Brainscape's Knowledge GenomeTM

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


See full index

Year 5 😊✌🏼 > Paeds > Flashcards

Paeds Flashcards

1
Q

Risk factors for meconium aspiration syndrome

A

post-term
maternal HTN
maternal PE
chorioamnionitis
smoking
substance abuse

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

Is trimethoprim safe during breastfeeding?

A

Yes

Trimethoprim passes into breast milk in small amounts and is unlikely to cause SE in your baby.

Over long time it may affect your baby’s folic acid levels. If you need to take trimethoprim for longer than a few weeks, talk to your doctor or pharmacist.

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

Name innocent murmurs found in childhood

A

Ejection murmurs (turbulent BF at the outflow tract of the heart)

venous hums (due to turbulent BF in the great veins returning to the heart; continuous blowing noise heard just below the clavicles)

Still’s murmur (low-pitched sound heard at the lower left sternal edge)

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

peak incidence of ALL

A

2-5 yo

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

Cyanotic congenital heart disease - when is it TGA and when TOF?

A

presenting in…
first days of life -> TGA
at 1-2 months -> TOF

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

What type of medication is dosulepin?

A

TCA

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

Which TCAs are more and which ones are less sedative?

A

More:
- amitriptyline
- clomipramine
- dosulepine
- trazodone (tricyclic related antidepressant)

Less:
- imipramine
- lofepramine
- nortriptyline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

causes of increased nuchal translucency?

A

Down’s syndrome
congenital heart defects
abdominal wall defects

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

features of foetal alcohol syndrome

A

flat philtrum
microcephaly
underdeveloped jaw
short palpebral fissure
thin vermillion border/hypoplastic (thin)upper lip
learning difficulties
cardiac malformations
epicanthic folds
growth retardation

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

when is CVS performed? When is amniocentesisi performed?

A

CVS: 11w - 13+6

Amnio: 15w +

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

Features of Edward syndrome

A

trisomy 18 (second most common autosomal trisomy)

  • micrognathia
  • low-set ears
  • rocker bottom feet
  • overlapping of fingers
  • heart/lung abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mx of meconium aspiraton syndrome

A

Born @ term with MSAF, clinically well, no hx of GBS -> observations, routine care, no abx needed

Born through MSAF + RFs + tachypnoea in the delivery room
-> can be mild, moderate or severe (latter 2 should be managed in tertiary care)
-> will include observation, monitoring sats, blood gases, FBC, CRP, blood cultures
- if needed abx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

mild MAS mx

A

= <40% oxygen for 48h

monitor blood gas and sats
monitor FBC and CRP, blood culture
nutritional support
abx only if RFs present

does not need to be in tertiary care centre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

moderate MAS mx

A

manage in tertiary care centre

= >40% oxygen for > 48h

CPAP
monitor ABG, dual O2 sats
FBC, CRP, blood culture
IV fluids
abx (IV ampicillin and gentamicin)
vent support if O2 requirement >60%

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

severe MAS mx

A

= need for assisted ventilaion

manage in tertiary care centre

PPHN +/-
monitor ABG, BP, dual o2 sat
FBC, CRP, blood culture
cardiac echo
work up for sepsis
start abx
nutritional support
inhaled NO for PPHN

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

What is PPHN?

A

persistent pulmonary HTN of newborn

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

Which abx would you give in MAS?

A

IV ampicillin AND gentamicin

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

Form or resp support in MAS

A

O2 therapy and non-invasive ventilation (e.g. CPAP) may be used in more severe cases

boluses of surfactant and inotropes given in moderate cases

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

Timing of onset of IgE and non-IgE cow’s milk protein allergy

A

IgE: within minutes (up to 2h) of ingestion

Non-IgE: 2-72h of ingestion

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

how common is cow’s milk protein allergy

A

affects 5-15% infants

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

Mx of cow’s milk protein allergy

A

breastfeeding: mum should avoid cow’s milk products (note it takes 2-3 weeks to eliminate cow’s milk from breastmilk)

formula: switch to hypoallergenic formula

consider calcium + vit D supplementation

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

how long does it take to eliminate cow’s milk from breastmilk?

A

2-3w

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

When should you refer a child with cows milk protein allergy to A&E?

A

if CVS / respiratory signs are present

anaphylaxis

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

Where should you refer children with CMA?

