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Phase 3a/4 > Paeds > Flashcards

Paeds Flashcards

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1
Q

name the 3 shunts in foetal circulation

A

foramen ovale
ductus arteriosus
ductus venosus

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2
Q

name the 4 left to right shunts

A

atrial septal defect
ventricular septal defect
atrio-ventricular septal defect
patent ductus arteriosus

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3
Q

describe an ASD and what are the most common types

A

hole connecting the 2 atria = leads to a shunt of blood moving from LA to RA = high pressure blood to lungs = RH failure and overload + pulmonary hypertension
ostium secundum = 80%
ostium primum = partial ASD

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4
Q

what are the symptoms of ASD

A

often asymptomatic in childhood or:
- sob
- difficulty feeding
- poor weight gain
older:
- recurrent chest - infections/wheeze
- heart failure

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5
Q

what are the clinical signs of ASD

A

fixed and widely split 2nd heart sound = pulmonary/aortic valves close at different times
ejection systolic murmur at left sternal edge in pulmonary area
possible palpitations

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6
Q

what investigations for ASD

A

chest XR = cardiomegaly wiht dilatation of pulmonary arteries
ECG = partial RBBB + right axis deviation
(partial ASD = left axis deviation)
echoCG = mainstay = shows anatomy

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7
Q

what is the management of ASD

A

small/asym = W&W
surgical closure/catheter closure
Anticoags in adults to prevent stroke complication

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8
Q

what is the most common cause of meningitis in the UK

A

neisseria meningitidis

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9
Q

what are the sepsis 6

A

WITHIN AN HOUR
1. high flow oxygen
2. blood cultures
3. obtain IV access + give IV ceftriaxone 80mg/kg
4. fluid resus of 20ml/kg 0.9% saline
5. measure lactate
6. measure urine

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10
Q

what is klinefelter syndrome and what are its features

A

XXY chromosomes = primary hypogonadism
- azoospermia + gynaecomastia
- reduced secondary sexual characteristics
- osteoporosis
- tall
- reduced IQ
** increased risk breast cancer

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11
Q

what is hypogonadotrophic hypogonadism

A

deficiency of LH and FSH

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12
Q

what is hypergonadotrophic hypogonadism

A

lack of response to LH/FSH by the gonads

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13
Q

what is the cause of hypOgonadotrophic hypogonadism and name some causes

A

= abnormal hypothalamus/pituitary function
- damage
- GH deficiency
- hypothyroidism
- hyperprolactinaemia
- serious chronic conditions (IBD/CF)
- excessive diet/exercise
- Kallman syndrome

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14
Q

what is the cause of hypERgonadotrophic hypogonadism

A

= gonads no response = no negative feedback = increased LH/FSH
- previous gonad damage
- congenital absence of gonads
- kleinfelters syndrome XXY
- turners syndrome XO

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15
Q

what is kallman’s syndrome

A

hypogonadotrophic hypogonadism
anosmia (no smell)
visual problems
craniofacial abnormalities

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16
Q

what is turners syndrome

A

45 X0
- often results in miscarriage
- lymphoedema hands/feet in neonate
- short stature (height 20cm below normal)
- gonadal failure
- webbing of neck/low hairline/big ears/high arched palate
- CVS malformations
- horseshoe kidney

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17
Q

name the causes of short stature

A

familial
constitutional delay in growth and development
malnutrition
chronic disease (IMD/CHD)
endocrine (hypothyroidism)
genetics (downs/turners)
skeletal dysplasia

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18
Q

how is constitutional delay in growth and puberty (CDGP) diagnosed

A

history/examination
XR of hand/wrist
bone age compared to actual age

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19
Q

name the causes of overgrowth with impaired final height

A

precocious puberty
congenital adrenal hyperplasia
hyperthyroidism
mcAlbright

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20
Q

name the causes of overgrowth with increased final height

A

androgen deficiency/oestrogen resistance
GH excess
Kleinfelter sydrome XXY/Marfan syndrome

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21
Q

what is psycho social short stature

A

seen over 3
emotional rejection/abuse associated
50% show reversible GH deficiency

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22
Q

what growth centile constitutes overweight and obese

A

overweight = BMI above 85th percentile
obese = BMI above 95th percentile

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23
Q

describe puberty in girls

A

breast bud first sign
early = under 8
late = over 13

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24
Q

describe puberty in boys

A

testicular enlargement first sign in boys
early = under 9
late = over 14

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25
Q

what genetic syndromes can cause short stature

A

turners
noonans
downs
russel-silver

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26
Q

causes of microcephaly

A

= familial
= autosomal recessive condition
= congenital infection
= acquired after insult to brain e.g. meningitis

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27
Q

causes of macrocephaly

A

= familial
= raised intercranial pressure
= hydrocephalus
= chronic subdural heamatoma
= tumour
= neurofibromatosis

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28
Q

causes of precocious puberty in girls vs boys

A

girls = usually early onset of normal puberty
boys = organic cause
- intracranial tumours
- adrenal cause

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29
Q

what is congenital adrenal hyperplasia

A

autosomal recessive
classic CAH = salt wasting type in boys 7-10 days = adrenal crisis
ambiguous genitalia = cliteral hypertrophy and labial fusion

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30
Q

describe the important causes of vomiting in neonates (5)

A

malrotation/volvulus = bilious
hirshprungs disease/meconium ileus = bilious
NEC = bilious
infection

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31
Q

describe the important causes of vomiting in infants (7)

A

GORD = feed associated
food intolerance = change in stools
pyloric stenosis = projectile
intussusception = 3-36 months/colicky, red currant jelly stools
strangulating hernia/obstruction = bilious
raised ICP = early morning
infection

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32
Q

describe the important causes of vomiting in older children (9)

A

appendicitis
strangulated hernia
pancreatitis
DKA - diabetes symptoms
meds/alcohol/drugs
post-op pain
psychiatric/eating disorder
pregnancy
infection - pyrexia

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33
Q

describe the investigations for acute vomiting

A

U&E
stool virology
abdo XR
surgical consultation
exclude systemic disease

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34
Q

describe the investigations for chronic vomiting

A

FBC
ESR/CRP
U&E
LFT

H.pylori serology
urinalysis

upper GI endoscopy
abdo USS
small bowel enema
brain imaging
test feed = pyloric stenosis

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35
Q

describe the investigations for cyclic vomiting

A

same as chronic +:
amylase
lipase
glucose
ammonia

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36
Q

what presentation is typical of pyloric stenosis

A

projectile vomiting at 2-7 weeks of age

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37
Q

what does bile stained vomiting suggest

A

intestinal obstruction
intessuseption
malrotation
strangulated inguinal hernia

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38
Q

what are the complications of vomiting

A

K deficiency
alkalosis
Na depletion
nutritional deficiency
FTT
anaemia

malloey-weiss tear
tear of small arteries
dental erosions and caries
oesophageal stricture/barrets oesoph

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39
Q

describe GORD in children

A

normal <12 months due to lower oesophageal sphincter immaturity

increased risk in neuromuscular kids (cerebral palsy)
effortless regurgitation
usually self-resolving

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40
Q

what is the best diagnostic test for GORD

A

24hr oesophageal pH monitoring

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41
Q

describe the management for GORD

A

upright position
feed thickeners
medication = antacid/H2 blocker/PPI
fundoplication if serious (rare)

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42
Q

what are the most common food allergens

A

cows milk
eggs
peanuts
wheat
soya
fish
shellfish
tree nuts

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43
Q

what are the clinical features of food allergy/intolerance

A

diarrhoea +/- bloody/mucus
vomiting
abdo pain
FTT
eczema
urticaria
red rash, particularly around mouth
asthma sympts/anaphylaxis if severe

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44
Q

what is the difference between a food allergy and an intolerance

A

food allergy = immunological response to food
intolerance = adverse reaction mediated by NON-immunological response = more common

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45
Q

describe cow’s milk protein allergy

A

most common allergy in infancy
Sx depend on site of inflammation:
upper GI = vomiting, pain
small intestine = diarrhoea, pain, FTT
large intestine = diarrhoea, acute colitis blood/mucus

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46
Q

what is the management of CMPA

A

limit cows milk protein intake *for mother if breastfeeding
give formula if bottle fed
dont give soya milk
after 6-12months consider cows milk challenge

