Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

3a 2023 > Paeds 1 - Cardio/Resp/GI/Infections etc > Flashcards

Paeds 1 - Cardio/Resp/GI/Infections etc Flashcards

1
Q

list some ways congenital heart disease might present

A
  • antenatal diagnosis by US
  • heart murmur
  • cyanosis
  • shock (low cardiac output)
  • cardiac failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the most common left to right shunting congenital heart lesions?

A
  • VSD
  • PAD
  • ASD

present BREATHLESS (acyanotic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the most common right to left shunting congenital heart lesions?

A
  • tetralogy of fallot
  • transposition of the great arteries

present BLUE (cyanotic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

which congenital heart lesion involves common mixing of oxygenated and deoxygenated blood?

aka - breathless and blue

A
  • AVSD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

give the two main causes of outflow obstruction in a well child
aka - murmur, but asymptomatic

A

pulmonary stenosis

aortic stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

give the main cause of outflow obstruction in a sick neonate

aka - collapsed with shock, as opposed to well but with a murmur

A

coarctation of the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the features of an innoSent murmur - the 5 S’s

A 
Soft blowing 
Systolic only (not diastolic) 
aSymptomatic
left Sternal edge
normal heart Sounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

explain the normal circulatory changes that occur at birth

A

with the first breath, the resistance to pulmonary blood flow falls and the volume of blood going through the lungs increases.
leads to a change in pressure making the foramen ovale close.
the ductus arteriosus (connects pulmonary artery to aorta) will usually close within first few hours/days - some babies rely on this duct to allow mixing of the blood if they have a defect, and will rapidly deteriorate once it shuts!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

when does the foramen ovale close?

A

at first breath - resistance to pulmonary blood flow falls, volume of blood going through lungs increases, change in pressure leads to closure of foramen ovale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

when does the ductus arteriosus close?

A

within first few hours/days - babies that were relying on mixing via ductus arteriosus may rapidly deteriorate once it shuts!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what symptoms might indicate a baby is in heart failure?

A

breathlessness - especially on feeding (/exertion)
sweating
poor feeding
recurrent chest infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what signs might indicate a baby is in heart failure?

A 
failure to thrive / faltering growth
tachypnoea, tachycardia
hepatomegaly
cool peripheries
heart murmur, gallop rhythm (third heart sound)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

give some causes of cardiac failure in a neonate

A

in neonates heart failure is usually due to obstructed systemic circulation (will be duct-dependent):

  • hypoplastic left heart
  • critical aortic valve stenosis
  • severe coarctation of the aorta
  • interruption of the aortic arch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

give some causes of cardiac failure in an infant

A

in infants heart failure is due to volume overload (‘high pulmonary blood flow’):
VSD
AVSD
large PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

if you suspect a neonate/infant is in cardiac failure, what investigations would be useful?

A

CXR - expect to see enlarged heart and pulmonary congestion (useful if unsure if resp v cardio issue)
ECG
Echocardiography to determine the underlying defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

give some causes of cardiac failure in a child/adolescent (i.e. not a baby!)

A

will see R or L heart failure.
Eisenmenger syndrome (R heart failure only)
Rheumatic heart disease
Cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what causes persistent cyanosis in an otherwise well infant?

A

some kind of structural heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what (broadly) might be causing cyanosis in a newborn infant with respiratory distress?

A

cardiac - the cyanotic congenital defects
resp - surfactant deficiency, meconium aspiration, pulmonary hypoplasia
persistent pulmonary hypertension of the newborn (PPHN)
infection - septicaemia from Group B strep (+ other organisms)
metabolic diseases - metabolic acidosis and shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is persistent pulmonary hypertension of the newborn (PPHN)?

A

failure of the pulmonary vascular resistance to fall after birth - pressure in pulmonary vessels remains high, preventing blood flow and limiting oxygenation of the blood -> leads to cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what investigations might you order to distinguish between causes of cyanosis/heart failure if echo is unavailable?

A

CXR + ECG
pre and post ductal sats (a difference indicates PPHN or R->L shunting)
4 limb BP (upper and lower limbs will be different in coarctation of the aorta)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the two types of ASD?

A

most common = ostium secundum defect, high in atrial septum

must less common = ostium primum, occurs much lower - common in Downs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how do you distinguish between ASD and PFO?

A

PFO only open when atrial pressure/volume raised - present in 1/3 of kids with congenital heart disease.
ASDs are large and always open (although usually asymptomatic in childhood!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what symptoms may be seen in ASD?

A

usually none!
might get recurrent chest infections/wheeze
in 30s onwards may get arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what signs will be seen in ASD?

A

ejection systolic murmur at upper left sternal edge - increased flow across pulmonary value due to L -> R shunt
fixed and widely split S2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the key investigation for diagnosing any structural heart defect?

A

ECHO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

management of ASD

A

if large, consider surgery (when age 3-5y) - to prevent cardiac failure/arrythmias later in life.
secundum defects often closed transcatheter.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what signs/symptoms might be seen if a baby has a small VSD?

A

asymptomatic!

signs - loud pansystolic murmur at lower L sternal edge, quiet pulmonary second sound (P2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how would you investigate and manage a small VSD?

A

Ix - CXR and ECG will be normal, can be seen on echo

Rx - none, resolves spontaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what symptoms will be seen if a baby has a large VSD?

A

heart failure with breathlessness and faltering growth after 1 week old
recurrent chest infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what signs will be seen if a baby has a large VSD?

A

tachypnoea, tachycardia, enlarged liver (heart failure signs)
active precordium (excessive movement of chest wall over heart)
soft pansystolic murmur/no murmur if v large defect
apical mid-diastolic murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what CXR signs would you expect to see in a large VSD?

A

cardiomegaly, enlarged pulmonary arteries, pulmonary plethora/strong pulmonary vascular markings, pulmonary oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what ECG findings would occur in ASD?

A

RVH + incomplete RBBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what ECG findings would occur in a large VSD?

A

biventricular hypertrophy - would occur by 2 months old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

how would you manage a baby with a large VSD?

A

diuretics and ACEi for heart failure
additional feeding/calories to grow them!
medium-sized defects often spontaneously close, but if there’s still a shunt at 4 years correct surgically before school starts
large defects - surgical correction at around 3-6 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is Eisenmenger’s syndrome?

A

obstructive pulmonary vascular disease that occurs due to significant L to R shunt - the pulmonary hypertension due to the shunt leads to permanent damage of the vessels.
this can lead to pressures equalising and the direction of blood flow shifting to R to L (reversed shunting).

it’s really bad!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the ductus arteriosus and when does it normally close?
at what point would you diagnose PDA?

A

connects aorta to L pulmonary artery, normally closes by 4th day of life.
PDA diagnosed if not closed after 1 month of life.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

give 3 risk factors for a PDA

A

preterm - although this is normal due to their prematurity
Downs
high altitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

how is a persistent PDA managed?

A

risk of pulmonary vascular disease or infective endocarditis is high - so surgical closure recommended.

usually done at 1 year. if diagnosed really early, ibuprofen (or indomethacin) may help close it without surgery, but typically surgical closure needed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what clinical features would you see in PDA?

A

continuous machine murmur beneath the L clavicle.
collapsing/bounding pulse (due to wide pulse pressure)

always asymptomatic - unless really severe and then you’d get heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how is a patent PDA (due to prematurity) managed?

A

(Indomethacin inhibits prostaglandin synthesis) oral/IV ibuprofen 10mg/kg, then 5mg/kg at 24 and 48hrs old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are the four features of Tetralogy of Fallot?

A
  1. Large VSD
  2. Overriding aorta
  3. Pulmonary stenosis
  4. RV hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

how might tetralogy of fallot present?