A

allergy testing and paediatric dietician (if IgE mediated is suspected or if non-IgE is severe)

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

What is severe non-IgE CMPA?

A

if measures taken for mild/moderate have not been effective and are severe

Sx to look out for:
- Skin: pruritus, erythema, atopic eczema
- GI: GORD, vomiting, loose stools, bloor or mucous in stools, abdominal pain or discomfort, infantile colic, food refusal or aversion, constipation, perianal redness, pallor or tenderness, faltering growth
- Resp: cough, wheeze, SoB

26
Q

Mx of IgE mediated CMPA

A

mild:
- excl BFing: mum to exclude milk products, take caclium and vit D
- if formula/mixed feeding, try extensively hydrolysed formula
- refer to allergy testing at specialist and a paediatric dietician

severe:
as above plus: consider elemental (amino acid) formula if extensively hydrolysed not effective
- ref to A&E is resp/CVS sx present as there is a risk of anaphylaxis

27
Q

Mx of non-IgE mediated CMPA

A

Mild:
- exclusively BFing:
exclude milk products from mum’s diet for 2-4w followed by home reintroduction to confirm dx (mum to take calcium and vit D supplementation)
-mixed/formula feeding: trial of extensively hydrolysed formula

(be wary of making this diagnosis as vomiting and diarrhoea are quite common)

severe:

28
Q

Mx of non-IgE mediated CMPA

A

Mild:
- exclusively BFing:
exclude milk products from mum’s diet for 2-4w followed by home reintroduction to confirm dx (mum to take calcium and vit D supplementation)
-mixed/formula feeding: trial of extensively hydrolysed formula

(be wary of making this diagnosis as vomiting and diarrhoea are quite common)

severe: sx not improving despite measures and are severe.
-> continue mx as per non severe
-> urgent referral to local paeds allergy service
-> urgent referral to dietician

ADVISE COW’S MILK FREE DIET UNTIL CHILD IS 9-12 MONTHS AND FOR AT LEAST 6 MONTHS IF NON-IgE MEDIATED ALLERGY IS CONFIRMED.

-> then commence milk ladder (available from allergy UK) to see if tolerance is acquired.

29
Q

Another term for non-IgE CMPA?

A

delayed CMPA

30
Q

Summarise the milk ladder

A

1) starts with wellcooked (baked) milk products (form of milk least likely to cause an allergic reaction; also flour binding with the baked milk makes it less allergenic. heating -> protein is changed into a less allergenic form)

2) then lightly cooked milk products (less baked) or heated milk products without flour are given

3) uncooked fresh milk can be tried when recommended.

31
Q

How should you monitor children (weaned infants/older children) affected by CMPA?

A

exclude CMP from their diet
offer nutritional counselling and paediatric dietician
regularly monitor growth
re-evaluate child every 6-12 months (incl. re-intorduction of milk using the milk ladder)

32
Q

How should you monitor children (weaned infants/older children) affected by CMPA?

A

exclude CMP from their diet
offer nutritional counselling and paediatric dietician
regularly monitor growth
re-evaluate child every 6-12 months (incl. re-intorduction of milk using the milk ladder)

33
Q

What can be heard in PDA?

A

continous machniery like murmur

left subclavicular thrill

34
Q

What are the symptoms of Rheumatic Fever>

A

remember: JONES criteria

J = Joints (migratory polyarthritis)
♥ = Pancarditis
N = Nodules
E = Erythema marginatum
S = Sydenham chorea

35
Q

What is rheumatic fever?

A

two to four weeks after an untreated infection with group A Streptococcus (GAS)

The pathogenic mechanisms that cause RF are not completely understood, but molecular mimicry between streptococcal M protein and human cardiac myosin proteins is thought to play a role.

36
Q

1st and 2nd line management of croup

A
  1. single dose oral dexamethasone 0.15 mg / kg

If oral not possible:
- IM dexamethasone 0.6 mg / kg
-inhaled beclomethasone 2 mg

37
Q

Supportive management in croup

A

analgesia and antipyretics (paracetamol/ibuprofen)
advice fluid intake

supplement oxygen if needed

nebulised adrenaline 1:1000 1 mg/ml if severe

Intubation rarely needed

38
Q

What are indications for admission in croup

A
  • oxygen requirement
  • features of moderate or severe illness
  • impending resp failure
  • RR > 60/min
  • toxic appearance
  • also consider admission in children with mild illness who have a lower threshold for admission (e.g CLD, hemodynamically significant heart disease, immunodeficiency, age under 3 months, inadequate fluid intake, factors affecting carer’s abilities and longer distance to healthcare in case of deterioration)

find out abo

39
Q

What virus causes croup and at what time of the year

A

Parainfluenza virus is responsible for 75% cases

most common in fall and winter.

