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Clinical Years / Progress Test > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

Developmental Milestones 2 months
- hearing/language
- social/emotional
- cognitive/visual/fine motor

A

coos and gurgles. turns head to sound

Begins to smile at people. Tries to look at parents. Sucks on hand to sooth

Begins to follow things with eyes
Begins to act bored

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2
Q

Developmental Milestones 8 months
- hearing/language
- social/emotional
- cognitive/visual/fine motor

A

Understands no. Mamama/dadada sounds

Stranger awareness. Has favourite toy

Transfers from one hand to another
Picks up cereal between thumb and index finger
Plays peek a boo

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3
Q

Developmental Milestones 18 months
- hearing/language
- social/emotional
- cognitive/visual/fine motor

A

Says 10 words
Says no and shakes head

Temper tantrums
Points to show something interesting

Follows 1 step verbal command
Scribbles on own

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4
Q

Developmental Milestones 3 years
- hearing/language
- social/emotional
- cognitive/visual/fine motor

A

Understands words such as in/on/under
Carries on a conversation using 2 to 3 sentences

Copies adults and friends
Takes turns in games
Shows concern friend crying

Does jig saw 3-4 pieces
Copies a circle with a pencil

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5
Q

cpr in children

A

15 compression s to 2 breaths

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6
Q

Croup (laryngotracheobronchitis) presentation and management

A

Common cause of acute respiratory distress in children 6 months to 3 years

Acute onset of seal-like barky cough in moderate to severe cases accompanied by stridor and sternal/intercostal indrawing
Fever
Viral cause (parainfluenza usually)
note majority of cases mild but if needed…

  • oral dexamethasone 0.15 mg/ kg as a single dose
  • Nebulised Adrenaline 5mls 1:1000 (mod or severe)
  • senior input
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7
Q

symptoms and management of foreign body aspiration

A

sudden onset of respiratory distress associated with coughing, gagging, or stridor. Unilateral wheezing suggests partial obstruction of the main or distal bronchi

management with flexible bronchoscopy or rigid if fails

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8
Q

signs of respiratory distress

A
  • increased RR
  • stridor
  • tracheal tug; retraction at the suprasternal notch
  • intercostal recession
  • subcostal recession
  • head bobbing
  • grunting
  • posture

impending respiratory failure and exhaustion will develop a low respiratory rate (for their age) and breath sounds including added sounds can diminish

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9
Q

differentials child in upper respiratory distress

A

Viral Croup
Epiglottitis (unlikely with haemophilia influenza vaccine)
Foreign body aspiration
Anaphylaxis
Bacterial tracheitis

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10
Q

laryngeal capillary haemangioma

A

slowly progressive airway obstruction / stridor since birth, particularly if the child has other capillary haemangiomas

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11
Q

gastro-oesophageal reflux disease in infants

A

silent symptoms or intermittent distress commonly after feeds and on lying flat, intermittent breathing difficulty with symptoms including stridor, episodes of colour change and / or recurrent chest infections, and behavioural changes such as back arching

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12
Q

stridor present since birth

A

Laryngomalacia or floppy larynx
soft stridor that worsens with feeds

monitor feeding and growth

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13
Q

epiglottitis

A

very rare cause of airway obstruction seen most in children 2-7

sudden onset of distressed child with muffled cough and voice, normal temp, drooling and leaning forward

needs emergency airway management
usually bacterial cause

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14
Q

bacterial tracheitis

A

differenital for epiglottis
younger age; 6 months to 14 months

fever present
sudden onset
hoarse voice and cough
drooling

needs emergency airway
broad spec Abx once airway secured

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15
Q

anaphylaxis presentation

A

Hypotension, Bronchoconstriction or Airway compromise in the setting of an allergic reaction

child pale and sweating (hypotensive), wheeze, stridor

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16
Q

what type of allergic reaction is a food allergy

A

type I hypersensitivity

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17
Q

sensitisation to allergen

A

for an allergy to occur a child must have previously encountered the allergen

Following exposure to an antigen the protein causes cross binding of two bound IgE molecules on the Mast Cell or Basophil surface. This process results in degranulation of the Mast Cell.

Histamine is released immediately causing the reaction

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18
Q

actions of histamine

A

localised irritation

vasodilation

bronchoconstriction

endothelial cell separation - resulting in urticarial rash

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19
Q

criteria for prescribing an Adrenaline Pen

A
  • History of Anaphylaxis
  • Previous cardiovascular / Respiratory involvement
  • Evidence of airway obstruction
  • Poorly controlled Asthma requiring regular inhaled corticosteroids
  • Reaction to a small amount of allergen
  • Ease of allergen avoidance

in less severe allergy, having antihistamine available can be sufficient

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20
Q

what is bronchiolitis

A

acute inflammation of the bronchioles usually caused by RSV
affects infants

initially subtle symptoms which worsen over 3-4 days

usually self limiting and needs supportive care but infants can become more unwell and need admission

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21
Q

symptoms of bronchiolitis

A

initial coryzal symptoms

progress to some or all of (day3-6)
- increased work of breathing
- typical cough
- poor/reduced feeding
- pallor
- exhaustion
- widespread wheeze and crackles
- fever (low grade)
- apnoea
- reduced oxygen sats
- tachycardia of bradycardia (more worrying)

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22
Q

symptoms bronchiolitis requiring admission

A
  • 50% feeding intake
  • pre-existing condition such as prematurity, CF
  • RR>70
  • O2 sats <92%
  • moderate resp distress
  • apnoeas
  • clinical dehydration
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23
Q

management of bronchiolitis in hospital

A

maintain oxygen sats

NG feed

if severely worsening; NBM, FBC, blood gas, biochem
IV fluids
orogastric decompression

consider CPAP if very severe
PICU?
consider Abx ?concurrent bac infection

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24
Q

accurate assessment of feeding in an infant

A

calculate the amount in mls/kg/day not ounces as reported by parents

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25
Q

minimum milk requirement for growth

A

150ml/kg/day in first month

100ml/kg/day after as long as meeting growth requirements

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26
Q

antenatal Hx

A

important in early childhood illness

maternal health
delivery
post delivery

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27
Q

systolic paediatric murmurs

A

Tetralogy of Fallot
VSD
pul/aortic stenosis

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28
Q

diastolic murmurs

A

pul or aortic valve regurge
mitral stenosis

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29
Q

symptoms/signs of HF in children

A

shortness of breath; tachypnoea and dyspnoea

poor feeding; can’t breathe and feed comfortably

tachycardia

hepatomegaly

poor pulses

acidosis

sweating

oedema only in children 3years+

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30
Q

management of HF in children

A

diuretics

ACEi

oxygen; with caution can close ducts

prostaglandins; prostin, to keep duct open

monitor diet/fluid intake

inotropes such as dopamine

sometimes catheter interventions, surgery last resort

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31
Q

diet in infants in HF

A

have higher energy requirements but need to control volume - high calorie feeds, supplements, frequent feeds less volume

sometimes need NG or if long term gastronomy

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32
Q

embryology of heart

A

forms from mesenchymal cells
4 chamber heart forms by 40 days

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33
Q

types of heart problems in children

A

congenital
- cyanotic
- acyanotic

acquired (rare)
- myocarditis (coxsackie B virus)
- viral pericarditis
- rheumatic heart disease

inherited
- HOCM
- marfans etc

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34
Q

presentation of congenital heart disease

A

antenatal; routine scan or FHx initiated scan

postnatal; routine check, symptomatic (cyanotic)

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35
Q

acyanotic CHD

A

majority septal defects; VSD, ASD

also
- aortic/pulmonary stenosis
- PDA
- coarctation of aorta
- mitral/tricuspid stenosis rare

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36
Q

VSD murmur

A

pansystolic

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37
Q

PDA murmur

A

continuous + bounding pulses

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38
Q

coarctation (narrowing) of aorta presentation

A

femoral pulses weak/absent

hypertension upper limbs

commonly associated with other heart defects

in newborns risk of necrotising enterocolitis

presents around 3 days. needs surgery and give prostin to keep a PDA open

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39
Q

cyanotic CHD

A

many but most important are
- fallot’s tetralogy
- transposition of great arteries (TGA)
- complete atria-ventricular septal defects

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40
Q

atrial-ventricular septal defect

A

atrial and ventricular septal defect

can be partial (no ventricular) or complete

higher incidence in trisomy 21

LAD on ECG

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41
Q

CHD and chromosomal syndromes

A

trisomy 21; 40% have CHD

trisomy 13 (Patau’s); 80% have CHD

trisomy 18 (Edward’s; 80-100% have CHD

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42
Q

DiGeorge syndrome

A

autosomal dominant condition. DiGeorge syndrome is associated with congenital heart disease.