A
  • in first 1-2 months of life with hypoxic spells OR a murmur
  • squatting on exercise in late infancy, due to hypoxic spells
  • often picked up antenatally on scans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

give the clinical signs of tetralogy of fallot

A

cyanosis ± clubbing (usually only in older kids)
loud and single S2
loud ejection systolic murmur maximal at lower L sternal edge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Delete

A 
boot shaped heart!
- RVH
- concavity on L heart border where normally the main pulmonary artery and RV outflow tract would create a convexity
- R sided aortic arch
diminished pulmonary vascular markings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how is tetralogy of fallot managed?

A

corrective surgery at 6 months - close the VSD, relieve RV outflow obstruction

if severe, may require shunt formation in the interim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is transposition of the great arteries?

A

aorta connected to R ventricle, pulmonary artery connected to the L ventricle
forms two parallel circulations, one of oxygenated blood and one of deoxygenated blood
this would be incompatible with life but defects exist allowing mixing e.g. VSD, ASD etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

how does transposition of the great arteries present?

A

profound cyanosis on first day or two of life - blue, sats <95%, collapsed
presents on day 2 due to closure of the ductus arteriosus which stops/reduces the mixing of the circulations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what signs would you see in transposition of the great arteries?

A

CYANOSIS - always.
loud S2
no murmur (unless VSD/PDA causing one)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how is transposition of the great arteries managed?

A

need to improve the mixing of circulations
prostaglandin (PG) E1 infusion to reopen ductus arteriosus
emergency balloon atrial septostomy via catheter is life-saving
corrective surgery performed at a few weeks of age (you basically just cut the great arteries and swap them over)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is a complete AVSD?

A

defect in middle of heart with single 5 leaflet valve between atria and ventricles - stretches across entire AV junction and tends to leak.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

when would most likely see a complete AVSD?

A

Downs syndrome

typically diagnosed antenatally on ultrasound.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

how does a complete AVSD present?

A

antenatally on US

cyanotic at birth, or heart failure at 2-3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

how is a complete AVSD managed?

A

diuretics/ACEis for heart failure

surgery at 3-6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is tricuspid atresia?

A

defect where only the L ventricle works - R is small and non functioning.
there’s ‘common mixing’ of oxygenated/deoxygenated blood in the L atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

how does tricuspid atresia present?

A

with cyanosis in newborn period, after the ductus arteriosus closes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how is tricuspid atresia managed?

A

surgically - palliative as there is no completely corrective surgical option

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what are the two main causes of outflow obstruction in a well child?

A

aortic stenosis, pulmonary stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is aortic stenosis (paediatric) and how does it present?

A

partly fused aortic valve leaflets.

presents with asymptomatic ejection systolic murmur at upper R sternal edge that radiates to neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

how is aortic stenosis managed?

A

if surgery needed - balloon valvotomy, possibly valve replacement in long term
before surgery/if no surgery needed, advise to avoid strenuous exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is pulmonary stenosis and how does it present?

A

partly fused pulmonary valve leaflets.

presents with asymptomatic ejection systolic murmur at upper R sternal edge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

how is pulmonary stenosis managed?

A

surgery - transvenous balloon dilatation or pulmonary valvotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what are the three main causes of outflow obstruction in a sick infant?

A

coarctation of the aorta
interruption of the aortic arch
hypoplastic left heart syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what is the general presentation of an infant unwell due to obstructive lesions?

A

really sick with heart failure and shock in neonatal period, unless lesion was diagnosed antenatally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what are the general principles of managing a neonate unwell due to obstructive lesions?

A

ABC resuscitation is key!
early prostaglandins
refer for early surgical intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what is coarctation of the aorta?

A

arterial duct tissue encircling the aorta just at the point of insertion of the ductus arteriosus - when this shuts, the aorta also constricts causing severe obstruction of LV outflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what are the clinical features of coarctation of the aorta?

A

normal exam on day 1.
then acute circulatory collapse on day 2 (after ductus closes!)
really sick baby, severe heart failure, absent femorals, severe metabolic acidosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

how is coarctation of the aorta managed?

A

once diagnosed, give a prostaglandin infusion to maintain ductal patency and transfer to cardiac centre for surgery ASAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is interruption of the aortic arch?

A

there’s no connection between proximal aorta and aorta distal to the ductus arteriosus - cardiac output relies on R to L shunt via duct.
normally a VSD as well.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

how does interruption of the aortic arch present?

A

shock as a neonate.

associated with DiGeorge syndrome (22q 11.2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

how is interruption of the aortic arch managed?

A

complete correction in first days of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what is hypoplastic left heart syndrome and how is it managed?

A

complete underdevelopment of entire L side of heart, detected at antenatal US.
surgery called Norwood procedure + further 2 surgeries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what is the only common paediatric cardiac arrhythmia?

can you name any others?

A

supraventricular tachycardia

others - congenital complete heart block, long QT syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what is supraventricular tachycardia and how does it present in children?

A

HR >220bpm, often up to 300bpm

typically asymptomatic, but infants may have heart failure - ensure an echo is done to rule out structure defects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what would you see on an ECG of a child with a supraventricular tachycardia?

A

narrow complex tachycardia - P waves discernible after QRS complex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

how is an acute episode of supraventricular tachycardia managed?

A

to restore sinus rhythm:
- vagal stimulation - ice cold compress to face, carotid sinus massage
- IV adenosine bolus - safe and effective
DC cardioversion only if the above fail.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what is rheumatic fever?

A

abnormal immune response to a preceding group A beta-haemolytic strep infection
v rare in developed world!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what are the clinical features of rheumatic fever?

A

polyarthritis, fever and malaise 2-6 weeks after pharyngeal infection.
arthritis is fleeting - lasts less than a week in individual joints (tends to affect knees and ankles)
50% of patients have pancarditis:
- pericarditis - friction rub and pericardial effusion
- endocarditis - murmurs
- myocarditis - heart failure

erythema marginatum (pink macules on trunk and limbs) = uncommon, painless, early

Modified Duckett Jones criteria used to diangose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

how is rheumatic fever managed?

A

bed rest and aspirin (suppresses fever and arthritis).

monthly IM ben pen is prophylactic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what is the main potential complication of rheumatic fever?

A

number one cause of valvular disease world wide! usually mitral valve - scarring and fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

when might you suspect infective endocarditis?

A 
children with congenital heart disease are at risk, but suspect in anyone with:
sustained fever
malaise
raised ESR
unexplained anaemia or haematuria

any kid with fever and significant cardiac murmur - think IE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

what are the clinical features of infective endocarditis?

A 
fever
malaise
anaemia/pallor
splinter haemorrhages
clubbing
neurological signs from cerebral infarct/CNS abscess
haematuria - glomerulonephritis
arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

how is infective endocarditis diagnosed?

A

combo of clinical and lab:

  • blood cultures - take 3+ within first 24h in hospital
  • echo to confirm presence of vegetations
  • raised ESR (useful for monitoring treatment)

strep viridans (alpha haemolytic strep) is most common cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

how is infective endocarditis treated?

A

high dose penicillin and an aminoglycoside - 6 weeks IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Environmental risk factors of respiratory infections in children: (3)

Personal & medical risk factors: (4)

A
  1. Parental smoking (esp maternal)
  2. Low SE status (large family, overcrowded, damp housing)
  3. Poor nutrition
  4. Male
  5. Congenital heart disease
  6. Immunodeficiency
  7. Underlying lung disease (bronchopulmonary dysplasia, CF, asthma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what are the different most common causes of a wheezy child, by age group?

