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paeds brief Flashcards

1
Q

wheeze is associated with ______

A

viral induced wheeze, asthma and bronchiolitis

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2
Q

what is apnoea

A

cessation of breathing for at least 10 seconds

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3
Q

what commonly causes sore throat

A
  • normally viral in children under 3
  • could also be caused by strep pyogenes (beta haemolytic strep)
  • epstein barr is a common cause of exudative tonsilitis
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4
Q

which criteria indicate the likelihood of a sore throat being caused by a bacrterial infection and what does it include

A
  • Centor criteria
    • tender lymphadenopathy
    • tonsilar exudate
    • fever
    • absence of cough
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5
Q

what is the treatment if strep throat is suspected

A

10 days of penicillin V

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6
Q

what is croup

A

acute laryngotracheobronchitis

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7
Q

what causes croup most commonly

A

parainfluenza virus

could also be RSV or bacterial

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8
Q
A
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9
Q

what age is croup most common

A

2

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10
Q

management of croup

A
  • most get better at home within 24 hours
  • children may require hospitalisation due to
    • more severe illness
    • being under 12 months old
    • signs of fatigue or resp failure
  • managemnet
    • single dose dex or nebulised budesonide
    • nebulised adrenaline if need to get to ITU
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11
Q

what organism causes acute epiglottitis

A

haemophilus influenzae type B

rare to HiB vaccination

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12
Q

age of acute eppiglotitis

A

1-6

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13
Q

management of acute eppiglottitis

A
  • do not
    • lie child down
    • examine throat
    • upset child (no bloods)
  • managed in resus room
  • examination of throat under anaesthetic
    • cherry red, swollen epiglottis on laryngoscopy
  • intubate
  • blood cultures
  • IV cefuroxime
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14
Q

what is bacterial tracheitis

A
  • rare but more common than epiglottitis
  • often seen as an acute deterioration after a vira infection
  • children systemically very unwell
  • no drooling
  • hoarse voice
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15
Q

what organisms commonly cause bacterial tracheitis

A

staphylococcus aureus

H. influenzae

strep spp.

neisseria spp.

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16
Q

management of bacterial tracheitis

A
  • secure airway
  • blood cultures
  • IV cefuroxime
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17
Q

distinguish croup, acute epiglottitis and bacterial tracheitis

A
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18
Q

organism for whooping cough

A

bordatella pertussis

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19
Q

how long can whooping cough last

A

3 months

(100 day cough)

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20
Q

what is the management of whooping cough

A

erythromycin given early reduces infectivity and complications but does not reduce duration of illness

managment is largely supportive but 1% will need hospital admission

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21
Q

what are the two types of LRTIs

A

bronchiolitis

pneumonia

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22
Q

what causes bronchiolitis

A
  • viruses rather than bacteria
  • most commonly RSV
  • less commonly
    • adenovirus
    • influenza
    • parainfluenza
  • rarely: mycoplasma pneumoniae
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23
Q

what would an X ray of bronchiolitis show

A

hyperinflation and patchy consolidation bilaterally

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24
Q

what is the management of bronchiolitis

A

supportive

oxygen

some may be ill enough to need ng feeds

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25
Q

what does pneumonia mean

A

inflammation of the lung parenchyma with consolidation within the alveoli

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26
Q

what organisms cause pneumonia

A
  • viruses (more common in children <2)
    • RSV
    • influenza
    • parainfluenza
    • adenovirus
  • bacteria
    • strep pneumoniae (most common)
    • s. aureus (common in CF)
    • pseudomonas (common in CF)
    • HiB (in unvaccinated)
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27
Q

what are the classic signs of consolidation on the lungs (pneumonia)

A

decreased breath sounds

dullness to percussion

crackles

bronchial breathing

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28
Q

what three features suggest bacterial pneumonia

A

polymorphoneuclear leucocytosis

lobar consolidation

pleural effusion

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29
Q

first line antibiotic for bacterial pneumonia

A

oral amoxicillin

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30
Q

what are the aims of asthma treatment

A

no daytime symptoms or waking in the night due to symptoms

no exacerbations

no need for reliever therapy

no limitations on activity

normal lung function

minimal side effects of therapy

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31
Q

what’s the difference between brown and blue inhalers

A
  • brown - preventors
    • ICS
  • blue - relievers
    • salbutamol
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32
Q

describe the steps of asthma therapy

A
  1. regular preventor
    • very low dose ICS
  2. initial add on preventor
    • inhaled LABA
  3. additional add on therapies
    • if no response to LABA stop it and increase ICS to low dose
    • if benefit from LABA but not enough then keep LABA AND increase ICS to low dose
    • if still inadequate add LTRA
  4. high dose therapy
    • increase ICS to medium dose
    • addition of theophyline
    • refer to specialist
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33
Q