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43
Q

sex chromosome aneuploidies

A

Turners 45XO
Klinefelters 47XXY
Triple X 47XXX
+ others

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44
Q

what is tested for on heel prick test

A

MCAD
HCU
Sickle cell
Isovalaric acidaemia
Cystic fibrosis
Hypothyroidism
Phenylketonuria

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45
Q

Kawasaki disease

A

inflammatory condition

swinging fevers resistant to paracetamol
lymphadenopathy
red eyes and tongue
rash
swollen feet and hands
platelet rise in 2 weeks

can cause coronary artery aneurysms; cardiac complications reduced by early aspirin and IV gammaglobulin

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46
Q

what can happen if VSD not treated

A

may close spontaneously but if left reversal of the shunt from L-R to R-L can occur which can lead to permanent pulmonary hypertension

VSD needs medical or surgical management

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47
Q

ASD management

A

needs closure

long term can result in arrhythmias or shunt reversal

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48
Q

pre term PDA

A

use NSAIDS for first 2-3 weeks
may close

if not surgery

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49
Q

4 components of tetralogy of fallot

A

pulmonary outflow obstruction

right ventricular hypertrophy

VSD

overriding aorta

baby presents with blue spells. needs surgery

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50
Q

innocent flow murmur

A

Many children will have an innocent flow murmur when they are pyrexic

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51
Q

differentials acutely breathless school age child

A

asthma
pneumonia
pneumothorax (unlikely)
foreign body aspiration
cardiac failure

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52
Q

acute severe asthma examination findings

A

Severe recession; sc/ic/ tracheal tug
Posture sitting forward; ‘Tripod’ position
Wheeze may be audible from end of bed

Hyperexpanded chest; Symmetrical expansion;
poor expansion if severe

trachea central cardiac apex in usual position
liver pushed down; edge palpable.
Resonant but equal
Air entry symmetrical; poor Air entry indicates increasing severity

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53
Q

severe pneumonia O/E

A

Respiratory distress with recession and tracheal tug

Wet cough; +/- Grunting

Expansion may be asymmetrical if severe unilateral pneumonia
Dullness over consolidation may be present

Reduced air entry +/-

Bronchial breathing / crackles over area of infection

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54
Q

what is Harrison’s sulcus

A

groove under ribcage seen in children with chronic respiratory disease e.g. severe asthma

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55
Q

sputum MC&S children

A

usually over 7 years can
if younger or cannot do a cough swab

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56
Q

investigations for chronic lung disease in a child e.g. bronchiectasis

A

CT chest

Measurement of serum immunoglobulin levels; assesses for primary immune deficiencies

Sweat chloride test; for CF

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57
Q

organs affected by cystic fibrosis

A

sinuses
lungs
skin - saltier sweat
liver
pancreas - exocrine and endocrine insufficiency
intestines - malabsorption
reproductive organs

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58
Q

CFTR protein

A

ion channel at cell membrane transporting ions such as chloride
loss of function results in altered secretions

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59
Q

diagnosis of CF

A

heel prick test approx day 5 in UK - measures a pancreatic trypsinogen elevated in CF babies

sweat test more accurate diagnosis esp in children >6 weeks

genetic testing analysis done to confirm

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60
Q

CF GI and liver complications

A
  • Meconium ileus (often first sign)
  • Constipation
  • Distal Intestinal obstruction
  • Neonatal cholestasis
  • fatty liver
  • cirrhosis
  • gallstones
  • cholecystitis
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61
Q

CF pulmonary management

A

Abx; oral/nebs/IV, prophylactic (start at birth) and treatment

mucolytics

physiotherapy

wheeze treatment

anti-fungals

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62
Q

extra pulmonary CF management

A

Creon for enzyme support + vitamins A, E, D, K (fat soluble)

management of constipation

insulin for CF diabetes

liver; ursodeoxycholic acid, vit K

salt supplements (lost in sweat)

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63
Q

presentation of CF if not diagnosed as neonate

A

poor growth and failure to thrive

fatty stools

recurrent respiratory problems (not in firth few months)

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64
Q

fetal circulation shunts

A

ductus arteriosus - between pulmonary artery and aorta to bypass lungs

foramen ovale - between R to L atria

ductus venosus - between umbilical vein and inferior vena cava to bypass liver

ducts are aided by high pulmonary vascular resistance in the foetus

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65
Q

how do fetal shunts change at birth

A

at first breath - alveoli fill with air and vascular resistance of the pulmonary circulation decreases
LA pressure exceeds RA pressure and the foramen ovale closes

circulating prostaglandins drop due to increased blood oxygenation - ductus arteriosus closes

ductus venous closes after cord clamped

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66
Q

PDA
- diagnosis
- management

A

may be picked up at birth with a murmur
can also present with failure to thrive, SoB, difficulty feeding - the L-R shunt causes increased pul pressure and HF
needs echo to diagnose

typically monitored until 1 year by which point may have closed or catheter surgery is performed

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67
Q

ASD symptoms/complicaitons

A

L-R shunt causes right heart strain and pul hypertension but is acyanotic because blood is always being oxygenated

eventually in Eisenmenger syndrome the pul pressure can exceed systemic and the shunt reverses to R-L causing cyanosis

murmur:mid-systolic, crescendo-decrescendo murmur loudest at the upper left sternal border with a fixed split second heart sound

may be picked up antenatally or later with symptoms/complciations

other complications are AF, stroke

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68
Q

VSD presentation

A

may be picked up antenatally or a murmur at newborn baby check

can also present with symptoms such as Poor feeding
Dyspnoea
Tachypnoea
Failure to thrive

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69
Q

CXR tetralogy of fallot

A

typically boot shaped heart due to RVH

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70
Q

“Tet spells” tetralogy of fallot

A

intermittent symptomatic periods where the right to left shunt becomes temporarily worsened, precipitating a cyanotic episode

usually when a child is physically exerting themselves, crying, laughing etc.

management: can try knees to chest/squatting. if failed
- oxygen
- IV fluids
- beta blockers/adrenaline/morphine

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71
Q

tetralogy of fallot management

A

prostaglandins can maintain ductus arteriosus

then heart surgery needed - mortality from surgery 5%

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72
Q

differentiating viral induced wheeze and asthma

A

factors favouring asthma
- personal or FHx of atopy
- interval symptoms (between viral infections ) of coughing at night, when playing or in cold

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73
Q

management of acute asthma child

A

Oxygen to maintain sats>94%

Salbutamol inhalers via a spacer device: starting with 10 puffs every 2 hours
Nebulisers with salbutamol / ipratropium bromide
Oral prednisone (e.g. 1mg per kg of body weight once a day for 3 days)
IV hydrocortisone
IV magnesium sulphate
IV salbutamol
IV aminophylline
if still not controlled contact ICU

work back down ladder as they get better

Antibiotics only if bacterial cause suspected

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74
Q

long term medical asthma therapy age <5

A

Start a short-acting beta-2 agonist inhaler (e.g. salbutamol) as required
Add a low dose corticosteroid inhaler or a leukotriene antagonist (i.e. oral montelukast)
Add the other option from step 2.
Refer to a specialist.

