
Q

How do you diagnose malrotation?

What is the treatment?

A

Upper GI contrast study is gold standard - look for LOSS OF C-shaped duodenum to indicate malrotation

Or AXR changes: double bubble, gastric and proximal duodenal dilatation…

Urgent surgical referral and laparotomy -> LAdd’s procedure + appendicectomy

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24
Q

Child with bile stained vomiting - diagnosis

A

Malrotation +/- volvulus until proven otherwise

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25
Non-bilious vomiting in neonates - differentials
Pyloric stenosis Infection - Sepsis, Meningitis, UTI Reflux Overfeeding
26
Typical presentation of hypertrophic pyloric stenosis
PYLORIC STENSOSIS: Typically first born boys, with non-bilious projectile vomiting (vomit past their feet) after each feed who are HUNGRY after! - family history of HPS - visible gastric peristalsis +/- palpable pyloric tumour ('olive') if stomach isn't too distended
27
When does pyloric stenosis typically present?
Peak 3-6 weeks old But can occur 10 days-11 weeks
28
What metabolic derangements do you see in pyloric stenosis and why?
Due to profuse vomiting -> losing water, HCL, NACL, K Metabolic alkalosis Hypochloraemia Hypokalaemia Normal serum na Acidic urine (paradoxical change - kidneys conserve Na as compensation)
29
What is intussception and what generally causes it?
Invagination of proximal into distal bowel - Peaks at 5-11 months - Physiological/idiopathic cause is most common (hypothesised that as babies wean, new antigen exposure causes payer's patches in terminal ileum to swell from inflammation and cause intussception) Less commonly can be due to pathological lead points
30
Classic presentation of intussception
Crampy (intermittent, also known as colicky) Abdominal pain (infant pulls legs into stomach to relax abdo wall) Vomiting Bloody 'red currant jelly' stools (LATE sign) Sausage shaped mass in RUQ and emptiness in RLQ.
31
What are 'anatomic' or 'pathological' lead points of intussception
Merkel's diverticulum Polyp Vascular malformation lymphoma
32
Complications of intussception if not treated early
Bowel obstruction, | Ischaemia, perforation, shock
33
How do you diagnose intussception?
Clinical suspicion -> US ('target sign') is first choice or AXR (?soft tissue mass ?absence of gas in caecal region)
34
Treatment intussception
<48 hour history in otherwise stable child = air enema reduction >48 history or peritonitic/septic child = laparotomy
35
Treatment pyloric stenosis
Fluid rehydration therapy and electrolyte replacement - 0.45% saline with 5% dextrose - Add K when baby is urinating Non-urgent surgical referral
36
Treatment exompathalous
Place baby in humidicrib wrapped in glad wrap (ensure blood supply of exposed bowel isn't twisted/compromised) NGT for GI decompression Fluid resus Urgent T/F to tertiary centre
37
DDX for acute scrotum (red, painful, tender scrotum) Immediate management
- testicular torsion - torsion of appendix testies - epididymo orchitis - idiopathic scrotal oedema Urgent surgical referral ?surgical exploration
38
Classic presentation of appendicitis
Colicky periumbilical pain migrating to RLQ and becoming constant Assoc w : - anorexia - fever - nausea - d&v
39
What are warning signs for appendicitis in kids?
abdo pain >24 hours diarrhoea >24 hours Infant preferring to lie still Suspected peritonitis if child doesn't allow abdo exam
40
What group most commonly have atypical presentations of appendicitis and how do you diagnose it?
Kids <5 yo Adolescent girls Need U/S diagnosis - May need to do bloods (CRP, WCC), but bloods are NOT ROUTINE in kids.
41
Long term effects of diptheria infection
Toxin causes nerve and heart damage | Mortality 1/15
42
Long term effects of tetanus infection
Toxin causes nerve and muscle changes resulting in paralysis, convulsions Mortality 1/10
43
Pertussis - effects of infection
Whooping cough. M&M highest in infants
44
Poliomyelitis - effects on infection
Febrile illness followed by paralysis in many (may become permanent) Mortality 1/20
45
HIB - effects of infection
Systemic infection - meningitis, epiglottitis, bone and joint infections Mortality 1/20
46
MMR
Measles encephalitis 1/2000, mumps encephalitis 1/200
47
Where to give vaccines to children?
• Children under 1 ○ Anterolateral thigh (if 3 vaccines given at once, space injections 2.5 cm apart with third vaccine in other thigh) • Children >1 ○ Mid-deltoid region of upper arm • NOT BUTTOCKS -> risk damage to sciatic nerve
48
Side effects of vaccines
* Local superficial inflammatory response -> redness, swelling at injection site * Mild transient systemic SX (crying, irritability, mild fever, febrile seizures) * Measles may be followed by mild, transient measles like illness (fever and brief rash 7-10s post immunisation) * anaphylaxis is v rare
49
What extra vaccines what an aboriginal/torres straight islander child receive?
BCG | Hep A vaccine
50
Vaccines given at 2,4,6 months
DTPa (Diptheria, tetanus, whooping cough) HIB IPV (inactive polio vaccine) HBV PCV (13v pneumococcal conjucate) RV (Rotavirus)
51
Vaccines given at 12 months
MMR (measles, mumps, rubella) HIB MenCCV
52
Vaccines given at 18mo
VZV (chickenpox) MMR (measles mumps rubella) DTP
53
Vaccines given at 4 years
DTPa (diphtheria, tetanus, pertussis) | Polio
54
Vaccines given at 10-15years
DTPa (diphtheria, tetanus, pertussis) VZV (chickenpox #2) HPV
55
Vaccines given at birth
HBV
56
Pattern of generalised seizure vs focal seizure
Generalised: wide spread all over brain, symmetric activity bilaterally Focal: starts in localised area of brain, unilateral
57
What is another term for focal seizure that is commonly used and how is this further classified based on consciousness?
Partial seizure - Simple partial seizure: consciousness intact (motor, somatosensory, visual/auditoary, autonomic, dysphasic) -Complex partial seizure (consciousness not intact)
58
How are generalised seizures further classified?
Tonic clonic Absence Myoclonic Atonic, Tonic etc
59
Do generalised seizures affect consciousness? Motor systems?
Yes, always involve consciousness AND motor manifestations!
60
What is the definition of a seizure vs of epilepsy
Seizure: Transient occurrence of signs and/or SX due to abnormal, excessive or hypersynchronous neuronal activity in cerebral cortex Epilepsy: Tendency to have recurrent unprovoked seizures (2 or more AFEBRILE seizures)
61
What types of seizures aren't included in the definition of epilepsies?
1. Single seizure events 2. Neonatal seizure 3. Febrile seizures 4. Acute symptomatic seizure (systemic illness, acute neurological insults)
62
Investigations for seizures in children
EEG (+/- video monitoring) MRI if… ◊ Suspected underlying cerebral abnormality ◊ Significant developmental delay ◊ Abnormal neurological findings on exam ◊ History of prior ne◊ Poorly controlled seizures CT only if suspected stroke, increased ICP, traumatic brain injury (never perform in otherwise well child)
63
Seizure mimics
○ Normal phenomenon § Sleep jerks § Tantrums § Inattention, day dreaming ○ Syncope and related episodes § Vasovagal § Breath-holding spells § Long QT syndrome ○ Parasomnias and related sleep disturbances § Night terrors, sleep walking, cataplexy, confusional arousals ○ Movement disorders § Tics, clonus, chorea, tremor ○ Behavioural and psychiatric disturbances § Mannerisms, psychogenic seizures, rage attacks ○ Migraine variants and NV episodes § TIA, complicated migraine, benign paroxysmal vertigo
64
How can absence seizures be provoked?
hyperventilation
65
what are febrile seizures often associated with? What ARENT they associated with?
Mostly assoc w URTI/UTI/viral exanthema Family history of seizures (30%) - same mutation in neuronal ion channel gene Age-limited predisposition to seizures (mostly 5mo-2yrs) NOT ASSOC W: CNS illness, prev afebrile seizure, incr mortality or later intellectual impairment
66
Medications for epilepsy
Sodium valproate Carbamazepine Lamotrigine Ethosuximide
67
DDX for generalised tonic clonic seizure (and what you would expect for each on history)
Focal seizure becoming generalised □ Preceding aura (note: NO aura with generalised TC) □ Todd's paresis (transient unilateral postictal weakness) □ Focal neurological deficits on exam □ HX of prior CNS illness/cerebral trauma Syncope □ Vasovagal setting □ Brief duration with rapid recovery Psychogenic seizure □ Eye closure during seizure □ Resistance to passive eye opening □ Intermittent or waxing and waning motor activity
68
what broad category of seizure if there is limb jerking/head turning/stiffening that is UNILATERAL?
Focal seizure! Not generalised because must be in one hemisphere only.
69
What type (lobe?) of focal seizure often gets confused for absence seizure?
Temporal lobe epilepsy
70
What type of (lobe?) focal seizure features hyperkinetic autisms (tapping, cycling, running in place)
Focal lobe epilepsy
71
Treatment of generalised vs focal epilepsies
Generalised seizures: Sodium valproate Focal: Carbamazepine
72
What is the best method of measuring temp in children and what is the upper limit of normal (degC)
Electronic thermometer in axilla Axillary > 37.2C
73
What is the definition of PUO?
Fever without focus for >2 weeks
74
What are the 3 main causes of PUO
1. infection (?encapsulated bacteria) 2. autoimmune 3. malignancy
75
What 3 main encapsulated bacteria infect kids
HIB Strep pneumonia Neisseria meningiditis
76
What do you do if a child comes in with a fever?
``` If child is : > 3months non toxic fever <14 days It is likely viral so DON'T do septic screen (possibly check urine ex: if <6 months) and review to ensure they don't deteriorate. ``` Otherwise they get a septic screen
77
What comprises a septic screen?
FBE, blood film Blood and urine cultures LP +/- CXR (if resp SX/signs)
78
What questions to ask on HX when a child comes in with fever
``` Localising symptoms: cough coryza headache photophobia diarrhoea, vomiting abdominal pain joint symptoms ``` Travel history Sick contacts Immunisation hx
79
SX, signs suggestive of a 'toxic' or unwell child
``` Lethargic Poor interaction Inconsolability Tachycardia, tachypnoea, Cyanosis, poor peripheral perfusion ```
80
Presentation of meningococcus
Rapid onset Fever Flu-like SX (malaise, lethargy, vomiting, headache, myalgia, arthralgia) Confusion Rash (petechial/purpura) Photophobia Neck pain/stiffness
81
Differentials for child presenting with fever and petechial rash (previously well, onset this am)
Meningococcus if unwell/shocked/toxic Viral infection (enterovirus, influenza) HSP ITP
82
15 month old presents with a non-itchy blanching erythematous rash (not on face) following 3 days of sudden-onset high-grade fever and a single febrile seizure. What's your top differential? Treatment?
HHV6 (roseola) No treatment required - self limiting.
83
Child presents with 'slapped cheek' rash on face and lacy rash on trunk and limbs following low-grade fever, malaise, or a "cold" a few days before the rash broke out. Differential? Treatment?
Parvovirus B19 No treatment required bc is viral +/- Paracetamol to bring down fever
84
What is a rare complication of parvovirus B19 infection in pregnant women? How common is this?