A

0 - 12m = bronchiolitis
12m - 3y = viral induced wheeze
3y+ = asthma (probably)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

give the common URTIs in kids

A

common cold (coryza)
sore throat (pharyngitis, tonsillitis)
acute otitis media
sinusitis (relatively uncommon)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

A kid with URTI. What complications might they present with?

A
  • Dehydration (difficulty feeding in infants (blocked nose obstructs breathing during feed))
  • Febrile convulsions
  • Acute asthma exacerbations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what are the ‘coryzal’ symptoms?

A

clear/mucopurulent nasal discharge and nasal blockage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what viruses typically cause coryzal symptoms

A

rhinoviruses, coronaviruses, RSV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what is the clinical picture of pharyngitis and what typically causes it?

A

inflamed pharynx and soft palate, enlarged and tender lymph nodes.
usually viral - adenoviruses, enteroviruses, rhinoviruses.

older child - might by group A beta haemolytic strep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what is tonsillitis?

A

a form of pharyngitis with inflamed tonsils +/- purulent exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what are the usual causative organisms in tonsillitis? how do you distinguish between viral and bacterial?

A

typically viral (rhinovirus, coronavirus, parainfluenza etc)

might see EBV (infectious mononucleosis), group A beta haemolytic strep

hard to distinguish clinically - more severe systemic symptoms in bacterial (headache, apathy etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what treatment is often given for bacterial tonsillitis?

A

penicillin

erythromycin if allergic to penicillin
avoid amoxicillin as can cause a rash if it’s EBV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

when might you admit a patient for tonsillitis?

A

if difficulty swallowing - give IV fluids and analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what is acute otitis media and who gets it?

A

middle ear infection

most common at 6-12 months age due to their short, horizontal Eustachian tubes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what are the clinical features of acute otitis media?

A

pain in ear and fever - examine tympanic membranes of any kid with fever!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what would the tympanic membranes look like in a kid with acute otitis media?

A

bright red and bulging, loss of normal light reflection.
might see acute perforation - pus in external canal.

recurrent otitis media –> scarring of tympanic membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

give some common causative organisms of acute otitis media

A

RSV, rhinovirus, pneumococcus, H. influenza, Moraxella catarrhalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

how would you manage acute otitis media?

A

pain - regular paracetamol/ibuprofen

amoxicillin can shorten duration - prescribe, ask parent only to use if still unwell after 2-3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what is glue ear and how does it present?

A

recurrent ear infections that have led to otitis media with effusion (OME)

often asymptomatic, may have reduced hearing - usually in a 2-7yo kid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what would you see down the otoscope if a child has glue ear/OME?

A

eardrum dull and retracted, visible fluid level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

delete

A

delete

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

how is glue ear managed?

A

generally resolves spontaneously

Grommet insertion if conductive hearing loss impacting speech development/school

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what type of hearing loss is seen in glue ear?

A

conductive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

what is the clinical picture of sinusitis in a child?

A

concurrent viral URTI, possibly a secondary bacterial infection - pain/swelling/tenderness over cheek

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

how might you manage a child with sinusitis?

A

abx if you suspect bacterial cause.

analgesia, topical decongestants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

what are the characteristic features of a laryngeal/tracheal infection? what is the major risk with these?

A

stridor, hoarseness, barking cough, dyspnoea (variable degree)

risk of airway obstruction!!! DO NOT EXAMINE THE THROAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

what is stridor?

A

rasping sound, predominantly on inspiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

how do you assess degree of airway obstruction in a child with suspected croup/laryngeal or tracheal infection?

A

degree of chest retraction (none/only on crying/at rest)
degree of stridor (none/only on crying/at rest/biphasic)

DON’T EXAMINE THE THROAT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

describe the basic acute management of upper airways obstruction in a child

A
  1. DO NOT EXAMINE THE THROAT
  2. observe for signs of hypoxia or deterioration
  3. consider oral dexamethasone or budesonide nebs before adrenaline
  4. if severe, use adrenaline nebs (bleep anaesthetist in case you have to intubate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

what’s the fancy name for croup?

A

laryngeotracheobronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

explain the pathology of croup

A

mucosal inflammation and increased secretions affect the airway - subglottic area oedema is the dangerous bit that can obstruct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

what are the causative organisms of croup?

A

95% viral (parainfluenza most common, or human metapneumovirus, RSV, influenza)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

who gets croup and when?

A

kids age 6m - 6y (peak @ 2y).

typically in autumn and spring.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

how does croup present?

A

barking cough, hoarseness, harsh stridor - all worse at night.
preceded by fever and coryza.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

how do you manage a kid with croup presenting with mild obstruction, no stridor, plus chest recession?

A

home care, with close observation by parent - supportive care as it’s self-limiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

how do you manage a kid with serious croup - stridor etc

A

ITU, oral dexamethasone (squirt into mouth with syringe), nebulised budesonide (adrenaline nebs if gets v bad), possible need to intubate.

supportive care - protecting airway - as it’s self-limiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

what is bacterial tracheitis?

A

similar to croup, but bacterial - very rare but dangerous!

Staph. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

how does bacterial tracheitis present?

A

similar to croup but with high fever - child appears toxic, with rapidly progressing airways obstruction and thick secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

how do you treat bacterial tracheitis?

A

IV abx ± intubation ± ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

what is epiglottitis?

A

an emergency! caused by Hib (suspect if not up to date with imms).
swelling of epiglottis and surrounding tissues, with septicaemia.
typically age 1-6y, but can affect any age.

122
Q

how does acute epiglottitis present?

A

high fever in an unwell child. intensely painful throat - prevents child speaking and swallowing (drooling saliva). soft inspiratory stridor.
child sits immobile, upright and with open mouth to optimise airway.
minimal/no cough - contrast to croup etc

123
Q

how do you manage a child with suspected acute epiglottitis?

A

DON’T lie them down or examine the throat!!

admit to ITU - intubate under GA, then do blood cultures and start IV abx (3-5 days e.g. cefuroxime).
remove tracheal tube at 24 hours.

rifampicin prophylaxis to close contacts.

124
Q

what organism causes whooping cough?

A

Bordatella pertussis

125
Q

describe the clinical presentation of whooping cough

A

1 week of coryzal symptoms (catarrhal phase).
then characteristic paroxymal cough followed by inspiratory whoop (paroxysmal phase - lasts 3-6 weeks).

worse at night. might cough until vomit, or get epistaxis/subconjunctival haemorrhage.

symptoms gradually reduce after 3-6 weeks but can persist for months (convalescent phase).

126
Q

what would you do to confirm a case of whooping cough?

A

culture/PCR of per-nasal swab

also will see marked lymphocytosis on blood film.

127
Q

how do you treat whooping cough?

A

erythromycin - give to close contacts as well.

imms - decrease risk of getting it but also reduce severity if you do get infected.

128
Q

what age group gets bronchiolitis and when?

A

90% are aged 1-9 months.

bonfire night -> valentines day

129
Q

what is the usual causative organism of bronchiolitis? can you list some others?

A

RSV - 80%

human metapneumovirus, parainfluenza virus, rhinovirus, adenovirus, influenza

130
Q

what are the clinical features of bronchiolitis?

A

coryzal symptoms preceding a dry cough and increased work of breathing/breathlessness.
feeding difficulties with increased dyspnoea = admit.

131
Q

what would you find on examination of an infant with bronchiolitis?

A 
sharp, dry cough
tachypnoea
subcostal and intercostal recession
hyperinflation of chest - prominent sternum, liver displaced downwards.
fine end-inspiratory crackles.
high-pitched wheezes - expiratory > inspiratory.
tachycardia
cyanosis/pallor
132
Q

what investigations would you perform for an infant with suspected bronchiolitis?