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47
Q

what is toddler diarrhoea

A

commonest cause of loose stool in preschool children
undigested veg in stool common
children are well and thriving
no treatment

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48
Q

what is encoporesis

A

involuntary faecal soiling or incontinence
= emotional disorder
= more common in boys
= can be secondary to constipation

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49
Q

what pattern indicates constipation

A

less than 3 stools per week
hard, large stool

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50
Q

what is hirsprungs disease

A

absence of meyenteric plexus of rectum and colon
usually presents in newborn as intestinal obstruction + delay in passing meconium w/n 24hr
diagnose with suction rectal biopsy
management is surgical

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51
Q

describe the red flags for constipation

A

no meconium w/n 48hrs = hirsprung/CF
neurological signs
vomiting = obstruction/hirscprungs
ribbon stool = anal stenosis
abnormal anus
abnormal lower back/buttocks
FTT
acute severe abdo distention/pain/bloating

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52
Q

what is the most common cause of a UTI

A

E.coli

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53
Q

what would pseudomonas on a urine microscopy result suggest

A

structural abnormality

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54
Q

what is foaming urine indicative of

A

heavy protein loss in urine

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55
Q

name the acyanotic congenital heart diseases

A

left to right shunts:
- atrial septal defect
- ventricular septal defect
- atrioventricular septal defect
- patent ductus arteriosus
Outflow obstruction:
- coarctation of aorta
- aortic stenosis
- pulmonary stenosis

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56
Q

name the cyanotic congenital heart diseases

A

transposition of the great arteries
tetralogy of fallot
tricuspid atresia

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57
Q

describe the diagnostic criteria for anorexia nervosa

A
  1. deliberately keeping weight below 85% expected = eating/exercise
  2. dread of getting fat
  3. endocrine effects = delayed menarche/menstruation stops
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58
Q

describe the epidemiology of anorexia nervosa

A

1 in 250 female
1 in 2000 males
mean age of onset 16-17

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59
Q

describe the aetiology of anorexia nervosa

A

social pressure
perfectionist character traits
low self esteem
reversing/halting effects of puberty
family attitudes
some genetic links
depression/anxiety
occupation (ballet)
past or present events

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60
Q

describe the screening tool for eating problems

A

SCOFF
do you make yourself SICK because uncomfortably full
do you worry youve lost CONTROL over eating
have you lost more than ONE stone in 3 months
do you believe youre FAT when others say youre thin
does FOOD dominate your life

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61
Q

describe the clinical signs of anorexia nervosa

A

dry skin
lanugo hair
orange skin/palms
cold hands/feet
bradycardia
oedema
postural hypotension
weak proximal muscles

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62
Q

what is the mneumonic for appendicitis

A

MAGNET
Migration of pain to RIF
Anorexia
Guarding
Nausea
Elevated temp
Tenderness in RIF

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63
Q

what are the 2 most common causes of acute abdominal pain in children

A

non-specific pain
appendicitis

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64
Q

how does malrotation typically present

A

within first few days of life (but can at any stage of life)
obstruction
green bilious vomiting
blood in vomit = ischaemic bowel
abdominal pain

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65
Q

what are the investigations and management for malrotation

A

urgent upper GI contrast study = barium meal
treatment is urgent surgical correction (Ladd’s procedure)

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66
Q

what is indicated with bilious or bloody vomiting in children

A

upper GI contrast study is needed

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67
Q

describe the presentation of intussuseption

A

2 months - 2 y/o
paroxysmal/severe colicky pain
pallor during pain episodes
sausage shaped mass on examination
redcurrant jelly stool - later presentation
abdominal distension and shock

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68
Q

what is the most common cause of intestinal obstruction in infants after neonatal period

A

intussuseption - ileocaecal most common

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69
Q

what route for fluids if iv access cant be abtained

A

interosseous (into femur)

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70
Q

what antibiotic can you not give to neonates and why

A

ceftriaxone = causes jaundice

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71
Q

what causes purpura

A

skin microvessel thrombosis leading to heamorrhagic necrosis
peripherals effected due to reduced perfusion to distal tissue in shock

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72
Q

what is the 1st line prophylaxis for meningitis

A

ciprofloxacin
rifampicin also acceptable

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73
Q

describe the contraindications/complications for rifampicin

A

effect oral contraceptives
cause jaundice
person on anticoagulants
person on seizure medication

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74
Q

what types of fluids can be used for maintenance in children

A

0.45% sodium chloride + 5% dextrose
0.9% sodium chloride + dextrose

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75
Q

what is the rate for maintenance fluids in children

A

100ml/kg for first 10kg
50ml/kg for next 10kg
20mls/kg for the rest

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76
Q

what fluid maintenance is given to babies on day 0

A

10% dextrose only

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77
Q

when is a fluid bolus given

A

hypoglycaemia - 10% dextrose 2ml/kg STAT
hypovolaemia (shock) - 0.9% saline (even in neonate) 20mls/kg STAT

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78
Q

how is the deficit calculated for dehydration fluids

A

% dehydrated x 10 x weight in kg

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79
Q

advantages of breast feeding

A

macronutrients for baby
free antibodies for infection
free
maternal bonding

reduce NEC risk in preterm
reduce risk of post menopausal breast cancers

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80
Q

disadvantages of breast feeding

A

unknown intake
mother has to do all
breast milk jaundice
transmission of drugs/infections
insufficient vit D/K in breastmilk

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81
Q

why is important to refeed slowly in anorexia

A

refeeding syndrome = body take up glucose and excrete sodium/potassium
refeeding hepatitis

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82
Q

describe the diagnostic criteria for ADHD in under 17 year olds

A

6/9 inattentive symptoms
6/9 hyperactive/impulsive symptoms
- present before 12 yr old
- developmentally inappropriate
- several symptoms in 2 or more settings
- clear evidence symptoms intefere/reduce QoL (social/academic etc)

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83
Q

describe some features of inattentive symptoms

A

easily distracted
not listening
difficulty sustaining attention during activities
forgetful in activities
difficult to follow instructions
difficult to organise tasks

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84
Q

describe some features of hyperactive symptoms

A

squirms/fidgets
cant remain still
run/climbs excessively
‘on the go’
talks excessively
cannot do tasks quietly

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85
Q

describe some features of impulsive symptoms

A

blurts out answers to questions
cannot wait their turn
interrupts or intrudes on others

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86
Q

describe the epidemiology of ADHD

A

4-7% school age children
males: females 4:1
overlaps with many other mental disorders

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87
Q

what are some risk factors for ADHD

A

foetal oxygen deprivation
maternal smoking
low birth weight
prematurity
heroin use in pregnancy
genetic component
low socioeconomic status
other psychiatric disorders - aspergers/odd/tics

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88
Q

describe the non drug management of ADHD

A

parent education and training
CBT to support social skills etc
regular routines
rewards and targets to reach for
school support

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89
Q

describe the drug management of ADHD

A

stimulants (increase dopamine) = as needed:
- ritalin = short acting
- delmosart = long acting
- elvanse
non stimulants (breakdown norepinephrine) = regular taking:
- atomoxetine (SNRI)
- guanfacine
** or combination **

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90
Q

what is the efficacy of ADHD drugs

A

70% benefit of stimulant medication
significant side effects - cardiac/anorexia/anxiety/depression

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91
Q

describe the prognosis of ADHD

A

30% grow out of it
15% remain meeting criteria by 25

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92
Q

describe the epidemiology of ASD

A

1 in 100
500,000 in UK
boys x4 to girls

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93
Q

what are the cardinal symptoms of Autism SD

A

combination of difficulties of:
1. communication/speech and language
2. social interaction
3. behaviour rigidity/routines/rituals

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94
Q

describe some of the communication features of ASD

A

lack of desire to communicate
communicate needs only
disordered/repeated speech
poor non verbal comms
no social awareness

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95
Q

describe some of the social interaction features of ASD

A

no desire to interact
lack of motivation to please others
affectionate on own terms
no understanding of social cues
inappropriate touching/eye contact
plays alone/stressful to be with others

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96
Q

describe some of the rigidity/imagination features of ASD

A

use toys as objects
cannot play imaginatively
resist change
playing same game over/obsessions
learn by rote not by understanding
follows rules exactly
inability to see others point of view