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75
Q

long term medical asthma therapy age 5+

A

Start a short-acting beta-2 agonist inhaler (e.g. salbutamol) as required
Add a regular low dose corticosteroid inhaler
Add a long-acting beta-2 agonist inhaler (e.g. salmeterol). Continue salmeterol only if the patient has a good response.
Titrate up the corticosteroid inhaler to a medium dose. Consider adding:
Oral leukotriene receptor antagonist (e.g. montelukast)
Oral theophylline
Increase the dose of the inhaled corticosteroid to a high dose.
Referral to a specialist. They may require daily oral steroids.

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76
Q

whooping cough symptoms

A

URTI caused by pertussis (children and pregnant women are vaccinated against)

typically starts with mild coryzal symptoms, a low grade fever and possibly a mild dry cough.
more severe coughing fits start after a week or more

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77
Q

whooping cough diagnosis

A

A nasopharyngeal or nasal swab with PCR testing or bacterial culture can confirm the diagnosis within 2 to 3 weeks

later can be tested for anti-pertussis toxin immunoglobulin G

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78
Q

whooping cough management

A

notifiable disease

management usually supportive
macrolide Abx can be helpful in early stages
close contacts are given prophylactic Abx

usually resolves in 8 weeks but can be long lasting and key complication is bronchiectasis

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79
Q

pyrexia and sepsis in children

A

apyrexia does not exclude sepsis

septic children often have normal or low temperatures

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80
Q

investigations suspected shaken baby

A

CT head - intracerebral haemorrhage?

skeletal survey

ophthalmology review - retinal haemorrhages?

metabolic testing - exclude glutaric aciduria associated with ICH

coagulation

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81
Q

clinical features of non-accidental head injury

A

Irritability
Poor Feeding
Increasing head circumference
Seizures
Reduced GCS
Full fontanelle
Anaemia
Retinal Haemorrhages

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82
Q

how does shaking baby cause injury

A

esp in a child under 6 months shaking can cause rupture to the small vessels crossing the subdural space, causing a subdural haemorrhage

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83
Q

What action should a doctor take if they have a child protection concern?

A

Refer to Social Services

Social Services will consider whether the child (and potentially siblings) requires a child protection medical assessment and needs to be safeguarded from impending harm.

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84
Q

child with bruising differentials

A

accidental injury

non accidental injury

immune thrombocytopenia
meningococcal septicaemia
leukaemia
Haemophilia A
Von Willebrands Disease

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85
Q

child with fractures differentials

A

accidental injury

non accidental injury

Osteogenesis Imperfecta
Copper Deficiency
Vit D defiency
Vit C deficiency
Ehlers Danlos and other hypermobility syndromes
JOBs syndrome

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86
Q

child with burns/scalds differentials

A

Accidental Injury
Non accidental injury
Bullous Impetigo
Scalded Skin Syndrome

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87
Q

red flag symptoms that indicate unlikely to be functional GI disorder of childhood

A

age <5years
weight loss/poor growth
blood in stools
regularly waking at night due to symptoms

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88
Q

causes of blood in stool in children

A

Infective – bacterial diarrhea eg campylobacter, salmonella

Inflammatory bowel disease

Tearing from anal vein

Polyp

Intussusception – acutely unwell

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89
Q

investigations IBD suspected

A

Hx and examination
bloods; FBC, U+E, LFT, CRP/ESR
Coeliac tests
stool MC&S
faecal calprotectin

if still suggestive; colonoscopy +/- small bowel barium studies

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90
Q

what typically causes Haemolytic Uraemia Syndrome
classical history

A

E Coli

Hx of severe diarrhoea, progressing to anaemia, thrombocytopenia, haematuria and raised creatinine

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91
Q

Kartagner’s triad

A

describes the three key features of primary ciliary dyskinesia. Not all patients will have all three features.

Paranasal sinusitis
Bronchiectasis
Situs Inversus

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92
Q

surgical causes abdo pain children

A

Appendicitis causes central abdominal pain spreading to the right iliac fossa

Intussusception causes colicky non-specific abdominal pain with redcurrant jelly stools

Bowel obstruction causes pain, distention, absolute constipation and vomiting

Testicular torsion causes sudden onset, unilateral testicular pain, nausea and vomiting

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93
Q

abdominal migraine

A

more likely in children compared to traditional migraine

abdo pain lasting >1 hour with possible associated Nausea and vomiting
Anorexia
Pallor
Headache
Photophobia
Aura

management similar to migraine in adults
acute; analgesia, low stimulus environment, triptan
preventative; Pizotifen, a 5-HT antagonist, consider propranolol

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94
Q

causes of constipation

A

majority idiopathic but consider CF, Hirschprungs, hypothyroidism

idiopathic contributed to by lifestyle factors including diet, activity, psychosocial problems

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95
Q

Encopresis/faecal incontinence

A

not pathological until >4years

usually a sign of chronic constipation where rectum loses sensation
other rarer causes include learning disability, abuse, psychosocial stress, cerebral palsy

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96
Q

constipation red flags

A

Not passing meconium within 48 hours of birth (cystic fibrosis or Hirschsprung’s disease)

Neurological signs or symptoms, particularly in the lower limbs (cerebral palsy or spinal cord lesion)

Vomiting (intestinal obstruction or Hirschsprung’s disease)

Ribbon stool (anal stenosis)

Abnormal anus (anal stenosis, inflammatory bowel disease or sexual abuse)

Abnormal lower back or buttocks (spina bifida, spinal cord lesion or sacral agenesis)

Failure to thrive (coeliac disease, hypothyroidism or safeguarding)

Acute severe abdominal pain and bloating (obstruction or intussusception)

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97
Q

management idiopathic constipation

A

diagnose without investigations if red flags excluded

  • correct reversible lifestyle factors
  • laxatives (movicol first line) should be weaned off as returns to normal
  • impaction may require disimpaction regime
  • encourage and praise toiletting
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98
Q

causes of vomiting

A

Overfeeding
Gastro-oesophageal reflux
Pyloric stenosis (projective vomiting)
Gastritis or gastroenteritis
Appendicitis
Infections such as UTI, tonsillitis or meningitis
Intestinal obstruction
Bulimia

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99
Q

red flags of vomiting

A

Not keeping down any feed (pyloric stenosis or intestinal obstruction)

Projectile or forceful vomiting (pyloric stenosis or intestinal obstruction)

Bile stained vomit (intestinal obstruction)

Haematemesis or melaena (peptic ulcer, oesophagitis or varices)

Abdominal distention (intestinal obstruction)

Reduced consciousness, bulging fontanelle or neurological signs (meningitis or raised intracranial pressure)

Respiratory symptoms (aspiration and infection)

Blood in the stools (gastroenteritis or cows milk protein allergy)

Signs of infection (pneumonia, UTI, tonsillitis, otitis or meningitis)

Rash, angioedema and other signs of allergy (cows milk protein allergy)

Apnoeas are a concerning feature and may indicate serious underlying pathology and need urgent assessment

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100
Q

physical risks of rapid weight loss

A

Refeeding syndrome risk, hypoglycaemia, risk of infection, cardiac arrhythmia.

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101
Q

What conditions can cause rapid weight loss in adolescents?