A
  1. PCR of nasopharyngeal aspirate
133
Q

how would you manage an infant with bronchiolitis?

A

humidified O2 via nasal cannulae if pulse ox indicates needed.
IV fluids if needed.

most recover within two weeks - some babies will get recurrent episodes.

134
Q

what prophylaxis can you offer high-risk prem babies for bronchiolitis?

A

monoclonal antibodies to RSV (palivizumab) via monthly IM injection

135
Q

what are the common causative organisms of pneumonia in a newborn?

A

group B strep, gran -ve enterococci

136
Q

what are the common causative organisms of pneumonia in an infant/toddler?

A

RSV, strep pneumoniae, H influenzae

137
Q

what are the common causative organisms of pneumonia in a child over 5?

A

M. pneumoniae, strep pneumoniae

at any age - always consider TB.

138
Q

what are the clinical features of pneumonia in a child?

A

fever and difficulty breathing
often preceded by an URTI
cough, poor feeding, generally ‘unwell’ child.

if there’s localised chest/abdo pain => pleural irritation => bacterial

139
Q

what would you expect to see on examination of a child with a pneumonia?

A

tachypnoea

also - nasal flaring, chest indrawing, possibly end-inspiratory coarse crackles over infected area.

140
Q

how would you investigate a suspected pneumonia in a child?

A

CXR can confirm diagnosis.

NPA can detect viral causes.

141
Q

how do you manage a child with pneumonia?

A

normally home management - admit if sats <93% with severe tachypnoea, difficulty breathing and feeding.

supportive care - O2, analgesia, IV fluids.

oral amoxicillin (IV for newborns/young infants)

142
Q

what is viral-induced wheeze?

A

commonly diagnosed in “chesty” kids when they’re too young for it to be asthma - kids have got small airways that are more likely to narrow and obstruct in response to viruses/other triggers

can split into episodic viral wheeze - kid gets wheezy when they have an URTI but symptom free in between episodes. non-atopic.

and multi-trigger wheeze - wheeze triggered by smoke, exercise, cold air etc - more associated with future asthma. associated with atopy.

143
Q

delete

A

delete

144
Q

delete

A

delete

145
Q

briefly describe the pathophysiology of asthma

A

combo of triggers, atopy and genetic predisposition –> bronchial inflammation –> bronchial hyperresponsiveness –> airway narrowing –> symptoms

146
Q

what are the clinical features of asthma?

A

polyphonic wheeze.
symptoms worse at night and first thing in the morning.
symptoms appear with triggers - but may have some interval symptoms.

personal/family hx of atopy
positive response to asthma Rx

147
Q

what investigations might be performed if you suspect a child has asthma?

A

peak expiratory flow!! - peak flow diaries usually used, helps identify diurnal variation and triggers.

may also do skin prick testing for specific allergens

148
Q

a child has been diagnosed as asthmatic - what initial treatment would the GP prescribe?

A

PRN salbutamol (SABA) - if using 3+ times per week, add an inhaled corticosteroid (ICS) e.g. beclometasone as a regular preventer

149
Q

a child has been using their ICS preventer inhaler for several weeks now but still uses salbutamol about 6 times a week - what is the next step?

A

consider montelukast (leukotriene receptor antagonist).

if older, add a LABA (salmeterol, formeterol)

150
Q

an asthmatic child comes to the doctor as they’re still using their salbutamol 5 times a week - they’re using a beclomethasone regular preventer and salmeterol - they’ve noticed some improvement since the salmeterol.

next step?

A

raise dose of ICS (beclomethasone).

as long as responding to LABA, keep that on.

if you hadn’t already added, montelukast could be trialled now.
need to refer for asthma specialist.

151
Q

an asthmatic child has been referred to your clinic as they’re using their salbutamol inhaler 8 times a week despite being on the max appropriate doses of PRN salbutamol, regular preventer (ICS, beclomethasone) and montelukast

next step?

A

oral steroids, on lowest feasible dose.

152
Q

what are the key principles behind moving patients up/down the asthma treatment guidelines?

A

move up if using PRN inhaler 3+ times per week.

if asthma well-controlled, always try to step down to see if they can remain symptomless on less treatment.

153
Q

describe the management of an acute asthma attack

A

OSHITME:

Oxygen - 15L 100% nonrebreathe
Salbutamol nebs
Hydrocortisone IV
Ipratropium
Theophylline
Magnesium sulphate
Escalate, consider ITU

give oral pred 3-5 days after acute attack

154
Q

what is the most common reason a child hasn’t seen an improvement in their asthma symptoms after starting a new inhaler?

A

they’re not using it right! always check inhaler technique

155
Q

list some environmental & medical causes of recurrent cough in a child

A
  1. recurrent resp infections
  2. post-specific resp infection e.g. pertussis
  3. persistent endobronchial infection
  4. asthma / CF / TB
  5. recurrent aspiration ± GORD
  6. inhaled foreign body
  7. active/passive smoking
156
Q

what is the mode of inheritance/genetic mutation for cystic fibrosis?

A

autosomal recessive
mutation in the cystic fibrosis transmembrane conductance regulator gene (CFTR) on chromosome 7 - codes for a cyclic AMP-regulated sodium/chloride channel

157
Q

describe how CF affects the airways

A

reduction in airway surface liquid layer leads to impaired ciliary function and retention of mucopurulent secretions.

also get chronic infection with pseudomonas aeruginosa

158
Q

what pathogens commonly affects CF patients

A

pseudomonas aeruginosa

  1. Can be very hard to get rid off - used to have CF parties in the past
  2. Staph Auerus also (may take prophylactic flucoxiccilin)
159
Q

how does CF affect the digestive tract?

A

intestines - thick viscous meconium produced, leads to meconium ileus
pancreas - ducts become blocked, leads to pancreatic enzyme deficiency and malabsorption

160
Q

how are most CF cases identified in the UK?

A

the Guthrie (heel prick test)

161
Q

what diseases does the Guthrie/heel prick test assess for?

A

sickle-cell
congenital hypothyroidism
CF
~~~
Inherited metabolic diseases:

galactosemia
branched chain ketonuria
MCADD
phenylketonuria

~~~

162
Q

describe the clinical features of CF

A

chronic infections (pseudomonas/staph aureus/H influenzae) due to viscous mucus in small airways –> leads to damage of bronchial wall, bronchiectasis and abscess formation –> persistent loose cough, producing purulent sputum

90% will have pancreatic exocrine insufficiency as well

163
Q

describe how pancreatic exocrine insufficiency affects people with CF

A

present in 90%
deficient in lipase, amylase and proteases
leads to maldigestion and malabsorption
leads to failure to thrive, passing of frequent large pale and offensive stools (steatorrhoea)

164
Q

delete

A

low faecal elastase

165
Q

how might neonates present with CF?

A

meconium ileus - intestinal obstruction - vomiting, abdo distension etc

166
Q

what 3 diagnostic tests are used in CF?

A
  1. Newborn blood spot testing
  2. Gold Standard: SWEAT TEST - salty sweat! raised Na+
  3. Genetic testing for CTFR mutations
167
Q

what are the 5 principles of managing a CF patient?

A
  1. Chest physiotherapy (clear mucus, reduce risk)
  2. Exercise
  3. High calorie diet (due to malabsorption)
  4. CREON Tablets (replace lipase)
  5. Prophylactic fluclox
168
Q

how do manage CF, from a respiratory perspective?

A

PHYSIO - exercises to be done at least twice a day, helps to clear secretions.
regular lung function tests.
prophylactic oral abx (fluclox) and rescue abx as required.
hypertonic saline/nebulised DNAse may help.

end stage = bilateral lung transplant.

169
Q

how do you manage CF from a nutritional perspective?