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97
Q

describe the management of ASD

A

education/information
parenting workshops - timetables etc
school liaison/support
manage comorbidities

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98
Q

what are the features of an ‘innocent’ murmur

A

4 S’s
Soft blowing murmer
aSymptomatic
left Sternal edge
Systolic murmur
short duration

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99
Q

name the congenital infections to be aware of

A

CHRISTS
CMV
HSV
Rubella
hIV
Syphillus
Toxoplasmosis

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100
Q

what do you give a pregnant lady with syphillis

A

IM benzylpenecillin

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101
Q

how do you treat toxoplasmosis in pregnancy

A

spiromycin

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102
Q

what causes epiglottitis and what are some red flag signs

A

haemophilus B
high fever
drooling saliva
soft stridor
tripod stance/mouth open

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103
Q

how is epioglottitis managed

A

do not examine throat
paeds emergency!!!!!
anaesthetis and ENT surgeon needed
keep child calm
prepare for intubation
once airway secures = blood cultures
TX: cefuroxime
3-5 day abx

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104
Q

what is prophylaxis for epiglottitis

A

rifampicin for household contacts

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105
Q

what is the treatment for croup

A

1st line = oral dose dexamethasone
severe:
nebulised adrenaline
oral prednisolone
nebs steroids

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106
Q

what age group does bronchiolitis effect

A

up to 1 year old
rare after 1

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107
Q

what preventative treatment is given for bronchiolitis

A

pavlizumab = for high risk
- premy
- CF
- chronic heart/lung disease

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108
Q

what are the most common causes of pneumonia in newborn

A

group B strep
gram negative enterococci
= from mothers genital tract

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109
Q

what are the most common causes of pneumonia in infants/young kids

A

bacterial
= strep. pneum
= h.influenza
= bordatella pertussis
= chlamydia
= s.aureus
viral
= RSV
= rhinovirus

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110
Q

most common causes pneumonia in over 5s

A

strep. pneumonia
chlamydia pneumoniae
klebsiella
mycoplasma

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111
Q

most common cause of pneumonia in immune comprpmised

A

pneumocystitis jiroveci
TB

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112
Q

describe the indications for hospitalisation in pneumonia

A

sats <93%
severe tachypnoea/difficult breathing
grunting
apnoea
not feeding
family unable to provide care

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113
Q

describe the antibiotic treatment for pneumonia

A

newborn = broad spec (benpen + gentamycin)
older children = oral amoxicillin/erythromycin

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114
Q

describe the presentation of otitis media and what are the typical causative pathogens

A

irritable/miserable child
pulling at ear
6 months - 12 months most common
RSV
rhinovirus
pneumococcus
h.influenzae

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115
Q

describe the examination findings of tympanic membrane for otitis media +/- effusion

A

red
bulging
lack of light reflection
+effusion:
= dull and retracted
= visible fluid level

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116
Q

how is otitis media treated

A

simple analgesics
80% spontaneous resolution
possible amoxicillin

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117
Q

what is glue ear and how is it treated

A

otitis media with effusion
recurrent OM infections = reduce hearing
most common cause conductive hearing loss in children
no Tx or grommets

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118
Q

what are the most common causes of tonsillitis

A

viral
group A beta haemolytic strep

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119
Q

what indicates more likely bacterial tonsilitis

A

headache
apathy
abdo pain
tonsillar exudate/pus
cervical lymphadenopathy

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120
Q

what are the causes of proteinuria in children

A

transient
orthostatic
increased glomerular perfusion pressure
reduced renal mass
hypertension
tubular proteinuria
glomerular abnormalities: GN, minimal change, abnormal BM

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121
Q

what is the most common cause of nephrotic syndrome in children + name 4 other causes

A
  1. minimal change disease
    - HSP/vasculitis
    - SLE
    - infections
    - allergens
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122
Q

what are the 3 categories of nephrotic syndrome and who is high risk for each

A

congenital - finnish people
steroid sensitive - boys/asian/atopic
steroid resistant

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123
Q

describe congenital nephrotic syndrome

A

first 3 months of life
rare but very serious
end stage renal failure and dialysis needed
high mortality

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124
Q

what are the features suggesting steroid sensitive nephrotic syndrome

A

age 1-10
no macroscopic haematuria
normal BP
normal complement
normal renal function
often resp infections precipitate

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125
Q

how is steroid sensitive nephrotic syndrome managed and what is the prognosis

A

60mg/m squared/day prednisolone 4 weeks every day
40mg/m squared/day 4 weeks alternate days
relapses can occur
if continue to adulthood may need methotrexate

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126
Q

what is the prognosis of steroid RESISTANT nephrotic syndrome

A

30% go to ESRF in 5 years
20% respond to cytotoxic meds
most spontaneously remit in 5 years

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127
Q

describe the classification for FTT

A

mild = fall across 2 centile lines
severe = fall across 3 centile lines

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128
Q

name the classification of causes of FTT

A

inadequate intake
difficulty feeding
malabsorption
increased energy requirements
inability to process nutrients

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129
Q

what are some organic causes of FTT

A

impaired suck/swallow - cleft palate/neuromotor dysfunction
cardiac disease = breathlessness
malabsorption = coeliac/CF/intolerance
chronic illness = liver/heart/renal
excessive calorie loss = vomiting/protein loss
increased calorie need = malginancy/CF
chromosomal = downs

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130
Q

what investigations for FTT

A

FBC
U&E
inflamm markers
coeliac antibodies
chest XR/sweat test for CF

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131
Q

what is the acute treatment for paediatric UTI

A

trimethoprim 3 day course
or
co-amoxiclav 5 day course
fluids
analgesia
adjust abx once sensitivities return

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132
Q

what are the fraser guidelines

A

used to assess if underage person is competent to consent to treatment:
1. can understand advice
2. cannot be persuaded to inform parents
3. likely to continue sexual intercourse without protection
4. physical and mental health suffer if dont get contraception
5. its in her best interest to receive contraception wihtout parental consent

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133
Q

what is the definition of osteoporosis in children

A

1 + vertebral crush fractures
2+ long bone fractures by 10
3+ by 19
bone density <2.5 SD below mean

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134
Q

describe the causes of osteoporosis in children

A

inherited:
- osteogenesis imperfecta
- haematological
acquired:
- drugs (steroids)
- endocrine disorder
- malabsorption
- inflammation/immobility

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135
Q

describe the pathophysiology of osteogenesis imperfecta

A

autosomal dominant
type 1 collagen defect
different types:
type 2 fatal
chest too small to allow breathing/multiple rib fractures/no lung function
= brittle bones
= fragiel bones

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136
Q

how does osteogenesis imperfecta present

A

bone fragility/fractures/deformity
bone pain
impaired mobility
poor growth

deafness/hernia/valvular prolapse

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137
Q

what is a distinctive feature of osteogenesis imperfecta

A

blue tinted sclera

138
Q

describe the XR features of osteogenesis imperfecta

A

wormian bones (wiggly black lines in skull) = bubble wrap feeling
bent bones
bowing of femur
complete chest collapse in type 2 fatal

139
Q

what is the treatment for osteogenesis imperfecta

A
  1. bisphosphonates = pamidronate
    - prefer given IV
    - increase lumbar spine/total body bone mass
  2. vitamin D supplements
  3. specialist MDT
140
Q

describe the types of OI

A

type 1 mild
type 2 fatal
type 3 severe
type 4 moderate

141
Q

describe the role of vitamin D

A
  • inreases Ca absorption from gut
  • increases Ca release from the bone
  • decreases Ca excretion by kidney
  • role in immune function
142
Q

what is rickets and what are the risk factors

A

soft bones due to vitamin D or calcium deficiency
can be genetic (X linked)
insufficient vit D in pregnancy
lack of sunlights
dark skin
lack of dietary vitamin D

143
Q

how does rickets present

A

bowed leg
hypocalcaemia convulsions
gross motor delay
swollen ankle
carpopedal spasm
incidental XR finding = splayed/frayed metaphyses

144
Q

how is rickets/vitamin D deficiency treated

A

vit D supplement 400mg per day reccomended
inactive form because they can convert it themselves

145
Q

how is estimated weight calculated

A

under 12 months = (age in months +9)/2
1-5 =(age in years +4) x 2
5-14 = age in years x4