If exposed to ParvovirusB19 in first half of pregnancy, baby can get fetal anaemia hydrops fetalis and fetal death (miscarriage) Occurs in 5% of pregnant women infected with parvovirus
85
What are the clinical features of measles?
4 day infectious prodrome (3 Cs) preceding rash: Cough, coryza, conjunctivitis Fever Koplik's spots Rash (red, blotchy, starts on the head and then spreads to the rest of the body) - lasts ~7d
86
2 year old with incomplete immunisations at creche with fever and cough, coryza, conjunctivitis progressing to descending, blotchy raised (papular) rash - diagnosis
Measles
87
Management for measles
MMR vaccine (2 doses) within 72 hours of exposure if >9mo IVIG if <9mo or >9mo but >72 hours post exposure
88
Differentials for diffuse erythematous rash (sunburn-like) in child
``` Toxic shock syndrome (Staph or strep) Scarlet fever/Invasive GAS Kawasaki disease Enteroviral infection Antibiotics ```
89
what is the most severe complication of measles?
Encephalitis -> fatal in 15%
90
What causes Scarlet fever?
Exotoxins from Group A Strep (pyogenies)
91
What infections does GAS cause?
``` Scarlet Fever Pharyngitis Toxic shock Necrotising fasciitis Acute rheumatic fever GN ```
92
Clinical presentation of scarlet fever
Exudative tonsillitis +/- pharyngitis Confluent erythematous sunburn-like rash Strawberry tongue Circumoral pallor
93
Treatment of scarlet fever
Penicillin (oral) - to treat GAS
94
What infectious agents cause toxic shock syndrome?
Exotoxins from staph aureus and strep pneumonia and strep progenies
95
Features of Kawasaki disease
Fever>5 days (unresponsive to antibiotics) Polymorphous rash Bilateral non-exudative conjunctivitis Mucus membrane changes (oropharynx injected, strawberry tongue, swollen lips) Swollen erythematous hands and feet with eventual desquamation Unilateral cervical lymphadenopathy >1cm
96
Treatment of kawasaki disease
IVIG and low-dose aspirin
97
Complication of kawasaki disease
Coronary artery disease (aneurysm) | Higher risk of IHD
98
Features of infectious mononucleosis (glandular)
``` FEVER Exudative pharyngitis Tonsillitis Lymphadenopathy Splenomegaly Palatal petechiae Rash ```
99
Management of mono
None | Steroids only if airway obstructed due to tonsillar enlargement
100
What is TTN? RF?
Tachypnoea of the newborn (TTN) = wet lung retention of fetal long fluid □ C-section without labour -> 'Cold' c-section = no maternal hormone surge hasn't caused resorption of fluid yet □ Breech delivery □ Male sex □ Birth asphyxiation □ Heavy maternal analgesia
101
characteristic CXR for TTN
Coarse streaking w fluid in fissures
102
Mx TTN
most babies settle in 24-48 hours with minimal handling and cot O2. CPAP if acidotic, low sats, working hard to breathe.
103
Signs of resp distress in a newborn
○ Tachypnoea (>60breaths/min) § In response to incr CO2 in order to breathe out and decr the CO2 ○ Expiratory grunt § Produced by exhalation against a partially closed glottis in order to increase PEEP and therefore keep alveoli open § May be interpreted as crying or moaning ○ Recession of intercostal spaces and suprasternum; in drawing of subcostal margin § Due to the increased resp effort generating more negative intrapleural pressure which sucks in the softer/more compliant chest wall during inspiration ○ Nasal flare § Flare during inspiration decreases airway resistance ○ Central cyanosis § Note - polycythaemic babies will appear cyanosed at relatively high O2 sats but babies with low Hb will not appear cyanosed until saO2 is v low. ○ Deranged temperature control ○ Low O2 saturation
104
Ix for resp distress in a neonate
``` BSL CXR FBE, blood film, UEC Blood culture VBG ```
105
What is infant RDS? Another name for it? Who gets it (RF)? Treatment?
= hyaline membrane disease § Occurs in pre-term infants due to surfactant deficiency in the alveoli Mx: Empirical abx because looks similar to sepsis! CPAP If need more, intubate and give surfactant (need intubation).
106
Characteristic CXR appearance of RDS/HMD
Hypo aeration, diffuse ground-glass appearance, air bronchograms
107
RF for meconium aspiration?
Post-term (>40 weeks) | Births involving fetal distress
108
what is the pathophys behind meconium aspiration syndrome?
Aspiration of substances leads to obstruction, atelectasis and chemical and mechanical pneumonitis
109
RF for neonate sepsis
Maternal GBS positive Maternal fever Prolonged rupture of membrane (>=18 hours)
110
Signs of pneumothorax
``` Most sensitive is transilluminator Tracheal deviation Chest asymmetry Unequal expansion Decr breath sounds unilaterally Resp distress ```
111
Abx coverage for neonatal sepsis (what bugs are you worried about?)
Gentamicin (listeria, e coli, HIB) | Benzyl-penicillin (GBS)
112
Differentials for resp distress
``` TTN/wet lung HMD/RDS Meconium aspiration syndrome Sepsis pneumothorax congenital pneumonia Cardiac (VSD, PDA, transposition, pulm HTN) Anatomical - although not usually in neonatal period (laryngomalacia etc) Drugs ? ```
113
RF for pneumothorax in neonates
Being on CPAP | Resp distress
114
Mx for MDS
NO evidence for suctioning airways (UNLESS baby is floppy or has no/inadequate respirations then it is reasonable to suction under direct vision using laryngoscope) Septic workup CPAP if needed/intubation
115
metabolic disturbances causing apnoeic episodes in premmies
Hypoglycaemia, hypocalcaemia, hypo/hypermagnesaemia
116
Define apnoea in neonates
§ No air flow occurs for >=20sec § No air flow for >=10sec + bradycardia or desat
117
General management of Respiratory distress in neonates
Observation - admit to neonatal nursery, incubator Monitor vital (HR, RR, saO2) Septic workup (FBE, blood film, blood cultures, CXR, vBG) Empiric antibiotics (gent and benpen) IV fluids (10% dextrose at 60ml/kg daily) Advice from senior physician! Additional resp support (CPAP, intubation)
118
Definitions for - term - pre term - post term
* term: ≥ 37 completed weeks' gestation * preterm: < 37 completed weeks' gestation * post-term: > 42 completed weeks' gestation
119
Definitions for - LBW - VLBW - appropriate weight for gestational age
• low birth weight (LBW): < 2500 g • very low birth weight (VLBW): < 1500 g - appropriate weight for gestational age; between 10th and 90th percentiles
120
3 things to look for on GI when examining a baby
1. pink (well perfused) 2. no incr WOB (resp effort) 3. active, good tone
121
when is bronchiolitis most common?
Up to 2 years of age | In winter/rainy season
122
Risk factors for bronchiolitis
Maternal smoking, pre-term delivery, chronic lung disease of prematurity, allergy, CHD, immunodeficiency
123
common causative agents of bronchiolitis
``` VIRAL always Rhinovirus #1 cause of mild bronchiolitis RSV #1 cause of SeVere bronchiolitis HRV Parainfluenza, influenza A/B Adenovirus ```
124
SX and signs of Bronchiolitis
``` Low grade fever § Tachypnoea § Mild dry cough § Expiratory wheezing § Hyperinflation § WOB § Fine inspiratory crackles § Difficulty feeding if severe ```
125
Mx of bronchiolitis
○ Mx - supportive (O2, fluids, nutrition)
126
What is the most common cause of wheeze in the first 2 years of life?
Viral bronchiolitis
127
Complications of Pertussis (whooping cough) who is most at risk?
Apnoea, severe pneumonia, encephalopathy, death Most at risk is <6mo
128
Clinical signs and investigations : Pertussis
§ Prodrome of a few days: nasal discharge and mild dry cough § Cough becomes more pronounced and characteristically 'whoop'ing § +/- severe vomiting and subconjunctival haemorrhages § Apnoea in young infants Ix: nasopharyngeal specimen: immunofluorescent Ab, culture
129
Treatment of pertussis
§ Admission for supportive therapy § Macrolide antibiotics if early in course of disease or v severe Sx § Treat household contacts § Contact precaution (until 5 days of antibiotics or illness for 3 weeks)
130
Most common causes of viral pneumonia in kids
``` parainfluenza influenza RSV Human metapneumovirus (HMV) Adenovirus Human rhinovirus ```
131
What does an x ray of viral pneumonia look like?
CXR: patchy, widespread bilateral infiltrates rather than lobar involvement
132
Clinical présentation of viral pneumonia
Dry cough Fever LOA
133
Complications of HIB
Epiglottitis | Meningitis
134
Risk factors for HIB
``` Age <5yo Indigenous Lower SES Male sex Congenital and acquired immunodeficiency ```
135
Causative agents of bacterial pneumonia
1. Strep pneumonia most common by far! 2. Staph aureus 3. Mycoplasma pneumonia 4. HIB Less common causes: - Group A beta haemolytic strep (pyogenies) - Klebsiella
136
Presentation of pneumococcal pneumonia Typical CXR findings
``` fever sob pleuritic CP wet cough tachypnoea grunting nasal flaring Reduced expansion, dull to percussion, reduced breath sounds, bronchial breathing on affected side ``` CXR: lobal opacification although can be patchy
137
What antibiotics to use for pneumococcal pneumonia?
Penicillin and third gen cephalosporin
138
lung complications of pneumonia what clinical features are the same, and what are different?
Pleural effusion Pneumothorax same - tracheal deviation and reduced breath sounds different - stony dull percussion and bronchial breathing above effusions.
139
what is the typical CXR appearance of mycoplasma pneumonia?
Central peribronchial opacification Extensive opacification of 1+ lobes Air bronchograms
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Presentation of staph pneumonia
``` □ Shorter acute HX than other forms of pneumonia (acute onset, rapid course) □ Appears more toxic □ High fever □ Marked tachypnoea □ Significant resp distress □ Non-specific chest signs ```
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Complications of staph pneumonia
``` LARGE pleural effusions Empyema Tracheal deviation Abscesses Air leaks (pneumothorax) ```
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Antibiotics for staph pneumoniae
IV flucloxacillin and third generation cephalosporin (cefotaxime) Vancomycin if MRSA suspected
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RF for staph pneumonaie
Low SES | Indigenous b/g
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Examples of ACYANOTIC heart defects
``` 1. L->R shunt VSD PDA ASD AVSD ``` ``` 2. Obstructive heart defects Pulmonary stenosis Aortic stenosis Coarctation of aorta Hypoplastic L heart syndrome ```
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Presentation of a VSD
Depends on the size 1. Small: pan systolic murmur @ L sternal edge rad to axilla BUT ASYMPTOMATIC at birth bc pressures between L and R heart are equal 2. Large: left heart dilatation leads to displaced apex, parasternal heave - SX of HF occur after lungs open up and L sided pressures > R. (poor feeding, FTT, tachypnoea, incr WOB, hepatomegaly) Note: L heart dilatation occurs because L heart has to work harder to generate the same CO w shunt present.
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what are the 2 most common types of CHD in kids?
