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PHASE 3A > PAEDS - cardio, resp, GI > Flashcards

PAEDS - cardio, resp, GI Flashcards

1
Q

define croup

A

acute infective URT disease affecting young children

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2
Q

epidemiology of croup
a) time of year
b) age

A

a) spring/autumn
b) 6m-2y

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3
Q

what causes croup?

A

MAINLY parainfluenza virus

others:
- influenza
- adenovirus
- respiratory syncytial virus (RSV)

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4
Q

RFs for croup

A
  • young
  • family hx
  • congenital/acquired airway narrowing
  • male gender
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5
Q

pathophysiology of croup

A
  1. upper resp tract infection causes oedema in the larynx
  2. swelling of larynx, vocal cords and trachea
  3. narrowing of subglottic region
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6
Q

classic presentation of croup

A

classic:
- cold-like sx in days preceding (prodromal)
- acute stridor
- barking seal like cough
- worse at night

other:
- hoarse voice
- low-grade fever
- if severe&raquo_space; resp distress

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7
Q

signs of croup with respiratory distress

A

seal-like barking cough with:
- recession
- agitation
- lethargy

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8
Q

investigations for croup

A

often clinical diagnosis

but consider:
- ABCDE
- ENT exam
- cervical lymph nodes exam
- lung auscultation
- CXR (to exclude other causes)

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9
Q

what classic CXR sign will be present in croup?

A

steeple sign (narrowing of trachea)

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10
Q

management of non-severe croup

A
  • normally self-limiting (<48h)
  • supportive with fluids and rest
  • sit child up during attacks
  • stay off school
  • can give single dose of oral dexamethasone (150mcg/kg) and repeat after 12h if required
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11
Q

what did croup used to be caused by before vaccinations? what did it lead to?

A

diptheria
led to epiglottitis > high mortality

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12
Q

stepwise management options in severe croup

A
  1. oral dexamethasone
  2. oxygen
  3. nebulised budesonide
  4. nebulised adrenaline
  5. intubation and ventilation
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13
Q

what dose of dexamethasone should be given in croup?

A

0.15mg/kg (single dose)

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14
Q

define childhood pneumonia

A
  • acute LRT infection
  • infection and inflammation of the parenchyma with consolidation
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15
Q

epidemiology of childhood pneumonia

A

relatively common - 14% of all deaths of children <5

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16
Q

common bacterial causes of childhood pneumonia (inc most common) (6)

A
  1. MOST = streptococcus pnuemonia
  2. second = H.influenzae type B (Hib)
  3. group A strep
  4. group B strep
  5. S.aureus
  6. atypical = mycoplasma pneumonia/tuberculosis
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17
Q

which children are likely to contract pneumonia caused by…
a) H.Influenzae type b
b) group B strep

A

a) pre or unvaccinated children

b) pre-vaccinated infants

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18
Q

how is group B strep pneumonia contracted in children

A

often during birth as it colonises the vagina

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19
Q

common viral causes of childhood pneumonia (inc most common) (4)

A
  1. most common = respiratory syncytial virus (RSV)
  2. parainfluenza virus
  3. influenza virus
  4. adenovirus
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20
Q

risk factors for childhood pneumonia (5)

A
  • young age
  • unvaccinated for Hib
  • immunocompromise
  • pre exisiting illness e.g. CF, measles
  • environment e.g. crowded home, parental smoking, indoor air pollution
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21
Q

pathophysiology of childhood pneumonia

A

inflammation of lung parenchyma (lung tissue) and sputum filling the airways and alveoli

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22
Q

signs and symptoms of childhood pneumonia

A
  1. cough (wet + productive)
  2. high fever (>38.5)
  3. lethargy
  4. delirium
  5. high RR
  6. tachypnoea
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23
Q

characteristic chest signs of childhood pneumonia (3)

A
  1. bronchial breath sounds (harsh, equally loud on inspiration and expiration)
  2. focal coarse crackles
  3. dullness to percussion
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24
Q

signs indicating sepsis secondary to childhood pneumonia (6)

A
  1. tachypnoea
  2. tachycardia
  3. hypoxia
  4. hypotension
  5. fever
  6. confusion
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25
Q

investigations for childhood pneumonia

A
  1. sputum cultures and throat swabs - bacterial causes
  2. viral PCR - viral causes
  3. CXR
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26
Q

what will a CXR show in childhood pneumonia?

A

dense/fluffy opacity occupying a portion of/a whole lobe

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27
Q

investigations if child with pneumonia has suspected sepsis

A
  1. blood cultures
  2. capillary blood gas analysis (monitor resp, metabolic acidosis, lactate)
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28
Q

management of childhood pneumonia
a) typical
b) atypical
c) penicillin allergy
d) sepsis

A

a) 1st line = dispersible amoxicillin
can also add oxygen

b) add a macrolide e.g. erythromycin, clarithromycin

c) use macrolides as a monotherapy

d) IV abx e.g. co-amoxiclav

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29
Q

what immunisations can be used to help prevent childhood pneumonia? (4)

A
  1. Hib
  2. pneumococcus
  3. measles
  4. whooping cough
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30
Q

define asthma

A

chronic inflammatory obstructive airway disease

characterised by bronchoconstriction and excessive secretion production

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31
Q

cause of childhood asthma

A

normally ATOPY - tendency to develop IgE mediated reactions to common aeroallergens

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32
Q

pathophysiology of childhood asthma

A

airflow limitation caused by
1. hypersensitive bronchoconstriction
2. mucosal inflammation
3. increased mucosal production

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33
Q

presentation of childhood asthma

A
  1. WHEEZE
    - episodic, intermittent exacerbations
    - diurnal variation (worse at night and early morn)
    - bilateral, widespread, “polyphonic”
    - improves w bronchodilators
  2. chest tightness
  3. dry cough w wheeze and SOB
  4. typical triggers
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34
Q

typical triggers for childhood asthma

A
  1. dust (house dust mites)
  2. animals
  3. cold air
  4. exercise
  5. smoke
  6. food allergens e.g. peanuts, shellfish, egg
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35
Q

diagnosis of asthma

if probability is:
a) low
b) intermediate/high

A
  • normally clinical
  • children usually not diagnosed until 2-3y

a) consider referral to specialist
b) trial of tx can be implemented, if improves sx then diagnosis is made

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36
Q

what investigations for asthma can be used if there’s intermediate possiblity/diagnostic doubt? (4)

A
  1. spirometry with reversibility testing (only in children >5!)
  2. direct bronchial challenge
  3. fractional exhaled nitric oxide (FeNO)
  4. peak flow variability with diary
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37
Q

medical therapy for asthma in children <5 (4 steps)

A
  1. start SABA e.g. salbutamol
  2. add low dose corticosteroid OR leukotrine antagonist (e.g. oral montelukast)
  3. add other option from step 2
  4. refer to specialist
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38
Q

medical therapy for asthma in children aged 5-12 (6 steps)

A
  1. start SABA e.g. salbutamol
  2. add regular low dose corticosteroid inhaler
  3. add LABA e.g. salmeterol
  4. titrate corticosteroid inhaler to medium dose. consider adding montelukast or oral theophylline
  5. increase corticosteriod to high dose
  6. refer to specialist
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39
Q

medical therapy for asthma in children aged 12+

A

same as adults!!

  1. start SABA e.g. salbutamol
  2. add regular low dose corticosteroid inhaler
  3. add LABA e.g. salmeterol
  4. titrate corticosteroid inhaler to medium dose. consider trial of montelukast, oral theophylline OR inhaled LAMA ie tiotropium
  5. titrate corticosteroid dose to high. combine additional tx from step 4. option of adding oral beta-2-agonist ie oral salbutamol. refer to specialist
  6. add oral steroids at lowest dose poss
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40
Q

presentation of acute asthma attack and auscultation findings

A
  1. progressively worse SOB
  2. signs of resp distress
  3. tachypnoea
  4. expiratory wheeze
  5. “tight” on auscultation, reduced air entry
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41
Q

asthma severity: category ‘moderate’

A
  1. peak flow 50-75% predicted
  2. normal speech
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42
Q

asthma severity: category ‘severe’

A
  1. peak flow 33-50% predicted
  2. saturations <92%
  3. unable to complete sentences in one breath
  4. signs of resp distress
  5. RR >40 in 1-5y, >30 in 5+
  6. HR >140 in 1-5y, >125 in 5+
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43
Q

asthma severity: category ‘life threatening’

A
  1. peak flow <33% predicted
  2. saturations <92%
  3. exhaustion and poor resp effort
  4. hypotension
  5. silent chest
  6. cyanosis
  7. altered consciousness/confusion
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44
Q

stepwise approach to managing moderate to severe cases of acute asthma

A
  1. salbutamol inhaler via spacer device
  2. nebulisers with salbutamol/ipratropium bromide
  3. oral prednisolone
  4. IV hydrocortisone
  5. IV mag sulphate
  6. IV salbutamol
  7. IV aminophylline
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45
Q

general staples of management for an acute asthma attack(4)

A
  1. supplementary O2
  2. bronchodilators e.g. salbutamol > ipratropium > magnesium sulphate
  3. steroids e.g. oral prednisolone or IV hydrocortisone
  4. abx if bacterial cause suspected
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46
Q

define viral-induced wheeze. what is it caused by?