what is the carrier rate of CF

A

1:25

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34
Q

incidence of CF

A

1:2500 live births

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35
Q

what is the most common CF mutation

A

three base pair deletion at F508

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36
Q

Common pathogens in CF chest infection

A
  • S.aureus
  • H.influenzae
  • Pseudomonas
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37
Q

what is the gold standard of CF diagnosis

A

pilocarpine ionotophoresis sweat test

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38
Q

what are the cornerstones of CF management

A

prevention of colonisation and infection of the lungs

effective mucocillary clearance

nutritional support

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39
Q

ear ache is usually caused by:

A

infection of the middle ear

otitis media

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40
Q

what is acute otitis media usually caused by

A
  • can follow viral URTI
  • can also be bacterial
    • s.pneumoniae
    • pneumococcus spp.
    • h. influenzae
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41
Q

management of otitis media

A

symptomatic treatment is usually sufficient

abx can reduce symptoms but not complications

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42
Q

what is conductive hearing loss usually due to

A

OME: otitis media with effusion aka glue ear

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43
Q

down’s syndrome is associated with which congenital heart disease

A

ASD

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44
Q

turner’s syndrome is associated with which congenital heart disease

A

coarctation of the aorta

bicuspid aortic valve

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45
Q

noonan syndrome is associated with which congenital heart disease

A

pulmonary stenosis

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46
Q

fetal alcohol syndrome is associated with which congenital heart disease

A

atrial septal defect

ventricular septal defect

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47
Q

describe the different types of cyanosis and what they mean

A
  • central cyanosis
    • blue lips, blue tongue
    • always pathological
  • peripheral cyanosis
    • blueness of hands and feet
    • can be normal in first 24hrs of life
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48
Q

hallmarks of innocent murmurs

A

an asymptomatic child

a normal cardiovascular examination

systolic or continuous

no radiation

variation with posture

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49
Q

what kind of murmur is always pathological and needs investigation

A

diastolic

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50
Q

clinical features of heart failure in infants

A

poor feeding and breathlessness

faltering growth

excessive sweating

recurrent chest infections

CVS signs

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51
Q

initial investigations for suspected heart failure

A
  • ecg
  • chest x ray
  • diagnosis normally needs echo
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52
Q

cxr finding of teratology of fallot

A

boot shape

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53
Q

cxr finding of transposition of great arteries

A

egg on side

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54
Q

what are the two cyanotic congenital heart conditions

A

teratology of fallot

transposition of great arteries

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55
Q

what is the most commonn congenital heart disease

A

vsd

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56
Q

complications of a left to right shunt

A

permanent irreversable pulmonary HTN

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57
Q

compare the three severities of VSD

A
  • small vsd
    • pansystolic murmur
    • no symptoms
    • may close spontaneously but if murmer persists to 12 months do echo to look for complications
  • medium vsd
    • has symptoms
    • treated with diuretics and ACE inhibitors
    • spontenous improvement often occurs and surgery can often be avoided
  • large
    • presents early with cardiac failure
    • medical management
    • then surgical correction
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58
Q

management of ASD

A

many close spontaneously before school age

management is to prevent heart failure and arrhythmias

transcatheter closure at age of 3-5

if very large might need surgical closure

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59
Q

when should the ductus arteriosus close

A

within hours of delivery

PDA diagnosed if duct doesn’t close in 1 month following birth

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60
Q

what are the clinical features of a PDA

A

bounding pulses

wide pulse pressure

continuous machinery hum murmer

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61
Q

management of PDA

A

ibuprofen to inhibit prostaglandin and encourage closure

can also be closed in first few months of life by cardiac catheterisation

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62
Q

clinical fetures of teratology of fallot

A

cyanosis

loud single S2

clubbing in older children if uncorrected

loud ejection systolic murmer

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63
Q

what are tet spells

A
  • in teratology of fallot when peripheral vascular resistance falls
  • increases right to left shunt
  • can be triggered by exertion, emotion, dehydration or illness
  • includes
    • worsenning cyanosis and pallor
    • distress/agitation
    • hypotonia
    • children squat
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64
Q

managmenet of TOF

A
  • treat ‘tet’ or hypercyanotic events with:
    • high flow oxygen
    • morphine
    • IV fluids
    • bicarbonate for acidosis
    • intubation and ventilation in severe cases
  • definitive treatment is surgical
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65
Q

managment of transposition of great arteries

A
  • initial aim is to promote mixing of blood
    • infusion of prostaglandin E1 to newborn
      • maintains patency of DA
    • emergency cardiac catheterisation and atrial septostomy
      • life saving procedures
  • definitive repair achieved with arterial switch surgery at a few weeks of age
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66
Q
A
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67
Q