1. VSD | 2. PDA
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What are SX of heart failure in a newborn?
tachypnoea SOB and sweating when feeding Failure to thrive Incr WOB
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Long-term complications of VSD
® Progressive AR if shunt is located close to aortic valve (aortic leaflets sucked/prolapses into defet due to high-velocity L->R flow) Pulmonary HTN due to Increased pulmonary pressures (L-> R shunt)
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What causes the ductus arterioles to close? when does this occur?
Closes in first 1-7 days post birth due to decreased circulating PGE2 and increased paO2, as well as muscle contraction
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What can cause the ductus arteriosus to fail to close?
Prematurity | Congenital malformation
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What is the treatment for a PDA in a premature infant?
Indomethacin or other NSAIDs (inhibit PGE2 to promote ductal constriction and closure)
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Why do you treat small PDAs and how? How does this differ from treatment of large PDAs?
Small PDAs are treated to prevent endocarditis rather than to treat symptoms or complications. Via transcatheter duct occlusion. Large PDAs need surgical ligation .
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How do PDAs present?
Small PDAs generally asymptomatic. May have continuous murmur at upper L sternal edge. Large PDAs present with L heart dilatation (displaced apex beat, parasternal heave) and progressive SX of heart failure. + Bounding pulses + Apical mid-diastolic murmur
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What investigations do you do if you hear a murmur in a baby?
CXR ECG ECHO is diagnostic
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Where do most ASDs occur?
fossa ovale (central part of atrial septum)
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How do ASDs present?
Small ASDs go undetected (low pressure gradient across atria) Large ASDs rarely symptomatic in childhood -may cause Atrial arrhythmias in adulthood, and reduced exercise capacity Because L->R shunt causes R heart enlargement -> - parasternal heave - ES murmur in pulmonary region with fixed splitting of A2 and P2
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What might an ECG of ASD show?
partial RBBB
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What is the treatment for ASD and when is it indicated?
Indicated if patient has RH enlargement Transcatheter or surgical closure
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Which congenital heart defect is most assoc w down syndrome?
AVSD
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How does AVSD present?
Partial AVSD - behaves physiologically and symptomatically like ASD Complete AVSD - presents like severe VSD (FTT, feeding difficulties, tachypnoea, WOB)
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Treatment of AVSD
almost always needs surgical closure
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What is the most common type of Acyanotic obstructive heart defect? What type of murmur is associated?
Pulmonary Stenosis Ejection systolic @ L upper sternal edge Radiating to back Ejection click earlier than with AS A2 and P2 widely split
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how does pulmonary stenosis present?
usually asymptomatic in children and infants Mild is benign, non-progressive finding Severe can lead to heart-failure
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What causes AS in children usually. What type of murmur?
Bicuspid aortic valve ES murmur over aortic area + radiation to carotids Ejection click later than PS Less splitting of A2 and P2 than PS
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How might AS present in kids
ES murmur Apical heave due to LV hypertrophy Gradual progression of SX (syncope, angina, dizziness on exertion, sudden death) Severe cases, HF evident at birth
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When do you treat AS in kids? How?
If symptomatic or ECG changes w exercise ``` Balloon valvuloplasty (trans-acth) or aortic valvotomy (surgical) ```
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what is coarctation of the aorta? What can it result in?
Stricture at distal part of aortic arch (max obstruction site close to aortic end of Ductus arteriosus) Can lead to severe cardiac failure in newborns with oliguria and acidosis
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When does cardiac failure onset in newborns with coarctation of aorta? How might this present on exam?
When ductus arteriosus closes because then there is NO blood flow to the rest of the body. Diminished/absent femoral pulses unequal BPs between L and R arm
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Treatment of coarctation of aorta
surgical repair as early as possible!!
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CXR findings of severe coarctation of aorta
Cardiomegaly Pulmonary congestion Abnormal appearance of aortic knuckle Rib notching (due to enlarged IC arteries bypassing obstructed segment of aorta)
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If a newborn has coarctation, what else might you expect?
other congenital heart defects such as : VSD PDA valvular abnormalities
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How does hypo plastic L heart syndrome present? What is it?
§ Infants present w severe cardiac failure or shock within first few days of life □ All periph pulses diminished or absent Small left ventricle (hypoplasia) - Underdevelopment of left heart + valves (often assoc w severe MS and AS)
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What is hypo plastic left heart syndrome always associated with
always assoc w PDA otherwise they would have died. Necessary to keep systemic circulation maintained (R->L shunt due to R ventricular blood shunting via PDA into aorta )
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Complications of Hypoplastic left heart syndrome
95% die within first few weeks of life if untreated Neurodevelopment impairment if children survive due to marked hypoxia and cyanosis in early days of life
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Treatment for Hypoplastic left heart syndrome
Immediate: PGE1 keeps PDA patient initially, until SURGERY can be performed. If untreated 95% die in first few weeks of life.
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Examples of cyanotic heart defects
The 4 Ts: 1. Tetralogy of ballot 2. Transposition of great arteries 3. Tricuspid atresia 4. Truncus arteriosus
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what is the most common cyanotic heart defect? What is it commonly assoc with?
tetralogy of fallot? | Syndromes -down syndrome
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What is the tetralogy of fallot and what 4 things comprise it?
Obstruction to RV outlfow tract + septal defect below obstruction such that blood can flow from RV to LV (R->L shunting) ``` § 4 anatomical defects: □ Overriding aorta □ RV hypertrophy □ Pulmonary stenosis □ VSD ```
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Clinical picture of tetralogy of fallot
Kids: Gradual, delayed development of cyanosis Delayed exercise tolerance, finger clubbing, growth retardation Development of compensatory polycythaemia Babies: 'tet' spells: cyanosis more obvious when baby is upset, crying (Baby may go floppy, lose consciousness)
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What do you suspect if a baby becomes cyanosed only when upset and crying, and on one occasion goes floppy and loses consciousness during such an episode? What do you do to manage this?
Tetralogy of fallot Treatment - soothe the baby
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Treatment for tetralogy of fallot in kids?
get older kids to squat to incr systemic vasc resistance and reduce R->L shunting Surgical closure of VSD and repair of PS
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what type of murmur do you hear, if any, in tetralogy of fallot and what is this due to?
Ejection systolic murmur over pulmonary region due to PS (not VSD)
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What changes would you see on CXR with tetralogy of fallot?
Normal heart size; 'boot shape' (upturned apex), reduced lung vascularity (fields look blacker)
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What is transposition of great arterities?
§ Aorta and pulmonary arterty connected to wrong side of heart and as a result venous blood is directed straight through into systemic circulation § 2 parallel circulations result with ® Systemic venous deoxy blood flowing through R heart back into aorta ® Pulmonary venous oxy blood flowing through L heart back into pulm circulation
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What does survival depend on with transposition of great arteriess?
§ Survival depends on mixing of blood between circuits via foramen ovale, ductus arterosus or septal defect
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Clinical presentation of transposition of great arteriess?
® Cyanosis present at birth and generally progresses gradually ® +/- metabolic acidosis from tissue hypoxia ® No murmur
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CXR findings for transposition of great arteriess?
mildly hypertrophied heart w contour 'egg on its side', increased pulmonary vascular markings
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Treatment for transposition of great arteriess?
® Balloon atrial septostomy (intra-cath) to forcefully create an ASD as an emergency procedure to improve systemic arterial O2 sat ® Surgical correction = arterial switch (transection and re-anastamosis of great arteries to appropriate ventricle) ® Perform within first few weeks of life so you don't get atrophy of LV
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Complications of kawasaki disease
risk of coronary artery aneurysms, myocardial ischemia or infarction
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What is myocarditis caused by and what are potential complication(s)? Treatment?
Triggered by common viral infection, is immune-mediated Compl: CCF, arrhythmias Treatment: supportive +/- IV IG or immunosuppressives
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What is the risk with long QT syndrome?
At risk of ventricular tachyarrhythmias (VT or VF) with sudden urges in adrenergic drive (exercise, morning alarm), which can lead to sudden death. Runs in family. ask about fam HX of sudden death Treatment: anti arrhythmic drugs, auto defib. implant
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Treatment for heart block
® Positive chronotropic agent (isoprenaline) ® OR Positive Inotropes ® Implantation of temporary or permanent pacemaker
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What are shockable rhythms?
VT and VF?
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How might SVT present? What do you see on ECG?
Babies - mild distress w tachypnoea and poor feeding. Kids - complain of palpitations ECG shows Wolf-Parkinson White syndrome (rapid regular tachycardia 200-300bpm with narrow QRS)
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Treatment for SVT
Vagal manoeuvres (valsalva) or IV adenosine to terminate an acute episode DC cardioversion if haemodynamically compromised
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When might you pick up heart block in a baby?
Uncommon but may pick it up on routine antenatal assessment (monitoring /ECG) w fetal bradycardia <60bpm
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pathophys of RHD What can it lead to?
Autoimmune: host immune response to strep Ag -> attacks heart, synovial membranes, other tissues (mainly damages heart VALVES) Can cause myocarditis, pericarditis leading to reduced ventricular function (CCF) and arrhythmias, and mitral and aortic stenosis/incompetence
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How does RHD present?
Follows acute rheumatic fever (strep infection of throat or tonsils) - Polyarthtiris, large joints - Carditis - NEW ONSET MURMUR - Sydenham chorea - Transient truncal skin rash (erythema marginatum) - Skin nodules over bony prominences - Fever
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Causes of nephrotic syndrome
Idiopathic (90%) - minimal change disease (85%) - FSGS (15%) Non-idiopathic (10%) - HSP - SLE - Membranoproliferazive GN - Membranous nephritis - Congenital nephrotic syndrome
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What are the key features of nephrotic syndrome?
Heavy proteinaemia Oedema Hypoalbuminaemia Hyperlipidaemia Note: may get some haematuria and FSGS can cause HTN. Don't generally get renal impairment
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Key features of nephritic syndrome
Haematuria Acute fluid overload Hypertension Renal impairment
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Complications of nephrotic syndrome
Hypovolaemia Infections Thrombosis (haemoconcentration and loss of antithrombin in urine)
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Signs of renal impairment
Oliguria Increased plasma creatinine Deranged UECs
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Potential results of acute fluid overload
oedema pulmonary oedema CCF
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When do you investigate isolated haematuria?
isolated haematuria is common and usually benign when there is no history of kidney disease. Further investigations only if it occurs in 3 diff specimens over period of 2-3 weeks
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Causes of nephritic syndrome
Idiopathic hypercalciuria ( excessive urinary calcium excretion) Thin basement membrane disease (benign familial haematuria) Proliferative glomerulonephritis (IgA nephropathy, post-strep GN, SLE, HSP)
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What is post-strep glomerulonephritis caused by and what is the typical presentation?