A

an acute wheezy illness caused by viral infection with RSV (respiratory syncytial virus)

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47
Q

who is typically affected by a viral-induced wheeze? why?

A

typically under 3y

very small diameter airway > slight narrowing caused by inflammation and oedema leads to a proportionally larger restriction in airflow (Poiseuille’s law)

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48
Q

risk factors for viral-induced wheeze

A

family history

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49
Q

how to differentiate between a viral induced wheeze and asthma

A

viral induced wheeze:
- presents <3
- no atopic hx
- only occurs during viral infections

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50
Q

signs and symptoms of a viral-induced wheeze

A
  1. transient and episodic wheezing episodes
  2. viral illness (fever, cough, coryzal sx) for 1-2 days preceding….
  3. SOB
  4. signs of resp distress
  5. expiratory wheeze throughout the chest
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51
Q

management of viral-induced wheeze
a) moderate
b) severe/life-threatening

A

SAME AS ACUTE ASTHMA

a) - nebulised salbutamol
- nebulised ipratropium bromide
- steroids e.g. oral pred or IV hydrocortisone
- abx if evidence of infection

b) stepwise:
- O2
- salbutamol inhaler via spacer device
- nebulisers with salbutamol/ipratropium bromide
- oral prednisolone
- IV hydrocortisone
- IV mag sulphate
- IV salbutamol
- IV aminophylline

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52
Q

what type of wheeze in children is never heard in asthma or viral-induced wheeze? what should you suspect in this case?

A

asthma/viral-induced will never cause a FOCAL WHEEZE

be cautious of airway obstruction e.g. inhaled foreign body or tumour

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53
Q

what examination is contraindicated in croup? why?

A

throat examination
can cause child to get agitated > rapid airway constriction

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54
Q

management of a child with croup if they have an audible stridor at rest

A

admit to paediatric ward - stridor at rest = red flag for admission

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55
Q

what is bronchiolitis?

A

a lower respiratory viral infection of the bronchioles

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56
Q

which virus causes bronchiolitis?

A

respiratory syncytial virus (RSV)

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57
Q

epidemiology of bronchiolitis:
a) who?
b) when?

A

a) common in <2y (mostly <6m)
b) winter and spring months

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58
Q

risk factors for bronchiolitis

A
  • breast fed for <2m
  • smoke exposure e.g. parents
  • siblings who attend nursery/school
  • chronic lung disease from prematurity
  • neuromusc disorder preventing clearance e.g. CF
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59
Q

physiological changes in bronchiolitis (4)

A
  1. proliferation of goblet cells > excess mucus
  2. IgE-mediated type 1 allergic reaction > inflammation
  3. bronchiolar constriction
  4. infiltration of lymphocytes, cytokines, chemokines
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60
Q

signs and symptoms of bronchiolitis

A

SX
- typically increasing over 2-5 days
- low-grade fever
- starts with coryzal sx e.g. nasal congestion, rhinorrhoea
- then chest sx e.g. cough, wheeze
- feeding difficulties

SIGNS
- inspiratory crackles
- expiratory wheeze
- hyperinflated chest

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61
Q

what lung sounds are heard in bronchiolitis?

A

inspiratory crackles
expiratory wheeze

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62
Q

investigations for bronchiolitis

A
  1. nasopharyngeal aspirate or throat swab - RSV rapid testing and viral cultures
  2. FBC
  3. blood/urine cultures (IF fever)
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63
Q

signs of respiratory distress in an ill child (8)

A
  1. raised RR
  2. use of accessory muscles e.g. sternocleidomastoid, abdo, intercostal
  3. recessions
  4. nasal flaring
  5. head bobbing
  6. tracheal tugging
  7. cyanosis
  8. abnormal airway noises e.g. grunting, wheezing, stridor
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64
Q

indications for an infant with bronchiolitis to be admitted? (9)

A
  1. <3m
  2. pre-existing condition e.g. prematurity, DS, CF
  3. 50-75% or less of their normal milk intake
  4. clinical dehydration
  5. RR >70
  6. O2 <92%
  7. moderate to severe resp distress
  8. apnoeas
  9. parents not confident in ability to manage at home
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65
Q

typical management of bronchiolitis

A

supportive at home - adequate fluid/milk intake, nasal suctioning, rest

if in hosp - O2, may provide NG feeding

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66
Q

what preventional vaccine can be given to babies who are at high risk if they get bronchiolitis? when is it given and who is high risk?

A

a) palivizumab
b) given monthly in high risk season (oct-mar)
c) babies with CF, immunocompromise, CHD etc

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67
Q

what is cystic fibrosis?

A

an autosomal recessive disease caused by a mutation in the CFTR gene

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68
Q

what does the CFTR gene code for? where in the body is implicated?

A

encodes the CFTR protein - a chloride (Cl-) channel found in epithelial tissues e.g. lungs, pancreas, intestines, sweat glands and reproductive organs

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69
Q

how is CF passed on genetically?

A

it is autosomal recessive so both parents need to be carriers for the child to demonstrate the disease

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70
Q

epidemiology of CF

A
  • 1/2 caucasian europeans are carriers
  • most common lethal genetic disease in caucasian population
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71
Q

briefly outline the pathophysiology of CF in the
a) lungs
b) pancreas
c) GI tract
d) reproductive tract

A

OVERALL - cells can’t transport Cl-

a) Cl- becomes trapped inside mucus-secreting cell rather than outside > less Cl- in mucus > water not attracted in > thickened mucus > impeded mucus clearance > chronic infection and inflammation

b) pancreatic duct is occluded in-utero > permanent damage to exocrine pancrease and insufficiency

c) small intestine secretes viscous mucus > bulky stools > bowel obstruction

d) 95% males infertile

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72
Q

presentation of CF in neonates (4)

A
  1. failure to pass first meconium
  2. bilious vomiting
    (both signs of meconium ileus (small bowel obstruction)
  3. failure to thrive
  4. prolonged neonatal jaundice
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73
Q

presentation of CF in infancy > childhood (5)

A
  1. failure to thrive
  2. recurrent chest infections (wet-sounding cough), chronic sinusitis
  3. pancreatic insufficiency - steatorrhea, diabetes
  4. nasal polyps
  5. chronic lung disease
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74
Q

when is CF normally identified? why?

A

in neonates - newborn screening (bloodspot test)

this is only a screening - still needs diagnostic testing

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75
Q

what is the gold std investigation for CF?

A

chloride sweat test - will be >60mmol/L

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76
Q

what happens when a sweat test is positive when investigating CF?

A

this is not sufficient to diagnose CF - need second test or identification of genetic mutation through genetic analysis

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77
Q

management for the respiratory sx of CF (4)

A
  1. 1st line = chest physiotherapy twice daily
  2. mucolytics e.g. DNase (reduces viscosity)
  3. inhaled bronchodilator e.g. salbutamol
  4. inhaled corticosteroid e.g. budesonide
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78
Q

management of pancreatic disease in CF

A
  1. pancreatic enzyme supplementation (creon)
  2. fat soluble vitamin (A, D and E) supplements
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79
Q

which bacteria are key colinisers in children with CF? which is particularly troublesome?

A

psuedomonas aeuruginosa (most troublesome, hard to treat and worsens prognosis)

staph aureus

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80
Q

how long should children with CF be on a course of antibiotics in the case of airway infections?

A

at least 2 weeks

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81
Q

what is the most likely infection a neonate will develop if the mother transmits group B strep?

A

neonatal sepsis

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82
Q

how is Pseudomonas aureginosa colinisation treated in children with CF?

A

aminoglycosides (e.g. gentamicin) or quinolones (e.g. ciprofloxacin)

think aureGinosa - Gent
Psuedo - cipro (sip)

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83
Q

what is acute epiglottitis?

A

a rare but serious infection of the supraglottis (upper part of larynx including epiglottis) that may cause airway compromise

an airway emergency in children!

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84
Q

what age group is most commonly affected by acute epiglottitis?

A

2-6 years old

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85
Q

most common bacterial cause of acute epiglottitis

A

haemophilus influenzae type B (Hib)

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86
Q

RFs for acute epiglottitis (3)

A
  1. non vaccination with Hib
  2. immunocompromised
  3. young age
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87
Q

signs and symptoms of acute epiglottitis

A
  • high fever
  • sore throat
  • dribbling
  • difficulty breathing
  • dysphagia
  • hoarse voice
  • muffled voice
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88
Q

which classic positioning do children display with acute epiglottitis?