rheumatic fever is a complication of what and how frequently does it occur

A

group A beta haemolytic strep

a sore throat

occurs in <1% of cases of strep throat

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68
Q

what age does rheumatic fever affect

A

5-15

use of antibiotics for bacterial throat infection have made it rare in UK

but is most common cause of cardiac valvular disease worldwide

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69
Q

what are the jones criteria and how can they be used

A
  • used to diagnose rheumatic fever
  • for diagnosis patient needs to meet required criteria AND have either of:
    • two major
    • one major and two minor
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70
Q

what are the required criteria of jones criteria

A
  • evidence of streptococcal infection. either:
    • positive bacterial throat swab
    • raised antistreptolysin O titre
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71
Q

what are the major criteria of the jones criteria

A
  • polyarthritis (can be fleeting)
  • erythema marginatum
  • subcutaneous nodules
  • carditis
  • chorea
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72
Q

minor criteria of jones criteria

A
  • fever
  • arthralgia
  • raised ESR, CRP or WCC
  • previous rheumatic fever
  • prolonged PR on ECG
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73
Q

ecg finding in rheumatic fever

A

prolonged PR

they may not have this

it is one of the minor criteria

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74
Q

acute management of rheumatic fever

A
  • bed rest
  • high dose aspirin
  • steroids for severe carditis
  • diuretics and ace inhibitors for heart failure
  • Abx for acute illness and for prophylaxis of endocarditis
    • for 5-10yrs
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75
Q

what is the most common complication of rheumatic fever

A

rheumatic valvular disease

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76
Q

any child with fever and a murmer what should you expect

A

endocarditis

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77
Q

what is the most common causative organism in endocarditis

A

strep viridans

this is alpha haemolytic streptococcus

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78
Q
A
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79
Q

diagnosis of endocarditis

A

cross sectional echocardiography can confirm diagnosis but cannot exclude

three blood cultures taken in first 24hrs of admission

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80
Q

treatment for infective endocarditis

A

4-6 weeks of IV abx

e.g. high dose ampicillin

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81
Q

investigations in a child presenting with abdominal pain

A
  • urinalysis
    • dipstick
    • mcs if indicated
  • bloods
    • fbc
    • crp
    • lfts if jaundiced
  • imaging
    • abdo x ray rarely useful
    • USS
      • can diagnose intussusception
      • can sometimes see appendicitis but cannot rule out
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82
Q

organic causes of recurrent abdo pain

A

recurrent UTI

renal calculi

Helicobacter pylori gastritis

IBD

malrotation with intermittent volvolus

gallstones

recurrent pancreatitis

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83
Q

compare dehydration and shock with the following features

Sunken eyes and depressed fontanelle

Mucous membranes

Skin turgor

Alertness

HR and RR

Urine output

Skin colour

Extremities

Cap refill

Blood pressure

A
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84
Q

7 red flags with vomiting

A

bilious vomiting

localised abdo pain

persistent fever

altered consciousness/bulging fontanelle

meningism

petechial rash

respiratory distress

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85
Q

vomiting blood in first few days of life could be

A

swallowing maternal blood

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86
Q

acute diarrhoea is most commonly caused by

A

gastroenteritis

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87
Q

what is a positive rovsing sign and what does it mean

A

palpation of the left iliac fossa causes pain in the right

appendicitis

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88
Q

bloody diarrhoea should raise suspicion of

A

Bacterial gastritis particularly HUS (e.coli)

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89
Q

constipation red flags (6)

A

starts in first few weeks of life

meconium passed >24 hours

abdo distension or bilious vomiting

faltering growth

delayed walking or lower limb neurology

child protection concerns

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90
Q

what age does colic most commonly occur

A

2 weeks until about 4 months

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91
Q

7 differentials for inconsolable crying in an infant

A

colic

GORD

cows milk protein allergy

incarcerated hernia

intussusception

otitis media

UTI

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92
Q

infantile colic managment

A

benign and has a good prognosis

sympathetic explanation of the condition is helpful but there is no evidence for medication