146
Q

what is the wet flag mneumonic and what are the equations

A

Weight = (age+4)x2
Energy = 4J per kg
Tube diameter = (age/4)+4
Fluid = 20ml x weight in medical, 10ml x weight in trauma
Lorazepam = 0.1mg x weight
Adrenaline = 0.1ml x weight of 1:10,000
Glucose = 2ml x weight of 10% dextrose

147
Q

what are some causes of seizures in children

A

epilepsy
febrile convulsions
hypoglycaemia/hypocalcaemia
head trauma
infection (meningo/enceph/abcess)
amphetamines/stimulants

148
Q

describe febrile convulsions

A

6 months - 6 years
high fever
simple = <15 mins
complicated = >15 mins
may reoccur, no lasting damage

149
Q

what are some causes of funny turns in children

A

breath holding attack
reflexive anoxic seizures
syncope
migrain
vertigo
arrythmias
fabricated by parent

150
Q

describe the distinctive features of temporal lobe seizures

A

strange warning feelings/aura
automatisms = lip smakcing/pacing
deja vu and jamais vu
impaired consciousness longer than absence

151
Q

how are seizures investigated

A

witness history/video
thorough history incl family history
EEG
blood tests
metabolic investigations

152
Q

what EEG features suggest absence seizures

A

3hrts spike and wave

153
Q

what is the treatment for absence seizures

A
  1. sodium valproate/ethosuximide
  2. lamotrogine
154
Q

what AED should be avoided in absence and myoclonic seizures

A

carbamezapine

155
Q

what are the blood result criteria for DKA

A

BM over 11
bicarb under 15
ketones over 3

156
Q

when are children’s hearing checked

A

newborn
starting school
if parents are concerned

157
Q

what are the 2 categories of hearing loss and the underlying pathology

A

conductive = obstruction in ear canal preventing sound from getting through, can be reversible
sensorineural = nerve damage, irreversible

158
Q

name some causes of conductive hearing loss in children (6)

A

congestion with cold most common
glue ear
ear wax
middle ear infection
perforated ear drum
structural abnormality

159
Q

name 3 risk factors of conductive hearing loss

A

down’s syndrome
craniofacial syndromes
cleft palate

160
Q

what is the exam finding of conductive hearing loss and how is it managed

A

better hearing through bone conduction
self limiting
ENT referral = grommets
hearing aids if permanent cause

161
Q

what are some causes of sensorineural hearing loss (7)

A

many unknown
genetic/syndromal
perinatal trauma/infection/hypoxia
CMV/rubella in pregnancy
meningitis
premature babies

162
Q

what is the examination findings in sensorineural hearing loss and how is it managed

A

hearing NOT better through bones
on audiology higher frequencies worst heard
= hearing aids
= cochlear implants
= aim to raise hearing so speech is audible

163
Q

which cases are cochlear implants reserved for

A

profound hearing loss
high frequency
bilateral loss
meningitis loss

164
Q

what are some long term affects of hearing loss

A

developmental delay
behavioural problems
impact on education/friendships/social life

165
Q

name 3 syndromes associated with hearing loss

A

ushers syndrome (sensorineural)
wardenbergs syndrome (sensorineural)
treacher-collins (conductive)

166
Q

what congenital infection most commonly causes hearing loss

A

cytomegalovirus
also:
rubella
syphillis
herpes

167
Q

when does hearing need to monitored

A

chemotherapy
cystic fibrosis treatment
CMV
head trauma
cleft lip/palate
any of the syndromes associated with hearing loss

168
Q

what is the difference between cyanotic breath holding spells and reflex anoxic seizures

A

cyanotic breath holding = stop breathing become blue and lose consciousness
= after crying
= involuntary
= tired/lethargic afterwards
reflex anoxic seizures = vagus nerve tells heart to stop beating = pale/unconscious/muscle twitches
= regain conc within 30 secs
= happens when child is startled/scared

169
Q

up to what age is a squint normal

A

up to 12 weeks

170
Q

what is strabismus and name some causes

A

misalignment of the visual axis
refractive errors = most common
cataracts
retinoblastoma
intra-occular problems

171
Q

what are the 2 types of squint

A

non-paralytic/concomintant = refractive error
paralytic = due to paralysis of motor nerves (rare)

172
Q

what tests can be done to detect a squint

A

corneal light reflex test = reflection of light should be in same position in both eyes
cover test = cover good eye and squinting eye will move

173
Q

name the 3 refractive errors seen in childhood

A

hypermetropia (long sighted)
myopia (short sighted)
amblyopia (lazy eye)

174
Q

what causes amblyopia and how is it treated

A

squint
refractive errors
ptosis
cataracts
treat early!! before 7 y/o
= glasses
= patching

175
Q

how is strabisumus treated

A

glasses
orthoptic exercises
surgery = strengthen or weaken
botox injections

176
Q

what infection most commonly presents with neonatal jaundice + investigations

A

= UTI
urine sample
blood cultures
CXR
FBC

177
Q

what type of jaundice in neonates is most worrying

A

persistent/prolonged

178
Q

what features suggest biliary atresia

A

pale stools
dark urine
off feeds/unwell
itching/scratch marks

179
Q

what is the gold standard investigation for suspected biliary atresia

A

ultrasound liver

180
Q

what counts as prolonged jaundice

A

> 14 days in term babies
21 days in premature

181
Q

what is an important complication of jaundice

A

kernicterus
excess bilirubin causes brain damage
non responsive/floppy/drowsy baby
permanent damage = cerebral palsy/learning difficulties/deafness

182
Q

what are the risk factors for neonatal hypoglycaemia

A

preterm
IUGR
diabetic mothers
large babies
polycythaemia
unwell babies

183
Q

how does neonatal hypoglycaemia present

A

jitters
irritable
apnoea
lethargy/drowsiness
seizures

184
Q

how is neonatal hypoglycaemia managed

A

regular blood glucose bedside monitoring
early and frequent milk feeding
if need top up = IV dextrose via central venous catheter

185
Q

describe an APGAR score

A

between 1 and 10
7-10 normal
cardio
resp
colour
reflexes
tone

186
Q

how does group B strep present in neonates and what is the mortality

A

pneumonia
septicaemia
meningitis (not as common)
mortality = 10%

187
Q

which women are high risk for GBS and are screened

A

pre-term delivery
previous baby with GBS
prolonged rupture of membranes
fever over 38 in labour
postpartum Abx given to high risk ladies

188
Q

how is conjunctivits in the newborn managed

A

usually just water/saline
if troublesome discharge could staph/strep = neomycin eye ointment
gonococcal infection (48hrs after birth)= treat with penicillin or cephalosporin, cleanse frequently
chlamydia (2 weeks after birth) = oral erythromycin for 2 weeks

189
Q

what are the features of juvenile myoclonic seizures

A

occurs in the teen years
early morning sudden myoclonic jerks = clumsy?
triggered by lack of sleep
often later develop generalised tonic-clonic (GTC) seizures
may be inherited as autosomal dominant
40% with absence seizures will develop JME

190
Q

a teenager spills their cereal every morning - what is this an indicator of

A

juvenile myoclonic epilepsy

191
Q

what are the side effects of sodium valproate

A

teratogenic
weight gain

192
Q

what is ebstein’s anomaly and when does it present

A

tricuspid valve is lower = larger RA, smaller RV
= poor flow to pulmonary vessels
associated with ASD = right to left shunt = cyanosis
presents couple days post natal = when PDA closes

193
Q

what are the clinical findings for ebsteins anomaly

A

ECG
= arrhythmia
= RBBB
= left axis deviation
CXR = cardiomegaly/RA enlarge
echocardiogram = definitive diagnosis

194
Q

how is ebsteins anomaly treated

A

treat arrythmia
treat heart failure
abx prophylaxis for IE
surgical to correct

195
Q

what findings are suggestive of a UTI

A

positive nitrites positive leucocytes
just positive nitrites
nitrites = better indicator of infection

196
Q

describe the treatment of a UTI in an infant

A

all <3 months old with fever = IV abx and sepsis screen
oral abx if over 3 months and well:
- trimethoprim
- nitrofurantoin
- cefalexin
- amoxicilin

197
Q

describe the need for ultrasound for UTI

A

all under 6 months first UTI = abdo USS within 6 weeks
children with recurrent UTI = abdo USS within 6 weeks
children with atypical UTI = abdo USS during the illness