A

the tripod position - sitting/standing while leaning forward with the hands on the knees/other surface

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89
Q

how is acute epiglottitis diagnosed?

A

if suspected do NOT try to examine the throat

diagnose by direct visualisation by a specialist - once in OP theatre and airway stabilised can perform laryngoscopy (will see swelling of supraglottic structures)

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90
Q

initial management of acute epiglottitis?

A
  1. immediate senior involvement including airway specialists e.g. anaesthetics and ENT
  2. endotracheal intubation may be needed
  3. IV abx - cefotaxime or ceftriaxone
  4. supplemental O2
  5. consider corticosteroids e.g. dexamethasone
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91
Q

later management of a child with acute epiglottitis (once no longer intubated)

A

oral amoxicillin

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92
Q

what criteria is needed to be passed for a child to be discharged following an acute asthma attack? (3)

A
  1. peak flow must be >75% expected
  2. have had inhaler technique checked and recorded
  3. be stable on discharge medications for at least 12-24h
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93
Q

what is the target oxygen saturation level in acutely asthmatic patients?

A

94-98%

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94
Q

define:
a) GOR
b) GORD

A

a) the passage of gastric contents into the oesophagus with/without regurgitation or vomiting

b) the presence of troublesome sx and/or complications of persistent GOR

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95
Q

what causes GOR/D in infants? (2)

A
  1. short/narrow oesophagus
  2. liquid diet and high caloric requirement puts strain on gastric capacity
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96
Q

risk factors for GOR/D in children (6)

A
  1. premature
  2. young infant (milk diet)
  3. parental hx
  4. obesity
  5. hiatus hernia
  6. neurodisability e.g. cerebral palsy
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97
Q

signs and symptoms of GOR/D in children

A

REGURGITATION and…
- distress e.g. excessive crying/crying while or after feeding
- milk coloured vomit
- hoarseness and/or chronic cough
- unexplained feeding difficulties e.g. refusing to feed, gagging, choking
- back arching
- faltering growth

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98
Q

what red flag features will NOT be present in GOR and suggest another pathology?

A
  • frequent projectile vomiting (pyloric stenosis)
  • bile stained vomit (obstruction)
  • blood stained vomit (GI bleed)
  • abdominal distension/tenderness (obstruction/acute surg condition)
  • bulging fontanelle (meningitis, RIP)
  • blood in stool (gastroenteritis, CMPA)
  • chronic diarrhoea (CMPA)
  • dysuria (UTI)
  • fever (infection)
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99
Q

how does reflux and GORD differ?

A

it is normal for babies to reflux feeds - they have an immature LOS so contents easily reflux into oesophagus

it becomes more troublesome (GOR/GORD) when this causes the baby to become distressed

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100
Q

how is GOR usually investigated? what about in severe cases?

A

normally doesn’t require investigations

in severe cases - can do barium meal and endoscopy

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101
Q

management for GOR/D in babies
a) mild GOR/D
b) problematic GOR/D

A

a) sometimes explanation, reassurance and practical advise is all that’s needed
- small, frequent meals
- burping regularly to help milk settle
- not over-feeding
- keep baby upright after feeding

b) if problematic can give
- gaviscon mixed with feeds
- thickened milk/formula
- PPIs e.g. omeprazole (only if others inadequate!)

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102
Q

a) what is the name of the rare condition associated with GOR that causes brief episodes of abnormal movements in infants?
b) what are its key features?
c) what is its prognosis?

A

a) Sanlifer’s Syndrome

b) key features are
- torticollis (forceful neck twisting)
- dystonia (twisting movements, arching of back of unusual posture)

c) normally resolves as reflux is treated

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103
Q

what is poor feeding? what age group is it most common in?

A

conditions in children <1 year that lead to impaired oral intake and are associated with medical/nutritional/feeding skill and/or psychosocial dysfunction

tends to be <1 but can be up to 3yo

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104
Q

common causes of poor feeding in children? (8)

A
  1. GORD
  2. malrotation
  3. intussusception
  4. Hirschsprung’s
  5. pyloric stenosis
  6. gastroenteritis
  7. infection
  8. metabolic conditions
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105
Q

RFs for poor feeding (5)

A
  1. prematurity
  2. developmental delay
  3. anatomical abnormalities of oropharynx/GI tract
  4. GI surgery
  5. trisomy 21
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106
Q

signs and symptoms of poor feeding

A

depends on cause! but general:

  • taking >30 mins to feed
  • inappropriate volume of feed
  • vomiting
  • abdominal pain/distension
  • colic
  • irritability/lethargy at mealtimes
  • refusing to feed
  • long term = faltering growth
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107
Q

how is poor feeding investigated? what should be considered?

A

process of ruling out possibilities!
consider…
- temporary exclusion of cow’s milk (CMPA)
- oesophageal 24hr pH/impedence study (GORD)
- upper GI contrast study (structural probs)
- trial of lactose-free diet
- TTG antibodies (coeliac)

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108
Q

how is poor feeding managed?

A

depends on cause

general
- feeding assessment
- advice/nutritional support if anatomical abnormalities
- surgery if obstruction
- thickener/anti-reflux formula
- dietary modification

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109
Q

what is pyloric stenosis?

A

congenital hypertrophy of the pyloric sphincter (opening from the stomach to the small intestine) causing gastric outlet obstruction (stomach can’t empty contents into duodenum)

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110
Q

epidemiology of pyloric stenosis (age, gender)

A
  • 4-8 weeks
  • more common in boys (4:1)
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111
Q

aetiology and RFs for pyloric stenosis

A

aetiology unknown!

RFs
- firstborn
- male
- family hx (especially on mum’s side)

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112
Q

pathophysiology of pyloric stenosis

A
  1. hypertrophy and narrowing of pyloric sphincter muscle
  2. gastric outlet obstruction
  3. excessive vomiting of stomach contents (can cause dehydration and electrolyte disturbance e.g. low Na2+ and K+)
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113
Q

signs and symptoms of pyloric stenosis

A
  1. FORCEFUL VOMITING
    - increased frequency over time
    - increased forcefulness over time
    - becomes projectile e.g. “hitting wall”
  2. loss of interest in feeding
  3. wave-like motion of abdomen shortly after feeding and just before vomiting
  4. weight loss (if delayed presentation)
  5. pale
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114
Q

what electrolyte complication can occur in pyloric stenosis? why?

A

hypochloric (low Cl-) metabolic alkalosis

baby is vomiting up hydrochloric acid from stomach

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115
Q

investigations for pyloric stenosis, including diagnostic

A
  1. test feed!!!
    - examined after feeding
    - peristalsis (rolling abdomen) seen
    - palpable pyloric mass “feels like an olive” in the RUQ
  2. blood gas analysis - hypochloric metabolic alkalosis
  3. abdominal USS (diagnostic!)
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116
Q

management for pyloric stenosis

A

laparoscopic pyloromyotomy (known as “Ramstedt’s operation”)

incision made in pylorus to widen canal

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117
Q

what is gastroenteritis?

A

transient infection of the gut, characterised by sudden onset of diarrhoea

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118
Q

epidemiology of gastroenteritis

A

v common
cause of morbidity in younger children
in UK - 10% of children <5y annually

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119
Q

most common cause of paediatric gastroenteritis:
a) in developed countries
b) bacterial
c) parasitic

A

a) rotavirus
b) Campylobacter jejuni
c) Giardia and Cryptosporidium

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120
Q

RFs for paediatric gastroenteritis (2)

A
  • travel
  • close contact with other infected ppl
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121
Q

signs and symptoms of gastroenteritis

A
  1. sudden change > loose, watery stools
  2. often accompanied by vomiting
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122
Q

what is important to assess when a child comes in with gastroenteritis?

A

dehydration!

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123
Q

possible signs of dehydration in a child with gastroenteritis (6)

A
  1. altered responsiveness e.g. irritable, lethargic
  2. decreased urine output
  3. sunken eyes
  4. dry mucous membranes
  5. reduced skin turgor
  6. sunken fontanelles
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124
Q

investigations for gastroenteritis

A

normally none needed!
assess dehydration

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125
Q

what is the mainstay of management in children with gastroenteritis?

A

preventing and/or correcting dehydration

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126
Q

management of a child with gastroenteritis if there is:
a) no dehydration
b) clinical dehydration
c) shock

A

a) prevent dehydration - continue breastfeeding, encourage fluid intake to compensate

b) fluid deficit replacement (50ml/kg), maintenance fluid, continue breastfeeding, consider supplementing with oral rehydration solution (ORS)

c) IV therapy - bolus 0.9% sodium chloride then replace fluid deficit over 24hrs

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127
Q

what advice should be given to a parent who’s child has gastroenteritis about returning to school?