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93
Q

infants at risk of severe GORD

A

preterm infants

infants with congenital oesophageal anomalies

infants with cerebral palsy

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94
Q

complications of GORD in infants and how many develop complications

A
  • 10% infants with symptomatic reflux develop complications
  • bronchospasm and wheeze
  • recurrent aspiration pneumonia
  • oesophagitis
    • could lead to haematemasis and anaemia
  • faltering growth
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95
Q

investigation of GORD

A
  • Diagnosed clinically
    • posseting
    • vomiting
    • crying after feeds
    • worse when lying down
  • sometimes to confirm diagnosis/assess severity
    • 24hr oesophageal pH monitoring in older kids
    • endoscopy if suspected oesophagitis
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96
Q

management of GORD

A
  • majority will resolve spontaneously by 18 months
  • following drugs can be used in severe reflux
    • H2 antagonists: ranitidine
    • proton pump inhibitors: omeprazole
    • prokinetic drugs: domperidone
      • reduce lower oesophageal sphincter pressure
  • surgery very rarely
    • nissen fundoplication
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97
Q

pyloric stenosis is due to

A

hypertrophy of the smooth muscle of the pyloric sphincter

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98
Q

complications of pyloric stenosis

A

weight loss

constipation

dehydration

mild jaundice

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99
Q

what is the characteristic electrolyte disturbance in pyloric stenosis

why

A

hypochloraemic hypokalaemic metabolic alkalosis

due to loss of gastric acid contents

then kidneys retain H ions at expense of potassium

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100
Q

managment of pyloric stenosis

A

correction of fluid and electrolyte abnormalities

difinitive treatment is ramstedt pyloromyotomy

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101
Q

what is the most common surgical emergency

A

appendicitis

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102
Q

common associated symptoms with appendicitis other than the pain

A

anorexia

nausea

vomiting

diarrhoea

constipation

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103
Q

diagnosis and investigations of appendicitis

A
  • usually clinical
  • FBC
  • CRP
  • abdo US may confirm but cannot exclude
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104
Q

management of appendicitis

A

appendicectomy

if there is diagnostic uncertainty, a period of observation may be indicated

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105
Q

what is mesenteric adenitis

A
  • inflammation of the intraabdominal lymph nodes that can mimic appendicitis
  • commonly follows viral infection
    • URTI
    • gastroenteritis
  • obs in hospital since diagnosis difficult
  • management is conservative
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106
Q

peak age of incidence of intussusception

A

5-10 months

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107
Q

commonest site of intussusception

A

ileum into caecum

108
Q

classical presenting triad of intussusception

A
  • paroxysmal abdo pain
    • screaming, becomes pale, draws legs to chest
  • abdo mass
    • sausage shaped
  • redcurrent jelly stool
    • late sign
    • compromise in blood supply to bowel causes blood and mucus to be mixed in
109
Q

what will the vomiting be like in intussusception if there is some

110
Q

US finding in intussusception

A

doughnut or target sign

111
Q

management of intussusception

A

air or barrium enemas

if this fails aroscopy or laparotomy will be needed

112
Q

what is hirschprung’s

A
  • aka congenital aganglionic megacolon
  • aganglionic segment between bowel and colon is contracted
  • more common in males and children with down’s syndrome
113
Q

hirschprung’s presentation

A
  • infants in neonatal period
    • delayed passage of meconium >48hrs
    • intestinal obstruction with bilious vomiting
  • older children
    • chronic severe constipation from birth
    • absence of faeces in narrow rectum
    • abdo distension
114
Q

diagnosis hirschprungs

A

confirmation is by absence of ganglion cells on suction biopsy of rectum

115
Q

management of hirschprungs

A

surgical resection of involved area of colon

anastamoses normally innervated bowel with anus

ladd’s procedure

116
Q

causes of small bowel obstruction

A

duodenal atresia (associated with downs)

malrotaion with volvolus

strangulated inguinal hernia

meconium ileus

118
Q

causes of large bowel obstruction

A

hirschprung’s disease

imperforate anus

rectal atresia

119
Q

what is the most causative virus of gastroenteritis

120
Q

how to calculate maintenance fluids

A

100mL/kg/24hrs for first 10kg

50ml/kg/24hrs for second 10kg

20ml/kg/24 hrs after that

121
Q

what proportion of IBD have their first presentation in childhood

122
Q

in the paediatric settin is crohns or UC more common

A

crohns is twice as common as UC

123
Q

compare crohns to UC

A
  • crohns
    • occurs anywhere from mouth to anus
    • transmural inflammation
    • granulomatous inflammation
  • ulcerative colitis
    • colon only
    • mucosa only involved
    • nongranulomatous inflammation
124
Q

complications of CD and UC

A
  • crohns
    • strictures
    • abscesses
    • fistulae
    • 5-6x increased risk of colon cancer
  • UC
    • toxic megacolon
    • risk of PSC
    • 20-30x increased risk of colon cancer
125
Q

diagnosis of IBD

A

colonoscopy and biopsy

126
Q

faecal calprotectin is a marker of what

A

inflammation of the gut

127
Q

chrons management

A
  • steroids to induce remission
  • immunosuppressive agents for maintenance
    • mesalazine
    • azithioprine
  • antitumour mabs
    • infliximab
  • surgery if medical treatment fails
128
Q