40
Q

What is the abnormality in osteogenesis imperfecta?

A

-> brittle bone disease, increased risk of fractures (type of skeletal dysplasia)

mutations in type I collagen lead to impaired osteogenesis (various genetic defects can lead to OI)

there are 2 types:
- type I is more common and milder
- type II is more severe and usually fatal in the 1st year of life

41
Q

How is osteogenesis imperfecta diagnosed?

A

DNA test

USS before birth and radiographic skeletal survey afterwards (to visualise fractures, causes, deformities)
Bone or skin biopsy to examine collagen

42
Q

Mx of osteogenesis imperfecta

A

no definitive treatment available

supportive measures: walking aids, wheelchairs, devices to improve mobility and function

bisphosphonates to increase cortical thickness and decrease # risk

surgery to improve mobility and correct associated skeletal defects

43
Q

Prevalence of osteogenesis imperfecta

A

1/10.000-20.000

1:1 m:f

44
Q

what is the life expectancy with osteogenesis imperfecta?

A

with mild forms -> normal

with very severe form (type 2) usually lethal in the first year of life

45
Q

Inheritance pattern of osteogenesis imperfecta

A

AD is most common but cam also be AR

46
Q

What are the features of osteogenesis imperfecta?

A

short stature
triangular face appearance
blue sclera
deafness (affected ossicles)
dentinogenesis imperfecta
scoliosis
frequent fractures
bone deformities
tendon instability
ligamentous laxity and joint hyper mobility

remember BITE: bones, I (eye - blue sclerae), teeth (dental abnormalities), Ears (hearing loss)

47
Q

How common is achondroplasia?

A

1:15.000 - 40.000

48
Q

what mutation is responsible for achondroplasia?

A

gain of function mutation in fibroblast growth factor receptor 3 gene on Chr 4

-> new sporadic mutations in ~80% (probability increases with the father’s age at the time of conception)

49
Q

What is the underlying pathophysiology in achondroplasia?

A

defective FGFR3 mutation -> inhibited chondrocyte proliferation -> endochondral ossification -> impaired longitudinal bone growth

50
Q

Outline the P-GALS assessment

A
  1. screening Qs
  2. Inspection
  3. Gait
  4. arms
  5. legs
  6. spine

also TMJ

51
Q

What Cobb angle is seen in scoliosis?

A

> 10 degrees

52
Q

what is scoliosis?

A

deformity of the spine
occurring during growth
characterised by a lateral curvature and simultaneous rotation of the vertebrae

53
Q

what gender is more affected by scoliosis?

A

females > male in idiopathic adolescent scoliosis

juvenile and infantile idiopathic scoliosis is more common in males.

54
Q

What is the management of SA in children?

A

2 weeks of IV flucloxacillin

followed by 4 weeks oral flucloxacillin

review by orthodontist, may need washout of the joint

55
Q

Causes of septic arthritis

A

haematogenous spread (most common)

direct contamination (iatrogenic, trauma)

Contiguous spread (septic bursitis, osteomyelitis)

56
Q

Management of scoliosis

A

referral to paeds ortho

  • back brace
  • PT
  • surgery may be indicated in some severe, rapidly progressing cases
57
Q

What is calculated in ?scoliosis?

A

Cobb’s angle

58
Q

What investigation for scoliosis?

A

X-ray spine

59
Q

What antibodies could be seen in someone with coeliac disease and IgA deficiency?

A

IgG

anti-tTG and anti-endomysial

60
Q

Antibiotiv options in whooping cough

A

ACE

azithromycin used if >1 month (for 21d)
Clarithromycin used if <1month
Erythromycin used if pregnant

can use co-trimoxazole if macrolides are contraindicated (but not in pregnancy or if <6 weeks old)

61
Q

What is the full name of GTN?

A

glyceryl trinitrate

Year 5 😊✌🏼 (53 decks)

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