A

Coeliac disease
Type 1 diabetes mellitus
Hyperthyroidism
Malignancy
Anorexia nervosa
Inflammatory bowel disease
Oesphageal problems eg achalasia
Severe depression/OCD/autism
Juvenile arthritis
Addisons

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102
Q

what assessments/tests would you want in a child with rapid weight loss?

A

Weight, height
HR, BP, BM, RR, CRT

ECG, U+E, phosphate, calcium, magnesium, LFTS, CRP, WCC, TFTS, coeliac screen, ESR.

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103
Q

course of action severe weight loss concerns of eating disorder

A

Admit to stabilise physically, commence vitamins (thiamine, Vitamin B complex, multivitamins) to prevent refeeding syndrome, regular observations + BM, monitoring bloods. Contact local eating disorders team, diet plan. IV fluids if hypoglycaemic or not drinking (10% dextrose+045% saline).

104
Q

Lanugo hair

A

fine hair growth in anorexia in response to loss of insulating fat

105
Q

short term treatment/weight gain plan anorexia nervosa

A

if weight height ratio <75% commence thiamine, Vitamin B complex and multivitamins

Aim for 0.5 kg-1kg per week weight gain

monitor blood especially phosphate; drop indicates refeeding syndrome

regular ECGs

Discharge when vital signs stable and weight gain occurring

106
Q

medium term plan anorexia nervosa

A

Multi-disciplinary treatment package in the community
- child psychiatrist oversees care + role of antidepressants for comorbidities
- dietician
- therapists + family therapist
- paediatrician to mentor physical health (risks of osteopenia/porosis esp if amenorrhea)

107
Q

main types of eating disorder young people

A

anorexia nervosa

bulimia nervosa

EDNOS - eating disorder not otherwise specified)

108
Q

What is weight for height ratio?

A

A method of assessing how appropriate that persons weight is for their height at a given age.
more accurate in children than BMI

109
Q

most significant mortality risks in anorexia nervosa

A

Sudden cardiac death
Suicide
Chronic emaciation + pneumonia

110
Q

causes of short stature in children/adolescents

A
  • familial note hypochondroplasia
  • constitutional/delay
  • psychosocial
  • chronic physical disease
  • malabsorption
  • endocrine
  • genetic/syndrome
111
Q

short stature; approach to diagnosing cause

A

general Hx + Hx of family

?diarrhoea ?abdo pain ?energy

examination: ?dysmorphic, ?limb size, ?skin lesions

parental heights + mid parental centile

blood pressure - renal failure can be missed cause

investigations; thyroid, creatinine, bone and liver profiles, FBC, CRP, glucose, coeliac screen

chromosomes esp girl ?turners

bone age vs actual age; is there just delay

112
Q

follow up short stature

A

usually not immediate medical diagnosis

follow up every 4 months and if cause identified can treat

keep safeguarding in mind

113
Q

first signs of puberty girls/boys

A

girls; breast development then pubic hair

boys; testicular enlargement followed by genital changes. later age than girls

114
Q

definition of delay puberty

A

no signs age 14 in boy or age 13 in girl

in boys testosterone to kickstart puberty sometimes offered

115
Q

precocious puberty

A

any signs before age of 8 in girl and 9 in boy

more likely to be pathological if under age 6

can be psychological distressing and can stunt adult height

can offer blockade with GnRH antagonist e.g. zoladex every 12 weeks injection

116
Q

thyroid disorders causing stunted growth

A

congenital hypothyroidism - should be detected on newborn heel prick test

2/3 of these have absent or ectopic thyroid gland - need lifelong replacement
other 1/3 gland is present but not producing - usually still needs replacing but sometimes starts producing thyroxine; trial cessation at age 3

acquired hypothyroidism - autoimmune condition can be seen in adolescent females

117
Q

physical features of dehydration in an infant

A

Sunken anterior fontanelle
dry mucous membrane
tachycardia
reduced capillary refill time
reduced skin turgor

118
Q

common causes of gastroenteritis in young children

A
  1. rotavirus - particularly winter and early spring
  2. adenovirus

if bacterial campylobacter is most common

119
Q

what infections can cause blood in the stool associated with diarrhoea and vomiting

A

Rotavirus
Intussusception
E. coli
Campylobacter
Shigella

120
Q

definition and typical presentation of intussusception

A

invagination of proximal bowel into a distal segment commonly involving invagination of ileum into caecum through the ileocecal valve

age 3 months to 2 years
paroxysmal severe colicky pain
pallor during painful episodes followed by lethargy

child may refuse to feed, vomit, and pass red currant jelly stools

121
Q

what infection is associated with haemolytic uraemia syndrome
management

A

E.Coli
associated with diarrhoea and blood in stool
can progress to HUS which is the most common cause of acute renal failure in children

treatment is mainly supportive; may include dialysis +/- IVIG if severe

122
Q

red flag features of vomiting

A

blood in vomit

bilious vomiting

projectile vomiting

abdominal tenderness or distention

blood in stool

bulging fontanelle

123
Q

young child vomiting with persistent or associated fever

A

may be associated with infections such as urinary tract infection or meningitis

124
Q

what does bilious vomiting indicate

A

intestinal obstruction

125
Q

what does haematemesis indicate

A

Oesophagitis, gastric ulcer, oral or nasal bleeding and vomiting up swallowed blood

126
Q

projectile vomiting under 2mo

A

pyloric stenosis

127
Q

vomiting with abdominal distention/tenderness

A

Intestinal obstruction, strangulated inguinal hernia, surgical abdomen

128
Q

vomiting with severe dehydration/shock

A

Severe gastroenteritis, systemic infection – UTI, meningitis, diabetes ketoacidosis

129
Q

vomiting with bulging fontanelle or fits

A

Raised intracranial pressure due to meningitis/ hydrocephalus

130
Q

vomiting with faltering growth

A

Gastroesophageal reflux, coeliac disease, chronic gastrointestinal conditions

131
Q

vomiting with paroxysmal cough

A

whooping cough

132
Q

what is a fluid challenge

A

if at risk of dehydration, give oral bolus of rehydration solution frequently in small amounts

5ml/kg of ORS after each large watery stool in children who are at risk of dehydration - consider giving via NG

continue to monitor input and output

continue breast feeding and other milk feeds

133
Q

what children are at risk of dehydration

A

low birth weight, age less than 1 year, had more than 2 vomiting episodes and more than 5 diarrhoeal episodes in the previous 24 hours

134
Q

usual duration of diarrhoea illness in children + how to manage simple illness

A

5-7 days and in most children, it stops in 2 weeks. The family should continue encouraging intake of usual fluids (breast milk or formula) and give 5ml/kg of ORS after passage or each loose stool

not attend nursery until 48 hours after last vomit or diarrhoea

135
Q

safety net simple gastroenteritis

A

contact healthcare professionals if child becomes unwell, appears pale/mottled, starts to vomit again (vomiting should not last longer than 3 days) has decreased urine output/wet nappies, irritable/lethargic and has cold extremities.