UC management

A

steroids

immunosuppressive agents needed

surgery when medical treatment fails - subtotal colectomy and ileostomy can be curative

129
Q

which HLA type is associated with coeliac and how close is the association

A

HLA-DQ2 is found in 95% of affected individuals

130
Q

investigations in coeliac

A
  • IgA tissue transglutaminase with total IgA
    • there may be IgA deficiency where IgG can be measured instead
  • definitive diagnosis is by duodenal/jejunal biopsy
    • villous atrophy
131
Q

jaundice with pallor indicates

A

a haemolytic episode e.g. G6PD deficiency

132
Q

what is marasmus

A

undernourishment causing a child’s weight to be significantly low for their age.

133
Q

causes of jaundice in first 24 hrs of life

A
  • excess haemolysis
    • immune
      • rhesus incompatibility
      • ABO incompatibility
    • non-immune (intrinsic red cell defects)
      • G6PD deficiency
      • Spherocytosis
  • congenital infections
    • TORCH, hepatitis and syphilis
134
Q

causes of jaundice between 24hrs and 2 weeks

A
  • most common cause is physiological jaundice
  • breast milk jaundice
  • infection
  • bruising
  • excess haemolysis
    • ABO incompatibiltiy
    • G6PD deficiency
    • spherocytosis
135
Q

causes of jaundice after two weeks of life

A
  • breast milk jaundice
  • infections
  • haemolysis
    • ABO incompatibility
    • Rh incompatibility
    • G6PD deficiency
    • Spherocytosis
  • biliary atresia
  • neonatal hepitits
  • hypothyroidism (should have been screened as newborn)
136
Q

treatment of biliary atresia

A

kasai procedure but many still require a liver transplant by the age of 20

137
Q

investigations for babies presenting with prolonged jaundice (more than 2 weeks)

138
Q

what is potter’s syndrome

A

bilateral renal agenesis

oligohydramnios due to lack of foetal urine

death

139
Q

vesicoureteric reflux is a major cause of

A

CKD in children

140
Q

what is the most common causative agent in UTI in children and what are some others

A
  • most common is e.coli
  • proteus
  • klebsiella
  • pseudomonas
  • enterococcus
141
Q

causes of acute nephritis

A
  • most commonly post-streptococcal glomerulonephritis
    • 10-14 days after a throat or skin infection
  • henoch schonlein purpura
  • IgA nephropathy
  • SLE
  • haemolytic uraemic syndrome
142
Q

acute nephritis is characterised by

A

haematuria

reduced renal function

hypertension

(there may be oedema and proteinuria but these are less common than in nephrotic syndrome)

143
Q

compare acute nephritis and nephrotic syndrome using

Aetiology

Gross haematuria

Hypertension

Oedema

Urinalysis

Serum C3 and C4

Anti-DNase B / antistreptolysin O titre

Treatment

144
Q

what is the triad for nephrotic syndrome

A

proteinuria

hypoalbuminaemia

oedema

145
Q

causes of nephrotic syndrome

A
  • minimal change disease (most common)
  • focal segmental glomerulosclerosis
  • membranous glomerulonephritis
146
Q

treatment for minimal change disease

A

4 weeks of high dose prednisolone

147
Q

what is the most common cause of AKI in a previously healthy child

A

haemolytic uraemic syndrome

148
Q

what is haemolytic uraemic syndrome

A

shiga toxin producing E.coli leads to red blood cell fragmentation in the kidney and thrombocytopenia

ABX ARE CONTRAINDICATED AS THEY INDUCE SHIGA TOXIN PRODUCTION

149
Q

management of undescended testis

A

carry an increased risk of malignancy, subfertility and torsion

treatment is by orchidopexy if they have not descended by 6 months

150
Q

distinguishing a hydrocoele from an inguinal hernia on examination

A

hydrocoele it is possible to get above it and it cannot be reduced

it transilluminates

151
Q

treatment for hydrocoele

A

usually no treatment needed as it will resolve spontaneously

152
Q

management of inguinal hernias

A

surgery promptly - the risk is strangulation

153
Q

differential diagnoses of an acute scrotum

A

epididymo orchitis

idiopathic scrotal oedema

torsion of the testicular appendix

154
Q

most common cause of ambiguous genitalia

A

congenital adrenal hyperplasia of an XX individual

155
Q

what is the commonest vasculitis in children

A

henoch schonlein purpura

156
Q

how does HSP affect the skin, joints, GI system and kidneys?