Group A beta haemolytic strep (progenies) ○ Follows 7-14 days after group A beta haemolytic strep throat infection or 3-6 weeks following strep skin infection ``` Presents w: MACROSCOPIC haematuria acute fluid overload (facial and leg oedema +/- papilloedema) HTN Lassitude, fever, loin pain ```
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Mx of post-strep GN
Oral penicillin for 10 days If fluid overloaded: fluid restrict, low salt diet, frusemide Dialysis if urea >50-60mmol/L, or hyperkalaemia or pulmonary oedema not controlled by diuretics and fluid restriction
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electrolyte changes in renal failure
Incr: K, phosphate, Mg, urea, creatinine, H Decr: Na, Ca Metabolic acidosis
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What is the clinical picture of IgA nephropathy
``` Macroscopic haematuria (haematuria often occurs at same time as intercurrent viral infections) ``` May present as acute renal failure with gross oedema and HTN May be asymptomatic
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Changes expected on positive SLE bloods
§ Serum C3 low | § ANA, anti-dsDNA positive
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Protein in urine can be normal in many kids. At what time doing a alb: creatinine spot test would you expect to see abnormally elevated results.
First morning void (Should be negligible if normal). In normal kids with no pathology, incr protein secretion occurs during the day, NOT overnight
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How does minimal change disease typically present
``` Children <10 Generalised oedema (facial puffiness, peripheral oedema, ascites) ``` NORMAL BP and renal function 30% have microscopic haematuria Normal C' levels
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Treatment for nephrotic syndrome
Steroids | Fluid restriction and low salt diet if fluid overloaded +/- albumin
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Complication of ascites
Spontaneous bacterial peritonitis (infection with encapsulated bacteria such as klebsiella, pseudomonas, e coli, staph aureus, strep pneumonia)
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When would you suspect FSGS in a kid with nephrotic syndrome What is the prognosis?
If they are steroid and/or immunosuppressant resistant If they have multiple relapses Prognosis is poor - 60% progress to ESKD over 10 years.
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Investigations for atopy
Skin prick testing is first line (needs specialist referral) Serological testing (lower specificity and sensitivity)
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What is cystic fibrosis?
Autosomal recessive disorder common in caucasian population caused by defect in CF transmembrane conductance regulator gene which codes for a Cl channel present on epithelial cells of the conductive airways and GIT
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How might cystic fibrosis be diagnosed?
Neonatal screening Meconium ileus Positive sweat test ([Cl]>40) In adulthood, presentation with pseudomonas pneumonia or male infertility (due to bilateral absence of vas deferens)
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What is the pathophys behind cystic fibrosis
Defective or absent Cl channel means that Cl is not getting pumped into secretions which would normally draw water in to thin secretions out, so as a result secretions are abnormally viscous. Thick meconium can get stuck and lead to meconium ileum (emergency! Ciliary dysfunction and damage due to thick mucus build up Leads to mucus buildup and inflammation and recurrent infection in lungs initially. Recurrent infections and mucus buildup lead to bronchiectasis Leads to thickened pancreatic secretions that block exocrine secretion from pancreas. protein and fat aren't absorbed -> poor weight gain, FTT, Steatthorea. Over time pancreas is damaged from backed up enzymes and can lead to acute or chronic pancreatitis. Eventually leads to pancreatic endocrine dysfunction leading to insulin-dependent diabetes
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Bugs that kids with cystic fibrosis are particularly prone to
Staph aureus (GP) and pseudomonas (GN)
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Chronic complications of Cystic fibrosis
Bronchiectasis from recurrent/chronic lung infections. Respiratory failure and death Nasal polyps Digital clubbing Infertility in men due to bilateral absence of vas deference Pancreatic failure Liver disease Growth delay Osteoporosis Urinary incontinence
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4 domains of development
○ Gross motor ○ vision and Fine motor ○ Social, emotional, daily living ○ Communication, language, hearing
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What are the 3 common features of all kids with cerebral palsy
□ Deformity, contracture, hip dislocation □ Tone and/or movement disorder □ Spasticity, dystonia, chorea etc NOT all kids w CP have intellectual disability!
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What should all kids w possible developmental delay/behavioural and attention difficulties get done (Inx-wise)?
Formal hearing and vision testing | speech assessment
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What does HEADSS stand for?
``` Home Education Activities (hobbies etc) Alcohol • A lot of kids your age start experimenting w drugs and alcohol - have you ever tried any alcohol, or drugs? ``` Drugs Sex/sexuality • Are you involved in a romantic relationship?? Suicide
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when do solids get introduced?
between 4 and 6 months
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when should babies be sleeping through the night by?
3-6 months .
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When to refer to speech and audiology assessment for a child with 'language' delay?
<50 words at 2yo or no 2 word combinations at 2yo | Doesn't understand simple instructions without gesture
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When to refer to speech and audiology assessment for a child with 'language' delay?
<50 words at 2yo or no 2 word combinations at 2yo | Doesn't understand simple instructions without gesture
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What are the 3 realms of problems that kids w Autism have?
1. problems w socialisation 2. problems w communication 3. repetitive or obsessive behaviours
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What is the mean IQ ?
IQ: mean 100 w SD of 15
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Differentials for developmental delay
○ Deprivation/abuse ○ Neurodegenerative disorder ○ Unrecognised epilepsy ○ Severe sensory or developmental disorders (ASD, ADHD, cerebral palsy) ○ Cultural differences, mental health disorders, ill health, refusal to participate ○ Movement difficulties
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what is the screening for down syndrome?
§ 1st and 2nd trimester serum markers □ Low alpha-fetoprotein and pregnancy associated plasma protein A □ High chorionic gonadotrophin levels □ Low blood oestriol levels § US findings - nuchal thickening, characteristic malformations
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characteristic dysmorphic features of down syndrome
§ Hypotonia § Eyes slated, epicanthic folds, brushfield spots § Tongue appears large § Ears small and poorly formed § Hands broad, simian crease (single palmar crease) Gap between first and second toes
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Diagnosis of down syndrome
Microarray or FISH (genetic testing showing trisomy 21)
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Common co-occurring malformations with Down syndrome
§ Congenital heart disease (tetralogy of fallot, AVSD etc) | § GI malformation (duodenal atresia, imperforate anus, Hirschsprung disease)
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Pathological Causes of constipation in kids
``` SC lesions Spina Bifida Intestinal neuropathy (Hirschsprung's) Cow milk protein intolerance Coeliac disease Cystic fibrosis Metabolic (hypothyroid, hypercalcaemia) Pyloric stenosis, malrotation +/- volvulus, incarcerated inguinal hernia Cerebral palsy Drugs ```
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Causes of delayed passage of meconium
``` Cystic fibrosis Malrotation +/- volvululus Fistula Imperforate anus Down Syndrome Hirschsprung's ```
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Functional causes of constipation in kids
Physiological/functional - withholding behaviour - pain - anxiety - diet - dehydration - change in lifestyle (weaning onto solids, toilet training, starting school)
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What is fecal incontinence associated with?
- Painful or frightening event assoc w defecation in early childhood - Limited attention or learning disability - Nocturnal enuresis/urinary incontinence - Constipation (overflow)
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Management of constipation in kids
1. Change behaviour (toilet sits, position on toilet, stool diary) 2. Diet - incr fluid and fibre, healthy diet 3. Education 4. Disimpaction if there is significant impaction that they are unlikely to pass 5. Laxatives Regular review and monitoring
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What are the mechanisms of action of the following laxatives: 1. Paraffin oil 2. Senna 3. Coloxyl 4. Movicol 5. Osmolax 6. Colonlytely
1. Paraffin oil - lubricant/softener 2. Senna - stimulant 3. Coloxyl - Softener 4. Movicol - osmotic 5. Osmolax - osmotic 6. Colonlytely - osmotic
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Exam and Ix for constipation
Exam - Neurological lower limb motor and sensory (neurological/spinal abnormalities) - Abdominal exam (faecal masses?) - Height, weight (FTT) - Spine and external exam of anal region (sacral teratoma, spina bifida, imperforate anus) Ix - none unless SX continue despite behavioural modifications and laxative therapy, then look into pathological causes
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what is the most common cause of constipation in kids?
Functional at >95% cases
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Causes of vomiting in neonates
Systemic infx/sepsis Bowel obstruction (anal atresia, duodenal atresia, Hirschsprung, meconium ileus w CF, incarcerated inguinal hernia) Hypoglycaemia Malrotation +/- volvulus UTI/renal disease Adrenal insufficiency (congenital adrenal hyperplasia, w ambiguous genitalia in females)
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Causes of vomiting in infants
``` infection lesions of GIT (malrotation, strangulated inguional hernia, pyloric stenosis) GORD Coeliac Gastroenteritis Intussception (3-12mo) ```
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Causes of vomiting in older kids
Migraine headache Sepsis Intracranial neoplasm (morning vomiting and headaches) Acute appendicitis and peritonitis (>5yo) Poisoning Psychological (anxiety, stress)
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SX and Treatment of overactive bladder
SX - frequency, incontinence, bed wetting, HOCKERING posturing +/- fecal incontinence often resistant to alarms and desmopressin, persisting beyond 10yo Treatment - regular toiling program + anticholinergic (oxybutynin)
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Investigations for urinary incontinence
U/S KUB (?Structural abnormality) Uroflow (filling or emptying problem?) Post-void U/S (?Residual volume)
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Treatment of monosymptomaatic NE
Alarms worn at night Wetting diary Desmopressin (synthetic ADH/vasopressin analogue) - used for those who ave not responded or are unsuitable for alarm. Child should NOT drink overnight (risk hyponatraemia)
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Treatment of polysymptomatic NE
Alarms Treat constipation/fecal incontinence and exclude UTI Anticholinergics (oxybutynin) Frequent, regular voiding
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Causes of daytime wetting without NE
``` Urge incontinence (overactive detrusor muscle) - urgency, freq, posturing, wetting ``` ``` Dysfunctional voiding (lack of coordination between detrusor and bladder neck activity w poor relaxation of external sphincter during voiding) ASsoc w high residual volumes, upper tract dilatation MX- teach pelvic floor/sphincter relaxation and optimal voiding techniques ``` ``` Neurological - neurogenic bladder (large of expressible bladders +/- NE ) Urological pathology (fistula, ectopic ureter) - constant rather than episodic bladders, may have NE too ```
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Risk factors for DDH
Female ○ Breech presentation ○ Positive family history of DDH Oligohydramnios
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Detection of DDH O/E and Inx
§ Ortolani - detects dislocated hip reducing during exam § Barlow - detects dislocating or subluxing during exam § Positive tests are ones in which 'clunk' is felt (click/popping) § Other signs to look for: □ Discrepancy in leg length □ Asymmetrical thigh skin folds (also present in 25% normal babies) ○ Ix: ultrasound <6months X-rays > 6 months
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Treatment for DDH | What happens if not treated early?
Tx: Pavlik harness. If not treated early, hip joint develops abnormally and open or closed surgical reduction is required
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What is DDH?
spectrum of disorders of hip instability producing subluxation or dislocation and imaging features of poor acetabular development
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Commonest organisms for meningitis
<2 years old § Group B strep (pyogenes) § E coli and other GNB § Listeria monocytogenes ``` >2 years old § above § Strep pneumoniae § Neisseria meningitis § HIB (in unimmunised children) ```
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Commonest organisms for encephalitis
Viruses - Enterovirus - HSV - Other herpes (EBV, CMV, HHV6, VZV) - Arbovirus Bacteria, fungal, parasite causes RARE
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Exam features of meningitis
Full fontanelle +/- neck stiffness Purpuric rash suggests meningococcal septicaemia
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Signs of encephalitis
Altered conscious state, focal neurological signs
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interpretation of CSF for viral vs bacterial meningitis
``` Bacterial Neutr=100-10000 (higher) Lymph<100 (lower) protein >1g/L (higher) glucose <0.4 ``` ``` Viral Neutr<100 (lower) Lymph 10-1000 (higher) Protein 0.4-1g/L (lower) Glucose normal ```
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MX of meningitis - encephalitis
Meningitis -Bacterial <2mo: IV Cefotaxime and benpen >2mo: IV ceftriaxone +/- dexamethasone (reduces risk of hearing loss) Enceph: viral -> acyclovir Analgesia Admission if bacterial meningitis or IV hydration required (bolus if shocked -> 2/3 maintenance) Monitor: - Neurological obs - BP readings - Weight and HC - UEC to monitor for electrolyte abnormalities whilst on IV fluids
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what does AVPU stand for?