136
Q

mechanisms of infectious diarrhoea

A

Secretory mechanism: ↓ absorption, ↑ secretion & electrolyte transport –> Watery stool. caused by Cholera, E. coli , Clostridium difficile and cryptosporidium (in HIV infection)

Mucosal Invasion: Inflammation, ↓ mucosal surface area and/or colonic reabsorption and ↑ motility –> stool with Blood and ↑ WBC’s. Caused by Rotavirus, campylobacter, Salmonella, shigella, Yersinia

137
Q

features of a gastroenteritis that suggest another diagnosis

A
  • Fever – temperature >38 degrees or higher in children younger than 3 months & >39 degrees or higher in children aged 3 months and older
  • Tachypnoea
  • Altered consciousness level
    -Neck stiffness
  • Bulging fontanelle in infants
  • Non-blanching rash
  • Blood and /or mucus in stool
  • Bilious vomit
  • Severe or localised abdominal pain
  • Abdominal distension or rebound tenderness
138
Q

mechanisms/causes of dehydration

A

isonatraemic - proportional loss of water and sodium

hyponatraemic - intake of large quantity of water, fall in serum sodium, resulting is shift of water form extracellular to intracellular compartment causes brain oedema and marked extracellular dehydration and shock

hypernatraemic - water loss exceeds the sodium loss with resultant increase in plasma sodium concentration. This can happen when there is low sodium diarrhoea or high insensible water loss. There is shift of water from intracellular to extracellular compartment and therefore less signs of dehydration and more features of hypertonia, hyperreflexia, convulsions, drowsiness

139
Q

when is stool microscopy and culture indicated in gastroenteritis

what other investigations are done

A

Recent travel abroad
The diarrhoea is not improving by day 7
Suspected septicaemia
Blood and /or mucus in stool
Immunocompromised child

blood culture if starting Abx
U+Es and glucose if dehydrated/starting fluids

140
Q

IV fluid treatment of shock

A

treat with fluid bolus 20 ml /kg of 0.9% sodium chloride by rapid intravenous infusion.
Give a second bolus of 20 ml /kg of 0.9% sodium chloride by rapid intravenous infusion if shock persists. Considers other causes of shock.

Once symptoms and signs of shock resolve, start rehydration using intravenous fluids

141
Q

what fluid is generally used for maintenance

A

0.9 % sodium chloride and 5 % dextrose

142
Q

how do you calculate volume of maintenance fluids for 24 hours

A

100ml/kg first 10kg

50ml/kg second 10kg

over 20kg 20ml/kg

143
Q

how should weight and U+Es be monitored in fluid therapy

A

Weight and u&e’s should be measured prior to commencing intravenous fluids and then at least every 24 hours if u&e’s are normal.
Measure blood glucose when starting intravenous fluids and at least every 24 hours or more frequently if there is risk of hypoglycaemia.

144
Q

when and what Abx are given for treatment of diarrhoea

A

Campylobacter – Erythromycin shortens the duration of illness and shedding of bacteria

Clostridium difficile – metronidazole or vancomycin

Nontyphoid salmonella, shigella , vibrio cholerae, Giardia, Yersinia and cryptosporidium

145
Q

what fluid is typically used for acute resuscitation

A

0.9% saline

146
Q

pyloric stenosis
- presentation
- investigation
- management

A

first few weeks of life, pale hungry baby with FTT and projectile vomiting + crying after feeds

diagnosis is by abdominal USS which shows pyloric hypertrophy
blood gas shows hypochloric metabolic alkalosis

treatment is laparoscopic pyloromyotomy (known as “Ramstedt’s operation“) - excellent prognosis

147
Q

post-gastroenteritis complications

A

Lactose intolerance
Irritable bowel syndrome
Reactive arthritis
Guillain–Barré syndrome

148
Q

coeliac disease presentation

A

can often be asymptomatic
may present when weaning starts

possible symptoms
Failure to thrive in young children
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis is an itchy blistering skin rash that typically appears on the abdomen

149
Q

coeliac disease diagnosis

A

Investigations must be carried out whilst the patient remains on a diet containing gluten
Check total immunoglobulin A levels to exclude IgA deficiency before checking for coeliac disease specific antibodies:

Raised anti-TTG antibodies (first choice)
Raised anti-endomysial antibodies

Endoscopy and intestinal biopsy show:
“Crypt hypertrophy”
“Villous atrophy”

150
Q

when to suspect IBD in children

A

children and teenagers presenting with perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia. They may be systemically unwell during flares, with fevers, malaise and dehydration
may have extraintestinal features such as eye, joint and skin symptoms

150
Q

when to suspect IBD in children

A

children and teenagers presenting with perfuse diarrhoea, abdominal pain, bleeding, weight loss or anaemia. They may be systemically unwell during flares, with fevers, malaise and dehydration
may have extraintestinal features such as eye, joint and skin symptoms

151
Q

what is biliary atresia
when to suspect
management

A

where a section of the bile duct is either narrowed or absent resulting in cholestasis

babies with a persistent jaundice, lasting more than 14 days in term babies and 21 days in premature babies
measure the bilirubin and conjugated only will be elevated

management is surgical

152
Q

causes of intestinal obstruction

A

Meconium ileus
Hirschsprung’s disease
Oesophageal atresia
Duodenal atresia
Intussusception
Imperforate anus
Malrotation of the intestines with a volvulus
Strangulated hernia

153
Q

presentation of intestinal obstruction

A

Persistent vomiting. This may be bilious, containing bright green bile

Abdominal pain and distention

Failure to pass stools or wind

Abnormal bowel sounds. These can be high pitched and “tinkling” early in the obstruction and absent later

154
Q

investigation is suspected intestinal obstruction

A

abdominal X-ray is first line - absence of air in rectum

155
Q

initial management intestinal obstruction

A

emergency referral to paediatric surgical unit

NBM, insert NG tube, IV fluids

156
Q

what is Hirschsprung’s disease

A

congenital condition where nerve cells of the myenteric plexus are absent in the distal bowel and rectum - absence of parasympathetic ganglion cells

length of lost innervation varies

157
Q

what family pattern does Hirschsprung’s disease occur in

A

usually in isolation but does have genetic associations

Downs syndrome
Neurofibromatosis
Waardenburg syndrome (a genetic condition causing pale blue eyes, hearing loss and patches of white skin and hair)
Multiple endocrine neoplasia type II

158
Q

how does Hirschsprung’s disease present

A

varies significantly depending on length of gut affected

can present with acute intestinal obstruction shortly after birth or more gradually developing symptoms:
- Delay in passing meconium (more than 24 hours)
- Chronic constipation since birth
- Abdominal pain and distention
- Vomiting
- Poor weight gain and failure to thrive

159
Q

what is Hirschsprung-associated enterocolitis (HAEC)

A

inflammation and obstruction of the intestine occurring in around 20% of neonates with Hirschsprung’s disease.

It typically presents within 2-4 weeks of birth with fever, abdominal distention, diarrhoea (often with blood) and features of sepsis.

It is life threatening and can lead to toxic megacolon and perforation of the bowel.

It requires urgent antibiotics, fluid resuscitation and decompression of the obstructed bowel.

160
Q

diagnosis and management of Hirschsprung’s

A

definitive diagnosis is with rectal biopsy

management is surgical removal of the affected bowel

161
Q

Intussusception
- diagnosis
- management
- complications

A

diagnosis; USS or contrast enema

management; therapeutic enemas can be used. if failed, surgical management

Obstruction
Gangrenous bowel
Perforation
Death

162
Q

appendicitis
- signs and symptoms
- diagnosis
- management

A

S&S
- anorexia, N&V
- Rovsing’s sign; palpation of LIF causes pain in RIF
- guarding
- rebound and percussion tenderness (suggest rupture and peritonitis)

diagnosis: clinical presentation and raised inflammatory markers but CT/USS can be used to rule out differentials

management: appendicectomy; better by laparoscopic

163
Q

when to suspect Kawasaki’s disease

A

fever >5 days
additional features:
- bilateral conjunctival injection without exudate
- erythema and cracking of lips, strawberry tongue, or erythema of oral and pharyngeal mucosa
- oedema and erythema in the hands and feet
- polymorphous rash
- cervical lymphadenopathy