A
  • skin
    • purpuric rash on extensor surfaces and buttocks
  • GI tract
    • abdo pain
    • GI bleeding
    • intussusception
  • Joints
    • arthralgia
    • swelling of large joints
  • Kidneys
    • glomerulonephritis
      • hypertension
      • microscopic haematuria
      • proteinuria
157
Q

what ig is responsible for HSP

158
Q

diagnosis of HSP

A
  • clinical diagnosis
  • normal platelet count and coagulation exclude other causes of purpura
159
Q

management of HSP

A

HSP is usually self limiting

treatment usually supportive with pain relief

steroids only if severe

160
Q

what is the most common cause of thrombocytopenia in childhood?

A

Idiopathic thrombocytopaenic purpura

161
Q

what’s the difference between IgE mediated allergies and non IgE mediated allergy

A
  • IgE mediated
    • asthma
    • acute allergy
    • alaphylaxis
  • non-IgE
    • cows milk protein allergy
    • eczema
  • IgE –> mast cell and basophil degranulation. classically have biphasic response with early and late component
  • non IgE –> less well understood
162
Q

investigating suspected allergies

A
  • there is no test for non IgE mediated allergies - just trial elimination and re-introduction
  • IgE allergy testing
    • Skin prick testing
      • wheal more than 3mm larger than negative control is a positive result
    • negative predictive value better than positive predictive value
      • so history important
163
Q

management of anaphylaxis

A
  • remove allergen
  • IM adrenaline (epinephrine) 1µg/kg 1:1000
  • if out of hospital an epi pen should be used
  • IV hydrocortisone
  • IV antihistamine (chlorphenamine)
  • back to back salbutamol nebs
164
Q

what does a maculopapular rash look like

A

has both macules and papules

i.e. areas that are flat and non-palpable as well as lesions that are fluid filled and raised

165
Q

examples of vesicular rashes

166
Q

examples of maculopapular rashes

A

viral exanthems like rubella, measles, roseola infantum

any viral infection

scarlet fever

kawasakis

167
Q

examples of haemorrhagic rashes

A

meningococcal sepsis

acute leukaemia

idiopathic thrombocytopenic purpura

Henoch-Schonlein purpura (usually legs and buttocks)

bleeding disorders

168
Q

three different varieties of eczema

A

atopic eczema

infantile seborrhoeic eczema

napkin dermatitis

169
Q

% of children affected by eczema

170
Q

management of eczema

A
  • step wise approach
    1. regular use of emollients
    2. topical steroids of appropriate potency
    3. topical tacrolimus and pimecrolimus
171
Q

what are the topical steroids in order of increasing potency

A
  • help every budding dermatologist
    1. hydrocortisone (least potent)
    2. eumovate
    3. betnovate
    4. dermovate (most potent)
172
Q

what is eczema herpeticum and what is the managment

A
  • secondary infection of eczema with HSV
  • potentially very serious
  • treatment with aciclovir
173
Q

what is infantile seborrhoeic eczema, where does it normally occur on the body, what age and what is the treatment

A
  • mild eczema
  • common in first 2 months of life
  • scaly and non itchy
  • initially on scalp - cradle cap
  • may spread to involve face, flexures and nappy area
  • treatments is with emollients and mild topical steroids
174
Q

rashes in the nappy areas can be due to

A

candidiasis

irritant contact dermatitis (nappy rash)

seborrhoeic dermatitis

175
Q

distinguishing true nappy rash from candidiasis

A
  • in true nappy rash the inguinal folds are spared since it’s the contact with urea that causes it
  • candidias will involve the skin folds
176
Q

management of nappy rash

A

frequent nappy changes

barrier creams

exposure to air can hasten recovery

177
Q

management of candidiasis

A

topical and oral antifungals such as nystatin

178
Q

bacteria for acne

A

propionibacterium acnes

179
Q

acne treatment

A
  • keratolytic agents
    • benzoyl peroxide
  • topical antibiotics
    • clindamycin
  • low dose oral antibiotics
    • doxycycline
  • vitamin A analogues
    • 13 cis retinoic acid
    • only prescribed by specialists
180
Q

what’s an important consideration with roaccutane

A

it’s teratogenic so councel teenage girls about this

181
Q

what is erythema multiforme

A

target lesions possibly with macules, papules and bullae

if there is mucous membrane involvement it’s called stevens-johnson syndrome

most commonly caused by HSV or EBV

self limiting and idiopathic

182
Q

erythema nodosum is caused by what

A

IBD

tuberculosis

strep infections

183
Q

what is the virus that causes molloscum and is it infectious

A

molloscipoxvirus

low infectivity

184
Q

management of molloscum

A

usually resolves spontaneously within 6 months to two years

185
Q

what is tinea capitis

A

scalp ringworm

itchy alopecia

occasional boggy inflammatory masses called kerion

186
Q

what is tinea corporis

A

body ringworm

187
Q

what is tinea pedis

A

athletes foot

188
Q

what are the tineas treated with

A
  • mild infections: treated with topical antifungal preparations such as clotrimazole or miconazole
  • severe infections: require systemic treatment with oral griseofulvin for several weeks
189
Q