``` A Alert V Responds to voice P Responds to pain - Purposefully - Non-purposefully - Withdrawal/flexor response - Extensor response U Unresponsive ```
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age range for epidiymitis
1) Only occurs immediately after birth (times when you have surges of androgens which open the vas) or in 14 + year olds
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what is the anatomical variant that predisposes boys to testicular torsion?
'Bell-clapper testes' - anatomical variant where the testes hangs on longer mesentary than usual so more prone to twisting (within tunica)
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How long do you have to save the testes from infarct with testicular torsion?
Have 6 hours with testicular torsion to save the testes from infarct
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What is another name for idiopathic scrotal oedema and what is it's typical presentation?
Allergic cellulitis Bilaterally red swollen skin w surrounding skin also red (inflammation not contained by tunica vaginalis) Often caused by flea bite on groin Often presents in middle of night, quick onset (<4-6h)
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MX of idiopathic scrotal oedema
Conservative - self limiting within 1-2 days
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DDX Left hemiscrotum is enlarged and blue - painless hard lump within scotum of a baby Ix?
Most commonly due to torsion of testes in utero DDX: testicular tumour Ix: Inguinal exploration to distinguish
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Enlarged non-erythematous right scrotal mass DDX How else might this present?
Cancer - probably rhabdomyosarcoma of cremaster muscle (cancer of spermatic cord) May also present as lower urinary tract SX -haematuria +/-urinary retention
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Primary vs secondary head injuries
Primary: - Contusion vs contre-coup - Axonal shearing - Injury to intracranial blood vessels (extradural/subdural/SA haematoma/intraventricular bleed etc) - Recognise patterns of injuries and blows to consciousness Secondary - Seizures - Hypoglycaemic state - Brain hypoxia, hypercarbia - Cerebral oedema -> Raised ICP
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Assessing a burns victim
ABCDE Airway - cervical spine needs demobilisation - ensure patent airway (+/- adjuncts +/- intubation) Breathing - O2 via mask, highest flow possible - RR and SaO2 - Expose chest for chest trauma/burns, observe chest movement (if burns are restricting chest expansion, consider escharotomy) Circulation + haemorrhage control - Pulses, CRT - IV fluid resusc - Elevate limbs if there are circumferential burns (may restrict perfusion) +/- escharotomy Disability - AVPU - Pupil size, symmetry, response Exposure - Minimise heat loss (warm room, blankets, cover wound, Baer hugger) - Expose fully, remove everything - Burn assessment (depth, % TBSA)
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Management of a burns victim
``` Dressing (clingfilm/paraffin/acticoat) Tetanus status Fluids (use TBSA% as guide) Analgesia Tubes (NGT +/- IDC if TBSA >10% +/- intubation) ```
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What is the most common cause of newborn jaundice? Why?
Physiological jaundice - As a foetus, unconjugated bilirubin is excreted by placenta. During transition to hepatic conjugation and excretion, all infants have raised bilirubin to some degree.
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When is newborn jaundice always pathological
If it occurs within first 24 hours after birth (suspect haemolysis or sepsis) Conjugated hyperbilirubinaemia
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Why does physiological newborn jaundice occur?
1. Incr RBC turnover (t1/2 less) - incr unconj bilirubin load 2. Defective hepatic uptake 3. Decr efficiency of conjugation (lower UDPG levels) 4. Breast milk jaundice (factors in milk cause incr enteric absorption of bilirubin)
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Mx of newborn jaundice
1. Observe/watch 2. Blue light phototherapy (converts bilirubin into water-soluble form that can be excreted in bile and urine) 3. Exchange transfusion (replace baby's blood w donor blood to decr bilirubin levels rapidly) SBR Levels at which these are performed are determined using standard hospital monogram Abi if sepsis suspected
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When do you use a lower SBR threshold for phototherapy and exchange transfusion?
Premature Asphyxiated infant Ill or haemolysing infant
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How long should physiological jaundice last?
~1 week, with peak SBR levels at 3 days in term babies. | Peak at 1 week in preterm babies
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Causes of pathological jaundice
1. Haemolytic 2. Incr Haem load (haemorrhage, polycythaemia, swallowed blood) 3. Impaired hepatic uptake and conjugation (Gilbert, hypothyroid, drugs etc) 4. Mixed (prematurity, sepsis, infants of diabetic mothers, asphyxia)
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Complication of jaundice
kernicterus (neuronal death caused by toxic unconjugated bilirubin crossing the BBB) -> manifests as bilirubin encephalopathy Can lead to death or survival with cerebral palsy (neurodevelopment impairment)
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Haemolytic causes of jaundice
Immune - ABO and Rh blood group incompatibility - Drug-induced Acquired - bacterial sepsis - congenital intrauterine info Hereditary - G6PD deficiency - Hereditary spherocytosis
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What is the genetic underpinnings (at risk group) for G6PD deficiency
X linked Mediterranean Asian ethnic groups
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DDX - asymmetrical scrotum When is this most obvious?
1. Varicocoeal if bag of worms appearance (Most obvious when patient is vertical rather than horizontal) 2. Undecended testes 3. Cancer 4. torsion of testes or appendix testis 5. Hydrocoeal (although may be bilaterally swollen, giving dumbbell appearance)
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What side are variocoeals more common and why is this?
Left side Because pampiniform plexus in scrotum becomes enlarged due to impaired drainage
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How do you diagnose a hydrocoeal? Tx?
Transilluminates No treatment required
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Sx of benzo poisoning
CNS depression (drowsy, coma) REsp depression Hypotension
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Mx benzo poisoning
Observation - vitals, sats, RR (intubation, IV fluids, inotropes if necessary) Call POISONS, get help from consultant, ICU Urine drug screen (benzos) Antidote - flumazenil - not generally used. only under discussion from specialist. +/- Social work/department of Human Services referral
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DDX depressed conscious state in a 2.5 year old
Ingestion/poisoning (drugs/alchohl/pesticides/poisons/medications such as benzos, opioids) Head trauma Sepsis/meningitis
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How do you evaluate paracetamol levels?
Serum paracetamol levels at 4 hours post ingestion (testing any earlier doesn't help)
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Pain management in kids (and what is the pain score) 1. mild 2. moderate 3. severe
1. mild (pain score 1-3) - Oral panadol (20mg/kg loading dose then oraly 15mg/kg q4h as req) - Oral panadeine (15mg/kg/dose q4h paracetamol and codeine) - Oral ibuprofin (helps bring down swelling, use if they are eating and drinking) - distraction/bheavioural techniques 2. Moderate (pain score 4-7) - Intranasal fentanyl and midaz (helps w anxiety) - Codeine once pain has settled to mild/moderate 3. Severe (pain score 8-10) - SC Morphine 0.15mg/kg/dose q4h - IV morphine, titrated 4 hourly
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What does bilirubin bind in the blood?
Albumin
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Things to ask on HX when assessing a jaundiced baby
Family history: - spherocytosis - G6PD/ethnicity - Previously jaundiced children - splenectomy - haemolytic anaemia Antenatal HX: - blood group - maternal diabetes Birth HX Trauma - bruises/cephalhaematoma/ventouse extraction
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What is the blood volume of a newborn baby?
10ml/kg | so around a can of coke's worth in a term 3.5kg baby!
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What is breast milk jaundice?
Hormones in breast milk (+ added affect of constipation) result in increased enterohepatic circulation so more bilirubin is absorbed back into blood rather than being excreted. Normal and physiological
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What is the most common haemolytic cause of newborn jaundice? What is the most severe cause?
ABO incompatibility Mother is usually type O with baby type A Rh disease is more severe
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How do you test for blood group incompatibility in jaundiced babies?
Direct coombs test - strongly pos in Rh disease - negative or weakly pos in ABO incompatibility
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What is
Gal-1-P UT deficiency leads to build up of Galactose which is toxic
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Newborn baby is jaundiced and has pale poos. what do you suspect and how do you investigate this? why is it important to treat early?
Biliary atresia US of liver/biliary tree to investigate for obstructive causes Investigate within 6 weeks otherwise results in irreversible liver damage
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Risks associated with ABO incompatibility
Fetal hydrops Jaundice -> kernicterus/bilirubin encephalopathy
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Causes of short stature (3) and how is bone age related to chronological age in each? is the growth velocity normal or abnormal in each?
1. Familial Short Stature (bone age = chronological age) Normal growth vel. 2. Congenital Delayed Growth (bone age < chronological age) Normal growth vel. 3. Pathological (endocrine PICNICS) Abnormal growth vel.
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Pathological causes of delayed growth
Endocrine PICNICS Endocrine - hypothyroid, GH deficiency, Cushing's disease, adrenal insufficiency Psychosocial Iatrogenic - exogenous steroids, spinal Chronic disease - GI (coeliac, IBD); renal (CKD, RTA), cardiac (CHD), JIA, tumour Nutritional disease Intrauterine growth restriction Chromosomal - Turner syndrome, Down syndrome, Prader Willi Skeletal abnormalities
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Types of allergies
IgE mediated Non-IgE mediated
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HX for allergies
Quality - specific symptoms experienced Severity of SX - medical req to control SX - medical visits and hospitalisation - ICU admissions - interference w sleep, sport, play Timing: seasonal, perennial, episodic; immediate onset or delayed? Context: triggers Any HX of anaphylaxis
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SX of anaphylaxis (Severe allergic reactions) Children vs young kids
MUST have resp involvement or involvement of 2+ body systems - difficult/noisy breathing - Drooling - SOB, resp distress, cough, wheeze, hoarse voice, clearing throat, swelling/feeling of tightness in throat - Dizziness or collapse +/- drooling, Angio-edema/swelling of lips, tongue, hives/urticaria - Young kids: pale and floppy
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SX of mild to moderate allergic rxn
Swelling of lips, face, eyes Hives/welts Tingling mouth Abdo pain, vomiting
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Action plan for mild to moderate allergic Rxn
Mild to moderate: - Stay with person and call for help - Locate epicene adrenaline autoinjector - Give other medications if prescribed (+/- H2 antag for SX relief of pruritus +/- oral steroid tablets for bronchospasm) - phone family/emergency contact - watch for any ONE of the signs of anaphylaxis indicating resp involvement
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Action plan for severe allergic Rxn
Severe - Lay person flat - Give epicene adrenaline auto injector (pull of blue safety cap, place orange end against mid-thigh and push down hard until you hear a click -> hold for ten sec, then remove epipen and massage the spot). Can be given through clothing. - Phone ambulance 000 phone family/emergency contact - Further adrenaline doses can be given if no response after 5 min if you have another auto injector available WHEN IN DOUBT GIVE ADRENALINE (and always give adrenaline before inhaler if in doubt as to whether it is anaphylaxis or asthma)
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What are the investigations for allergy?