164
Q

causes of non-blanching petechial/purpuric rash

A

meningococcal septicaemia

Henoch-Schonlein Purpura

Idiopathic thrombocytopaneia purpura

Non-accidental injury

165
Q

suspected meningitis actions

A

A-E and sepsis 6

obtain IV access and call seniors

fluid, Abx and oxygen IN
blood cultures, lactate and urine output OUT

bloods for FBC, CRP, Blood culture, lactate, whole blood real-time PCR testing for Meningococcus and Pneumococcus

LP if not contraindicated but shouldn’t delay Abx being given - third gen cephalosporin

166
Q

suspected meningitis Abx
- under 3 months
- over 3 months

A

under 3 mo - IV ceftriaxone with amoxicillin for listeria cover
over 3 mo - IV ceftriaxone

167
Q

What bacterial causes of meningitis are more prevalent in
- under 3 mo
- 3 mo to 5 years
- over 5 years

A

under 3 mo - listeria, E. coli, Group B strep

3mo-5yrs; Niesseria Meningitides, Streptococcus pneumoniae, Haemophilus influenza B

over 5 (same as adults) - niesseria or strep pneumonia

168
Q

what are the most likely viral causes of meningitis

A

enteroviruses (85%, especially coxsackie and echovirus).
Other viruses include adenovirus, mumps, EBV, CMV, Varicella zoster, Herpes Simplex virus, HIV.

169
Q

risk factors for bacterial meningitis

A
  • asplenia
  • basal skull fracture
  • attendance at daycare/crowding
  • low family income
  • children with facial cellulitis, periorbital cellulitis, sinusitis, and septic arthritis
  • maternal infection and pyrexia at delivery
170
Q

Indications for Dexamethasone in suspected/confirmed Meningitis

A
  • Frankly purulent pus
  • CSF wcc > 1000/microlitre
  • Raised CSF wcc with CSF Protein > 1g/l
  • Bacteria on Gram stain

give with first dose of Abx and never more than 12 hours after
usually given qds for 2-4 days under senior clinician

171
Q

where should the needle enter in an LP

A

into the L4/L5 intervertebral space, With the child on his/her side with the child’s back in a vertical position then the L5 vertebrae is vertically below the iliac crest. The L4 L5 disc space is just above

172
Q

when is LP contraindicated

A
  • unstable child; signs of shock or respiratory insufficiency
  • signs or symptoms of raised ICP
  • extensive or spreading purpuric rash
  • bleeding disorder
  • after convulsions if not yet stabilised
  • local infection at the LP site
173
Q

acute complications of meningitis

A
  • seizures
  • raised ICP
  • metabolic disturbance
  • coagulopathies
  • anaemia
  • coma
  • death
174
Q

long term complications meningitis

A
  • hearing impairment
  • psychosocial problems
  • epilepsy
  • developmental/learnign difficulties
  • neurological impairment

children need general paediatrician follow up + audiology assessment within two weeks

175
Q

which pathogen in meningitis has the worst prognosis

A

group B streptococcus pneumonia
highest mortality and highest res of neurological complications

176
Q

slapped cheek syndrome

A

fever and bright red clearly demarcated rash on cheeks
otherwise generally well
caused by parovirus

177
Q

antenatal Hx and UTI risk

A

abnormalities such as renal pelvis dilatation, cysts, or poor production of amniotic fluid (oligohydramnios) may indicate antenatal renal abnormalities predisposing to infection.
Prematurity may indicate an increased overall infection risk

178
Q

how can urine be obtained from an infant

A

clean catch sample is best method

if not possible can catheterise or suprapubic aspiration which should be ultrasound guided

179
Q

management if UTI detected on dipstick

A

if nitrites and leukocytes +ve start antibiotics

if one positive start if clinical UTI

send samples for microscopy, culture and sensitivity (M,C&S)

180
Q

what is checked for on a dipstick

A
  • leukocytes
  • nitrites
  • blood (tumour, trauma, infection)
  • protein (tubular or glomerular disease)
  • ketones
181
Q

In Renal disease, what are the significant levels of proteinuria?

A

> 20 mmol/ml - This may be significant, and may indicate tubular disease

> 200 mmol/mg - This is nephrotic range

182
Q

complications of minimal change nephrotic syndrome are recognised in childhood?

A
  • spontaneous bacterial peritonitis
  • infection with streptococci
  • recurrence
183
Q

what parameters make a diagnosis of Minimal Change Nephrotic Syndrome less likely (meaning further investigations would be indicated)?

A
  • abnormal renal function
  • haematuria
  • hypertension
184
Q

when in gestation do the kidneys form?

A

5 weeks with glomeruli still forming until 34 weeks

185
Q

What is the commonest congenital renal anomaly?

A

renal hypoplasia

186
Q

Definition of atypical UTI; increased risk of renal screening

A
  • seriously ill
  • poor urine flow
  • abdominal or bladder mass
  • raised creatinine
  • septicaemia
  • failure to respond within 48 hours
  • non E coli
187
Q

Definition of recurrent UTI; requires investigations for an underlying cause

A

2 or more upper UTI
1 upper and 1 or more lower UTI
3 or more lower UTI

188
Q

what features make an upper UTI more likely compared to lower?

A

Bacteriuria and fever of 38oC or higher +/- loin tenderness
Bacteriuria, loin pain/tenderness and fever of less than 38oC
Age less than 3 months

usually no systemic features in lower UTI

189
Q

what developmental anomaly can underly UTIs

A

vesoureteric reflux - in 35% of cases in children

others; hydronephrosis, duplex system or obstructive lesions

190
Q

management simple lower UTI

A

oral antibiotics for 3 days according to local guidelines, usually trimethoprim, nitrofurantoin, cephalosporin or amoxicillin. Parents should be asked to bring the children back if they remain unwell after 24-48 hours

191
Q

management upper UTI

A

considered for admission to hospital. If not admitted oral antibiotics such as cephalosporin or co-amoxiclav should be given for 7-10 days

192
Q

antibiotic prophylaxis UTI

A

not after first one but consider for recurrent or if structural abnormality such as VUR

193
Q

investigations in atypical or recurrent UTI symptoms

A

3 investigations are used selectively depending on the age of the child and presence of atypical or recurrent UTI symptoms: Ultrasound scan, MCUG and DMSA.

194
Q

indications for renal ultrasound in UTI

A
  • Infants less than 6 months with confirmed UTI (acutely if infant has atypical or recurrent UTI)
  • Children more than 6 months old only in the presence of atypical UTI
195
Q

when is Micturating cystogram (MCUG) used in UTI

A

identify any vesicoureteric reflux (VUR), bladder abnormalities and posterior urethral valves within a few weeks after treatment of UTI
catheterizing the child in order to fill the bladder with a radio-contrast agent then taking x-rays as the infant voids urine..

Indications:

Infants younger than 6 months with atypical or recurrent UTI
Consider in children older than 6 months if dilatation on ultrasound, poor urine flow, non-E coli infection or family history VUR

196
Q

when is DMSA used in UTI

A

DMSA in 4-6 months after infection
radionucleotide scan used to assess renal function and identify any scarring of the kidneys due to the UTI - predisposes to HTN

Healthy renal tissue takes up the isotope. Unhealthy or scarred tissue doesn’t take up the isotope and appears as a filing defect on DMSA scan. DMSA may be inaccurate if performed shortly after an infection.