A

oral enteric coated pancreatic replacement therapy.
high kcal diet (150% of RDAs)
fat soluble vitamin supplements.
screen for impaired glucose tolerance once they reach adolescence.

170
Q

how does periorbital cellulitis present?

A

fever with erythema, tenderness and oedema of eyelid - usually unilateral.
might follow local trauma or spread from a paranasal sinus infection.

171
Q

how do you manage a child with periorbital cellulitis?

A
  1. Refer to hospital JIC orbital cellulitis
  2. prompt IV abx to prevent progressing to orbit (would then have proptosis, painful/limited occular movement, reduced visual acuity)
172
Q

what is strabismus/squint?

A

when one eye is misaligned in relation to another

affect 2-3% of children in UK

173
Q

what is the most common type of childhood squint?

A

Congenital/infantile squint - most commonly an esotropia (convergent squint).
develops within the first six months of life and is usually idiopathic in a child with otherwise normal health.

174
Q

why do squints develop?

A

because there is lack of coordination which prevents the gaze of both eyes being directed at the same point in space

175
Q

give some causes of a squint

A

Idiopathic.
Refractive errors, especially hypermetropia.
Other causes of poor visual acuity in one or both eyes - incl congenital cataract and retinoblastoma.
Neurodevelopmental conditions and syndromes.
cranial nerve palsies, brain lesions and muscle diseases - rare in kids.

176
Q

how might a squint be managed?

A

Glasses to correct any refractive error.
Occlusion therapy to treat amblyopia (lazy eye - eye patch)
Surgery (or in some cases injection of botulinum toxin) to correct misalignment of eyes.

treatment basically helps correct or reduce squint. in some, normal vision can be restored.

177
Q

what’s the difference between regurgitation and posseting?

A

posseting is the return of small amounts of milk with burps/wind
regurgitation is larger more frequent loss
both are ‘non-forceful’ return of milk (differs from vomiting)

posseting is normal, regurg might mean GORD

178
Q

what would bile-stained vomit in a child indicate?

A

intestinal obstruction

179
Q

what might haematemesis in a vomiting child indicate?

A

oesophagitis, peptic ulcer, oral/nasal bleeding

teenagers - mallory-weiss tears (drinking/bulimia)

180
Q

what might projectile vomiting in first few weeks of life indicate?

A

pyloric stenosis

181
Q

what might abdo distension in a vomiting child indicate?

A

obstruction - including strangulated inguinal hernia

182
Q

what might blood in the stool of a vomiting child indicate?

A

intussusception, gastroenteritis (salmonella/campylobacter)

183
Q

what might failure to thrive in a vomiting child indicate?

A

reflux, coeliac disease, other chronic GI conditions

184
Q

define gastro-oesophageal reflux - what causes it? why is it common in infants?

A

the involuntary passage of gastric contents into the oesophagus

due to inappropriate relaxation of the lower oesophageal sphincter (LOS) due to functional immaturity

common as infants have a fluid diet, are horizontal most of the time, and have a short intra-abdominal oesophagus

185
Q

what’s the usual prognosis of GORD in an infant? when might you be more worried?

A

usually resolves by 12 months of age - they then have an upright posture, matured LOS and more solid diet!

worry if - failure to thrive (due to severe vomiting), oesophagitis, aspiration

186
Q

what investigations would you do if you suspected GORD in an infant?

A

usually none - clinical diagnosis

COULD do - 24h oesophageal pH monitoring, endoscopy with oesophageal biopsies

187
Q

how would you manage GORD in an infant? give answers for mild vs more significant

A

mild - reassure, add thickener (E.g. carobel), hold upright after feeds

significant - ranitidine (H2 receptor blocker) or gaviscon (omeprazole, PPI)

if no response - consider cow’s milk protein allergy

188
Q

what is pyloric stenosis and how does it typically present?

A

hypertrophy of pyloric muscle causing gastric outlet obstruction

presents at 2-7 weeks old, boys > girls

189
Q

what are the clinical features of pyloric stenosis?

A

vomiting that increases in frequency and forcefulness over time, becoming projectile in nature.

initially hungry after vomits, but might become dehydrated and lose interest in feeds.

will see weight loss if delayed presentation.

190
Q

how would you go about diagnosing pyloric stenosis?

A

give a test feed of milk, will calm them to allow examination
might see visible gastric peristalsis across abdomen.
olive sized mass in RUQ - pyloric mass.

USS if in doubt.

191
Q

how would you treat a baby with pyloric stenosis?

A

IV fluids - rehydrate, correct electrolyte disturbance.

pylomyotomy - open/laparoscopic - division of hypertrophied muscle down to mucosa.

192
Q

what are the symptoms of acute appendicitis in a child?

A

anorexia, vomiting, abdo pain (central and colicky then localised to RIF

v. uncommon if <3 yrs

193
Q

what are the signs of acute appendicitis in a child?

A

low grade fever
abdo pain aggravated by movement
persistent tenderness with guarding of RIF (McBurney’s point)

194
Q

what is intussusception and what age group does it usually affect?

A

invagination of proximal bowel into a distal segment - usually ileum passing into caecum through the ileocaecal valve

3 months - 2 years

195
Q

what are the possible complications of intussusception?

A

stretching and constriction of mesentery, resulting in venous obstruction –> engorgement and bleeding from bowel mucosa –> fluid loss, bowel perf, peritonitis, gut necrosis

need prompt diagnosis, immediate fluid resus and urgent reduction!!

196
Q

how does intussusception present?

A

paroxysmal severe colicky pain and pallor - during pain episodes, baby becomes pale and draws up legs
refuse feeds, may vomit (might be bile stained depending on site of intussusception)
sausage shaped mass in abdomen
redcurrant jelly stool - blood stained mucus
abdo distension and shock

197
Q

how would you manage an infant with an intussusception?

A

immediate IV fluid resus
XR abdo / USS (more useful than XR)
interventional radiology - rectal air insufflation

25% will require surgery - if air insufflation unsuccessful or signs of peritonitis

198
Q

what is Meckel’s diverticulum and how does it present?

A

small bulge in the small intestine present from birth - remnant of the omphalomesenteric duct - contains ectopic gastric mucosa or pancreatic tissue.
mostly asymptomatic - might have severe rectal bleeding (somewhere between bright red and malaena)

199
Q

how is Meckel’s diverticulum diagnosed and treated?

A

shows up on Technetium scan - technetium picks up gastric mucosa so shows up as spot on the scan.

treatment is surgical resection

200
Q

what happens in malrotation of the bowel?

A

during rotation of small bowel, if the mesentery isn’t fixed at the duodenojejunal flexure or in the ileocaecal region then the rotation goes wrong - end up with a shorter base and predisposition to volvulus

201
Q

how does a child with malrotation of the bowel present? how should they be managed?

A

obstruction with bilious vomiting, usually in first few days of life.

needs urgent surgery + pass an NG tube

202
Q

what is abdominal migraine?

A

bit of a vague ‘diagnosis’ of recurrent abdo pain - might be associated with headaches.
midline abdo pain w/vomiting and facial pallor + personal/family hx of migraine.

203
Q

what are the 3 ‘symptom constellations’ (?) you might see in a child with recurrent abdo pain lasting at least 3 months?

A

IBS - by far most common
peptic ulcer/functional dypepsia
abdominal migraine

204
Q

what are some characteristic symptoms of IBS in a child?