Ig E mediated: Skin prick testing: positive if welt >3mm Serology: measure allergen-specific Ig-E levels (more expensive and lower sensitivity and specitifiy but widely available) Both in conjunction with clinical history Immunotherapy --------------------- Non-IgE mediated and/or IgE mediated: Food challenge is gold standard but only perform at RCH (controlled environment)
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When is immunotherapy indicated as treatment for allergies?
For IgE-mediated inhalant or venom allergic disease only | Rhinoconjunctivitis as main indication
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Atopic diseases
Eczema (Allergic dermatitis) Asthma Allergic rhinoconjunctivitis (hayfever) Anaphylaxis
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What might you see on exam of someone with allergic rhino conjunctivitis?
- Mouth breathing - Inferior nasal turbinates pale and swollen - Clear nasal discharge - Conjunctivitis -itchy, red eyes w incr lacrimation
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Causes of failure to thrive (5)
1. *MAY BE PSYCHOSOCIAL* so take thorough social hX - blunts GH response 2. Inadequate intake - Neglect - Low SES - Poor diet - micronutrient deficiencies - inability to suck/swallow 3. Inadequate digestion, absorption - coeliac - CMPA - CF - pancreatic, cholestatic issue - Giardiasis - Diabetes 4. Incr metabolism - Carcinoma - Hyperthyroid - Chronic disease (resp, cardiac, renal, GI) 5. Prenatal issues - prematurity - maternal illness/drugs/smoking - IUGR - chromosomal abnormalities
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Investigations for short stature/FTT
Bone scan Bloods: FBE, UEC, LFTs - TFT, coeliac serology - Nutrition: CMP, Fe, vit D, B12, folate, IGF
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MX for short stature
1. education/reassurance 2. change diet 3. treat any underlying pathology 4. +/- GH therapy 5. psychosocial support
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How might pain present in a neonate? vs young child
``` Tachycardia Tachypnoea Restless/writhing/squirming Irritable Poor feeding ``` Young child: miserable, crying/screaming, lack of function, can verbalise pain
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What is a smegma?
Combination of desquamated skin cells, skin oils and moisture collects around the clitorus or under the foreskin of males. Looks like localised collection of pus but there are no signs of inflammation and it is normal in toddlers due to the foreskin separating gradually from penis between ages of 2 and 5!
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Ballinitis presentation Aetiology?
- Red, swollen, painful penis, often presenting in middle of night. - Common in 1-3 year old during period of separation of foreskin - Infection by e. coli or candida in pockets between inner layer of foreskin and penis (where smegma form)
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Treatment and prevention Ballinitis
Treatment: high dose topical antibiotics (eye ointment) squirted under foreskin every 2 hours until it's fixed (clears in 4-6 hours) Prevention: wash regularly in salt water (cooking salt in bath)
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What is parafimosis? Treatment
Foreskin trapped behind corona forming tight band of constricting tissue which causes venous obstruction and swelling of glans Treatment: urological emergency! Manipulation of glans within foreskin under laughing gas
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What is phimosis? When is treatment warranted and what is treatment? What are complications if not treated?
Inability to retract the skin covering the head (glans) of the penis May appear as a tight ring or 'rubber hand' of foreskin around tip of penis, preventing full retraction. Can be physiological (self-resolves around 5-7 years of age) or pathological (due to scarring, infection, inflammation). If there is ballooning of foreskin during urination/difficulty urinating, or infection, treatment (topical steroids +/- circumcision) may be warranted. Complications: renal failure due to complete obstruction of urinary tract
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What is hypospadias? | What is treatment?
Developmental condition where the meatus isn't at the tip of the penis. Instead, the hole may be any place along the underside of the penis. The meatus (hole) is most often found near the end of the penis ("distal" position) (80%), often occurring with dorsal hood of foreskin and chordee Tx: urological surgery within 6 weeks
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What is chord What is associated with? Tx?
Penis curves up or down at junction of head and shaft of penis, most obvious during erection Can be assoc w hypospadias Tx: surgery in infancy
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What is epispadius? What is it associated with?
URethra opens in top of penis rather than the tip | Assoc w dorsal chordee (penis curves up) and rarely with bladder exstrophy
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When do you intervene surgically in an umbilical hernia
If it persists beyond 2 years of age (under 2 years it should resolve spontaneously)
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What is the most common cause for boys needing renal transplant in childhood?
Posterior urethral valve (developmental abnormality) Leads to urinary obstruction -> renal failure
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Systemic effets of anorexia
Hypotension Arrhythmias Long QT Decr grey matter (reversible) Decr bone density - growth delay/arrest Hypothermia Delayed/interrupted puberty Long term effects on sexual/reproductive health
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Treatment anorexia
CBT | Maudsley family based treatment
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Features of ADHD
Developmental problem w deficits in: 1. Inattention 2. Impulsivity 3. Overactivity Tx: - Stimulant medication (ritalin) - Psychosocial/behavioral strategies involving positive parenting, teachers, counselling
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When does ODD typically present and what os the risk of not treating it? Tx?
Typically surfaces at primary school but can be younger May progress to conduct disorder if untreated Tx: psychological strategies 1. Assess current motivation to change 2. CBT 3. Family interventions
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IgE vs non-IgE mediated allergies
IgE mediated: - Sx appear within 1-2hrs but typically within min - Sx: hives, urticaria, angeioedema, resp distress ex: tree nuts, raw egg Non-IgE mediated - T cell mediated - Sx appear >2 hours after ingestion - Sx: GI and skin related (vomiting, diarrhoea) - ex: cow's milk allergy, soy milk, rice, FPIES
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How is a skin prick test conducted?
Allergen introduced under epidermis Measure wheel at 15min Controls: histamine (expect pos) and saline (expect neg) Wheal => 3mm above saline control is positive result
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Indications for food challenge
– Non-IgE mediated – IgE mediated BUT low suspicion of allergy w uncertain history w +ve SPT/RAST (serum specific IgE) w OR good history w -ve SPT/RAST
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High risk groups for anaphylaxis
□ HX anaphylaxis □ Multiple food and drug allergies □ Poorly controlled asthma □ Underlying lung disease
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What is FPIES
Type of non-IgE mediated food allergy Food protein induced enterocolitis syndrome - occurs in infants and young children - profuse vomiting and diarrhoea 2-4 hours after first exposure to allergen
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Mx of allergic rhinitis
Avoidance/ reduction measures Drugs: oral antihistamines (end gen), intranasal corticosteroids (fluticasone) Allergy immunotherapy
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What are the 4 types of child abuse?
``` Physical Emotional Neglect Sexual +/- family violence witnessing ```
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What do you do if you suspect child abuse?
Mantatory reporting if you have reasonable grounds to suspect it is causing harm to child and parents have failed or are unlikely to protect them. Look up number to call on child protection website. 'Child FIRST' referral
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What sort of injuries might indicate child abuse?
Bruising (esp on buttox, ears and peri-orbital) Posterior rib fractures and epicondylar fractures from shaking
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DDX midline neck lump in a child
1. thyroglossal cyst (will elevate on protrusion of tongue and swallowing) 2. Thyroid lump 3. Thymus lump
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Features of psoriasis in children - Appearance - Location - Complication(s)
□ Deep salmon red colour, silver scaly plaques Commonly on extensor surfaces, scalp, nails, umbilicus In childhood get more post-strep guttate pattern on trunk Complications: arthritis (1/10)
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What is tinea and what is it's typical appearance?
Tinea is ringworm. fungal infection. | Typical appearance is spreading ring rash
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What virus causes roseola?
Human Herpes Virus 6 and 7
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Systemic complications of port-wine stain birth
CCF Brain PHACES Hypothyroid
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Possible causes of hair loss in kids
Alopecia Areata (autoimmune hair loss in patches) Tinea Wapitis (focal hair loss w underlying scaly erythematous lesions)
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Treatment of atopic eczema
Face - topical hydrocortisone and steroid-sparing medications (weaker) Body - topical methylprednisilone (stronger) Regular emollients Treat secondary infection (ex: staph) Identify and remove any potential allergens and irritants
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Treatment of psoriasis (3)
1. Topical - Keratolytics (salicylic acid) if scaly - Steroids - Emollients - Vitamin D and A (retinoids) 2. Phototherapy in older kids not responding to steroids 3. Systemic (difficult, severe, resistant cases) - Retinoids (vit A) - Methotrexate
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ABCs of a paediatric behavioural history - red flags of each
Antecedent (trigger) - Red flags: no clear/reasonable trigger, occurring in multiple environments Behaviour - Red flags: developmentally inappropriate, regression, multiple concerning behaviours * ASK SPECIFICALLY ABOUT: eat, sleep, play* Consequences (what happens after; how does this affect the child and those around them and functioning) - Red flags: harmful to self and others, affecting functioning of child and/or family
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What do you suspect if a baby has a massively distended abdomen AT BIRTH - hasn't passed meconium - vomiting bile What if they were only distended a day or 2 after birth?
Distended at birth: think meconium ileum in a child w F Distended a day or 2 after birth: think - distal bowel obstruction (anorectal anomalies/imperf anus) - hershsprung's disease (rectal stimulation will give sudden gush of merconium)
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What condition is duodenal atresia associated with? How would this present?
30% risk of down syndrome w duodenal atresia Bowel obstruction WITHOUT distended abdomen (empty hypogastrium with distended epigastrium dye to duodenal/jejunal obstruction) in a nutritionally deficient baby (thin, pale, ribs visible)
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Classic x-ray finding of duodenal atresia
Double bubble sign - distended stomach and duodenum separated by pyloric valve (Have complete closure of portion of lumen of duodenal so get ballooning of lumen proximal to this)
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What is hirschsprung's disease?
A form of megacolon occurring when part or all of large intestine have no ganglion cells therefore are in constant state of contraction, causing distal bowel obstruction Presentation: failure to pass meconium within 48 hours od devilry +/- abdo distension, vomiting, explosive stools following rectal stimulation, bloody diarrhoea
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What do you suspect in a baby who is unable to swallow and is constantly dribbling/drooling saliva? How do you examine for this?
Oesophageal atresia (drooling baby until proven otherwise) Passing catheter through mouth and seeing how far it travels will establish whether oesophagus is non-patent or not
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What BMI percentile cut off qualifies as FTT? Overweight? Obese?
<5th centile: FTT 85-95th centiles: overweight >95th centile: obese
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Features of turner syndrome
XO karyotype - Short girl relative to family - Pubertal failure - Webbed beck - hearing, renal defects - CHD, HTN
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Endocrine causes of short stature
Hypothyroid most commonly (elevated BMI, constipation, sluggish behaviour etc) Cushing's disease (GC excess) - elevated BMI GH deficiency
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What is a form of skeletal dysplasia and how is this generally picked up?
Achondroplasia (dwarfism) - Autosomal dominent, picked up antenatally on ultrasound
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Red flags for investigating short stature
abnormal growth velocity signs of chronic disease on systems review/exam abnormally short for family <1st centile Obvious dysmorphic/syndromic features
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What is the definition of failure to thrive?