198
Q

describe the risk factors for DDH

A

1st child
breech presentation from 36 weeks
breech at birth
multiple pregnancy

199
Q

name the tests to screen for DDH

A

ortolani test = abduct hips to see if hips dislocate anteriorly
barlow test = pressure on knees/femur to see if femoral head dislocate posteriorly
clicking = normal
clunking = need ultrasound

200
Q

how is DDH investigated

A

ultrasound of hips for all children with findings or risk factors
XR useful in older children

201
Q

describe the management for DDH

A

pavlik harness if under 6 months = keeps hips flexed and abducted
regular review
surgery if harness fails or >6 months old

202
Q

describe the features of ulcerative colitis (CLOSE UP)

A

Continuous inflammation
Limited to colon/rectum
Only superficial mucosa
Smoking is protective
Excrete blood/mucus
Use AMINOSALICYCLATES
Primary sclerosing cholangitis

203
Q

describe the features of Crohns (NESTS)

A

No blood/mucus
Entire GI tract
Skip lesions
Terminal ileum most common and Transmural
Smoking risk factor

204
Q

what is pyloric stenosis and how does it present

A

hypertrophy and narrowing of pylorus = peristalsis of the stomach sends contents up oesophagus = vomiting in first few weeks of life
- thin
- pale
- FTT
- hungry
- PROJECTILE vomiting
firm round mass in upper abdomen (olive-like)
metabolic alkalosis from loss of stomach acid

205
Q

how is pyloric stenosis managed

A

Dx = abdominal USS
laparoscopic pyloromyotomy (Ramsted’s operation) = widens pylorus

206
Q

what is gastroenteritis and what are the most common causes

A

inflammation from stomach to intestines with nausea, vomiting and diarrhoea
most common causes = viral:
rotavirus
norovirus

207
Q

what is biliary atresia and how is it treated

A

narrow or absent bile duct = cholestasis = no bile excreted = buildup of conjugated bilirubin = jaundice >14 days (term bb) >21 days (prem bb)
treat with surgery = Kasai portoenterostomy = attach small intestine to liver
often need full liver transplant

208
Q

what is oesophageal atresia

A

congenital abnormality = blind ending oesophagus
can have >1 fistulae connecting trachea as well = tracheo-oesophageal fistulae (TOF)
associated with other anomalies = VACTERL syndrome

209
Q

how does oesophageal atresia +/- TOF present

A

first few hours from birth:
respiratory distress
choking
feeding difficulties
frothing at mouth
NG tube not possible
overflow of saliva
aspiration can occur

210
Q

how is oesophageal atresia investigated and treated

A

CXR to assess lung fields + if theres TOF
imaging renal tract = assess urogenital tract
‘gap-o-gram’ to assess length of oesophagus
Mx: correct abnormality
= surgery
= supportive feeding and hydration

211
Q

what is duodenal atresia and how does it present

A

gap or narrowing in duodenum
present with bile green vomiting after feeds within first few days of life
association with downs syndrome

212
Q

how is duodenal atresia diagnosed and treated

A

abdo XR = 2 large air sacs (double bubble)
surgical management

213
Q

describe the causes of clubbing in children

A

hereditary
infective endocarditis
cyanotic heart disease
cystic fibrosis
liver cirrhosis
IBD
TB

214
Q

what are the most common causative organisms for chest infections in cystic fibrosis

A

staph aureus = flucloxacillin long term to prevent
pseudomonas = hard to treat, worse prognosis
= tobramycin or ciprofloxacin

215
Q

describe the management of hypoglycaemia in T1DM

A

too much insulin = low blood sugar
pale/irritable/hungry/tremor/sweating
treat with rapid acting insulin (lucozade) followed by long acting (toast/biscuits)
severe = IM glucagon and IV dextrose
nocturnal hypoglycaemia very common

216
Q

describe the complication of hyperglycaemia in T1DM

A

BM too high but not DKA = alter insulin regimen

217
Q

what is mesenteric adenitis

A

inflammation of lymph glands of the mesentery = umbilical/RIF abdominal pain
common in children/teenagers
fever/nausea/diarrhoea/cold sympts just before
painkillers and supportive care

218
Q

describe the pathophysiology of viral induced wheeze

A

children under 3 have smaller airways, smaller diameter
virus = oedema and inflammation = airways constrict and narrow
wheeze + lack of ventilation = respiratory distress

219
Q

what is the difference between viral wheeze and asthma

A

viral wheeze:
children <3
no atopic history
only during viral infections

220
Q

what is the presentation and management of viral induced wheeze

A

coryzal sympts roughly 2 days before wheeze
shortness of breath
signs of respiratory distress
widespread expiratory wheeze
management same as acute asthma management

221
Q

what causes whooping cough and how does it present

A

bordatella pertussis gram neg bacteria
coryzal sympts and dry cough then develop paroxysmal coughing attacks with loud inspiratory whoop
coughing can cause fainting, vomiting, pneumothorax
children may not make whooping sound

222
Q

how is whooping cough diagnosed and treated

A

nasal/nasopharyngeal swab PCR tested/cultured
cough >2 weeks = can test for anti-pertussis toxin IgG
notify public health
supportive care
macrolides good in vulnerable people (erythromycin/clarithromycin etc)
contact tracing

223
Q

what is diptheria and how does it present

A

cornyebacterium diptheria causes mucosal membrane inflammation
severe sore throat
mild pyrexia
lymphadenopathy
tachypnoea
grey membrane over tonsils

224
Q

how is diptheria diagnosed and treated

A

throat swab = irregular gram +ve rods
treat with antitoxin
isolation for the individual to prevent spread

225
Q

what is scarlet fever

A

disease caused by strep pyogenes (group A strep)
highly contagious - aerosol or direct contact spread
most common ages 2-8

226
Q

how does scarlet fever present

A

sore throat/fever/nausea/vomiting
pin point sandpaper-like blanching rash on trunk developing 12-48 hours after initial sympts - spreads to rest of body
possible strawberry tongue + cervical lymphadenopathy

227
Q

how is scarlet fever diagnosed and managed

A

clinical diagnosis
oral antibiotics e.g. phenoxymethylpenicillin for 10 days
notify public health
isolation

228
Q

describe the complications of scarlet fever

A

otitis media
peritonsillar abcess
acute sinusitis
rheumatic fever
acute post strep GN

229
Q

what is congenital diaphragmatic hernia

A

birth defect of diaphragm = abdominal organs pushed into chest cavity = pulmonary hypoplasia and pulmonary HTN
causes severe respiratory distress at birth
Bochdalek most common type
treated surgically to repair hernia while child is intubated
40-62% mortality rate

230
Q

what is meconium aspiration syndrome

A

respiratory distress in newborn due to presence of meconium in the trachea
if born in meconium stained amniotic fluid = at risk of developing
diagnosis confirmed through CXR
management is supportive
ECMO and NO may be needed if persistent pulmonary HTN

231
Q

what are some risk factors for meconium aspiration syndrome

A

gestation >42 weeks
maternal Hx of HTN/preeclampsia/smoking/substance abuse
foetal distress
oligohydramnios

232
Q

describe retinopathy of the newborn

A

retinal vessel growth stimulated by hypoxia
if exposed to too much oxygen = excessive abnormal blood vessels and scar tissue form = causes retinal detachment

233
Q

describe the diagnosis of retinopathy of the newborn

A

screening for all born <32weeks or <1.5kg
performed by opthalmologist at 30-31 wk gestational age if born <27wks
4-5wk of age if born >27wk
happen every 2 weeks until around 36 weeks gestation
examination = retinal vessels and signs of plus disease

234
Q

how is retinopathy of the newborn treated

A

transpupillary laser photocoagualation = stops new blood vessels developing
cryotherapy also option

235
Q

describe transient tachypnoea of the newborn

A

newborns present with tachpnea and respiratory distress due to delayes absorption of lung fluid following birth
risk factors:
- C sections
- maternal asthma and smoking
- premature infants
- male sex
- PROM
frequently resolves within 72 hours

236
Q

how is transient tachypnoea of the newborn diagnosed and treated

A

clinical diagnosis
ABG to assess gas exchange
pulse oximetry
supportive treatment for resp distress
rule out pneumonia and meconium aspiration