A

do not return until 48 hours after last diarrhoea episode

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128
Q

which cardiac defects are associated with these genetic syndromes?
a) Down’s syndrome
b) Edwards’s syndrome
c) Patau’s syndrome
d) Turner’s
e) DiGeorge
f) Noonan syndrome
g) Marfan syndrome

A

a) AVSD
b) VSD
c) patent ductus arteriosus
d) coarctation of the aorta
e) arch, truncal abnormalities
f) dysplastic pulmonary valve
g) aortic root dilation

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129
Q

which septal defects are…
a) acyanotic
b) cyanotic?

A

a) VSD, ASD, AVSD, PDA

b) transposition of great arteries, tetralogy of fallot, severe Ebstein’s anomaly

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130
Q

what is the role of the…
a) ductus venosus
b) foramen ovale
c) ductus arteriosus

in foetal circulation?

A

a) shunts oxygenated blood from the placenta in the umbilical vein towards the foetus’ heart, bypassing the liver

b) shunts O2 blood from the RA to the LA (bypasses lungs)

c) connects pulmonary artery with the aorta (again bypassing the lungs)

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131
Q

briefly describe where O2 blood from the placenta and deoxygenated blood from the foetus’ body travels in foetal circulation

A
  1. blood from placenta > right heart > left heart > body
  2. some to lungs BUT majority shunted through PDA > descending aorta (right heart)
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132
Q

what cardiac and respiratory changes occur in the foetus after birth?

A
  1. baby’s first breath
  2. O2 is pulmonary dilator > pulmonary resistance falls allowing blood into lungs
  3. foramen ovale closes (increased pul blood flow increases LA pressure and decreases RA pressure)
  4. ductus arteriosus closes after a few days
  5. aortic pressure rises
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133
Q

infusion of what helps to maintain ductal patency in neonates e.g. before surgery?

A

prostaglandin E1 (Alprostadil)

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134
Q

what is the most common cyanotic congenital heart disease?

A

tetralogy of fallot

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135
Q

4 cardiac features of tetralogy of fallot

A
  1. pulmonary stenosis
  2. ventricular septal defects
  3. right ventricular hypertrophy
  4. aorta overriding the VSD
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136
Q

clinical features of tetralogy of fallot (4)

A
  1. pulmonary stenosis
  2. heart failure (before age 1)
  3. tet spells
  4. squatting
  5. cynaotic - blue
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137
Q

investigations and key findings in tetralogy of fallot (3)

A
  1. cardiac auscultation - HARSH SYSTOLIC EJECTION MURMUR over pulmonary and left sternal area
  2. cxray - boot-shaped heart
  3. echocardiogram (diagnostic)
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138
Q

how is tetralogy of fallot managed?

A

neonates: prostaglandin infusion (maintain ductus arteriosus allows blood to flow from aorta into pulmonary arteries)

surgery

beta-blockers

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139
Q

what is transposition of the great arteries (TGA)?

A

where the aorta is connected to the right ventricle and the pulmonary artery is connected to the left ventricle

O2 blood recirculates only in pulmonary circulation, deoxygenated systemic blood bypasses lungs

incompatible with life

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140
Q

what does survival depend on for infants born with TGA? why?

A

whether there is a PDA, VSD or ASD, as these will allow blood to mix

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141
Q

how does TGA present?

A

cyanosis in FIRST 24H
tachypnoea
tachycardia
failure to thrive

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142
Q

what is the main RF for TGA?

A

maternal diabetes

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143
Q

investigations and findings for TGA

A

bloods and gas - metabolic acidosis, decreases PaO2

CXR - ‘egg on a string’

diagnostic = echo

144
Q

management for TGA

A

emergency prostaglandin infusion and surgical correction

145
Q

what is the most common septal defect?

A

ventricular septal defect (VSD)

146
Q

what is VSD? what is it’s pathophysiology? how does this explain why it’s an acyanotic defect?

A
  • hole in the septum between the R and L ventricle
  • pressure is higher in L ventricle
  • so blood shunts from L to right
  • O2 blood then re-enters pulmonary circulation
    = pulmonary OVERcirculation
  • O2 blood still flowing around body but inefficient!
147
Q

presentation of VSD and its classical sign on ausculation

A
  • sweating
  • fatigue
  • poor weight gain
  • tachypnoea/SOB
  • on auscultation = pan systolic murmur at LLSE
148
Q

investigations and findings for VSD

A
  1. CXR - may have cardiomegaly, pulmonary oedema, plural effusion
  2. echo (GOLD STD)
149
Q

how is a VSD managed? when is surgical intervention indicated?

A
  • MOST will close by themselves
  • increase caloric intake
  • diuretic (furosemide) to decrease fluid in circ
  • ACE-Is
  • digoxin

surgery if significant or causing complications later in life

150
Q

what condition does VSD increase a child’s risk of?

A

infective endocarditis

151
Q

what is ASD?

A

atrial septal defect - hole between left and right atrium causing L>R shunt

152
Q

why is ASD commonly asymptomatic?

A

because the L>R shunt is at at a lower pressure than in a VSD - less pul circulation overload

153
Q

classical presentation of ASD on auscultation?

A

split double (split, fixed 2nd heart sound) + soft ejection systolic murmur

154
Q

main RF for ASD

A

maternal rubella

155
Q

if a child with ASD is symptomatic, how may they present?

A

chest pain, exercise intolerance

156
Q

how is ASD diagnosed?

A

gold std = echo

157
Q

how are ASDs <5mm managed?

A
  • conservative: should close spontaneously within 12m of birth
  • if heart probs, give diuretics e.g. furosemide
158
Q

how are ASDs >1cm managed?

A

surgery

159
Q

what is ASVD? what comorbidity is it strongly associated with?

A
  • malformation of the atrioventricular septum connecting all 4 heart chambers
  • essentially an ASD and a VSD
  • strong association w Trisomy 21
160
Q

signs and sx of AVSD

A

sx:
- tachypnoea
- poor feeding
- sweating
- failure to thrive

signs:
- hyperactive precordium
- thrill
- gallop rhythm
- HF > hepatomegaly and generalised oedema/crackles

161
Q

definitive management of ASVD?

A

surgery!!!
lifelong FU needed

162
Q

what is Eisenmenger’s syndrome? what causes it to happen?

A
  • if a septal defect e.g. VSD is left untreated
  • constant L>R shunt
  • increased strain on R side of heart > increased pressure on pulmonary artery > pulmonary HTN > increased pressure in RA > overcomes pressure in LA
  • shunt REVERSES and becomes R>L
163
Q

what will happen to a baby with Eisenmenger’s syndrome

A

will become blue as septal defect has become cyanotic

164
Q

what is coarctation of the aorta?

A

narrowing of the aorta distal to the left subclavian artery - at top of descending aorta

165
Q

what pathophysiological changes occur as a result of coarctation of the aorta?

A
  • severe obstruction of blood flow in descending aorta
  • significant afterload on LV
  • compensatory ventricular hypertrophy
166
Q

how does coarctation of the aorta present?

A

relatively asymptomatic!

  • headaches
  • on exertion claudication and cool peripheries
167
Q

investigations and findings for coarctation of the aorta (2)

A
  1. chest xray- dilated aorta and rib knotching
  2. ECG - left ventricular hypertrophy
168
Q

how is coarctation of the aorta managed?

A

balloon angioplasty (opens aorta)

169
Q

what is Ebstein’s anomaly?

A

incorrect positioning (low insertion) of the tricuspid valve separating the R atrium and ventricle > blood leaks from V to A > LARGE A and SMALL V

170
Q

most common cause of heart failure in children

A

congenital heart defects (CHD)

171
Q

what can the causes of paediatric heart failure be split into?

A

overcirculation

pump failure

172
Q

list some ‘overcirculatory’ causes of paediatric heart failure (4)

A
  1. L>R shunt e.g. VSD, ASD, patent ductus arteriosus
  2. parallel circulation e.g. transposition of the GAs
  3. conditions causing increased cardiac output e.g. anaemia
  4. mitral and aortic regurgitation
173
Q

list some examples of ‘pump failure’ causes of paediatric heart failure (4)

A
  1. aortic stenosis/pul stenosis
  2. inflammatory e.g. myocarditis, HIV-related, Chaga’s disease
  3. dilated cardiomyopathy
  4. rhythm disturbance e.g. complete heart block
174
Q

signs and symptoms of HF in:
a) new-borns
b) infants
c) older/adolescents

A

a) nonspecific e.g. tachycardia, high RR

b) tachypnoea, feeding difficulties, irritability with feeding, sweating

c) fatigue, effort intolerance, dyspnoea, orthopnoea, abdominal pain, oedema, ascites

175
Q

investigations and findings for paediatric HF (6)

A
  1. bloods - BNP elevation
  2. urine tests
  3. CXR - enlarged heart
  4. ECG
  5. Echo - enlarged chambers
  6. cardiac catheterisation
176
Q

other than treating the underlying cause, how can paediatric HF be medically managed?