Failure to thrive is being <3% for weight or dropping 2 or more percentile tracks
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what are the three main complications in kids of renal failure?
Anaemia Metabolic bone disease (renal osteodystrophy and hyperparathyroidism) Poor growth
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what is haemolytic uraemia syndrome?
microangiopathic
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What is the most common cause of AKI?
Pre-renal cause (hypo perfusion due to septic shock, hypovolaemia, haemmhorage, severe dehydration etc)
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Which electrolyte reflects water balance in the body?
[Na] w normal range 135-145mmol/L [Na] high: dehydrated [Na] low: over-hydrated
365
What is a severe complication of SiADH? Around what [Na] does this occur?
Water retention from ADH release -> Cerebral oedema -> raised ICP -> hyponatraemic encephalopathy and brainstem herniation Occurs around [Na] 120 in kids
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What are the clinical signs of dehydration and what % body weight of fluid is lost with each? - Mild - Moderate - Severe
Mild (<4%) -none Moderate (4-6%) - delayed cap refill - increased RR - mildly decr tissue turgor - sunken eyes and fontanelles - oliguria/decr wet nappies Severe (>=7%) - cap refill >3sec - mottled skin - irritable, decr conscious state, hypotensive - deep, acidotic breathing - decr tissue turgor
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How do you evaluate fluid status in a child?
Daily weights (Loss of body weight in g = estimated fluid deficit in ml) Fluid charts (daily intake and losses) Daily UEC and BSL monitoring Clinical signs
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When replacing a fluid deficit, over how long should you replace that deficit?
Over 24 hours | UNLESS they are hypo or hypernatraemic, then replace over 24-72 hours
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Why is NGT preferred over IV rehydration in kids?
Less likely to cause electrolyte imbalances
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What fluid do we use for rehydration in children and neonates?
Children: normal saline with 5% dextrose Neonates: normal saline with 10% dextrose
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What is the 4/2/1 rule of fluid resus? When might you stray from this and why?
First 10kg body weight: 4ml/kg/hr Second 10kg: 2ml/kg/hr Over 20kg: 1ml/kg/hr 1/2 or 2/3 maintenance for kids w severe illness due to SiADH causing fluid retention (meningitis, encephalitis, head trauma, surgery, resp issues)
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What can happen if serum [Na] changes too rapidly?
Cerebral oedema, seizures and permanent brain damage Central pontine myelinosis occurs as a consequence of a rapid rise in serum tonicity following treatment in individuals with chronic, severe hyponatremia
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What referral(s), if any, would you give a chid w school-based learning and behaviour problems?
Educational psychologist to test: - Vision - Hearing - Cognitiion
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When do you refer for speech therapy and audiology assessment?
<50 words at 2yo No 2 word combinations at 2.5yo No understanding of simple instructions without gesture
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Differentials for an irritable baby who is sleeping poorly
Colic GORD/physiological reflux Poor maternal/child relationship Cow's milk protein allergy
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Features of colic
``` PURPLE CRYING Peaks at 6-8 weeks Unexpected Resists soothing Pain-like face Long-lasting (crying for >5 hours a day at times) Evening (sleep deficit is at peak) ```
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When might a child have lactose intolerance?
Never BORN with lactose intolerance - all kids under 3 have high levels of lactase. They may only have it secondary to coeliac, IBD, giardiasis, CMPA which destroy the intestinal brush border which attaches to lactase
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What may the presentation of CMPA be? What are the rates of resolution?
Regurgitation, vomiting after feeds Stool changes (diarrhoea/constipation, blood) Skin/eczematous rash FHX atopy 50% resolve by 1yo; 80% by 3yo
379
Management of physiological reflux in infants
Raise head of head Thicken formula Omeprazole is just a bandaid - decreases acidity but doesn't prevent reflux.
380
What is the character and location of a pulmonary flow murmur?
Pulmonary area +/- radiation to axilla Soft blowing ejection systolic murmur
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Systolic murmurs in kids | ejection vs pan systolic
Ejection: - innocent pulmonary flow murmur - AS - PS - Bicuspid aortic valve Pan systolic: - MR - VSD
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Diastolic murmurs in kids Early Mid Late
Early: - AR - Pulmonary Regurg Mid - MS - Large VSD Late - MS (with atrial contraction)
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What does APGAR stand for?
Appearance (colour) - pale or blue/body pink extremities blue/pink Pulse rate - absent/<100/>100 Grimace (reflex irritability) - none/some/vigorous, cry Activity (tone) - floppy/some flexion/good flexion Respiratory rate - apnoeic/irregular/active crying
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Where do you place the SaO2 probe on neonates and what does this represent?
R hand or wrist | = pre ductal pulse oximetry
385
When is peak surfactant produced in babies and below what age is it not enough to keep alveoli patent?
Peak at 37 weeks (term) Not enough surfactant to keep alveoli open below 32 weeks
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risk factors for hypoglycaemia in neonates
Maternal/gestational diabetes Delay in feeding Preterm Growth retarded and sick infants
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What affect does prematurity have on the kidneys?
Kidneys are unable to reabsorb phosphate which results in demineralisation of bones in order to increase serum [Ph]
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How do you test for bone disease of prematurity Mx?
Ix: test blood ALP and urine Phosphate levels Mx: Ph and Ca supplements
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When do you expect each of the following shunts to close: 1. Ductus venous 2. Foramen vale 3. Ductus arteriosus
1. Ductus venosus - Over 3-7 days 2. Foramen ovale - Functionally closes in first few breathes of life (but is not fully closed in 50% children by 5yo) 3. Ductus arteriosus - 3-4 days in 95% term babies
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Causes of apnoea in premies
1. Apnoea of prematurity is most common in otherwise well bubs (caffeine as Mx) 2. Infection (empirical antibiotics until infx is ruled out!) - lung disease - hypoxia - academia - drugs - metabolic disturbances (hypoglycaemia, hypocalcaemia, hyper/hypomagnasaemia) - Intracranial haemmhorage - polycythaemia w hyperviscosity - Necrotising enterocolitis - CHD (PDA)
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RFs for prematurity
1/2 of premature births don't have RFs 1. Maternal factors - previous preterm - extremes of maternal age - low pre-pregnant weight/malnourished - acute illness - pre-eclampsia/eclampsia - previous miscarriage or termination of pregnancy - HX infertility - IVF 2. Fetal factors - fetal anomalies - polyhydramnios 3. Placenta and membrane difficulties 4. Social - Low SES - psychological stress - Alch, drugs, smoking
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Complications of prematurity (acute)
Resp - RDS/HMD - apnoea of prematurity Cardiac -PDA Neurological - intraventricular haemmhorage - periventricular leukomalacia - Cerebral palsy Hepatic - Hypo/hyperglycaemia - Jaundice Renal - Bone disease of prematurity - electrolyte imbalances (hypo/hypernatraemia, hyperkalaemia, metabolic acidosis) GI - feeding difficulties - NEC Infection due to immature immune system Temp instability
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Late/chronic effets of prematurity
Delayed growth (usually catch up Retinopathy of prematurity Chronic lung disease of prematurity Neurodevelopment delay (CP, blindness, deafness)
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Most common cause for IUGR?
placental compromise
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Gross Motor milestones
Head lag minimal at 6-8 weeks Rolling at 3-5 mo Sitting at 6 months Crawling at 9 mo Walking at 12 mo Jumps BY 3 years Balances on one foot BY 4.5 years
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Red flag for gross motor
Not walking by 18mo
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Fine motor milestones
Palmar grasp by 6mo Inferior pincer by 9mo Pincer grip, stacks 2 cubes ~ 12mo Handedness 18mo Spontaneous scribbling by 2years Imitates vertical line by 3 years Copies face/ladder by 4.5 years
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Social and daily living skills milestone red flags
No interest in other children/help w dressing at 24 months NO interactive play with peers at 3 years No imaginative role play by 4 years
399
Paracetamol overdose treatment in kids
1. If dose ingested is possibly >10g or >200mg/kg, start NAC 2. measure paracetamol concentration 4 hours post-ingestion 3. If above treatment threshold, continue NAC 4. repeat paracetamol concentration, UECs, LFTs on completion.
400
Main infectious agents of cellulitis Ix Mx
S aureus and Strep progenies (consider HIB in unimmunised children <5yo) Ix: blood cultures Mx: Flucloxacillin po or IV if fever, rapid progression +/- ceftriaxone to cover HIB if unimmunised, <5yo
401
What is Prader-willi syndrome?
Behaviourial/developmental disability featuring food seeking, ODD and OCD, mild features of ASD as children - incr risk of psychosis, T2DM, OSA, scoliosis as adults Excessive appetite and lack of satiety -> risk of obesity Genetic - loss of paternally expressed genes
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Features of autism
1. Problems w socialisation - poor eye contact - difficulties w gestures - not responding to name - failure to socialise w others 2. Problems w communication - limited use of language - no imaginative play or social imitative play 3. Repetitive or obsessive behaviours - repetitive play - inflexible, repetitive use of language - unusually obsessions w inflexible and limited interests - self-stimulating behaviours (toe walking, hand flapping, jumping in place, making sounds, grinding teeth etc)
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What is 'croup'? Presentation Aetiology MX
Laryngotracheobronchitis Presentation: barking cough +/- stridor on exertion (at rest = severe) Aetiology: Parainfluenza Mx: supportive treatment for most kids - If stridor at rest, single dose of oral DEX then Observe for half an hour post steroid administration. Discharge once stridor-free at rest. - If severe: O2, IM/IV dex, neb adrenaline, intubation or tracheostomy If good improvement, observe for 4 hours post adrenaline. Consider discharge once stridor free at rest. If deterioration/no improvement, give further adrenaline and consider admission or transfer as appropriate.
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Complications of viral URTIs
- Otitis media - Acute sinusitis - Bacterial superinfection - Progression to LRTI (bronchitis, croup, bronchiolitis, pneumonia) - Asthma exacerbation
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What are the bag bugs you have to watch out for that can cause pharyngitis? Defining features
1. EBV - exudative tonsillitis assoc w cervical lymphadenopathy and generalised flu-like SX 2. HSV-1 Mucosal ulceration 3. Enteroviruses (Coxsackie A/B, echoviruses) - assoc w oral ulcers and rash 4. Strep throat (pyogenies) - exudative tonsilitis, strawberry tongue, widespread erythematous rash, tender enlarged cervical lymph nodes, high fever
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Presentation: bilateral swelling, tenderness, pain in parotid glands What is the diagnosis?
Mumps.
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Most common causative agent of acute otitis media. What would you see on ear exam? How do you treat?