237
Q

describe the causes of primary nocturnal enuresis

A

= child has never had a dry night
overactive bladder
fluid intake prior to bedtime
failure to wake due to deep sleep/weak signals
psychological distress and stress
secondary

238
Q

what is the management for primary enuresis

A

reassurance - probably resolve
lifestyle changes - less fluid b4 bed etc
encouragement and positive reinforcement
treat underlying factors
pharmacological tx

239
Q

what is secondary enuresis and what are the causes

A

= child begins wetting bed after dry period of at least 6 months
UTI
constipation
T1DM
new psychosocial stress
maltreatemnt
abuse/safeguarding

240
Q

describe the pharmacological treatments for enuresis

A

desmopressin = ADH = reduces volume of urine produced by kidneys
oxybutinin = anticholinergic reducing contractility of bladder
imipramine = tricyclin antidepressant may relax the bladder

241
Q

what is nephritis and what is it caused by and what are the features

A

inflammation of nephrons
caused by post strep GN and IgA nephropathy
= nephritic syndrome
1. reduction in kidney function
2. haematuria
3. proteinuria (not as much as nephrotic syndrome)

242
Q

describe the diagnosis and treatment of post strep glomerulonephritis

A

1-3 weeks post Beta strep infection e.g. tonisilitis
supportive management with 80% full recovery
impaired renal function = may need antihypertensives and diuretics for oedema

243
Q

describe the diagnosis and treatement of IgA nephropathy causing nephritis

A

aka Berger’s disease
related to HSP
renal biopsy will show IgA deposits
usually teenagers/YA
supportive management and immunosuppressent medications (steroids/cyclophosphomides)

244
Q

what is status epilepticus and how is it managed

A

medical emergency = seizure >5 mins or >3 in and hour
ABCD approach:
- secure airway
- oxygen
- cardiac/resp functino
- blood glucose
- IV lorazepam
- IV phenobarbital/phenytoin
- transfer ITU

245
Q

describe junior myoclonic epilepsy

A

occurs in teen years
triggered by lack of sleep
early morning myoclonic jerks (arms/shoulders)
often later develop GTC seizures
may be autosomal dominant inheritance

246
Q

describe petit mal seizures

A

brief staring spells lasting a few seconds at a time
abrupt onset and termination
child may be unaware
1/3rd will have 1+ tonic clonic convulsions

247
Q

describe acute chest syndrome and how it is managed

A
  1. fever/resp sympts
  2. new infiltrates seen on CXR
    can be infective or non infective cause
    = medical emergency with high mortality
    treat underlying cause:
    - antibiotics/antivirals
    - blood transfusions
    - incentive spirometry
    - artificial ventilation
248
Q

whats the most common cause of meningitis in neonates

A

group B strep contracted during birth

249
Q

how might meningitis present in a neonate/baby

A

non specific
hypotonia
poor feeding
lethargy
hypothermia
bulging fontanelle

250
Q

how is meningitis investigated

A

clinical examination
kernig’s test = lift bent leg then straighten from knee = pain
brudzinski’s test = gently lifting head and neck off bed = involuntary hip/knee flexion
lumbar puncture

251
Q

what level is a LP performed at

A

L3-L4 intervertebral space

252
Q

describe the causes of acute glomerulonephritis

A

common:
post infectious GN
HSP
IgA nephropathy
less common:
SLE
Membranoproliferative GN
focal segmental glomerulosclerosis

253
Q

name the causes of headaches in children

A

tension
migraines
ENT infection
analgesic headache
vision problems
raised intracranial pressure
brain tumours
meningitis/encephalitis
carbon monoxide poisoning

254
Q

describe tension headaches

A

very common in children
band-like, symmetrical, gradual occur and resolve
NO visual problems
resolve within 30 mins
triggered by stress/dehydration/hunger

255
Q

how are migraines managed in children

A

rest/fluids/low stimulus environment
paracetamol/ibuprofen
sumatriptan
antiemetics
prophylaxis in severe cases:
propranolol (CI in asthma)
pizotifen (cause drowsy)
topiramate (teratogenic)

256
Q

what is abdominal migraine

A

common in young children - go on to develop migraines
central abdo pain >1 hour
normal examination
nausea/vom
anorexia
headache
pallor

257
Q

what is gowers sign and when is it seen

A

to stand from lying down, child pushes hips up and out like downward dog and walks hands up legs = due to proximal muscle weakness in muscular dystrophy

258
Q

what causes duchennes muscular dystrophy

A

defective gene for dystrophin on X chromosome = X linked recessive inheritance

259
Q

describe DMD

A

boys around 3-5 with weakness around pelvis muscles
progressive weakness
life expectancy 25-35
cardiac and respiratory complications

260
Q

describe beckers muscular dystrophy

A

dystrophin less severely affected
presentation at 8-12 yr old
longer life expectancy

261
Q

describe myotonic dystrophy

A

genetic disorder presenting into adulthood
progressive muscle weakness
prolonged muscle contractions (unable to let go shaking hand)
cataracts
cardiac arrhythmias

262
Q

what is facioscapulohumeral muscular dystrophy

A

progressive weakness around face, shoulders, arms
sleep with eyes slightly open and unable to purse lips

263
Q

what is emery dreifuss muscular dystrophy

A

presents in childhood
contractures elbows/ankles
progressive weakness/wasting of muscles starting in upper arms/lower legs

264
Q

what is west syndrome

A

= infantile spasms
rare disorder
onset around 6 months old
cluster of full body spasms
ppor prognosis = 1/3rd die by 25
treat with prednisolone and vigabatrin

265
Q

what is friedreich’s ataxia

A

autosomal recessive neurodegenerative disease
associated with cardiomyopathy/diabetes
onset before adolescence
- progressive ataxia
- ascending weakness and loss - of vibration/proprioception
- scoliosis
- cardiomyopathy/arrhythmias

266
Q

what presents identically to friedreichs ataxia

A

vitamin E deficiency

267
Q

how is freidreichs ataxia diagnosed and managed

A

nerve conduction studies
ECG/echocardiogram
exclude vitamin E deficiency
MDT treatment - mainly supportive with physios and occupational therapists
treatment of cardiac issues
life expectancy 40-50

268
Q

what is neurofibromatosis and what is the difference between type 1 and 2

A

autosomal dominant genetic disorder causing tumours to form on nerve tissue
type 1 (more common) = recklinghausens disease = neurofibromas grow on nerves and compress nerves/tissue
type 2 = bilateral acoustic neuromas develop causing hearing loss

269
Q

describe the difference in presentation between neurofibromatosis 1 and 2

A

type 1
cafe au lait spots
freckling
dermal fibromas
nodular neurofibromas
lisch nodules (eyes)
short stature/microcephaly

type 2
cafe au lait spots
deafness
vertigo
tinnitus
signs of raising ICP

270
Q

how is neurofibromatosis managed

A

supportive and monitoring progress in all areas
treat comlications e.g. HTN/epilepsy/ADHD

271
Q

describe some risk factors for neural tube defects

A

family history
chromosomal disorders
inadequate folate intake
folic acid antagonists (methotrexate)
anti-epilepsy drugs

272
Q

describe the types of neural tube defect

A

anencephaly = absence of major portion of brain, skull and cap = cranial end of neural tube fails to close
cephaloceles = brain matter herniate through skull
spina bifida occulta (most common) = neural tube fail to close at caudal end but isolated laminar effects = usually only tuft of hair etc
spina bifida cystica = defect of lumbar/sacral vertebrae = can be incidental/myelomeningocele/asymmetrical LMN weakness and wasting and limb deformity

273
Q

how are neural tube defects diagnosed

A

MRI/CT scan
USS antenatally
prenatal screening = measure maternal alpha fetoprotein
second trimester USS most accurate

274
Q

what is tuberous sclerosis and how does it present

A

wideranging multisystem disorder = harmatomas in many organs
commonly brain/skin/kidney
commonly present in childhood with SKIN changes and EPILEPSY
renal angiomyolipomas/lung tumours
cognitive and behavioural problems
treat and support each problem individually

275
Q

describe extradural haemorrhage in children

A

rare due to plasticity of skull
= bleeding between dura and skull
due to fractured temporal/parietal bone damaging middle meningeal artery
history of trauma/head injury with loss of consc followed by lucid period before deterioration
headahce/nausea/vomiting
CT = lemon shape
avoid LP
may need mannitol to reduce intracranial pressure
may need burr holes