A
  1. diuretics e.g. furosemide
  2. inotropes e.g. epinephrin (increase contractility)
  3. ACEis (reduce afterload)
  4. digoxin
177
Q

what is rheumatic fever?

A

an autoimmune systemic illness caused by an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection

178
Q

who is most commonly affected by rheumatic fever?

A

children in developing countries

179
Q

briefly describe the pathophysiology of rheumatic fever. what antibodies are involved?

A
  1. strep A releases toxins including M proteins
  2. B cells produce anti-M protein antibodies
  3. these antibodies cross-react with other tissues e.g. heart, brain, joints and skin
180
Q

what is the name of the granulomatous nodules found in rheumatic heart fever?

A

Aschoff bodies

181
Q

what ALWAYS precedes the signs and symptoms seen in rheumatic fever?

A

a recent (2-4w) infection with strep A e.g. sore throat/scarlet fever

182
Q

how is a diagnosis of rheumatic fever made?

A

evidence of recent strep infection accompanied by…
- 2 major criteria
- 1 major with 2 minor criteria

183
Q

what are the minor and major criteria for rheumatic fever?

A

MINOR (RAPP)
- Raised ESR/CRP
- Arthralgia
- Prolonged PR interval
- Pyrexia

MAJOR (SPECS)
- Sydenham’s chorea (often late)
- Polyarthritis
- Erythema marginatum (bright pink/red circular lesions with defined borders and central clearing)
- Carditis and valvulitis
- Subcutaneous nodules

184
Q

what is sydenham’s chorea?

A

a neurological complication of rheumatic fever characterised by rapid, uncoordinated jerking movements affecting the face, hands and feet

185
Q

management of rheumatic fever (3)

A
  1. oral abx 1st line = benzathine benzylpenicillin
  2. anti-inflammatories - NSAIDs
  3. tx of complications e.g. HF
186
Q

how does the frequency of stool passage change from infants under 6m to children older than 3y?

A

3x per day for infants, decreases to 1x a day after 3y

187
Q

what is encopresis?

A

involuntary faecal soiling/incontinence secondary to chronic constipation

188
Q

pathogenesis ‘cycle’ of functional constipation in children (4)

A
  1. painful defecation
  2. voluntary withholding
  3. prolonged fecal statis, re-absorption of fluids, increased size and consistency of stools
  4. more pain

and then the cycle continues

189
Q

NICE guidelines suggest a diagnosis of constipation can be made when 2 or more of the following are present in children <1 year…

A
  1. stool pattern
    - <3 stools a week
    - hard large stool
    - rabbit droppings
  2. symptoms with defecation
    - distress
    - bleeding
    - straining
  3. history
    - prev constipation
    - prev/current anal fissure
190
Q

NICE guidelines suggest a diagnosis of constipation can be made when 2 or more of the following are present in children >1 year…

A
  1. stool pattern
    - <3 stools a week
    - overflow soiling
    - rabbit droppings
    - large infrequent stools that block toilet
  2. symptoms with defecation
    - poor appetite improving with passage
    - abdo pain
    - retentive posturing e.g. straight-legged, tiptoeing, back arching
    - straining
    - anal pain
  3. history
    - prev constipation
    - prev/current fissure
    - painful bowel movements + bleeding
191
Q

causes of constipation in children (9)

A
  1. dehydration
  2. low-fibre
  3. medications e.g. opiates
  4. anal fissure
  5. over-enthusiastic potty training
  6. hypothyroid
  7. Hirschsprung’s
  8. hypercalcemia
  9. learning disabities
192
Q

investigations are often unnecessary for constipation, but when may they be indicated and what would they be?

A

IF organic cause suspected/child remains constipated despite medical tx

  • bloods (TFTs, serum calcium, coeliac panel)
  • sweat test (CF)
  • abdo xray
  • anal mamometry
  • rectal biopsy
  • spinal imaging (if neuro cause suspected)
193
Q

what constipation ‘red flags’ suggest an underlying disorder?
a) timing
b) passage of meconium
c) stool pattern
d) growth
e) neuro/locomotor
f) abdomen
g) other

A

a) reported from birth/first few weeks of life
b) >48h
c) ‘ribbon’ stools
d) faltering growth
e) previously unknown/undiagnosed weakness in legs, locomotor delay
f) distension
g) concern of child maltreatment

194
Q

what presentation suggests idiopathic constipation as opposed to an underlying disorder?
a) timing
b) passage of meconium
c) stool pattern
d) growth
e) neuro/locomotor
f) abdomen
g) diet

A

a) starts AFTER first few weeks of life
b) <48h
c) not ribbon
d) generally well, weight and height ok
e) no neuro or locomotor probs
f) no distension
e) changes in infant formula, weaning, insufficient fluid or diet intake

195
Q

what does a child need to be assessed for prior to starting constipation tx?

A

faecal impaction

196
Q

factors suggesting faecal impaction

A
  1. sx of severe constipation
  2. overflow soiling
  3. faecal mass palpable in abdomen
197
Q

tx of constipation if faecal impaction is present

A

first line = polyethylene glycol + electrolytes (Movicol Paediatric Plain)

198
Q

what laxatives can be used to treat paediatric constipation?

A

osmotic laxatives e.g. Movicol Paediatric Plain, stimulant laxatives e.g. Senna, other e.g. lactulose if not working

199
Q

non-medical tx for constipation

A
  • do NOT use dietary interventions alone
  • regular toileting and behavioural interventions e.g. reward scheme
200
Q

management options for constipation in very young children
a) not yet weaned (<6m)
b) weaned

A

a) give extra water in between feeds, abdominal massages, bicycling legs

b) offer extra water, diluted fruit juices and fruits (if not effective consider lactulose)

201
Q

what is the most common cause of abdominal pain in children requiring surgery

A

appendicitis

202
Q

uncomplicated vs complicated appendicitis?

A

complicated - inflammation of appendix without signs of necrosis/perforation

uncomplicated - inflammation progressed to focal or transmural necrosis and/or perforation

203
Q

3 common causes of appendicitis in children

A
  1. faecalith (hardened lump of poop)
  2. lymphoid hyperplasia (dense collections of lymphocytes, reaches max size in adolescence)
  3. pinworm infection
204
Q

pathophysiology of appendicitis

A
  1. obstruction to entrance of appendix
  2. but appendix continues secreting mucus/fluids from intestinal lumen mucosa
  3. fluid and mucus builds up
  4. pushes on afferent nerve fibres
  5. flora and bacteria in appendix trapped
  6. WBCs invade > pus builds up
205
Q

presentation of uncomplicated appendicitis

A
  • loss of appetite
  • nausea and vomiting
  • low-grade fever
  • abdominal pain: initially central and colicky, then localising at right iliac fossa (McBurney’s)
  • pain aggravated by movement
206
Q

presentation of complicated appendicitis

A
  • appendix mass
  • generalised guarding (perforation)
  • fever
  • weakness
  • rebound tenderness
207
Q

investigations for appendicitis including 1st line imaging

A
  1. bloods
    - FBC (raised WCC)
    - U&Es (may be deranged)
    - CRP (raised)
  2. urinalysis (rule out UTI)
  3. first-line imaging = ultrasound
208
Q

signs of appendicitis on USS (3)

A
  1. non-compressible appendix (6mm diameter)
  2. wall thickening
  3. may see appendicolith (hard lump made of minerals and faeces)
209
Q

ddx for paediatric appendicitis

A
  1. mesenteric adenitis (usually preceded by sore throat)
  2. meckel’s diverticulitis (rectal bleeding)
  3. gastroenteritis (more general pain)
  4. UTI
210
Q

management of uncomplicated and complicated appendicitis

A

uncomplicated - appendicectomy

complicated - IV fluids, appendicectomy, surgical drainage

for BOTH - laparoscopic approach, pre-operative abx therapy

211
Q

complications of appendicitis (2)

A
  1. perforation
  2. abscess formation
212
Q

which hernia types are the most common in children?

A

inguinal and umbilical

213
Q

a) when do inguinal hernias present?
b) in who?

A

a) infancy, mostly appear in first 6m of life
b) mostly boys

214
Q

what causes inguinal hernias in children?