Indications:

All children with recurrent UTI
Children under 3 years with atypical UTI

197
Q

how do urinary infections present in children

A

can be quite non-specific
more specific with age - older children more classic triad of dysuria, frequency and haematuria

Abdominal pain
Haematuria
Bedwetting/enuresis
Constipation
Febrile convulsion
Dysuria

198
Q

definition of enuresis

A

involuntary discharge of urine by day or night or both, in a child aged 5 years or older, in the absence of congenital or acquired defects of the nervous system or urinary tract

199
Q

how is nocturnal enuresis defined

A

primary - child never achieved continence

secondary - child was dry for at least 6 months before

200
Q

possible underlying causes of enuresis

A
  • neglect/abuse
  • disturbed sleep/wake cycle
  • constipation
  • diabetes mellitus
  • UTI if recent onset
  • rarely neurological disease
201
Q

enuresis management techniques

A
  • general fluid intake management and toileting patterns
  • reward systems for agreed behaviours (not for dry nights)
  • enuresis alarm
  • desmopressin can be used for short term eg. sleepovers
202
Q

bilateral dilated kidneys in a neonate

A

in a male child can mean posterior urethral valves – this is a very serious condition which if untreated can cause renal failure due to obstruction

203
Q

scarlet fever
presentation
immediate management

A

reaction to group A strep toxins
most common age 2-6 years

presentation:
fever: typically lasts 24 to 48 hours
malaise, headache, nausea/vomiting
sore throat
‘strawberry’ tongue
rash

commence Abx immediately 10 days of pen V

204
Q

complications of scarlet fever

A

otitis media: the most common complication

rheumatic fever: typically occurs 20 days after infection

acute glomerulonephritis: typically occurs 10 days after infection

invasive complications (e.g. bacteraemia, meningitis, necrotizing fasciitis) are rare but may present acutely with life-threatening illness

205
Q

presentation of immune thrombocytopenia purpura

A

petechial and purpura often after a viral illness

206
Q

surgical sieve for anaemia

A

V-acute bleed? haemorrhgaic disease of newborn?
I- malaria, helminth infection, transient aplastic anaemia secondary to parvovirus, inflammatory bowel disease, severe cow’s milk protein enteropathy
T- acute bleed i.e. following an accident or non-accidental injury worsened by a clotting disorder
A- pernicious anaemia very rare in children , coeliac, haemolytic anaemia, haemolytic uraemic syndrome
M- G6PD deficiency
I- IDA
N- leukaemia
C- inherited pure red cell aplasia (Diamond Blackfan Anaemia), thalassaemia sickle cell, spherocytosis, fanconis anaemia, clotting disorders, congenital infectionsions ie parvo B19
D- physiological anaemia of the newborn
E - menstruation, medication ie nitrofurantoin

207
Q

when does sickle cell disease present

A

after 6 months when fatal haemoglobin is replaced

208
Q

what is Henoch Schonlein Purpura

A

an IgA vasculitis that presents with a purpuric rash affecting the lower limbs and buttocks in children
often triggered by a recent infection and most common under 10 years

4 main features:
- purpuric rash (100%)
- joint pain (75%)
- abdominal pain (50%)
- renal involvement (50%)

209
Q

abdominal complications HSP

A

gastrointestinal haemorrhage, intussusception and bowel infarction

210
Q

renal involvement HSP

A

affects the kidneys in around 50% of patients, causing an IgA nephritis.
This can lead to microscopic or macroscopic haematuria and proteinuria.
If there is more than 2+ of protein on the urine dipstick the child has developed nephrotic syndrome and will have a degree of oedema

211
Q

HSP management

A

exclude other causes of purpura!
then supportive management:
- steroids debatable for abdo pain/renal involvement
- closely monitor urine dip and BP for 6 months

most fully recover 4-6 weeks. small proportion develop renal failure

212
Q

what are Kernigs and Brudzinkis signs

A

Kernigs +ve = Pain on lower leg extension with hip flexed

Brudzinkis +ve = Involuntary flexion of the knees and hips with neck flexion

213
Q

differentials child with seizure and reduced consciousness

A

febrile seizure
encephalopathy
encephalitis/meningitis
sepsis/shock
brain tumour
metabolic disorder
epilepsy
poisoning/intoxication

could be post ictal - only if returns to normal within an hour

214
Q

Indications for urgent head CT or MRI in seizure

A

Encephalopathic or coma
Suspected raised intracranial pressure
Progressive neurological deficit

215
Q

Indications for elective MRI head in seizure

A
  • In a child under 2 year of age at onset
  • hard focal neurological signs
  • a focal epilepsy
  • associated significant learning difficulties
  • an epilepsy resistant to full doses of 2 appropriate drugs
216
Q

EEG urgent and non urgent indications in seizure

A

Urgent Indications:
suspected non-convulsive status
Non traumatic encephalopathy
Coma of unknown cause

Elective standard EEG if:
strong suspicion of epilepsy (to support classification)
developmental or language regression

NOT generally after a first afebrile seizure or febrile seizures

217
Q

causes of delayed walking

A

central - delayed maturation, global developmental delay, any cause of hemiplegia, cerebral palsy

peripheral - spinabifida

muscular and neuromuscular e.g. DMD

environmental

orthopaedic e.g. DDH

metabolic/hormonal - hypoT, rickets

218
Q

what is cerebral palsy

A

Static brain injury pre or shortly post birth, causing a motor and coordination dysfunction, usually with neuroimaging changes

219
Q

neonatal causes of tachypnoea

A

sepsis

cardiac

respiratory

metabolic

pain - either acidosis causing compensatory tachypnoea or a raised ammonia which acts as a respiratory stimulant causing tachypnoea

220
Q

main groups of inborn errors of metabolism causing hyperammoniaemia

A

urea cycle disorders and the organic acidaemias

221
Q

Urea cycle disorders

A

ammonia level is markedly raised and often over 1000 micromols/L and there is liver dysfunction

blood gas often shows a respiratory alkalosis due to the ammonia acting as a respiratory stimulant

222
Q

organic acidaemia

A

mixed picture of metabolic acidosis and hyperammonaemia - less high than urea cycle disroders

The first pointer to diagnosis is a metabolic acidosis that does not respond to standard fluid resuscitation and then the finding of a raised anion gap caused by the presence of the abnormal organic acid.

Methylmalonic acidaemia and propionic acidaemia are the 2 most common organic acid disorders.

223
Q

presentation in born errors of metabolism

A

presents neonatally

often reduced consciousness

blood gas abnormalities and often altered anion gap

can be very sick and need specialist review

224
Q

definition of global developmental delay

A

A child has global developmental delay if they have a significant delay in milestones in two or more areas

225
Q

definition of cerebral palsy

A

A disorder of tone, posture and movement, caused by a non-progressive brain lesion in a developing brain

226
Q

types of cerebral palsy

A

spastic (UMN signs)
ataxic
dyskinetic aka choreoathetoid

in reality is often mixed

227
Q

medications which can be used to help manage increase tone in children with cerebral palsy?