A

abdo pain worse before/relieved by defecation
explosive, loose or mucus-y stools
bloating
feeling of incomplete defecation (tenesmus)
constipation - that might alternate with normal/loose stools

205
Q

explain how you’d differentiate between peptic ulcer and functional dypepsia in a child

A

do a 13C breath test to check for h pylori
treat with PPI + h pylori eradication if indicated
failure to respond to this = upper GI endoscopy
if that’s normal = functional dyspepsia

206
Q

what is the most common cause of gastroenteritis in children? name a couple of others

A

rotavirus

adenovirus, norovirus, bacterial (much less common)

207
Q

name some bacterial causes of gastroenteritis in children

A 
Campylobacter jejuni
Shigella
Salmonella
Cholera
E. Coli
208
Q

how would a child with gastroenteritis due to camylobacter typically present?

A

severe abdo pain + diarrhoea

209
Q

how would a child with gastroenteritis due to shigella or salmonellae typically present?

A

dysentery type picture - blood and pus in stool, pain, tenesmus

210
Q

how would a child with gastroenteritis due to cholera or E coli typically present?

A

profuse and rapidly dehydrating diarrhoea

211
Q

what is the concern with a child with gastroenteritis?

A

dehydration –> shock

212
Q

what factors increase a child with gastroenteritis’s risk of dehydration?

A
  • infant, especially if <6 months or low birthweight (greater insensible fluid loss + greater basal fluid requirements
  • 6+ diarrhoeal stools in prev 24h
  • vomited 3+ in prev 24h
  • unable to tolerate (or not been offered) extra fluids
  • evidence of malnutrition
213
Q

list the components of a dehydration assessment in a child

A
  • general appearance
  • level of consciousness
  • skin colour - pale, mottled
  • pale extremities
  • sunken eyes
  • dry mucous membranes
  • tachycardia, tachypnoea, low BP
  • peripheral pulses
  • cap refill time (should be < 3s)
  • skin turgor
  • sunken fontanelle
214
Q

what investigations might be done for a child with gastroenteritis?

A

if septic, blood/mucus in stool or immunocompromised - do a stool culture.
might check U&Es and glucose
if start abx - should do blood cultures first

215
Q

how would you manage a child with gastroenteritis?

A
  • encourage oral fluids
  • dioralyte - little and often
  • consider NG dioralyte if refusing orally
  • if shocked give fluid resus
  • IV fluids - replace deficit, plus maintenance
  • gradually introduce usual foods after recovery
  • don’t return to school/childcare for 48h, encourage handwashing
  • anti-diarrhoeals and abx rarely used
216
Q

briefly describe the pathology of coeliac disease

A

immune system overreacts to the gliadin bit of gluten - causes damage to the villi of the proximal small intestine - increased cell loss from villous tips, eventually end up with a flattened mucosa

217
Q

describe the classical presentation of coeliac disease in a child

A

8-24 months - after weaning onto wheat-containing foods.
Failure to thrive, abnormal stools, buttock wasting and general irritability.

but - children are more likely to present less acutely, later in childhood

218
Q

how is coeliac disease diagnosed?

A

serology for IgA tissue transglutaminase antibodies + endomysial antibodies

small intestinal biopsy - increased intraepithelial lymphocytes and villous atrophy, plus crypt hypertrophy

plus - symptoms go away when you withdraw gluten, and they catch up on growth!

219
Q

how is coeliac disease managed?

A

gluten free diet - involve dietician

monitor growth

220
Q

how does Crohn’s disease present in a child?

A
  • growth failure, delayed puberty
  • general ill health - fever, lethargy, weight loss
  • random signs - oral lesions, perianal skin tags, uveitis, arthralgia, erythema nodosum
  • classical stuff - abdo pain, diarroea, weight loss
221
Q

what might you find on blood tests of a child with Crohn’s disease?

A

raised ESR and CRP
iron-deficient anaemia
low albumin

222
Q

how does Crohn’s affect the bowel?

A

usually the distal ileum and proximal colon
initial areas of acutely inflamed, thickened bowel - then you get strictures and fistulas between loops of bowel and skin/other organs

223
Q

how is Crohn’s definitively diagnosed?

A

endoscopy + biopsy - shows non-caseating epitheliod cell granuloma

224
Q

how would you induce and maintain remission from Crohn’s disease in an infant?

A

nutritional therapy - whole protein modular feeds (polymeric diet) for 6-8 weeks

systemic steroids if that doesn’t work.

to maintain remission - immunosuppressants (azathioprine, methotrexate)

225
Q

describe the characteristic presentation of ulcerative colitis?

A
  • rectal bleeding, diarrhoea, colicky pain
  • may get weight loss/growth failure
  • erythema nodosum, arthritis
226
Q

how would you diagnose UC in a child?

A

endoscopy and biopsy - after excluding infectious causes

you would see continuous colitis from rectum, extending proximally - mucosal inflammation, crypt damage and ulceration

227
Q

describe the management of UC in children

A

induction and maintenance of remission with aminosalicylates (mesalazine), topical steroids.
if more severe - azathioprine, systemic steroids.

really severe - colectomy with ileostomy or ileorectal pouch.

228
Q

define constipation

A

decreased frequency or increased pain on defecation

229
Q

list some causes of constipation in babies that should be considered

A

Hirschprung’s disease, anorectal abnormalities, hypothyroidism, hypercalcaemia

also - dehydration, decreased oral intake, anal fissure (causes pain)
in older children, could be an issue with toilet training / stress

230
Q

what would you find on the abdominal examination of a constipated child?

A

hard palpable mass, often in a well child

231
Q

what might happen if a child has long-standing constipation?

A

rectum becomes over-distended, lose feeling of need to defecate - may have involuntary soiling as contractions of full rectum inhibit internal sphincter (overflow, may be diarrhoeal)

232
Q

describe the management of a child with constipation

A
  • reassure and explain
  • evacuate overloaded rectum - use Movicol (macrogol laxative, contains polyethylene glycol and electrolytes) - escalating dose until impaction resolves and then maintenance
  • add stimulant laxative if needed (e.g. sodium picosulphate)
  • ensure sufficient fluids, high fibre diet and encourage child to sit on toilet after meals (physiological gastrocolic reflux)
  • star charts!
233
Q

what is hirschsprung’s disease?

A

congenital abnormality involving abnormal innervation of large bowel - absence of parasympathetic ganglion cells in rectum (may extend to colon).
results in constantly constricted colon - functional obstruction at birth.

234
Q

how does Hirschsprung’s disease present?

A

failure to pass meconium within 24h of birth - abdo distension and bile-stained vomiting develops

235
Q

how is Hirschsprung’s disease diagnosed and treated?

A

rectal biopsy - absence of ganglion cells in mesenteric plexus, plus presence of acetylcholinesterase-positive nerve trunks

treatment - surgery - affected sections of bowel removed and ends are anastomosed.

236
Q

what is infantile colic?

A

baby has recurrent episodes of inconsolable crying + drawing up of legs - usually from around 2 weeks old -> 4 months.
no treatment or anything - just differentiate from cow’s milk protein allergy and GORD - movement can help soothe.

237
Q

define failure to thrive

A

poor weight gain in infancy - falling across centile lines

238
Q

what can cause failure to thrive?

A

global main cause is poverty.

feeding technique can be an issue - check latching, teat of bottles etc. be on look out for evidence of maltreatment, NAI etc.

also - organic causes - coeliac, cow’s milk protein allergy, etc etc etc

239
Q

what is the anatomical cause of inguinal hernias in babies/children?

A

patent processus vaginalis (passage which ushers the descending testicle into the scrotum)

240
Q

If a baby presents with a bulge lateral to pubic tubercle during crying, what is the likely cause and how should it be managed?

A

inguinal hernia - repair promptly - six/two rule:
< 6 weeks = operate within 2 days
< 6 months = within 2 weeks
< 6 years = within 2 months

241
Q

what is “toddler’s diarrhoea” and what causes it?