276
Q

describe subdural haemorrhage in children

A

bleeding between dura and arachnoid mater due to tearing of bridging veins between cortex
often due to acceleration-deceleration of head/blunt head trauma = shaking baby/abuse
headache/possible loss of conc
CT (with contrast) = banana shape
opthalmology for retinal haemorrhages if shaken baby suspected
mannitol/burr holes/surgery
craniotomy/clot evacuation

277
Q

describe subarachnoid haemorrhage in children

A

rare!
caused by trauma = ?child abuse
severe headache sudden onset
nausea/vomiting/loss of consc/neuro deficits
CT = star shaped
surgical intervention

278
Q

what is hereditary spherocytosis and how does it present

A

RBC sphere shaped = autosomal dominant
common in northern europe
jaundice
anaemia
gallstones
splenomegaly
haemolytic crises = symptoms more severe
aplastic crises = parvovirus = no bone marrow response so severe anaemia/jaundice

279
Q

how is hereditary spherocytosis diagnosed and managed

A

family history and clinical features
blood film = spherocytes
MCHC = raised
reticulocytes = raised due to rapid RBC turnover
Tx: folate supplement and splenectomy
removal of GB if stones persistant problem
transfusions during severe crises

280
Q

what is G6PD deficiency

A

= defect in G6PD enzyme
more common mediterranean/middle east/african
X linked recessive pattern = males affected
causes crises triggered by:
infections
medications
fava beans
crises = RBC attacked by reactive oxygen species = haemolysis

281
Q

how does G6PD deficiency present and diagnosed

A

** neonatal jaundice **
anaemia
intermittent jaundice
gallstones
splenomegaly
Heinz bodies on blood film = denatured Hb within RBC
G6PD enzyme assay for diagnosis

282
Q

how is G6PD managed

A

avoid triggers:
antimalarial
ciprofloxacin
nitrofurantoin
trimethoprim

283
Q

what is thalassaemia

A

autosomal recessive genetic defect in protein chains of Hb
alpha (chrom 16)
= depletion of alpha chains
= more severe if more genes affected
= african/asian pop
beta (chrom 11)
= depletion beta chains
= no. genes affects NOT = severeity
= european pop

284
Q

how can thalassaemia present

A

microcytic anaemia (low MCV)
fatigue
pallor
jaundice
gallstones
splenomegaly (increased RBC breakdown)
pronounced forehead/malar eminences (bone marrow expands to produce extra RBC)

285
Q

how is thalassaemia diagnosed

A

FBC = microcytic anaemia
haemoglobin electrophoresis = globin abnormalities
DNA testing for genetic abnormality

286
Q

how is alpha thalassaemia managed

A

monitor for FBC and complications
blood transfusions
splenectomy
bone marrow transplant

287
Q

how is beta thalassaemia managed

A

minor = monitor mild microcytic anaemia
intermedia = significant anaemia = blood transfusions, may require iron chelation
major = 2x deletion genes = severe anaemia and FTT = regualr transfusion/iron chelation/splenectomy/BM transplant

288
Q

what is a common complication of thalassaemia

A

iron overload
= monitor ferritin levels
= limit transfusions and perform iron chelation
effects:
fatigue
liver cirrhosis
infertility
impotence
heart failure
arthritis
diabetes

289
Q

what is haemophilia

A

inherited condition X linked recessive
type A = more common = lack of factor VIII
type B = lack of factor IX
prothrombin time normal
partial thromboplastin time increased
presents with bleeding/bruising/haematomas e.g. prolonged umbilical bleeding in neonate
mild to severe disease presentation

290
Q

how is haemophilia managed

A

replace missing clotting factors with regular infusion
type A = factor VIII
type B = factor IX

291
Q

what is idiopathic thrombocytopenic purpura ITP

A

spontaneous low platelet count causing purpuric rash
caused by type 2 hypersensitivity reaction = antibodies destroy platelets
can be triggered
presentation:
bleeding
bruising
petechial/purpuric rash (non blanching)

292
Q

how is ITP managed

A

urgent FBC for plt count = confirm Dx
exclude other causes e.g. leukemia
usually no treatment required
plt <10 or actively bleeding:
prednisolone
IV Ig
blood transfusions
platelet transfusion (only temporary)

293
Q

what are the complications and advice for ITP

A

chronic ITO
anaemia
intracranial and subarachnoid haemorrhage
GI bleeding
= avoid contact sports
= avoid NSAIDs/blood thinners/bleeding procedures

294
Q

what is perthes disease

A

disruption of bloodflow to femoral head = avascular necrosis = affects epiphysis of femur
4-12 y/o with common 5-8y/o
no clear cause
revascularisation + healing of femoral head can lead to soft and deformed femoral head = early OA

295
Q

how does perthe’s disease present and how is it diagnosed

A

slow onset + no Hx of trauma
pain in hip/groin
limp
restricted movement
referred pain to knee
- XR (can appear normal)
- bloods to exclude other causes
- technetium bone scan
- MRI

296
Q

how is perthes disease managed

A

severity varies
conservative Mx in younger/milder
bed rest
traction
crutches
analgesia
= reduce risk of damage/deformity when healing
= physio/regular XR/surgery in severe cases

297
Q

describe slipped upper femoral epiphysis and its presentation

A

head of femur displaced along the growth plate
8-15y/o (12y/o common) and boys>girls
Px
adolescent obese male undergoing growth spurt with Hx minor trauma
- hip/groin/knee pain disproportionate to minor trauma
- RoM hip
- painful limp
examination = prefer external rotation of hip with PAIN with internal rotation of hip

298
Q

how is SUFE diagnosed and managed

A

bloods = normal/to exclude
xr of both hips AP and frog leg
= in situ fixation with cannulated screw
= internal fixation across growth plate

299
Q

describe osgood-schlatter disease

A

inflammation at tibial tuberosity at patella tendon insertion due to stress from activity and exercise
= multiple small avulsion fractures = cause visible lump below knee = tender and inflamed
pain in anterior knee
pain worse by activity/pressure
once healed = non tender and hard lump

300
Q

how is osgood-schlatter disease managed

A

reduction in physical activity
ice
NSAIDs
stretching/physiothreapy
symptoms usually resolve - may have small lump under knee

301
Q

what is chondromalacia patellae

A

= softening of articular cartilage of patella seen on MRI
= patellofemoral pain syndrome
inflammation and pain in and around patella
caused by compressive forces from exercise or long periods of knee flexion
common in sporty and active adolescents/YA
treat with physio/analgesia

302
Q

what is patellar tendonitis

A

= ‘jumpers knee’
inflammation at patellar tendon due to overuse
adolescents = sinding-larsen johansson disease = chronic stress injury
= anterior knee pain and tenderness
XR may be normal
USS examination of choice = shows swelling
rest/analgesia/physio to treat

303
Q

what is osteochondritis dissecans

A

pathological process affecting subchondral bone of children with open growth plates
affects knee mainly
trauma/male/overuse/family hx = risk factors
= vague aching pain/oedema/formation of loose bodies in joint/latching and catching joint
XR show loose body
USS/CT showing lesions
MRI best for evaluation
Tx = analegesia/physio/surgery

304
Q

what is achondroplasia

A

= dwarfism
= FGFR3 gene on chromosome 4
= autosomal dominant inheritance
homozygous gene mutation = fatal in neonatal period

305
Q

what are the features of achondroplasia

A

disproportionate short stature (4 ft)
short limbs
short digits
bow legs
disproportionate skull
foramen magnum stenosis (cervical cord compression/hydrocephalus)
recurrent otitis media due to cranial abnormalities
obesity
obstructive sleep apnoea

306
Q

what is molluscum contagiosum

A

viral skin infection caused by type of poxvirus
small flesh coloured papules with central dimple
appear in crops of lesions
spread through direct contact/shared linens
avoid scratching/breaking skin as can cause additional infection
clear up spontaneously up to 18months
can treat with potassium hydroxide/benzoyl peroxide/imiquimod
surgical removal is option but can cause scarring