A

failure of the processus vaginalis to close once the testes have moved through the inguinal canal into the scrotum

215
Q

RFs for
a) inguinal hernia
b) umbilical hernia

A

a) family hx
b) down’s syndrome, prematurity, familial tendency

216
Q

presentation of an inguinal hernia

A

bulge or swelling in groin
- in boys, may be seen in scrotum
- may only be seen during crying/straining

217
Q

presentation of an umbilical hernia

A
  • bulge at umbilicus, size of pea-plum
  • painless
  • v obvious when crying/straining
218
Q

investigations for paediatric hernias

A

normally clinical diagnoses

219
Q

which children presenting with an inguinal hernia require emergency surgery? why?

A

children that present in first few months of life - due to risk of strangulation

ALSO those with an irreducible hernia

220
Q

which children presenting with an inguinal hernia are at lower risk of strangulation? so what is the management?

A

children >1 year old
can have elective (rather than emergency) surgery

221
Q

how are umbilical hernias usually managed?

A
  • 95% close spontaneously
  • surgery rarely required as strangulation rare
222
Q

when is surgery indicated for umbilical hernias?

A

IF pain in hernia OR child is age >4

223
Q

what is infective endocarditis?

A

infection of the endocardium (lining of the heart), often involving the heart valves

224
Q

which children is IE commonly seen in?

A

those with hx of congenital/acquired heart disease e.g.
- ventricular septal defects
- patent ductus arteriosus
- TOF

225
Q

give 2 common bacterial causes of IE

A
  1. staphylococcus aureus
  2. streptococcus viridans
226
Q

which bacteria are associated with causing IE following:
a) dental procedures
b) GU/GI surgery

A

a) strep viridans
b) enterococci

227
Q

presentation of IE

A

with a history of CHD/cardiac surgery/prosthetic material…

  1. persistent low grade fever
  2. heart murmur/change in murmur
  3. splenomegaly

(cutaneous manifestations uncommon in paeds)

228
Q

what are the 2 main investigations of choice for IE?

A
  1. blood cultures - multiple samples from multiple sites
  2. ECHO - identifying vegetations
229
Q

which criteria is used to diagnose IE?

A

Modified Duke’s Criteria

230
Q

what combo of major/minor criteria must be met for IE to be diagnosed?

A

either:
2 major
1 major + 3 minor
5 minor

231
Q

major Duke’s criteria for IE diagnosis (2)

A
  1. positive blood culture
  2. positive ECHO findings of vegetation
232
Q

minor Duke’s criteria for IE diagnosis (6)

A
  1. predisposition - heart condition
  2. fever >38
  3. vascular phenomena e.g. arterial emboli, conjunctival haemorrhage
  4. immunologic factor e.g. glomerulonephritis, RF
  5. positive blood culture not consistent with IE organisms
  6. positive ECHO not meeting major criteria
233
Q

examples of ECHO findings suggesting tx of IE needs to be surgical (3)

A
  1. vegetation >15mm
  2. valve perforation/rupture
  3. heart failure
234
Q

medical tx for IE if bacteria cause is…
a) streptococci
b) penicillin resistant
c) enterococcus

A

a) IV penicillin/IV ceftriaxone for 4 weeks

b) add gentamicin for first 2 weeks to above regimen

c) 4–6 weeks IV penicillin and gent

235
Q

what is the infective endocarditis pathophysiological triad?

A
  1. endothelial damage
  2. platelet adhesion
  3. microbial adherence
236
Q

brief pathophysiology of coeliac disease

A
  1. repeated exposure to protein gluten
  2. inflammation and villous atrophy of small bowel mucosa
  3. malabsorption
237
Q

when do children normally present with coeliac disease? why?

A

normally before 3 years old, following intro of gluten into the diet

238
Q

which genes are strongly associated with coeliac disease? (2)

A
  1. HLA-DQ2
  2. HLA-DQ8
239
Q

presentation of coeliac disease in children (“classic” and “common”)

A

“classical”
- faltering growth/failure to thrive
- abdominal distension
- diarrhoea
- foul-smelling, floating stools
- irritability

“common”
- mild, non specific GI sx
- anaemia: fatigue, pallor
- growth faltering

240
Q

1st line and gold std investigations for coeliac disease

A

1st line = bloods
- serology IgA-TTG blood test (+ve)
- FBC and blood smear (low Hb, folate, ferritin, B12)

gold std = duodenal biopsy and histology

241
Q

what will be seen on histology of the duodenum in a child with coeliac disease?

A

villous atrophy, crypt hypoplasia, intraepithelial lymphocytes

242
Q

what is there a slight increased risk of in coeliac children who don’t adhere to a gluten-free diet?

A

small bowel lymphoma

243
Q

define failure to thrive

what are the NICE definitive guidelines in terms of falls in weight if birth weight was:
a) below the 9th centile
b) between the 9th and 91st centile
c) above the 91st centile

A

poor physical growth and development

a) fall in weight across one or more centile spaces
b) fall in weight across two or more centile spaces
c) fall in weight across three of more centile spaces

244
Q

what are the 5 categories for causes of failure to thrive?

A
  1. inadequate nutritional intake
  2. difficulty feeding
  3. malabsorption
  4. increased energy requirements
  5. inability to process nutritiom
245
Q

inadequate nutritional intake causes of failure to thrive

A
  1. maternal malabsorption if breastfed
  2. Fe deficiency anaemia
  3. family/parental problems
  4. neglect
  5. availability of food ie poverty
246
Q

difficulty feeding causes of failure to thrive

A
  1. poor suck e.g. due to cerebral palsy
  2. cleft lip/palate
  3. genetic e.g. abnormal facial structure
  4. pyloric stenosis
247
Q

malabsorption causes of failure to thrive

A
  1. CF
  2. coeliac
  3. cow’s milk intolerance
  4. chronic diarrhoea
  5. IBD
248
Q

inability to process nutrients causes of failure to thrive

A
  1. type 1 diabetes
  2. metabolic errors
249
Q

which key areas need to be assessed when investigating failure to thrive?

A
  1. pregnancy, birth, development and social hx
  2. feeding/eating history - breast/bottle, feeding times, volume, food choices, aversion, meal time routines, appetite
  3. observe feeding
  4. mums physical and mental health
  5. parent-child interactions
  6. growth chart plot and mid-parental height centile
250
Q

initial investigations for a child failing to thrive

A
  1. urine dipstick
  2. coeliac screen
251
Q

management of failure to thrive if caused by difficulty breastfeeding

A
  • support from midwife, health visitors, peer groups
  • supplement with formula
252
Q

management of failure to thrive if inadequate nutrition is the cause

A
  • encourage regular structured meals and snacks
  • reduce milk consumption to increase appetite for other foods
  • review by dietician
  • additional energy dense foods
  • nutritional supplement drinks
253
Q

define…
a) Crohn’s
b) UC

A

a) a transmural (across whole wall), focal, subacute or chronic inflammatory disease most commonly affecting the distal ileum and proximal colon

b) a recurrent, inflammatory and ulcerating disease involving the mucosa of the colon

254
Q

risk factor for paediatric IBD

A

family history

255
Q

pathophysiology of Crohn’s:
a) location
b) type of inflammation
c) continuous or discontinuous?
d) granulomas or not?
e) rectal involvement
f) gut complications
g) classic associating condition

A

a) mouth to anus (most common is distal ileum and prox colon)
b) transmural inflammation
c) discontinous
d) granulomas
e) rectal sparing
f) fissures, fistulas, abscesses and strictures COMMON
g) perianal disease

256
Q

pathophysiology of UC:
a) location
b) type of inflammation
c) continuous or discontinuous?
d) granulomas or not?
e) rectal involvement
f) gut complications
g) classic associating condition

A

a) colon only - in children, most common is pancolitis (whole colon)
b) mucosal inflammation
c) continuous
d) NO granulomas
e) NO rectal sparing
f) abscesses and strictures RARE
g) primary sclerosing cholangitis (PSC)

257
Q

signs and symptoms of UC in children

A

(in children, sometimes persistent poor growth is only sign of disease)

  1. rectal bleeding
  2. diarrhoea
  3. colicky pain
  4. extra-intestinal - erythema nodosum, arthritis
258
Q

signs and symptoms of Crohn’s in children

A

(sometimes in children persistent poor growth is only sign of disease)

  1. delayed puberty
  2. classic presentation = abdominal pain, diarrhoea and weight loss
  3. general ill health e.g. fever, lethargy
  4. extra-intestinal - oral lesions, perianal skin tags, uveitis, arthralgia, erythema nodosum
259
Q

investigations (including gold std) for IBD

A
  1. bloods - FBC (may be anaemic), LFTs, ESR and CRP (raised)
  2. stool microscopy and culture - rule out infection
  3. faecal calprotectin (faecal inflamm marker, raised)
  4. gold std = colonoscopy with biopsy and histology
260
Q

what will be seen on histology of the colon in:
a) Crohn’s
b) UC

A

a) granulomas, skip lesions, cobblestone appearance, fistula formation

b) mucosal inflammation, crypt abscesses and ulceration

261
Q

ddx for paediatric IBD

A
  • gastroenteritis
  • coeliac disease
  • IBS
  • lactose intolerance
262
Q

managing paediatric crohn’s:
a) inducing remission
b) maintaining remission

A

a) 1st line = corticosteroid therapy, fluids
2nd line = immunosuppression e.g. mesalazine or bio agents e.g. infliximab

b ) first line = azathioprine (monotherapy)
alternative = methotrexate

263
Q

what medication should be avoided in acute IBD attacks? why?