how is scabies diagnosed

A

identification of mites or ova in scrapings from burrows or vesicles

190
Q

what is the treatment of scabies

A

permathrin cream 5% applied to whole body

two treatments 1 week apart

can take several weeks for the pruritis to subside after successful treatment as hypersensitivity persists - this can be treated with oral antihistamines

191
Q

what is pediculosis capitis

192
Q

summarise glasgow coma scale

193
Q

what is the difference between general and focal seizures

A

general - abnormal electrical activity originates from both hemispheres

focal - abnormal electrical activity originates from one hemisphere

194
Q

features of tonic clonic seizures and are they generalised or not

A
  • tonic phase
  • clonic phase
  • loss of consciousness
  • postictal drowsiness

can be febrile seizures

they are generalised

195
Q

features of absence seizures and are they generalised or focal

A

brief unawareness lasting a few seconds

no loss of posture

immediate recovery

may be very frequent

associated with automatisms - blinking and lip smacking

196
Q

what is the peak age of onset of childhood absence epilepsy

A

peak onset 6-7 years

197
Q

describe childhood absence epilepsy

A

absence seizures typically lasting 5-15 seconds but there may be up to several 100 a day

episodes induced by hyperventilation

198
Q

what do you see on an EEG in childhood absence epilepsy

A

generalised bilaterally synchronous three per second spike wave discharges

199
Q

what is the management and prognosis of childhood absence epilepsy

A

prognosis is good with spontaneous remission in adolescence

sodium valproate and ethosuximide are first line but medication is not required for infrequent absences

200
Q

what is another name for infantile spasms

A

west syndrome

201
Q

what is the peak onset of west syndrome

A

4-6 months

202
Q

describe the seizures in west syndrome

A

sudden flexor spasms of the head, trunk and limbs

followed by abduction and adduction of the limbs

remember that this will be happening in a baby under 6 months age

203
Q

what will the EEG show in west syndrome?

A

hysparrhythmia

204
Q

what is the management and prognosis of west syndrome

A

prognosis poor

seizures often intractable

often learning difficulties

treatment is with adrenocorticotrophic hormone or vigabatrin

205
Q

what age do febrile convulsions occur

A

6 months to 6 years of age

206
Q

what is the most common cause of seizures in childood

A

febrile convulsions

207
Q

what are the clinical features of febrile convulsions

A

1-2 minutes typically

generalised, tonic clonic

208
Q

what three things would make a febrile convulsion ‘complex’ rather than ‘simple’

A
  • any three of the following make it complex:
    • longer than 15 minutes
    • focal
    • recurring within 24hrs
209
Q

management of febrile convulsions

A

identification and treatment of underlying infection

regular anti-pyretics

prolonged convulsions treated as per status

210
Q

prognosis following febrile convulsion

A
  • in simple prognosis is good
  • child may have another febrile convulsion in their life but generally grow out of this by 6
  • slightly higher risk of developing epilepsy than the rest of the population
    • even more so if it was a complex seizure
211
Q

what is the insulin dose when managing DKA in children

A

0.1 units/kh/hr

212
Q

what is the treatment of kawasakis

A

IV Ig and high dose PO aspirin

213
Q

causative organism in osteomyelitis in children

A

staph aureus

214
Q

what is the management of oteomyelitis

A

IV cefuroxime or IV flucloxacillin

6 weeks of treatment - switch to PO once improving

215
Q

OGTT result in a) diabetes b) impaired glucose tolerance

A

diabetes: >11.1mmol/l

impaired glucose tolerance: 7.8-11mmol/l

216
Q

criteria for diagnosis of JIA

A

more than 6 weeks of pain and stiffness in a joint with no other cause found and they are under 16 years of age

217
Q

what is CAH

A

AR disease - most common cause of insufficient cortisol and mineralocorticoid secretion

218
Q

why do you give aspirin to children with kawasakis

A

they have high platelets - thrombocytosis - so they are at risk of thrombosis

219
Q

management of pneumonia

A

IB ben pen if acutely unwell

PO amoxicillin if stable

220
Q

fasting plasma glucose in a) diabetes b) impaired glucose tolerance c)euglycaemia

A
  • a) diabetes >7mmol/l
  • b) impaired glucose tolerance: 5.7-7mmol/l
  • c) euglycaemia 3.5-5.6mmol/l
221
Q

characteristic electrolyte finding in congenital adrenal hyperplasia

A

salt losing adrenal crisis

hyponatraemic hyperkalaemic metabolic acidosis

no aldosterone so losing salt and retaining potassium

222
Q

name a condition of hypogonadotropic hypogonadism with total anosmia

A

kallman syndrome

223
Q

what is the cause of kallman syndrome

A

failure in the correct production or activity of gonadotropin-releasing hormone by the hypothalamus. This results in low levels of the sex hormones testosterone in males or oestrogen and progesterone in females.