Strep pneumonia most common (H. influenza and moraxella catarrhalis) See red bulging TM, presence of middle ear fluid Analgesics. Limited value in treating w antibiotics as pain resolves in 2-7days
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Maintains of MX of URTIs
- self-limiting and don't require pharm. intervention unless they are complicated - influenza and pneumococcal vaccine as prevention - reduce exposure to tobacco smoke - hygiene to reduce transmission rates
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Features of asthma SX Signs
SX: Wheeze and SOB Responsive to salbutamol Chest tightness, coughing (worse at night and in morning) Signs: - tracheal tug, WOB - prolonged exp. phase - exp wheeze - tachypnoea - decr RR and absent wheeze, decr breathe sounds in severe asthma
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Asthma management plan (and what features define each stage?) 1. mild 2. moderate 3. severe 4. critical
1 dose salbutamol: 6 puffs if <6yo or 12 puffs if >6yo 1. mild: 1 dose salbutamol and review after 20min. If good response, D/C on salbutamol PRN. Poor response, treat as moderate 2. Moderate (incr WOB, disrupted sentences, tachycardia): Salbutamol 1 dose every 20min for 1 hour. review 10-20 min after 3rd dose to determine freq of next dose. O2 if saO2<92% 3. Severe (agitated/distressed, marked WOB and limitation of speaking ability): Salbutamol 1 dose every 20min for 1 hour -> if responding, incr time between doses. If not responding, continue dosing even 20min. + o2 as above. +/- atrovent via MDI/spacer every 20min for 1 hour only. +/- IV Mg sulfate +/- IV aminophylline 4. Critical (silent chest, confused/drwosy, no talking) - O2 - Continuous nebuliser salbutamol - Nebulised iprotropium (3x in 1st hour only) - IV methylpred - IV Aminophylline and MgSulfate +/- ICU admission + 3 days oral pred with each (2mg/kg `day 1 then 1mg/Kg day2,3)
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Signs of salbutamol toxicity?
Tachycardia, tachypnoea, metabolic acidosis. Can occur with both IV and inhaled therapy. Lactate commonly high.
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Stridor -differentials - Inx?
Acute - most common acute cause in kids is CROUP - retropharyngeal abscess - peritonsillar (quinsy) abscess - laryngeal trauma Persistent - laryngomalacia most common cause of persistent stridor - subglottic stenosis - subglottic haemangioma INX: only if stridor is persistent with an expiratory component (severe) = bronchoscopy
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Differentials for wheeze
Since birth: - airway malacia (tracheomalacia or bronchomalacia) Gradual onset SX - Asthma - Recurrent viral-induced wheeze - Cystic fibrosis - Cardiac causes Sudden onset SX - LRTI (bronchiolitis, viral pneumonitis, bacterial bronchitis) - Inhaled foreign body
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RF for TB infection
``` Emigrants from developing countries Low SES Indigenous Immunodeficiency <5yo ```
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Chronic cough DDX and first line IX
Asthma Viral or bacterial URTI or LRTI Cardiac (pulm HTN, pulm oedema) Bronchiectasis (CF, primary ciliary dyskinesia, immunodeficiency, foreign body etc) Aspiration Chronic/less common infx (Tb, pertussis, mycoplasma, atypical pneumonia) Interstitial lung disease (rheumatic diseases, cytotoxic, drugs, radiation) GOR Psychogenic FIRST line Ix: CXR and spirometry if >6yo
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Presentation of bronchiectasis
□ Chronic moist or productive cough, WORSE in mornings □ Clubbing □ Chest wall abnormalities (hyperinflation, pectus carinatum) □ Inspiratory creps
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Mx of cystic fibrosis
1. Antibiotics to reduce bacterial colonisation and biofilm formation of resp tract 2. Physio to promote mucociliary clearance 3. Vaccines: pneumococcal and influenza 4. High energy diet and pancreatic supplements (Creon) 5. Vitamin and salt supplements +/- lung and liver transplants at end-stage
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DDX diarrhoea
Osmotic - IBS - Laxatives Secretory - Gastro (ETEC, cholera) Inflammatory - IBD - Surgical (appendicitis, interception) - Sepsis, UTI - NEC Motility - Hyperthyroid - Diabetic neuropathy Malabsorption - Coeliac - Cystic fibrosis - Giardia - CMPA
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Red flags for diarrhoea
SX of Dehydration (dizzy, decr urine output, lethargic) Prolonged diarrhoea Blood in stool Systemically unwell FTT Bilious commits Acute abdo (severe abdo pain and tenderness)
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When do do a renal U/S for kids w UTIs
If <6mo: U/S during acute infection if atypical UTI or recurrent UTI OR within 6 weeks if responds to treatment within 48 hrs If >6mo: U/S during acute infection if atypical UTI only OR within 6 weeks if recurrent UTI only . If responds to treatment within 48 hrs no need for imaging.
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Features of atypical UTIs
- Seriously ill/septicaemia - Poor urine flow - Abdo or bladder mass - Raised creatinine (deranged renal fun) - Failure to respond to Ab treatment within 48 hours - Non-ecoli isolated
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Acute management of UTIs
<3mo: IV antis >3mo, pyelo/upper UTI: PO cephalosporin or augmentin (7-10days) >3mo, cystitis/lower UT: PO cephalosporin, trimethoprim (3 days)
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Causes of non-blanching rashes
Viral most common (but higher % bacterial than w blanching rashes) - enterovirus, influenza ``` N. Meningitidis Other bacteria (Strep pneumonia, HIB) ``` HSP, ITP, DIC Leukaemia Mechanical trauma
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Causes of blanching rashes
``` VIRAL most common cause Enterovirus Adenovirus Coxsachie virus Rhinovirus RSV Measles Parvovirus B19 (itchy) Bacterial - toxic shock syndrome ```
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How does parvovirus cause fetal anaemia?
bone marrow suppression which decr production of erythrocytes
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what about fevers can cause febrile convulsions?
Rate of temp rise rather than the degree of temperature itself
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Steven Johnson syndrome results due to what causes? what is the classic presentaiton
Flu-Like symptoms as prodrome followed by red/purple rash that spreads and forms blisters (skin, mucous membranes, genitals, eyes) Main cause: mycoplasma infection - drug reactions (anti epileptics) -
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Causative agents of osteomyelitis/septic arthritis Management?
Staph aureus #1!! Strep pyogenies and haemophilus influenzae Mx: 1. REFER TO ORTHO for aspiration +/- athrotomy and washout 2. IV fluclox 3. Elevate and immobilise limb
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Rule of 2s of Meckel's diverticulum
``` 2% population 2:1 male:female 2 feet above ileocecal valve 2 inches long 2% patients develop complications over lifetime, typically before age of 2. ```
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How can mocker's diverticulum present?
``` Abdo pain (Related to bowel obstruction, Meckel's diverticulitis or perforation) GI bleeding SX of bowel obstruction ```
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What does a high reticulocyte count indicate? | Low reticulocyte count?
® Incr -> indicates marrow response to ?haemolysis ® Decr -> indicates lack of marrow response -> ? Deficiency in necessary iron or vitamins OR ? Inability to respond (marrow aplasia or infiltration)
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Causative agents of osteomyelitis/septic arthritis Management?
Staph aureus #1!! Strep pyogenies and haemophilus influenzae Mx: 1. REFER TO ORTHO for aspiration +/- athrotomy and washout 2. IV fluclox 3. Elevate and immobilise limb
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Rule of 2s of Meckel's diverticulum
``` 2% population 2:1 male:female 2 feet above ileocecal valve 2 inches long 2% patients develop complications over lifetime, typically before age of 2. ```
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How can meckel's diverticulum present?
``` Abdo pain (Related to bowel obstruction, Meckel's diverticulitis or perforation) GI bleeding SX of bowel obstruction ```
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What is HUS?
STEC (also known as VTEC) infection can cause bloody diarrhoea, fever, abdo pain, vomiting and sometimes haemolytic uraemic syndrome. Infection usually results from consuming contaminated food or water, or from contact with infected animals or people. HUS is a severe condition characterised by kidney failure, bleeding and anaemia. It can sometimes be fatal. -> bruising/petechial rash (low Plts), haemolytic anaemia, reduced consciousness, reduced urination, HTN, seizures.
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Definition of failure to thrive
Infant's weight below 3rd centile or >2SD below population mean Weight crossing 2 major centile lines with time
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Risk factors for FTT
Prematurity | IUGR
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Causes of FTT | What 2 are most common
Reduced intake (most common) 1. Inadequate caloric intake (poor feeding etc) 2. Psychosocial - maternal depression/poor maternal-child bond - difficulties at home Incr metabolism - Chronic or intercurrent illness, infections (UTI, Thyroid, CF, CHD, CRF, chromosomal, atopy, Tb, HIV etc) Reduced nutrient absorption - Coeliac - CMPA - IBD
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What are some methods of increasing caloric intake in infants with FTT
Dietary advice and monitoring Breast-fed infant: Supplementing breastfeeds with EBM or formula afterwards Formula-fed infant: - Increase forumla concentration or add glucose polymer (extra calories) to bottle - introduce solids or add calories to solids
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Indications for an epipen
- anaphylaxis - also has asthma as well as allergy - geographical distance from emergency medical services
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Indications for Food challenge
- uncertain HX | - borderline skin prick testing (~3mm)
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What organism causes meningococcaemia? What is different about managing this condition as a cause for sepsis and/or meningitis?
Neisseria Meningiditis Notifiable disease! - patient req isolation until 12hours IV antis - notify the Department of Human Services - Rifampicin prophylaxis to all close contacts (household, day-care, intimate relations in pst 7 days)
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Emergency management of severe anaphylaxis
Adrenaline - 0.5mc Adrenaline IM, give every 5 min if not responding Airway - intubation + neb adrenaline if required +/- oral corticosteroids and nebulised salbut for bronchospasm B - high flow O2 C - circulation (supine w legs elevated to prevent collapse) Exposure - H2 antagonists for skin involvement
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DX and MX of eosinophilic esophagitis
DX: gastroscopy and biopsy histology MX: food avoidance (dairy, wheat, egg, soy triggers), swallowed aerosolised CS
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Emergency fluid rhesus in shocked patients
Give boluses of 10-20ml/kg of 0.9% sodium chloride (normal saline), which may be repeated once (Give second 20ml/kg bolus if required to a total vol of 40ml/kg) ® If persisting hypotenseion after second bolus, give inotropes (Adren/NA in 500ml 0.9% normal saline)
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Prophylactic antibiotics for sepsis
<1mo: benpen and cefotaxime | >1mo: flucloxacillin and ceftriaxone
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What is HSP and how does it typically present?
Most common vasculitis of childhood Purpura + abdo pain + arthralgia +/- renal involvement (haematuria/proteinuria/hypertension) Often preceded by viral URTI
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Dx and Mx of HSp
Dx: urine test Mx: supportive (paracetamol +/- NSAIDs, oral or IV corticosteroids relieve joint and abdo pain)
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features of colic
Completely benign, normal part of development ``` Peaks at 2 months (Begins: 2 weeks of age and continues until about 3-4 months of age). Unexpected Resists soothing (INCONSOLABLE crying) Pain-like face Long-lasting (up to 5 hours of crying) Evening ```
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Newborn that appears normal but has resp distress when NOT crying. Pink when crying but makes vigorous resp efforts and becomes dusky when stops crying. What is the likely explanation and how would you diagnose this?
Choanal atresia. Infants are obligate nose breathers until 4 months of age - choanal atresia occurs when an infant has a structurally non-patent nose. DX by inability to pass a feeding tube through nostril or clouding of cold metal under infant's nose?
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Contraindications to vaccines
Known allergy to ingredient Previous anaphylaxis Immunocompromised