A

anti-motility drugs e.g. loperamide - can precipitate toxic megacolon

264
Q

when is surgery indicated in paediatric crohns? give some surgical options

A

for those with failed medical management or severe complications e.g. strictures, perforation

options include:
- ileocaecal resection
- small bowel resection
- perianal disease surgery

265
Q

GI and extraintestinal complications of crohn’s

A

GI
- fistula e.g. rectovaginal
- strictures
- recurrent perianal fistula
- malignancy

extra
- malabsorption and osteoporosis secondary to this
- gallstones and renal stones

266
Q

what investigation should not be perforemd during an acute chron’s flare? why?

A

colonoscopy = risk of perforation

267
Q

medical management of mild-moderate UC (induction and maintenance)

A

induction - mesalazine
maintenance - mesalazine

268
Q

medical management for moderate-severe UC (induction and maintenance)

A

induction - corticosteroids
maintenance - anti-TNF e.g. infliximab OR azathioprine

269
Q

hospital management of an acute severe UC flare (3)

A
  1. IV corticosteroids
  2. fluid resus
  3. prophylactic heparin and stockings (due to prothrombotic state of IBD flares)
270
Q

lifestyle/general management for paeds IBD

A

refer to IBD nurse specialists, consider enteral nutritional support if growth concerns, consider low residue diet

271
Q

complications of UC (3)

A
  1. toxic megacolon
  2. colorectal adenocarcinoma
  3. pouchitis (inflammation of ileal pouch following surgery)
272
Q

define marasmus
how does it differ from Kwashikor

A

marasmus = acute malnutrition as a result of insufficient intake of protein AND calories

it is total calorie insufficiency, as opposed to Kwashikor which results from sufficient caloric intake but insufficient protein

273
Q

aetiology and RFs of marasmus

A

aetiology - poverty, biological e.g. HIV, AIDs, infectious disease

RFs - low social status, no maternal education, war/natural disaster

274
Q

general presentation of marasmus
in children
in infants

A
  1. overt loss of adipose tissue and muscle
  2. weight-for-height value LOW
  3. failure to thrive
  4. infants - irritability, apathy, sunken fontanelles
275
Q

what signs of vitamin deficiency may a child with marasmus present with? (4)

A
  1. vit A - dry eyes, Bitot spots (keratin deposits in eye)
  2. Fe deficiency anaemia - koilonchyia, glossitis
  3. hypocalcemia - Chvostek/Trousseau signs
  4. calcium and vit D - rickets, deformities long term
276
Q

3 steps for managing marasmus

A
  1. resus and stabilisation - rehydrate, prevent infection, avoid refeeding syndrome
  2. nutritional rehabilitation - gradual increase in intake, vaccines
  3. FU and prevention of recurrence
277
Q

what would be the visible differences seen in a child with marasmus vs kwashikor?

A

marasmus - loss of muscle mass, thin
kwashikor - ascites, moon face

278
Q

what is kwashikor? what is it characterised by?

A

severe acute malnutrition characterised by severe protein deficiency, causing fluid retention (bilateral pitting oedema in absence of another medical cause)

279
Q

RFs for kwashikor

A
  1. monotonous corn based diet
  2. recent weaning
  3. recent infection e.g. measles
  4. diarrhoea illness
  5. rural communities, Africa
  6. endemic food insecurity/famine
280
Q

under what circumstances may kwashikor present in developed countries?

A

in association with TB, HIV or severely restricted diet e.g. in autism and behavioural disorders

281
Q

classical presentation of kwashikor

A
  1. weight loss
  2. muscle wasting
  3. OEDEMA of belly (ascites), feet and ankles
282
Q

investigations for marasmus/kwashikor

A

primarily clinical diagnosis but can do it to look for underlying conditions/rule out dix

urine - rule out nephrotic syndrome and GN (will be no proteinuri/haemturia)
FBC - low Hb
U&Es - deranged
serum protein and albumin - low/normal
blood glucose — hypoglycemia
CXR - TB may co-exist
urine, blood, stool cultures and malaria screen

283
Q

management options for kwashikor

A

if in community - ready-to-use therapeutic food (RUTF), broad spec abx e.g. amoxicillin

in hospital - regular milk-based liquid food, emperical abx, vitamin A supplementation

284
Q

risk factor for IBS in children

A

parental hx

285
Q

which age group is most commonly affected by IBS in the paediatric population?

A

teens

286
Q

brief pathophysiology of IBS

A

altered gut reactivity (motility and secretion) due to environmental effects like stress/certain foods

287
Q

signs and sx of IBS

A

ABC
A - abdo discomfort
B - bloating/distension
C - change in bowel habit

Other
- mucus in stool
- loss of appetite
- nausea
- altered stool passage e.g. straining, urgency, incomplete evacuation

288
Q

signs and sx of IBS

A

ABC
A - abdo discomfort
B - bloating/distension
C - change in bowel habit

Other
- mucus in stool
- loss of appetite
- nausea
- altered stool passage e.g. straining, urgency, incomplete evacuation

289
Q

investigations for IBS

A

diagnosis of EXCLUSION:
1st line = bloods
- FBC
- ESR and CRP
- coeliac serology

stool sample e.g. faecal cal protection
abdo imaging
upper endoscopy/colonoscopy if IBD suspected

290
Q

management of non-severe IBS (2)

A
  1. dietary modifications (limiting lactose, probiotics, high fibre NOT indicated in paeds)
  2. stress management
291
Q

management of severe IBS

A

medical tx, same as adults:
1. pain/bloating - antispasmodic e.g. buscopan
2. constipation - laxative e.g. senna
3. diarrhoea - antimotiltiy e.g. loperamide

292
Q

what is Hirschprung’s disease?

A

a congenital condition of the colon, leading to functional obstruction

293
Q

aetiology/pathophysiology of Hirschsprung’s disease

A
  1. ganglion cells in the colon fail to develop (normally in rectosigmoid area)
  2. lumen tonically contracted
  3. peristalsis halts
  4. obstruction
294
Q

when is Hirchsprung’s commonly diagnosed?

A

within the first year of life, most commonly first few DAYS

295
Q

risk factors and other conditions associated with Hirschsprung’s disease

A

associated with Down’s syndrome, multiple endocrine neoplasia

RF = male sex, genetics e/g/ Trisomy 21, sibling with HSD

296
Q

how does Hirschsprung’s disease present?

A
  1. failure to pass meconium in first 24 hours
  2. abdo distension
  3. bilious vomiting (bright green)
  4. failure to thrive

other = constipation, explosive passage of liquid/foul stools, fever

297
Q

1st line and gold standard investigations for Hirschsprung’s

A

1st line = abdominal x-ray (can also do contrast enema)
gold std = rectal biopsy

298
Q

what findings would indicate Hirschsprung’s disease on:
a) x-ray
b) contrast enema
c) rectal biopsy

A

a) distended colon (automatically ruled out if no distension)

b) contracted distal bowel, dilated proximal bowel, transition zone

c) absence of ganglion cells, thickened unmyelinated nerves, increased Ach activity

299
Q

differential diagnoses for Hirschsprung’s disease (5)

A
  1. intussusception
  2. constipation
  3. pyloric stenosis
  4. CF (meconium ileus)
  5. small left colon syndrome
300
Q

what is the classical triad of Hirschsprung’s disease?

A
  1. failure to pass meconium
  2. abdominal distension
  3. bilious distension
301
Q

initial and definitive management of Hirschsprung’s disease

A

initial = IV abx, NG tube insertion and bowel decompression
definitive = surgical

302
Q

what is a serious complication of Hirschsprung’s disease surgery?

A

enterocolitis (infection)

303
Q

what are the two surgical options for Hirschsprung’s?

A
  1. single-stage pull through procedure (single-stage RESECTION)
  2. 3-stage procedure
304
Q

what is colic defined as?

A

excessive crying in the first few months of life

305
Q

epidemiology of colic
- how common?
- when is prevalence highest?