A

Baclofen
Diazepam
Botulinum toxin

228
Q

what is Gower’s sign

A

pt uses hands and arms to walk to and then up the body in order to stand
sign of weakness of the proximal muscles

seen in Duchenne Muscular Dystrophy

229
Q

Duchenne Muscular Dystrophy

A

most common muscular dystrophy in northern Europe and is due to an abnormality of the dystrophin gene
X linked disorder

measure CK +genetic testing to diagnose

Steroid treatment has been shown to delay the progression

can also present with early neurological signs due to expression of dystrophin protein in the brain

230
Q

long term complications of conditions such as DMD

A

Reduced mobility, loss of ambulation

Scoliosis – spinal surgery will be needed if scoliosis significant

Feeding problems – may cause malnutrition – gastrostomy feeds may be required

Cardiac involvement (depending on condition, but common in DMD)

Respiratory weakness- nocturnal non-invasive ventilation may be required

231
Q

side effects of steroids in children

A

Increased appetite – with weight gain
Behavioural deterioration – especially if pre-existing problems
Hypertension
Growth failure
Gastrointestinal irritation
Bone thinning

232
Q

at what times are DKA most likely to occur in T1 DM

A

At diagnosis

During a growth spurt/puberty

Insulin omission for any reason

(DKA usually develops over 24 hours but can develop faster particularly in young children or patients on insulin pumps)

233
Q

how does DKA present

A

may initially have polyuria, polydipsia, weight loss, excessive tiredness

more specific to DKA symptoms are nausea or vomiting, abdominal pain, hyperventilation, dehydration and reduced level of consciousness

234
Q

when should a suspected DKA be sent immediately to an acute paediatric facility (HDU)

what needs measuring on arrival

A

child not known to have diabetes with glucose level is above 11 mmol/litre and suggestive symptoms

child known to have diabetes with any symptoms of DKA - but only need transfer if ketones elevated or can’t measure

on arrival measure
capillary blood glucose, capillary blood ketones (beta-hydroxybutyrate) capillary or venous pH and bicarbonate

235
Q

DKA diagnostic criteria

A
  1. Acidosis (indicated by blood pH below 7.3 or plasma bicarbonate below 18 mmol/litre) and
  2. Ketonaemia (indicated by blood beta-hydroxybutyrate above 3 mmol/litre

Diagnose severe DKA in children and young people with DKA who have a blood pH below 7.1.

236
Q

what is the main cause of morbidity and mortality in childhood DKA

A

from cerebral oedema due to rapid correction
The aim of therapy is very gentle and slow correction to avoid cerebral oedema

237
Q

initial management DKA

A
  • inform senior clinician
  • explain to child and parents
  • fixed rate insulin infusion
  • IV fluids
  • may need potassium
  • avoid hypo by adding dextrose when glucose is coming down
  • monitor for signs of cerebral oedema

can give O2, consider ABX and consider NG tube

238
Q

what is Kussmaul breathing

A

deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney failure.

In metabolic acidosis, breathing is first rapid and shallow but as acidosis worsens, breathing gradually becomes deep, labored and gasping.
It is this latter type of breathing pattern that is referred to as Kussmaul breathing.

239
Q

what needs recording once DKA diagnosed

A

blood gas - pH and pCO2, lactate
monitor ketones
level of consciouss
vital signs
clinical evidence of dehydration + weight
plasma sodium, potassium, urea and creatinine plasma bicarbonate

240
Q

when should you think about sepsis in a child with DKA

A

has any of the following: fever or hypothermia, hypotension, refractory acidosis, lactic acidosis.

241
Q

what fluids and when should be given in DKA
how much

A

only give oral fluids if alert, not nauseated or vomiting, and not clinically dehydrated
otherwise give IV and if IV don’t let them have oral until ketosis is resolving
give the fluid gradually - not a bolus unless can consider in severe
Use 0.9% sodium chloride without added glucose until the plasma glucose concentration is below 14 mmol/litre.
Ensure that all fluids (except any initial bolus) administered to children and young people with DKA contain 40 mmol/litre potassium chloride, unless they have renal failure.

first 48 hours adding the estimated fluid deficit to the fluid maintenance requirement
assume if pH>7.1 5% deficit
if <7.1 assume 10% deficit

maintenance if they weigh less than 10 kg, give 2 ml/kg/hour if they weigh between 10 and 40 kg, give 1 ml/kg/hour if they weigh more than 40 kg, give a fixed volume of 40 ml/hour - this is reduced volume to avoid cerebral oedema

242
Q

when should insulin be started and how

A

fixed rate insulin infusion start 1-2 hours after fluids started
use a soluble insulin infusion at a dosage between 0.05 and 0.1 units/kg/hour

243
Q

when should normal insulin be restarted

A

subcut at least 30 minutes before stopping intravenous insulin. For a child or young person with DKA who is using insulin pump therapy, restart the pump at least 60 minutes before stopping intravenous insulin

244
Q

signs of cerebral oedema
when to treat and how

A

assess for oedema if any of headache, agitation/irritability, increased BP or fall in HR

treat with mannitol or hypertonic sodium chloride if a child with DKA has any of deterioration in level of consciousness abnormalities of breathing pattern (for example respiratory pauses), oculomotor palsies, pupillary inequality or dilatation
escalate

245
Q

potassium in DKA

A

insulin moves potassium which can lead to hypokalaemia
if falls below 3mmol/L consider temporarily suspending the insulin infusion and discuss with ICU

246
Q

potassium in DKA

A

insulin moves potassium which can lead to hypokalaemia
if falls below 3mmol/L consider temporarily suspending the insulin infusion and discuss with ICU

247
Q

basic types of insulin regimen in T1DM

A
  1. Multiple daily injection basal–bolus insulin regimens: injections of short-acting insulin before meals, together with 1 daily injection of long-acting insulin.
  2. Continuous subcutaneous insulin infusion (insulin pump therapy): a programmable pump and insulin storage device that gives a regular or continuous amount of insulin (usually a rapid-acting insulin analogue or short-acting insulin) by a subcutaneous needle or cannula.
248
Q

optimal target ranges for short-term plasma glucose control

A

Fasting plasma glucose level of 4–7 mmol/litre on waking

a plasma glucose level of 4–7 mmol/litre before meals at other times of the day

a plasma glucose level of 5–9 mmol/litre after meals

a plasma glucose level of at least 5 mmol/litre when driving

measure 5x a day - more in illness or activity

249
Q

management of mild to moderate hypoglycaemia

A

Give fast-acting glucose (for example, 10–20 g) by mouth and recheck BM within 15 minutes
repeat if persists

once resolved give oral complex long-acting carbohydrate to maintain blood glucose levels

250
Q

treatment of severe hypoglycaemia

A

if in hospital with IV access; give 10% intravenous glucose.

if no access give intramuscular glucagon or a concentrated oral glucose solution (for example Glucogel). Do not use oral glucose solution if the level of consciousness is reduced as this could be dangerous

251
Q

what complications monitoring should children with T1DM have

A

Thyroid disease at diagnosis and annually thereafter until transfer to adult services

Diabetic retinopathy- annually from 12 years

Moderately increased albuminuria (albumin:creatinine ratio [ACR] 3–30 mg/mmol; ‘microalbuminuria’) to detect diabetic kidney disease- annually from 12 years

Hypertension- annually from 12 years.

Be aware of the following rare complications and associated conditions with type 1 diabetes:

Juvenile cataracts
Necrobiosis lipoidica
Addison’s disease.

In addition Children and Young People with Type 1 DM get screened for Coeliac Disease at diagnosis

252
Q

what is Meckel’s diverticulum

A

congenital diverticulum of the small intestine

most common cause of massive GI bleeding requiring a transfusion in children between the ages of 1 and 2 years

presents with rectal bleeding, can cause obstruction and may be painful

253
Q

investigation and management of Meckel’s diverticulum

A

‘Meckel’s scan’ should be used if haemodynamically stable
uses 99m technetium pertechnetate

mangamenet is surgical removal

254
Q

traffic light system paediatric history

A
  • colour
  • activity; playing normally?
  • respiratory; any difficulty breathing?
  • hydration/circulation; feeding? drinking? nappies?
  • other; have they felt hot? recorded temperatures? rashes?
255
Q

APGAR score + what are the domains

A

assesses health of newborn baby at 1, 5 and 10 minutes looking at pulse, respiratory effort, colour, tone and irritability
A score of 0-3 is very low score, between 4-6 is moderate low and between 7 - 10 means the baby is in a good state

256
Q

when is neonatal jaundice physiological or pathological

A

first 24 hours pathological

2-14 days physiological

> 14 days (21 in premature) pathological

if pathological screen for haemolytic anaemia and sepsis screen

Clinical Years / Progress Test (24 decks)

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