307
Q

describe scabies

A

tiny mites (sarcoptes scabiei) burrow under skin cauing intense itching and small red dots rash
finger webs common area
easily spread so ask about contacts with itching
treat with permethrin cream = need to be applied to entire body and left for 8-12 hours then washed off
= repeat after a week
oral ivermectin single dose option for difficult to treat
all household needs treatment and deep clean all linens and carpets
crotamiton cream for itching

308
Q

what are crusted scabies

A

norwegian scabies
serious infestation with scabies in immunocompromised
can present like psoriatic plaques with no ithcing
may require hospital treatment and isolation

309
Q

what is impetigo

A

superficial bacterial skin infection
caused by staph aureus
also can be caused by strep pyogenes
VERY infectious = no school during infection

310
Q

what is non-bullous impetigo

A

occur around nose/mouth
exudate dries = golden crust
treat with topical fusidic acid
oral flucloxacillin to treat more widespread
advise measures to avoid spread

311
Q

what is bullous impetigo

A

always caused by staph aureus = epidermolytic toxins that break down skin proteins = fluid vesicles form then burst = golden crust
painful and itchy
more common neonates + <2y/o
can have systemic symptoms
swabs to confirm Dx
flucloxacillin treatment
very contagious = isolation needed

312
Q

what are the complications of impetigo

A

cellulitis
sepsis
scarring
post strep GN
staph scalded skin syndrome
scarlet fever

313
Q

what is erythema multiforme

A

erythematous rash caused by hypersensitivity reaction
caused by viral infections and medications e.g. HSV/mycoplasma pneumonia
widespread itchy red rash with target lesions
sypmts abrupt onset + mild fever/stomatitis/muscle aches/flu-like sympts
Tx underlying cause
mild and should resolve spontaneously

314
Q

what is staphylococcus scalded skin syndrome (SSSS)

A

staph aureus release toxins break down skin proteins = infection
affects children <5
generalised patches of erythema –> fluid blisters (bullae) –> burst and scar = scalded
Nikolsky skign = gentle rubbing of skin causes it to peel away = confirm SSSS
+ systemic symptoms
tx by hospital admission + IV fluids and IV Abx

315
Q

what is ringworm and what are the different types

A

fungal infection
aka tinea or dermatophytosis
tinea capitis = on scalp
tinea pedis = foot/athletes foot
tinea corporis = body
tinea cruris = groin
onchomycosis = fungal nail

316
Q

how does ringworm present

A

itchy/erythmatous/scaly/well demarcated rash
capitis = hair loss/dryness
pedis = between toes
** check toes if ringworm = athletes foot common**

317
Q

how is ringworm diagnosed and managed

A

clinical diagnosis + response to antifungals
possible to scrape and culture
treat with antifungals
- clotrimaxole
- miconazole
- ketoconazole
mild topical steroid help with inflammation and itching
advice to avoid/prevent future infections

318
Q

what is tinea incognito

A

more extensive fungal skin infections
caused by use of steroids to treat fungal infection = suppresses immune response = infection grows

319
Q

what causes chicken pox and how does it present

A

varicella zoster virus = highly contagious
presents with fever first
itch
general fatigue/malaise
rash - widespread/red/raised/vesicular
once scabbed = not contagious

320
Q

how is chicken pox spread

A

highly contagious
spread through direct contact with lesions or infected droplets from cough/sneeze
symptomatic 10 days03 weeks after exposure

321
Q

what are the complications of chicken pox

A

bacterial superinfection
dehydration
conjunctival lesions
pneumonia
encephalitis
virus can lay dormant in sensory dorsal root ganglion cells = later = shingles or ramsay hunt syndrome

322
Q

how is chicken pox managed

A

mild/self-limiting
aciclovir considered in immunocompromised patients/>14 presenting <24hr/neonate
itching = calamine lotion/antihystamine

323
Q

what causes hand foot and mouth disease and how does it present

A

coxsackie A virus
3-5 day incubation
upper resp tract symptoms and fever
1-2 days = small mouth ulcers with blistering red spots across body (hand/foot/mouth)
painful mouth ulcers + on tongue

324
Q

how is hand foot and mouth disease managed and what are the complications

A

diagnosis = clinical appearance
supportive management
resolve in week-10 days
highly contagious = careful
dehydration/bacterial superinfection/encephalitis

325
Q

what is roseola infantum

A

sixth disease/3 day rash
caused by herpesvirus 6/7
high fever sudden development
rash over body excluding face (often after fever subsides)
sore throat
lymphadenopathy
supportive management

326
Q

what is erythema infectiosum

A

aka slapped cheek syndrome
caused by parvovirus B19
can be passed from mother to baby via placenta
may be asymptomatic or non specific coryzal sympts
symptom free 7-10 days then rash appear on cheeks
can present with arthropathy
management = symptomatic

327
Q

what are the complications of erythema infectiosum

A

transient aplastic crisis in those with sickle cell/thalassaemia/hereditary spherocytosis/iron deficiency anaemia
can cause immunocytopenia in immunodeficient patients
can cause meningoencephalitis in immunocompromised
DANGEROUS IN PREGNANCY

328
Q

what are the features of osteosarcoma

A

= bone cancer
10-20 y/o
most commonly femur (tibia/humerus)
** persistent bone pain, especially at night **
bone swelling/palpable mass/RoM

329
Q

describe the diagnosis of osteosarcoma

A

very urgent direct access XR in 48 hours if unexplained bone pain/swelling
if XR suggest osteosarcome - urgent specialist assessment 48hrs
blood test = raised ALP
CT
MRI
bone scan
PET scan
bone biopsy

330
Q

describe the features of osteosarcoma on XR

A

poorly defined lesions in bone
destruction of normal bone
fluffy appearance
periosteal reaction = sunburst appearance

331
Q

how is osteosarcoma managed

A

surgical resection of lesion with limb amputation
adjuvant chemo
MDT team
main complication = pathological bone fractures and metastasis

332
Q

what is a wilm’s tumour and how does it present

A

= nephroblastoma = cancer of kidneys
presents 0-5 y/o
asymptomatic abdo mass
adbo pain
haematuria
UTI
HTN

333
Q

how is wilm’s tumour diagnosed and managed

A

FBC
renal function
electrolytes
urinalysis
USS show distortion of renal pelvis
renal angiography
CT/MRI for staging
Tx = nephrectomy followed by chemo
routine postop radiotherapy is stage 3
prognosis = 90% survive long term
increased risk of second tumours in wilms survivors

334
Q

what is a rhabdomyosarcoma

A

malignancy of connective tissue where abnormal cells arise from primitive muscle cells
most common around head/neck
bladder (20%)
muscles/limbs/chest (15-20%)
= highly malignant and grow rapidly
87% patients are <15 (rarely affect adults)

335
Q

what are the risk factors of rhabdomyosarcoma

A

neurofribromatosis
fetal alcohol syndrome
parental use of marijuana/cocaine
exposure to XR

336
Q

how does rhabdomyosarcoma present

A

expanding lump/swelling = may be painful
nose - nasal obstruction/discharge
eyes = swelling eyeball
adbdomen = pain/change in bowel habit
bladder = haematuria

337
Q

how is rhabdomyosarcoma diagnosed

A

non resolving lumps in children = investigated for cancer
bloods = anaemia/raised ALT
urinalysis = haematuria
XR/CT/MRI
bone scan look for mets

338
Q

how is rhabdomyosarcoma managed

A

surgery for all lesions if possible
chemo (vincristine/cyclophosphamide etc)
post-op radiotherapy
prognosis = 60% children/teens cured

339
Q

describe retinoblastoma

A

embryonal tumour of retina = most common eye malignancy in children
inutero-5 y/o onset
40% = hereditary (AD)

340
Q

how does retinoblastoma present and what are the key differentials

A

abnormal pupil (leukocoria)
strabismus
deterioration of vision
red/irritated eye
Ddx:
cataracts
hamartomas
choroiditis

341
Q

how is retinoblastoma diagnosed and managed

A

any child showing indication = red reflex performed
exam under anaesthesia
bidimensional ocular USS/MRI
evaluate presence of mets
genetic counselling
Mx: urgent opthamology referral
1. surgery
2. chemo
3. radiation
99% survival in UK
invasion of optic nerve most significant prognostic factor

342
Q

what are the most common types of brain cancer in children

A

astrocytoma most common = most are low grade, slow spread
medullablastoma = most common high grade, fast spreading

Phase 3a/4 (6 decks)

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