A
  • V COMMON
  • prevalence highest in <6 weeks, generally common <12m
306
Q

aetiology of colic

A

unknown - possibly to do with gas production/abnormal motility and pain signalling/inflammation

307
Q

RFs for colic (4)

A
  1. family tension
  2. parental anxiety/depression
  3. inadequate parent-infant interaction
  4. misinterpretation of crying
308
Q

what are the Rome IV diagnostic criteria for colic? (2)

A
  1. infant <5m when symptoms start AND stop
  2. recurrent, prolonged periods of infant crying/fussing/irritability with non-obvious causes and cannot be settled by caregivers
309
Q

other signs of colic

A
  • crying in late afternoon/evening
  • fist clenching
  • drawing knees to abdomen
  • arching back when crying
310
Q

what types of crying are red flags when diagnosing colic? (2)

A
  1. weak, continuous cry
  2. abnormally high-pitched cry
311
Q

how should colic be investigated?

A

full examination to rule out ddx - observations, weight plotting, physical exam, observe carer interactions, maternal breast exam

if no abnormalities besides inconsolable crying, further ix not indicated

312
Q

ddx for colic
a) acute (6)
b) chronic (5)

A

a) - intussusception
- pyloric stenosis
- incarcerated/strangulated hernia
- trauma/NAI
- sepsis
- hydrocephalus

b) - hunger/dehydration
- inadequate winding
- constipation
- GORD
- non-IgE mediated food allergy

313
Q

management for colic including strategies and advice for parents/carer

A
  1. SELF-LIMITING - normally resolves by 5 months
  2. reassurance
  3. strategies - hold baby when crying, gentle motion, white noise, warm bath, optimise winding technique
  4. advise - continue breastfeeding, rest when baby is asleep, reassure baby can be left in safe place if carer unable to cope
314
Q

when is a referral re colic indicated?

A
  1. parent/carer unable cope despite reassurance/advice
  2. suspected faltering growth
  3. symptoms persist >5m
  4. suspected underlying cause
315
Q

complications of colic

A
  • child maltreatment
  • early breastfeeding cessation
  • family/relationship difficulties
  • carer sleep deprivation/depression/fatigue/stress etc
316
Q

what is cow’s milk protein allergy (CMPA)? which proteins is cow’s milk made up of?

A

multisystem disease caused by an adverse immune reaction to one or more cow milk proteins (caseins and whey)

317
Q

before what age do most cases of CMPA present by?

A

1 year old

318
Q

what are the two types of CMPA? give a brief pathophysiology

A
  1. IgE-mediated
    - production of specific IgE antibodies against the cow’s milk proteins
    - exposure to CM proteins > release of cell mediators e.g. histamines
  2. Non-IgE mediated
    - T-cell mediated response
319
Q

causes of CMPA (3)

A
  1. atopy
  2. IgA deficiency
  3. IgG subclass abnormalities
320
Q

RFs for CMPA (3)

A
  1. atopy (comorbid asthma, atopic eczema)
  2. family hx of food allergy or atopy
  3. male sex
321
Q

symptoms of CMPA present up to X hours following cow’s milk ingestion

A

2 hours

322
Q

IgE mediated CMPA symptoms (GI, skin, resp)

A

GI
- oral pruritis
- nausea, vomiting and diarrhoea
- colicky abdo pain

skin
- pruritis
- erythema
- acute, localised urticaria
- acute angioedema (eyes, lips, face)

resp
- URT e.g. nasal itching, sneezing, congestion, conjunctivitis
- LRT e.g. cough, tight chest, wheeze, SOB

323
Q

Non-IgE mediated CMPA symptoms (GI, skin, resp)

A

GI
- GORD
- loose/frequent stools
- blood/mucus in stools
- abdo pain
- colic
- food refusal/aversion
- perianal redness
- pallor and tiredness
- faltering growth in conjunction with one or more above

skin
- pruritis
- erythema
- atopic eczema

resp
- JUST LRT sx e.g. cough, tight chest, wheeze, SOB

324
Q

investigations for CMPA - what is diagnostic?

A
  1. allergy testing e.g. skin prick, serum-specific IgE test
  2. diagnostic = ELIMINATION DIET
325
Q

ddx for CMPA

A

GORD

326
Q

management of CMPA in a formula-fed infant (first line and alternative)

A

first line replacement = extensive hydrolysed formula (EHF) milk

if no response/severe CMPA - give amino-acid based formula (AAF)

327
Q

management of CMPA in a breast-fed infant

A
  1. continue breastfeeding
  2. eliminate cow’s milk protein from maternal diet
  3. consider prescribing calcium supplements to breastfeeding mums
  4. use eHF milk when breastfeeding stops
328
Q

at what age do children often become milk tolerant after having:
a) Ige mediated CMPA
b) non-IgE mediated CMPA

A

a) by 5 years old
b) by 3 years old

329
Q

what is biliary atresia?

A

a rare liver disease of newborn babies where a section of the bile duct is either narrowed or absent

330
Q

when can biliary atresia develop?

A

in utero OR in neonatal period

331
Q

aetiology of biliary atresia

A

idiopathic

332
Q

RFs for biliary atresia (3)

A
  1. genetics
  2. viral infection
  3. immune dysregulation
333
Q

pathophysiology of biliary atresia - which type of bilirubin is involved?

A
  1. inflammation of biliary tree > discontinuous/obliterated bile ducts
  2. ducts get blocked
  3. results in cholestasis > bile cannot be transported from liver to bowel
  4. bile builds in liver
  5. prevents excretion of CONJUGATED bilirubin
334
Q

signs of biliary atresia

A

SHORTLY AFTER BIRTH…
1. significant and persistent jaundice
2. pale stools +/- dark urine
3. failure to thrive
4. weight loss
5. ascites
6. hepatomegaly
7. bruising

335
Q

investigations for biliary atresia - what is gold std?

A
  1. bloods
    - serum total bilirubin
    - serum conjugated bilirubin (RAISED)
    - FBC
    - LFTs (deranged)
  2. new-born screen - rule out CF
  3. gold std - abdominal USS
335
Q

what may be seen on abdo USS in biliary atresia?

A
  • potential hepatosplenomegaly
  • absent/multiple spleen
  • ascites
  • triangular cord sign
337
Q

differential diagnoses for biliary atresia

A
  • other biliary obstruction e.g. tumour
  • hepatic viral infection e.g. CMV, HSV, hepatitis B
338
Q

what defines persistent jaundice in…
a) term babies
b) premature babies

A

a) > 14 days
b) > 21 days

339
Q

what is the first-line surgical management for biliary atresia?

A

Kasai procedure (replumbing bile duct into bowel)

340
Q

definitive management for biliary atresia

A

liver transplant

341
Q

what is toddler’s diarrhoea?

A
  • chronic (>14 days) NON SPECIFIC diarrhoea
  • functional aka child is otherwise healthy
342
Q

what is the most common cause of chronic diarrhoea in children aged 1-5?

A

toddler’s diarrhoea

343
Q

signs and symptoms of toddler’s diarrhoea - what distinguishes it from pathological chronic diarrhoea?

A
  • abnormal defecation frequency/consistency
  • foul-smelling, watery, contains mucus with undigested food
  • are NOT failing to thrive, have good nutritional state
  • short mouth-anus transit time
  • minority may have abdo pain
344
Q

how is toddler’s diarrhoea diagnosed?

A

clinically - thorough history and physical examination will be unremarkable

345
Q

what is the difference between acute vs chronic diarrhoea?

A

acute = <14 days

chronic = >14 days

346
Q

how is toddler’s diarrhoea managed? what age can you reassure parents it will go away by?

A

reassurance - normally self-limiting, most cases go away by age 5

347
Q

what is a choledochal cyst?

A

a rare congenital disorder where there are cystic dilatations at single/multiple segments of the biliary tree

348
Q

what population is predominantly affected by choledocal cysts?

A

asian children

349
Q

RFs for choledocal cysts (3)

A
  1. female sex
  2. young age
  3. asian
350
Q

brief pathophysiology of choledocal cysts

A

bile flow is blocked > builds up in liver

351
Q

signs and symptoms of choledocal cysts
what does it present similarly to?

A

presents similarly to biliary atresia

triad of jaundice, abdominal pain and palpable abdominal mass

infants <12m may have vomiting and pale stools

352
Q

3 imaging investigations for choledocal cysts - what is gold std?

A
  1. abdominal USS
  2. CT choliangiography
  3. gold std = magnetic resonance cholangiopancreatography (MRCP)
353
Q

management of choledochal cysts

A

surgery - cyst resection and restoration of bile flow

354
Q

ddx for choledochal cysts

A

biliary atresia

355
Q

what is neonatal hepatitis syndrome?

A

inflammation of the liver occurring in early infancy (1-2m) caused by a range of diseases

356
Q

what are the categories of causes of neonatal hepatitis syndrome? (9)

A
  1. congenital infection (MOST COMMON)
  2. anatomical/structural
  3. metabolic
  4. genetic
  5. neoplastic
  6. vascular
  7. toxic
  8. immune
  9. idiopathic

PHASE 3A (11 decks)

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