A

most common cause of persistent loose stools in a well and thriving preschool child - maturational delay in intestinal motility causes intermittent explosive loose stools (often with undigested vegetables in it - grim) - thought to be to do with dodgy diet - aim for high in fat (whole milk), normal (not high) fibre, not loads of fruit juice

242
Q

what is cow’s milk protein allergy?

A

usually transient intolerance to cow’s milk in babies - colic symptoms, GORD, diarrhoea (±blood/mucus), failure to thrive

243
Q

how do you manage a child with suspected cow’s milk protein allergy?

A

if exclusively breastfed - get mum to cut out cow’s milk

if bottle - hypoallergenic formula (hydrolysed or amino acid)

244
Q

what causes Kwashiorkor, how does it present and how would you manage it?

A

low intake of PROTEIN and essential amino acids - malnutrition
signs - poor growth, diarrhoea, apathy, anorexia, oedema, skin/hair depigmentation, distended abdomen.
Rx - gradually increasing high-protein diet + vitamins

245
Q

what is marasmus and how does it present and how would you manage?

A

lack of CALORIES + discrepancy between height and weight. associated with HIV.
signs - distended abdomen, diarrhoea, constipation, infection, low albumin.
parenteral nutrition to rehydrate and restore renal function. then balanced diet with vitamins.
head circumference and stature may remain poor.

246
Q

what is biliary atresia/how does it present?

A

rare but serious. apparently healthy babies with jaundice, yellow urine and pale stools - either destruction/absence of extrahepatic biliary tree.
persistent jaundice from day 2 after birth, predominantly conjugated hyperbilirubinaemia.
spleen palpable in week 3 or 4.

247
Q

how is biliary atresia managed?

A

surgery - OK prognosis with early referral but late presentation means will need liver transplant by 1 year old.
refer all term babies jaundiced beyond 2 weeks!
US can be helpful for diagnosis.

248
Q

what are the two main (rare but treatable) causes of persistent obstructive neonatal jaundice?

A

biliary atresia and choledochal cyst

249
Q

choledochal cysts - what are they, symptoms, management

A

congenital cysts on the bile duct - cause neonatal obstructive jaundice persisting for >14 days, enlarged liver.
Rx - surgical excision

250
Q

what is meningitis?

A

inflammation of the meninges covering the brain.
raised WCC in CSF.
usually viral but can be bacterial.

251
Q

what is bacterial meningitis?

A

bacterial infection of meninges following bacteraemia.
damage caused due to host response instead of organism itself –> inflammation mediators, activated leukocytes, endothelial damage –> raised ICP, cerebral oedema, reduced cerebral blood flow

252
Q

give some causes of bacterial meningitis

A

pathogens carried in nasal passages, invade meninges via bloodstream.
over 50% are meningococcal - Group B most common variety, vaccinated in childhood imms (MenB).

neonates - 3 months:
Group B strep, E coli, listeria monocytogenes

1 month - 6 yrs:
neisseria meningitidis
streptococcus pneumoniae - quite rare
haemophilus influenzae type B - rare due to HiB vaccine.

> 6 yrs:
N. meningitidis, Strep pneumonia

253
Q

give some causes of viral meningitis, how does it present compared to bacterial and how is it diagnosed?

A

enteroviruses, HSV, VZV
usually less severe than bacterial.
confirmed by PCR of CSF (there’s also specific changes to sugar/protein levels in CSF I think?)

254
Q

what are the clinical features of meningitis?

A

can be non-specific - irritability, poor feeding, vomiting, fever, drowsiness.
purpuric rash (non-blanching - glass test) if meningococcal sepitcaemia - bad news!
bulging fontanelle in infants
neck stiffness and photophobia in older kids
seizures - be careful diagnosing febrile convulsions.

255
Q

what investigations should be performed if you suspect a child has meningitis?

A

LP - examine CSF, PCR, MC&S
blood cultures and PCR before start abx
throat/nasal swabs

NB - LP contraidicated if signs of raised ICP, coagulopathy or sepsis

256
Q

how would you manage a child with bacterial meningitis?

A

cefotaxime or ceftriaxone.

if in community and child has purpuric rash - give IM benzylpenicillin and transfer urgently to hospital

give prophylactic rifampicin (or ciprofloxacin/ceftriaxone) to contacts - eliminates nasopharyngeal carriage

Passmed: >3mth = cef’. < 3mth = IV amoxicillin + iv cef’

Steroids if bacterial - dexamethasone

257
Q

give some complications/sequelae of meningitis

A

sensorineural deafness, subdural effusion, cerebral oedema, local vasculitis, cerebral infarcts (seizures), hydrocephalus, cerebral abscess

258
Q

what pathogens typically cause periorbital cellulitis?

A

staph aureus, group A strep

H. influenzae if young/unimmunised

259
Q

describe the transmission of chicken pox

A 
Varicella Zoster (VZV) infection - highly infectious vis droplet transmission, direct contact or contact with soiled materials.
average incubation period = 14 days.
infectious from 2 days pre rash --> all lesions encrusted.
260
Q

what are the clinical features of chicken pox?

A

preceded by short period of coryza, then itchy vesicular rash - starts on head and trunk then spreads out over 3-5 days.
in immunocompromised kids can get a secondary staph infection of vesicles.

261
Q

how is chicken pox diagnosed?

A

clinical diagnosis.

can isolate virus from vesicular fluid if needed but don’t normally bother.

262
Q

how is chicken pox managed?

A

usually symptomatic.
if immunocompromised - IV acyclovir or varicella zoster Ig (this is also given to new babies if mum has VZ or herpes in 7 days before/after birth, plus any exposed premature babies).
might also use valcyclovir in adolescents/adults - disease is much more severe than if they’d contracted in childhood.

263
Q

describe the transmission of glandular fever/infectious mononucleosis

A

Epstein-Barr Virus.
droplet transmission or directly via saliva (kissing disease).
most people asymptomatically infected in childhood. symptomatic infection is most common in adolescents.
incubation period 30-50 days

264
Q

what are the clinical features of glandular fever?

A

fever, malaise, pharyngitis, cervical lymphadenopathy.

might see petechiae on palate, sparse maculopapular rash.

265
Q

how is glandular fever diagnosed and managed?

A

clinical diagnosis usually

heterophil antibody test (Monospot test) - NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm.

management is symptomatic.

266
Q

what is Kawasaki’s disease? why is it important?

A

uncommon systemic vasculitis occurring in kids age 6m - 4 yrs.
important because they are at high risk of developing coronary artery aneurysms afterwards - early recognition is important.

267
Q

what are the clinical features of Kawasaki’s disease?

A

prolonged fever and rash is the general gist.

Fever >5 days, plus 4 of 5 out of:

  • conjunctival infection
  • mucous membrane changes - pharyngeal injection, red dry cracked lips, strawberry tongue
  • cervical lymphadenopathy
  • rash
  • extremities - red and oedematous, then peeling
268
Q

how would you manage a child with Kawasaki’s?

A

single dose of IVIG plus high dose aspirin, continued at low dose for 6-8 weeks.

refer for echocardiography monitoring - coronary artery aneurysm formation, usually occurs in first 4-6 weeks of illness - repeat echos at intervals throughout next year.

269
Q

what causes primary immunodeficiency? when should you consider it?

A

uncommon - X linked or autosomal recessive disorders e.g. SCID.
consider if they have SPUR infections - Severe, Prolonged, Unusual or Recurrent

270
Q

how would you investigate and manage a child with a possible primary immunodeficiency?