224
Q

glood goes through what to reach the baby from the placenta

blood goes through what to reach the placenta from baby

A

placenta –> umbilical vein –> baby

baby –> umbilical artery –> placenta

225
Q

what are the bacterial prophylaxis drugs

A

rifampicin

ciprofloxacin

226
Q

treatment for ESBL e.coli

227
Q

treatment of precocious puberty

A

GnRH superagonists suppress the pulsatility of GnRH action

228
Q

HbA1c in a) diabetes b) impaired glucose tolerance c) euglycaemia

A
  • diabetes: >6.5%
  • impaired glucose tolerance 5.7-6.4%
  • euglycaemia 4-5.6%
229
Q

biochemical diagnosis of CAH

A
  • raised lecvels of 17-alpha-hydroxy-progesterone
  • biochemical abnormalities:
    • hyponatraemic hyperkalaemic metabolic acidosis with hypoglycaemia
230
Q

how do you treat mycoplasma pneumoniae pneumonia

A

erythromycin

clindamycin

231
Q

managmenet of conductive hearing loss

A

wait - it normally goes away

grommett insertion

232
Q

what do you see in the bloods of kawasaki

A

high: crp, esr, wcc and platelets

233
Q

croup treatment

A

beclamethasone

234
Q

what mode of inheritance is osteogenesis imperfecta

235
Q

where is the defect in osteogenesis imperfecta

A

in the genes for type 1 collagen

236
Q

two genes involved in type 1 diabetes

A

HLADR3

HLADR4

237
Q

what is the inheritance pattern for spherocytosis

A

autosomal dominant

238
Q

treatment for UTI in children

A

IV cefuroxime

PO trimethoprim if stable

239
Q

when is the brainstem myelinated and what can this do to prems

A

32/34 weeks gestation

can cause apnoea of prematurity

240
Q

treatment for apnoea of prematurity

A

nasal cpap

caffeine to stimulate

241
Q

acute otitis media organisms

A

s. pneumoniae
h. influenzae

242
Q

meningitis organisms by age and antibiotic therapy

243
Q

why are prem babies at greater risk of infection

A

IgG transfer happens in the last 3 months of pregnancy

244
Q

what syndrome is associated with biliary atresia

A

down’s syndrome

245
Q

what is first line treatment for retinoblastoma

A

laser therapy

246
Q

what chromosomw is the rb1 gene on

247
Q

first line for focal seizures

A

carbamazepine

248
Q

criteria for tonsillectomy

A

>7 episodes of acute tonsilitis in a year

OSA or sleep deprived breathing

249
Q

common causes of diarrhoea

A

adenovirus

rotavirus

giardia

250
Q

what test for lactose intollerance

A

hydrogen breath test

251
Q

what is lactose hydrolysed into

A

glucose and galactose

252
Q

skin change from coeliac

A

dermatitis herpeteformis

253
Q

treatment of giardiasis

A

three days high dose metronidazole

254
Q

analgesia for paediatric fracture

A

paracetamol

oromorph

255
Q

coeliac HLA

A

DQ2 and DQ8.

256
Q

what is hypospadias

A

When the urethral opening is on the under side of the penis.

257
Q

which abx to reduce risk of neonatal infections in a pre-term baby

A

Benzylpenicillin (50mg/kg BD).
Gentamicin (5mg/Kg OD).

258
Q

when can you start feeding a prem baby

A

35 weeks - this is when suckling reflex develops

259
Q

medication for general seizures

A

Ethosuxamide or Sodium Valporate.

260
Q

ethosuxamide side effects

A

rash

nausea

d&v

261
Q

sodium valproate side effects

A

weight gain

hair loss

teratogenic

262
Q

what can absence seizures evolve into

263
Q

signs of JME

A

Clumsiness and GTCS that occur shortly after waking and are often provoked by sleep deprivation.

264
Q

demographics of students affected by ADHD

A

4 - 7 % of school age children

Male : Female = 4:1

265
Q

name an ADHD med

A

methylphenidate - it’s a stimulant

formative 3b (18 decks)

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