A

start investigations with FBC and serum Igs

management involves antibiotic prophylaxis, Ig replacement therapies, bone marrow transplants, gene therapy (SCID)

271
Q

give some causes of secondary immunodeficiency

A

drugs - cytotoxic agents (e.g. chemo), steroids

another disease - intercurrent infection, malignancy, HIV, nephrotic syndrome

272
Q

what causes measles?

A

infection with a single-stranded RNA virus (Morbillivirus)

not vaccinating kids!
highly infectious, transmitted by droplet spread, incubation period 10 days.

273
Q

describe the clinical features of measles

A

fever, cough, coryza and conjunctivitis - then Koplik’s spots (white lesions) on buccal mucosa (pathognomic, but only present in some cases).
3 or 4 days later - erythematous maculopapular rash which becomes blotchy and confluent.

CCCK

274
Q

how would you manage a child with measles?

A

diagnosis confirmed by specific IgM in serum samples taken 3 days after rash appeared - notifiable.
symptomatic treatment.
need to be off school for a week after appearance of the rash.

275
Q

what are some complications that might occur in a child with measles?

A

acute - febrile convulsions, otitis media, tracheobronchitis, pneumonia.

rarely - severe encephalitis. 40% of these will have neurological sequelae.

276
Q

what is rubella?

A

aka German measles.
infection with rubivirus.
MMR vaccine!
mild childhood disease, only important re. maternal infection and congenital rubella

277
Q

what are the clinical features of childhood rubella (i.e. not congenital)?

A

often subclinical.
incubation period of 14-21 days, low grade fever, then pink-red maculopapular rash - starts on face and spreads over whole body - but only lasts a couple of days.

278
Q

how would you diagnose and treat childhood rubella?

A

clinical diagnosis.
can detect rubella IgM in saliva if necessary.
supportive treatment.
MMR vaccine! live attenuated vaccine.

279
Q

what is congenital rubella?

A

occurs when mother is infected with rubella during pregnancy - extend of foetal damage is determined by its gestational age at onset - in first 8-10 weeks risk is hight, beyond 18 weeks risk is minimal.

280
Q

what features might a baby affected by congenital rubella have?

A

deafness, congenital heart disease, cataracts.
hearing impairment is the main thing really - sensorineural deafness.
also - growth retardation, heaptosplenomegaly, retinopathy, glaucoma.

281
Q

how would you manage a pregnant woman with exposure to rubella?

A

test for antirubella IgG and IgM - vaccinate after delivery.

can offer termination if highly likely woman is infected in first 8-10 weeks.

282
Q

what is erythema infectiosum?

A

slapped cheek disease.
infection with parvovirus B19 - DNA virus.
transmitted via respiratory secretions, from mother to fetus or by contaminated blood products.

283
Q

what are the clinical features of slapped cheek disease/erythema infectiosum? how is it diagnosed/managed?

A

often asymptomatic.

fever, then a week later red appearance on face, progresses to symmetrical lacy rash on extremities and trunk.
Dx - clinical
Rx - supportive

284
Q

what is staphylococcal scalded skin syndrome? how is it treated?

A

life-threatening, toxin mediated manifestation of localised skin infection.

epidermolytic toxins produced by bacteria cause blistering (disruption to epidermal granular cell layer) - appearance of scalding.
Rx - IV flucloxacillin and pay attention to fluid balance

285
Q

what is scarlet fever?

A

occurs in kids with streptococcal pharyngitis - organism (group A strep) produces a toxin which causes characteristic rash - widespread, erythematous rash starting on trunk that becomes puncatet and desquamates after 7-10 days.

286
Q

what are the clinical features of scarlet fever?

A
  • tonsillitis
  • strawberry tongue
  • palatal petechiae
  • fever
  • rash - widespread, erythematous, starts on trunk, becomes punctate and desquamates after 7-10 days
287
Q

how do you diagnose and treat scarlet fever?

A

clinical diagnosis - can isolate streptococcus from a throat swab if needed
Rx - penicillin or erythromycin.

288
Q

how does TB present in kids?

A

kids <4 y more at risk of disseminated disease e.g. TB meningitis, bone TB etc.

main symptoms of active TB included prolonged cough, weight loss, anorexia, fever

289
Q

how is TB tested for?

A

Mantoux test.
culture is ideal but hard to get from kids - early morning gastric washings.
on XR - consolidation, hilar/mediastinal lymphadenopathy

290
Q

how is TB treated?

A 
6 months of 4 drugs - RIPE
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

last two just for first two months.

BCG given to immigrants from countries with high incidence, contacts of TB, babies in certain parts of country with high TB.

291
Q

what are the four common nematodes affecting children?

A
  • enterobius vermicularis - threadworm
  • ascaris lumbricoides - roundworm
  • ancylostoma duodenale - hookworm
  • toxocara canis
292
Q

how does threadworm present? how do you diagnose/treat?

A

v common in preschool - faecal oral transmission. eggs laid in perianal area at night, causes scratching, eggs then carried under fingernails to the mouth - autoinfection.

present with perianal pruritus and vulvovaginitis.
diagnosis - apply sellotape to perianal region in morning and look for eggs on it with magnifying glass.
Rx - two doses of piperazine two weeks apart, or single dose of mebendazole for kids >2 years.

293
Q

describe the transmission of polio?

A

enterovirus with three antigenic types.
faecal-oral transmission, incubation period of 7-21 days.
exists only in a few countries now - vaccination working towards eradication woo!

294
Q

what are the clinical features of polio infection?

A

90% asymptomatic.
some have minor illness - fever, malaise, headache.
some have CNS involvement / paralytic polio - virus attacks anterior horn cells of spinal cord leading to paralysis.
notifiable disease.

295
Q

how is HIV transmitted to children? how is it diagnosed?

A

vertical transmission - intrauterine, intrapartum or via breastfeeding.
if current treatment given, vertical transmission occurs in < 1%.

newborns to HIV-infected mothers will have circulating maternal HIV abs until 15-18 months - so can’t diagnose based on antibodies till after this.
at < 18 months - HIV viral cultures (gold standard but not available widely) or PCR for viral genome.

296
Q

describe the clinical manifestation of HIV in kids?

A

incubation period from infection to disease is shorter in perinatally affected kids than for adults - but treatment has reduced mortality and hospital admissions.

they get lots of infections, lymphadenopathy, hepatosplenomegaly, failure to thrive/wasting, encephalopathy, severe bacterial infections and weird opportunistic infections etc etc

297
Q

how is paediatric HIV managed/prevented?

A

antiretroviral treatment once symptomatic/low CD4 count.
lots of psychological treatment for child, mum and rest of family.

prevention - zidovudine given during pregnancy and delivery, then to neonate in first weeks, reduces risk of vertical transmission. birth via C section recommended unless maternal viral load is low.

298
Q

what is hand, foot and mouth disease and what is the most common viral cause?

A

disease beginning with fever, irritability, malaise, then you get rash on palms/soles of feet and around mouth.
Coxsackie A16 - transmitted by nasopharyngeal secretions.
symptomatic treatment only.

299
Q

what are the features of a life-threatening asthma attack?

A 
92 33 CHEST
sats < 92% 
PEFR < 33% predicted
Cyanosis
Hypotension
Exhaustion - "reduced/poor respiratory effort"
Silent chest
Tachypnoea

also altered consciousness, agitation

300
Q

what are the features of a severe asthma attack?

A

SpO2 < 92%
PEFR 33-50% predicted
Too breathless to talk or feed / can’t complete full sentences (once at talking age!)
Heart rate > 140/min if age 2-5y, >125 if >5yrs
Respiratory rate > 40/min (2-5y), >30 (>5y)
Use of accessory neck muscles

301
Q

what rash might you see on the shins in association with streptococcal infections?

A

erythema nodosum - tender, erythematous, nodular lesions

3a 2023 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions