Brainscape's Knowledge GenomeTM

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


See full index

Phase 3a > PAEDIATRICS > Flashcards

PAEDIATRICS Flashcards

1
Q

Describe the different levels of neonatal respiratory support

A
  1. Non-invasive
    - Incubator oxygen - ambient
    - High flow oxygen (nasal cannula - humidified if >2L/min)
    - cPAP (continous positive airway pressure) this prevents the lungs collapsing, but supports spontaneous ventilation
    - NIPPV (nasal intermittent positive pressure ventilation) this is cPAP but with intermittent ventilator breathing at a set pressure
  2. Invasive ventilation (endotracheal tube)
    - volume targetted ventilation
    - high frequency osscilation ventilation
    - synchronised intermittent mandatory ventilation (dont use with prem, risk of Intraventricular haemmorhage)
  3. Surfactant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Signs of neonatal respiratory distress syndrome

A

Tachypnoea
Increased work of breathing (recessions, nasal flaring, grunting)
Cyanosis

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

Complications of cPAP and invasive ventilation in neonates

A

Pneumothorax
Bronchopulmonary dysplasia
Tracheomalacia (invasive ventilation)

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

What should be given to neonates that have been receiving ventilation for 8 days to prevent bronchopulmonary dysplasia.
What needs to be monitored with this medication.
When is this contraindicated.

A

Dexamethasone.

BP should be monitored, as steroids increase BP.
CI if on NSAIDs.

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

What is the cause of RDS in premature neonates

What is the cause in term babies

A

Prem babies - under developed dense lungs.

Term babies - deficiency in protein surfactant B

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

What long term condition can neonates on oxygen and ventilation therapy develop and why
What are the features on a CXR

A

Bronchopulmonary dysplasia
Because of pressure & volume insult to the lungs from mechanical ventilation
And, oxygen toxicity
And, sometimes infection

Both of above cause injury to lungs - inflammation/ repair - leads to decreased alveolarization and vascularisation. Get large simplified alveoli + dysmorphic pulmonary vasculature

CXR see widespread opacification (consolidation from scarring), lung hyperinflation, sometimes cystic changes (large alveoli)

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

List some of the side effects of oxygen therapy to be considered when prescribing for neonates

A

Bronchopulmonary dysplasia
Convulsions
Retinal damage (retrolental fibroplasias - vasoconstriction of retinal vasculature because of high oxygen)
Infection (drying of mucosa & secretions)
Atelectasis

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

What is a blood profile worrying for kernicterus

A

Very high unconjugated bilirubin

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

List the differential diagnosis & investigations for a baby that developed jaundice hours after borth

A

Haemolytic disease of the newborn - coombs test, group & save, cross-match blood, LFTs
Infection - Congenital CMV, Hepatitis, GBS & Sepsis: full septic screen including viral serology
Inherited causes - gilberts, crigler-najjer. Family Hx, LFTs

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

List the differential diagnosis & investigations for a baby that has developed jaundice 5 days after birth

A

Physiological jaundice
Breast feeding jaundice
Dehydration

Bloods: FBC, LFTs including bilirubin, treat according to level of unconjugated bilirubin & monitor every 6 hours until you know the level is falling

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

List the differential diagnosis & investigations for a term baby that developed jaundice 3 days after birth and is still affected at 1 month

A

GIO-HBD
Genetic - gilberts, C-J etc. Bloods- LFTs, look for raised conjugated bilirubin profile
Infection - UTI, hepatitis etc (bloods, & urine microscopy)
Obstruction - biliary atresia - imaging & raised conjugated blood profile
Hypothyroid - TFT
Haemolytic causes - still consider this in case missed?
Breast feeding - by exclusion
Dehydration - clinical exam, feeding hx, calculate infants fluid requirements & compare

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

What is the treatment for haemolytic disease of the newborn

A

Phototherapy, IVIG, exchange therapy if needed

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

What is the pathology of haemolytic disease of the newborn

A

Mum is Rh -ve
Baby is Rh +ve

Can be other causes between mum & baby blood groups

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

How long after birth should a newborn take their first breath

A

6 seconds

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

How long after the first breath should a newborn establish breathing

A

30 seconds

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

What are the causes of failure to establish breathing in term neonate

A

Continuous birth asphyxia
Traumatic birth
Maternal analgesic/ anesthetic
Congenital malformations that interfere with breathing

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

List some of the common causes of birth asphyxia

A

Placental abruption

Cord prolapse

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

Outline the steps in neonatal resuscitation

When would you begin this

A

Floppy newborn, no first breath (10 seconds), or gasping

1.Clean, dry, heater
2.Suction mouth and nose, tactile stimulation
ASSESS - chest movement, HR >100
3.Mask ventilation - 5 inflation breaths (2-3 seconds each - be careful not to do breaths too quickly bc can then fill stomach with air)
Start with ambient (21%) oxygen
ASSESS
If HR >60 and movement of chest wall - continue, with escalating O2 if needed.
If HR >60 but no chest wall movement - intubate
4. Intubation and artificial ventilation
5. If HR <60, chest comparessions
Central below nipple line. 3:1.
6.If not responding, consider drugs, adrenaline etc

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

What should you be continuously monitoring during neonatal resuscitation

A

Chest wall movement
Heart rate
Oxygen saturation
Colour

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

What are the normal physiological mechanisms that support the first breath

A
  1. Labour - initiates resorption of lung fluid
  2. Birth canal - pushes fluid out of lungs = decreased intrathoracic pressure and lowers pulmonary vascular resistance
  3. First breath - clears final bits of fluid. Increases oxygen tension - this causes DA to close.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

If a term floppy baby starts having seizures what are you concerned about and what is the management

A

Asphyxia and HIE

cooling - heaters off during resuscitation

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

What is the difference between gastroschisis and exomphalos, how do differences effect management

A

Both ventral wall defects
Gastroschisis - lateral folding does not complete by end of week 4. This leaves a ventral wall defect where the bowel is exposed and grows into amniotic cavity. Because ventral wall hasn’t fused, the bowel only has visceral peritoneum covering it. Water and fluid loss here when born - must wrap in cling film to prevent this.

Exomphalos - lateral folding completes. Week 6 physiological herniation of the bowel into umbilical cord happens (bc liver grows and no space for bowel). By week 10 it should retract back into abdominal cavity. If it does not get exomphalos. Because bowel is covered, heat and water loss not as much of a problem as with gastroschisis, but still needs to be kept warm and be monitored for fluids. Associated with more congenital defects.

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

What are the main concerns regarding exomphalos

A

Genetic defects and syndromes

High mortality rate (15%)

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

Why is green bilious vomitting in a newborn a medical emergency

A

Sign of small bowel obstruction

If the cause is a volvulus, this can lead to gut death within 6 hours and baby can die. Surgical emergency.

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

List some of the common GI malformations in neonates

A

Oesopheal atresia (tracheo-oeosophgeal fistula)
Pyloric stenosis (projectile vomit)
Duodenal atresia (bilious vomiting if above sphincter of oddi)
Jejunal atresia
Ileial atresia
Malrotation (and volvulus)
Hirschsprungs disease
Anorectal atresia (rectal-bladder, urethre fistula, rectal-vaginal fistula)

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

What gut malformation is associated with downs

A

Duodenal atresia (1/3 have downs)

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

Causes of congenital hypothyroid

A

Maldescent of thyroid (from base of tongue to larynx)
Hypohormonogenesis (inbuilt error of hormone synthesis)
Panhypopituitarism
Iodine deficiency
Hashimotos thyroiditis

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

Complications of congenital hypothyroid

A

Learning difficulties

Neurodevelopment delay

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

Management of congenital hypothyroid

A

Life long thyroxine

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

What is the normal physiology of the thyroid gland during pregnancy

A

B-HCG stimulate TS receptors
Also get increase in thyroid binding globulin
= increase in Total T4 and T3 (not free T4 or T3)

First trimester increased physiological thyroid requirement.
Autoimmune status usually decreases during pregnancy (meaning some Graves patients may be able to come off meds entirely)
Hashimotos need regular monitoring and thyroxine adjustments during first trimester so that increased thyroid levels are met

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

What are the risks to the fetus with a mother with Graves

A 
Thyrotoxicosis 
Thyroid storm - tachy, AF
Miscarriage 
Prem labour
Small for dates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How would you manage a neonate with suspected thyrotoxicosis (mum is known to have Graves)

A

Bloods:
Cord blood or infant blood - measure TSH, total t4 and t3, TSA
If confirmed by bloods can start on carbimazole and BB

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

How would you manage a neonate with hypoglycaemia

A

Regular blood sugar monitoring (must be >2.6)
Regular feeds (1 hourly)
If not correcting, IV dextrose

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

Causes of neonatal hypoglycaemia

A

Gestational diabetes
SGA (underdeveloped liver - low glycogen stores)
Prem baby (as above)

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

Signs of hypoglycaemia in neonate

A

Jittery, irritability, lethargy, drowsiness, seizures

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

What do you need to rule out in a child with constipation before you start movicol

A

Intestinal obstruction

Movicol is contraindicated with this

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

When is clean prep used and what is it

A

Used before colonoscopy

It is a very high dose of movicol (110 g, normal sachet dose in paeds 6g)

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

Outline the management of chronic constipation and prevention of fecal impaction in children

A
  1. Osmotic laxitives
    Lactulose, movicol (increasing doses, depending on age). Can have treatment (2-6 sachets) and maintenance doses (2-4)
  2. Disimpaction regime
    Movicol up to 8-12 sachets over 12 hours depending on age of child.
  3. Possibly clean prep - if need to have colonoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What can you prescribe for children with urinary incontinence at night

A

Desmopressin (Anti diuretic hormone)

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

Outline the different assessment you would do in children with a suspected UTI

A

<3 months: MSU + USS - paeds management
3 - 6 months: no focus - dipstick + MSU. Focus but not resolving - dipstick + MSU. If typical UTI, USS within 6 weeks
6 months+: no focus - dipstick + MSU. Focus but not resolving - dipstick + MSU. No need for USS unless atypical.

Refer to paeds for any atypical UTI.

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

What assessment should all children with a fever under 3 months get

A 
Septic screen 
Bloods - inflammatory markers + CRP, blood culture
LP
MSU + USS
CXR (sometimes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

List some features of an atypical UTI in children

A 
Recurrent 
Systemic features 
Unusual pathogen 
Does not respond to UTI
FHx of GU abnormality/ renal disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What imaging investigations are done with children with atypical UTI

A

USS - structure of GU tract
DMSA - renal scarring
MCU - emptying and reflux

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

What concerns are there about infants and children who get UTIs

A

Veso-uteric reflux
Renal scarring & damage
Renal disease as adult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

When should you do urinalysis in a child >3 months with a fever

A
  1. If no source of infection

2. If source but not responding to treatment

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

What conditions can present with a measles rash

A 
Measles
Rubella 
Roseola infantum 
Scarlet fever
Kawasaki disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What prophylactic antibiotic coverage is used in CF patients with pseudomonas aeruginosa

A

Azithromycin

Tobramycin in acute

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

Outline the management of CF

A

Respiratory: Regular physio
Inhalers - bronchodilators (salbutamol), steroids (corticosteroids, prednisolone), mucolytics (saline neb), anti-inflammatories (azithromycin)
Pancreas: enteric coated pancreatic enzymes, high calorie diet (150%), fat soluble vitamins
Acute management: coverage for gram positive and negative organisms, and pseudomonas aeruginosa coverage

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

What is a common pathogen that CF patients need ABx coverage for

A

Pseudomonas

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

What medication can be given to infants with bronchiolitis with immunodeficieny

A

Ribavirin (anti-viral against RSV)

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

What can be used to prevent RSV bronchiolitis in children with CF

A

Palivizumab

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

What is the management of bronchiolitis

A

Oxygen therapy (correct sats, >92% acceptable)
Hydration - may need NG tube
cPAP if respiratory distress not managed with O2
Can use neb steroids and adrenalin if severe but not routinely
Ribavirin for immune compromised, and those with underlying lung or heart disease

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

What are the indications of admission in an infant with bronchiolitis

A

Hypoxemia
Respiratory distress
Feeding difficulties

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

What are the RFs, signs and symptoms of bronchiolitis

A

Age - most common in 3-6 months old, but consider in any <2s
November - May - seasonal
Prematurity / Bronchopulmonary dysplasia
Exposure to second hand smoke
Signs/ symptoms: increased WOB (nasal flaring, grunting, recessions), hypoxaemia, tachypnoea, wheeze, difficulties feeding, preceeding by corzay symptoms, cough, crackles.
Check throat to exclude bacterial infection.

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

What are the differentials for bronchiolitis

A

Pneumonia, Bacterial bronchiolitis, viral induced wheeze

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

How long does bronchiolitis last

A

10-14 days acute illness, cough and wheeze may persist for weeks after this

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

What investigations should you do for bronchiolitis

A

Pulse oximetry
Can do ELISA testing for viral antibody but not often
If severe:
Chest XR if considering pneumonia (heard crackles on chest, but bronchiolitis can look like pneumonia on CXR sometimes), also to look for lung collapse, pneumothorax
Blood gases if concerned about respiratory failure

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

What are the differentiating factors between bronchiolitis and pneumonia

A

Temperature - higher in pneumonia >40
No wheeze in pneumonia
CXR focal consolidation would suggest pneumonia

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

What is HSP

A

Immune related vasculitis. Can be chemical (drug) or infection related. Often follows URT strep infection.

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

What should you rule out in a child with erythematous swelling around one eye

A

Probably peri-orbital cellulitis, want to rule our orbital cellulitis. Can do this clinically by checking visual acuity in both eyes, pain with eye movements and proptosis. Must do CT scan to confirm if infection is in orbital space.

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

What can cause periorbital cellulitis

Why is it an emergency

A

Sinusitis
Dental infection
Some trauma to skin around eyes
Emergency as it can cause orbital cellulitis and that can cause blindness

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

What is meningococcal disease, what are its two manifestations

A

N meningitidis
Meningococcal septicaemia
Meningitis

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

What is the difference in management and treatment of an ill child under 5

A

Antibiotics
Investigation and empirical treatment
Newborns - benpen and gent
Newborn - 3 months - cefotaxime and amoxicillin
3 months plus - cefotaxime only
Investigate and empirically treat all under 3 month olds with any red flags
Investigate and empirically treat all over 3 month olds with any red flags - meningococcal disease, shock, unrousable
?investigations and treatment in over 3 months old in amber/ green categories only

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

What is a port wine stain, how does it look

A

Capillary malformation. Permanent. Usually flat red mark at birth, can develop lumps in it and have cobble stone appearance.
Describe as red naevus (birthmark)
Unusally physically benign but may cause cosmetic concerns
If on forehead, scalp or around eye - need to consider Sturge-Weber syndrome
If around eye can also increase risk of glaucoma
Post wine stain on the back can be linked to spina bifida

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

What is a haemangioma, what are the different types and what is the difference in prongosis

A

Vascular tumour.
Congenital - present from birth. Some of these dont have a shrinking stage. Some will disappear by 18 months.
Infantile - develop in first few weeks of life. These disappear by 4 years.
Only need to be concerned if near eye or airway.

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

If you need to treat a haemangioma, what would you use

A

Beta blockers

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

How many cafe au lait spots are suggestive of NFT1

A

5 or more

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

Is there ever an indication to treat milia

A

If it is severe and you think there is a risk of a staph aureus infection

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

What is erythema toxicum

A

Benign neonatal rash. No treatment.
Macular rash with white spot in middle.
Its an indication of immune system development/ activation.

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

What are your main differentials for a maculopapular rash

A

Viral:
Measles (koplick spots; CCCK)
Rubella (no koplick spots, possibly no cough)
Rosela infantum (petichae on uvula, forchheimer)
Possibly smallpox - this is more of a papular rash on extremities
Possibly Mumps - in small number of cases

Bacterial:
Beginning of menigococcal rash can be maculopapular
Kawasakis disease (staph or strep) can have a maculopapular rash

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

What signs/ features help you to differentiate between different causes of a maculopapular rash

A 
Onset pattern - head to trunk (measles, rubella), trunk first (scarlet fever)
Other symptoms (pharengitis - Scarlet fever, koplick spots, any red flag features for meningococcal disease, unrousable, fatigued etc, vesicular rash hand foot and mouth - enterovirus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What questions should you always ask in any acutely sick child

A 
Activity level:
Feeding/ drinking
Urine output 
Irritable/ restless
Lethargy/ sleeping more 
Unrousable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the differentials for a peticheal / pupuric rash

A

Meningococcal disease

HSP

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

What symptoms distinguish viral from bacterial pharengitis

A

Cough
Cervical Lymphadenopathy
Fever
Tonsillar exudate

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

What is acute rheumatic fever

A

Autoimmune disease that follows Group A strep infection

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

What first line investigations should you do for a child with ?HSP

A

Urinalysis - dip and MSU - look for RBC, protein, cast cells
24 hours protein - look for proteinuria - sign of nephrotic syndrome
Higher the proteinuria the greater the risk of nephritis
2nd line invx- serum creatine and electrolytes
IgA, coagluation, renal biopsy, USS

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

What are the manifestations of HSP

A

Skin - urticarial then maculopapular then petechial rash
Abdomen - coliky pain
Joints - arthralgia, swelling
Kidney - micro/ macroscopic haematuria, nephrotic syndrome

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

What is the treatment of HSP

A

Usually resolves on its own within 4 weeks
Only treat with steroids if severe abdo pain, vomitting, nausea, or if nephrotic/ nephritic syndrome. If renal function declining can step up to high dose immunosuppressants and plasmapheresis.

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

Which post-infectious rashes are treated with steroids or ivigs

A

Kawasakis (Ig cross reacts = vasculitis) - IVIg
HSP (Ig deposits) - steroids
No rheumatic fever - steroids and IVIg not found to help

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

What is the management of rheumatic fever

A

Analgesics for arthralgia
ACE inhibitors and diuretics for carditis
Possibly surgery for carditis
IVIg may help with chorea but not first line at moment

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

What is a kerion

A

Allergic reaction to fungus on scalp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the features of candida nappy rash

A

Skin fold inclusive

Satellite pustules / spots beyond main rash

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

What are the differentials for a napkin rash

A 
Atopic dermatitis (skin fold sparing, scalded red)
Candida infection (skin fold including)
Seborrhoeic dermatitis (look for cradle cap)
Psoriasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the treatment for candida nappy rash

A

Nappy free time
Emollient/ barrier - sudocrem
Can use topical antifungal clotrimazole, and 1% hydrocortisone if necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the treatment for atopic dermatitis nappy rash

A

Nappy free time
More regular nappy change/ time without nappy
Emollient/ barrier cream - sudocrem

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

What are some differentials for ringworm (tinea corporis)

A

Granuloma annulare - this does not have a scaly eddge/ any dry skin like ringworm does. May take years to go. No treatment. Cause not well understood.

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

How would you describe the various tinea rash’s (fungal skin infections)

A

Corporis - annular (O shaped), expands peripherally with central clearance. Dry, scaly skin. Raised, scaly border.
Capitis - annular lesion, hair loss. May have kerion - red inflammation - reaction of immune system to fungal infection.
Pedis - athletes foot
unguium - fungal nail infection. Yellow brittle toe nail. Treatment must continue to 3-4 months until all infected portions of the nail have grown out.
Must take sample and do culture to confirm.
Can treat with topical antifungal - in children this should be clotrimazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

How is oral thrush in newborns treated

A

If mild, no treatment needed. Should pas in a few days.
If not passed after 7 days, can try oral miconazole gel.
RF for oral thrush - mum on abx, more candida from breastfeeding.
Baby can pass thrush to mum via breastfeeding.

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

What is the main complication of congenital toxoplasmosis infection

A

Long term neurological disability
Retinopathy
Can have blueberry muffin rash

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

What are the causes of reflux in infants

A

Underdeveloped sphicter, does not relax properly and close
Lay flat most of the day and after feed
Large abdomen

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

What are the common causes of regurgitation/ vomitting in infants

A

reflux

over feeding

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

What are the uncommon causes of regurgitation/ vomitting in infants

A

Pyloric stenosis
Infection - urine, respiratory, gastroenteritis
Intestinal obstruction

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

What are the common causes of vomitting in children

A

Infection - gastroenteritis, resp, whooping cough, UTI, meningitis, appendicitis
Anatomical - obstruction, strangulation, pyloric stenosis, hirschsprungs disease
Raised ICP
Food intolerance - cows milk, coaeliac

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

What investigations would you consider for a child presenting with vomitting

A 
urine MCS
Abdominal XR if ?surgical/ anatomical cause 
USS if ?surgical/ anatomical cause 
Bloods - FBC, CRP if ?infection
MRI ?tumour
LP if ?meningitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the common causes of acute abdominal pain in children

A

Medical:
Gastro - constipation, IBD, gastroenteritis
Other infections - UTI, pyelonephritis, hepatitis, Respiratory infection/ lower lobe, TB
Infection + = HSP
Bleeding - Sickle cell, HSP
Metabolic - DKA,
Gynae

Surgical:
Appendicitis, intestinal obstruction, malrotation (infant presentation), testicular tortion, hernia, meckels diverticulitis, trauma

Other: hip & spine

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

Investigations for acute abdominal pain

A

Urine dip + MCS
Abdominal XR
Bloods - FBC, CRP (if ?infection)
Blood sugars - DKA

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

What are some red flag features associated with acute abdominal pain in children and what do they mean

A

Bilious vomiting - intestinal obstruction
Redcurrent jelly stool - intussusception
Vomitting - any infection, appendicitis, UTI, resp
Fever - any infection

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

List some useful signs to elicit on examination in a patient with acute abdominal pain

A 
Fecal mass - constipation 
Sausage mass - intussuseption 
Right iliac fossa pain - appendicitis 
Hernia 
Loin tenderness - pyelonephritis 
Suprapubic pain/ tenderness - UTI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What tests should you do in children with appendicitis to check about peritonitis

A

Ask if its painful when they jump, cough or laugh

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

What is mesenteric adenitis

A

Non-specific abdominal pain resulting from swelling of mesenteric nodules, accompanied by respiratory tract infection and cervical lymphadenopathy
Diagnosis can only be made on laparotomy/ laparoscopy
Can present similarly to appendicitis

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

What are the symptoms of appendicitis

A

Anorexia
Vomitting
Abdominal pain, central then localises to RIF
Pain aggrevated by movement - walking, coughing, jumping
Tenderness/ guarding RIF, mcburney’s point
Flushes face with oral fetor
Low grade fever 37.2 - 38

Absence of cough and polyuria

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

How do you diagnose appendicitis in children

A

Tests and imaging not very reliable
It is a progressive condition, regular monitoring and clinical review every few hours will enable diagnosis.
Can do abdo XR, bloods (raised neutrophils), USS, but all can be normal and still have appendicitis.
If child can sit up unsupported and hop, appendicitis is unlikely.

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

What investigation should you do for any child with dark green billious vomitting

A

Urgent upper GI contrast to assess for intestinal malrotation - unless vascular compromise

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

What is malrotation when does it usually present

A

Usually first few days of life

Can present later as volvulus

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

What are the clinical features of malrotation

A

Green bilious vomitting
Abdominal pain
Tenderness from peritonitis or ischemic bowel

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

How can meckles diverticulum present

A

Rectal bleeding or intestinal obstruction

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

What investigations should you do for a child with suspected coeliacs disease

A

Bloods - FBC, signs of anaemia and malabsoption
Coeliac Serology- anti-TTG, and anti-endomysial antibodies
Endoscopy - look for villous atrophy

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

What are the symptoms of coaeliacs disease

A 
Abdominal pain 
Abdominal distension
Diarrhoea 
Failure to  thrive, short stature
Anaemia 
Fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the different types (causes) of diarrhoea

A

Secretory (infection, water secreted into lumen)
Osmotic (malabsorption, food allergy, milk)
Inflammatory (IBD)
Motility (IBS, endo - thyroid)

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

When are investigations indicated in a child with diarrhoea, what investigations would you do

A

Blood or mucus in stool
Any suspicion that they are septic
Would do stool sample and bloods if suspect sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is the management of infective diarrhoea in children

A

Only treat with abx, if abnormal/ nasty pathogen (c diff, psuedomonas, shigella), dont treat common bacterial infections eg campylobacter, salmonella with abx.
The main treatment is dehydration assessment and fluid support - maintenance and deficit replacement.

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

What are the different thresholds for fluid deficit

A

<5% - no signs of clinical dehydration
5-10% - signs of dehydration but not shock
>10% - signs of shock

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

List some examples of how you assess dehydration in children

A 
Conscious level 
Urine output
Skin colour 
Skin turgor 
Extremities 
Eyes
Mucous membranes
Heart rate 
Breathing 
Peripheral pulses
CRT
Blood pressure 
Fontanelle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What is post-gastroenteritis syndrome

A

When a child gets diarrhoea after reintroducing normal diet. It is caused by post-infection intolerance. Usually resolves if you treat diarrhoea again with fluids and reintroduce, but some continue to have food intolerance long term.

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

How much milk should a newborn baby have

A

150-200 ml per kg of their weight
14-22 oz of formula milk for day, extra oz per month. eg 1 month 1, 2 month 2, 3 month 3, 4 month 4 etc

You can start by offering your baby 1 to 2 ounces of infant formula every 2 to 3 hours in the first days of life if your baby is only getting infant formula and no breast milk. Give your baby more if he or she is showing signs of hunger. Most infant formula-fed newborns will feed 8 to 12 times in 24 hours.

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

What is toddlers diarrhoea

A

Very common. Diarrhoea in toddler, no systemic symptoms, thriving.
Due to increased gut motility.
Manage with reducing fruit and fibre, higher fat diet.
Sometimes loperamide in extreme cases.

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

What are some of the causes of abdominal distension in children

A

Air - obstruction, malabsorption
Ascites - liver, kidney, hypoproteinaemia
Solid masses - neuroblastoma, Wilm’s, adrenal tumour
Cysts’ - polycystic kidney, hepatic, dermoid, pancreatic

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

What investigations should you do for IBD

A 
CRP
ESR
FBC
Albumin
Acid glycoprotein 
Definitive diagnosis is endoscopy/ colonoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is the management of IBD in children

A

Polymeric diet
Steroids if ineffective
Can use other immunosuppresants such as methotrexate, azathioprine if needed to prevent
remission
Anti-TNF when conventional methods have failed

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

What is the most common cause of solid tumour in under 5s

A

Neuroblastoma

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

What are the causes of hepatomegaly in children

A

Malignancy - leukaemia, neuroblastoma
Metabolic - hurlers
Other blood - sickle cell and haemolytic anaemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What are the causes of splenomegaly in children

A

Malignancy - leukaemia
Metabolic - hurlers
Other blood - sickle cell and haemolytic anaemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What are the symptoms of neuroblastoma

highly malignant

A

Abdominal distension
Abdominal pain - may lead to constipation
Difficulties walking
Can check urinary secretion of catecholamines as it can be in adrenal glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What serology test should you use to diagnose coaeliacs disease in a child with IgA deficiency

A

Ig anti gliadin antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What autoimmune diseases overlap with coaeliacs

A

Type 1 diabetes, hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What allergies can cause failure to thrive

A

Cows milk protein allergy
Lactose
Fructose
Gluten - coeliacs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What investigation should you ALWAYS consider in any child with GI symptoms?

A

Urine sample dip/ MSU.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What is the pathophysiology of migraine

A

activation and sensitization of trigeminovascular pathways

Brain state of altered excitability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Can you have aura without headache

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Is headache a feature of abdominal migraine

A

No
The features are central midline abdominal pain, in bouts of 1-72 hours (same-ish as migraine), moderate to severe, nausea and vomitting. Plus some vosomotor symptoms. Well between episodes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is torticollis

A

Tilting of the head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

what is a craniopharygioma

A

Pituitary tumour in children. Originates from embryonic tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What are some red flag features of secondary headaches in children and why

A

SOL - headache worse lying down, in the morning, may wake at night - think about a pressure headache.
Change in personality, mood, school performance
Any other focal neurology - visual field defects, diplopia, squint, facial nerve palsy. Gait. Torticollis. Growth failure (pituitary tumour). Papilloedema (late sign). Cranial bruits, may be heard in AV malformations but rare.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What are the causes of secondary headaches in children

A

SOL / raised ICP
Head or neck trauma
Cranial or cervical vascular disorder (haemorrhage of AV malformation)
Raised ICP (idiopathic)
Substance abuse or withdrawal
Infection - meningitis, encephalitis
Disorder of homeostasis - hypercapnea or HTN
Disorder of facial or cranial structures - sinusitis
Psych disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Summarise the causes of secondary headaches in children

A

Mass - SOL
Infection - meningitis
Vascular - malformations/ haemorrhage
Trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What is the management of headaches in children

A

Nothing can cure a primary headache. But there is symptoms relief.
Rescue - analgesics (paracetamol, NSAIDs), antiemetics (prochlorperazine), tryptans (serotonin agonists, vasoconstrict) - caution/ not licensed <12 years.
Prevention (if very frequent) - beta-blockers (not if asthmatic), 5-HT antagonists, Na+ blockers (valproate or topiramate).
Psychosocial support - aimed at managing triggers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

When should you investigate a headache in a child

A

When they have red flag symptoms only, Do brain imaging if red flags

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

List some uncommon forms of migraine

A 
Basilar artery migraine
Familial 
Sporadic hemiplegic migraine
Abdominal migraine 
BPPV - ask about vertigo 
Cyclical periods of vomitting - may be precursor to migraine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

List some of the important questions to ask about migraine

A

What is child like between attacks - asymptomatic? Persistent features are a red flag, eg vomitting
Nausea and vomitting
Photo / phono phobia
Aura - visual, sensory, motor - must be followed by headache within 1 hour. Must last 5-60 minutes.
Pulsatile.
1-72 hours.
Worse with activity.
Triggers.
Positive negative features.
Sequential symptoms and duration important.
Sudden onset focal neurology with negative features - think about a stroke or vascular event.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

List some common childhood epileptic seizures

A

Idiopathic (70-80%) - cause unknown, presumed genetic
Secondary - cerebral dysgenesis/ malformation, vascular occlusion, cerebral damage eg HIE, congenital infection
Cerebral tumour
Neurodegenerative disorders
Neurocutaneous syndromes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

List some common non epileptic seizures in children

A 
Febrile
Metabolic - hypoglycaemia, calacemia, mg, na+
Head trauma
Meningitis/ encephalitis 
Poisons/ toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What are the causes of seizures in children

A

Epilespy (disease that causes lower threshold for seizures - these ones are recurrent unprovoked attacks)
Non-epileptic (seizure not related to lower threshold)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What is neuroblastoma

A

Malignancy that is extra-cranial. Malignancy of embryonic tissue - tends to be of sympathetic nervous system. Peripheral. Can metastasise to CNS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What is sturge-webber disease

A

Vascular malformation disease
Port wine stain
Malformation in brain on same side as stain - seizures, muscle weakness, visual problems, glaucoma (if port wine stain is near the eye)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What is a leptomeningeal angioma

A

Capilliary malformation in the brain associated with struge-webber disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Which childhood epilepsies are benign and usually disappear with puberty

A

Typical absence seizures

Other IGE seizures have life long liability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

What is the difference between the criteria for adult and child migraine

A

In children is it a bilateral or frontal headache
1-48 hrs
Nausea/ vomitting
+ photo, phono, vertigo or abdominal pain (2 of these)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What considerations for children need to be made if prescribing sumatriptan

A

Must be over 12yrs or >30kg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What serotonin antagonist can be used as prophylaxis for migraine in children

A

pizotifen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What are the causes of raised ICP in children

A 
Meningoencephalitis (infection)
Bleeds - subdural/ extradural (trauma)
Head injury 
Ketoacidosis 
Tumours 
Thrombosis
Reye's
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What should you always do on an acutely unwell child before you LP

A

CT to rule out pressure gradient

Look at basal cisterns - if raised pressure here (mass), doing LP will lead to coning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What is the management of raised ICP in children

A
  1. Mannitol
  2. Dexamethasone
  3. Fluid restriction and diuresis avoiding hypovolemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Is juvenile myoclonic epilepsy generalised

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Give the different routes and names of different benzodiazepines used in prolonged seizure

A

Lorazepam IV
Midazolam buccal
Diazepam rectal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

When can AED therapy be discontinued

A

After 2 years seizure free

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Give some examples of alternative management to AEDs for childhood epilepsy

A

Ketogenic diet
Vagal nerve stimulation
Surgery - if EEG and MRI is concordant with seizure type, can resect some of the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Outline first and second line AED therapy for generalised and focal seizures

A 
Generalised
1. Valproate, then Carbamazepine
2. Lamotrigine, topiramate
Focal 
1. Carbamazepine, then Valproate 
2. Topiramatem levetiracetam, gabapentin etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

List some generic lifestyle advice that must be given to children with epilepsy

A

Have showers over baths
Do not swim alone in deep water
Contraception and sexually active teenagers
Avoid activities that could lead to injury if seizure takes place
Alcohol use and effect of AEDs/ seizure threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What is the definition of status epilepticus

A

Continuous seizure lasting >5 minutes
or
Seizure without conscious recovery in between

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What are the causes of congential hypothyroid

A

Dysgenesis (gland does not form properly, eg fails to descend from tongue down to neck)
Dyshormonogensis (metabolic error in thyroid production)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What is the difference between a learning difficulty and disability

A 
Difficulty = obstacle, but retained IQ
Disability = loss of function, impaired IQ
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Describe the difference between difficulty, impairment and disability

A 
Difficulty = obstacle in achieving a function, but normal function still achievable 
Impairment = loss or abnormal function, often a physical cause
Disability = restrictions that arise as a result of loss of function, eg unable to walk to school
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What IQ threshold is required for cognitive impairment in children

A

<70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What is cerebral dysgenesis

A

Broad term to describe a fetus whose brain is not developing properly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What is periventricular leucomalacia

A

Form of white matter brain injury
Hypoxia causes necrosis of white matter tracts near ventricles (white matter softens = leuco- malacia) then is replaced with fluid filled spaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What age range (for when brain injury occurs) is used for the diagnosis cerebral palsy

A

Up to 2 years

After this it is acquired brain injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What is the most common cause of cerebral palsy

A

Antenatal vascular occlusion (80%)
Ischemic birth injury is second (10%)
Post-natal (10%)
Genetic syndromes, congenital infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What are the different types of cerebral palsy, how do these relate to symptoms

A

Cerebral cortex - spasticity (UMN)
Basal ganglia - dyskinesia (extra pyramidal)
Cerebellum - ataxia
Multiple areas - mix of two or more of above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

List some of the non motor symptoms of cerebral palsy

A 
Cognition
Communication 
Perception 
Sensation 
Behaviour 
Seizure
Secondary MSK problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

What are the two features of autism

A

Impaired/ deficit in social communication and social interaction
Poor imagination/ rigidity/ ritualistic behaviour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

When is autism likely to present

A

2-4 years with impaired social interaction, speech and language disorder and imposition of routines with ritualistic behaviour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

When is the newborn hearing test done

A

Anytime in the first 4-5 weeks post birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

What are the causes of social/ emotional/ behavioural delay in children

A

Autism spectrum disorder
Learning difficulty
Environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

What are the causes of speech and language developmental delay in children

A 
Hearing loss (conductive - recurrent otitis media with effusion, grommets - or sensorineural)
Cerebral palsy (problem with oral production of speech)
Learning difficulty (severe = global delay, moderate speech and language delay only)
Environment 
Normal variant/ familial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

What are the causes of speech and language disorder in children

A

Autism spectrum disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

What are the causes of motor delay in children

A

Cerebral palsy

Learning disability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

What is the management of autism

A

Early behavioural intervention + speech therapy - aim is to enhance motor, social and living skills
Parent training - education and support
School support - possibly school for learning disabilities
Treat comorbidities
Can use some meds: risperidone (aggression), melatonin (sleep), SSRIs (repetitive behaviours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

What are the different types of hearing loss and the causes of these in children

A

Sensorineural - genetic, congenital infection (CMV), HIE, hyperbilirubinaemia, postnatal infection (meningitis etc), head injury, drugs (furosemide), neurodegenerative disorders
Conductive - recurrent otitis media effusion, more common in syndromes etc Downs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

What is a red flag for vision problems in new born

A

Loss of red light reflex
No smile by 6 weeks, no fix and follow
Random eye movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What are the causes of squint in children

A

Refractive errors (lens)
Retinoblastoma
Cataract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What are the different types of squint, which one can reflect sinister pathology (SOL)

A

Non-paralytic - lens, correction by glasses (squint in all gaze directions)
Paralytic - SOL, paralysis of motor nerves. Varies with gaze direction (type of eye movement - essentially more of a lower motor nerve palsy picture)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What is the most common ocular malignancy in children

A

Retinoblastoma

Autosomal dominance inheritance pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What is the management of viral induced wheeze in children

A

If sick enough to admit to ward - oral pred for 3 days
If not scoring/ responds to bronchodilators - try bronchodilators + LTRA or high dose ICS if needed (lower dose ICS don’t work as well)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What is the management of croup

A

Mild - oral dexamethasone or prednisolone

Severe - minimal interference - can try neb adrenalin and oral steroids, if concerned, ITU for intubation

185
Q

How would you stratify risk in a child with stridor

A 
Continuous or intermittent with being upset 
Harsh or soft 
Hoarse or muffled/ no voice 
Drooling 
Fever
186
Q

What is the different management of stridor based on mild-moderate-severe

A

If it is mild (only when child is upset, its loud, they have an audible hoarse voice) can be managed with oral steroids (dex or pred)
If it develops from mild into moderate, can give neb adrenalin
If suspect moderate/ severe do not approach child and do an ITU referral

187
Q

What are the differential diagnoses for a child with stridor

A

Croup (parainfluenza virus)
Bacterial tracheitis (often hx of croup with deterioration)
Epiglottitis (H influenzae)
Diptheria can sometimes cause laryngotracheal diptheria (but usually higher up, nose and throat)

188
Q

What is the management of asthma in children

How is this different to adult management

A

Bronchodilator (reliever SABA)
Preventer (1st: ICS, 2nd: LTRA, 3rd: LABA If LTRA doesn’t work - stop this before LABA)
Adults LTRA then LABA - adult doses

189
Q

What is the difference in management in a child under 5 with suspected asthma vs over 5 with confirmed asthma

A

Only that you do an 8 week trial of moderate-dose ICS to see if there is any benefit or not. If there is and symptoms come back after stopping ICS (must come back within 4 weeks), then use ICS as 1st line preventer. If becomes uncontrolled ICS + LTRA. Over 5 start a low dose ICS.

190
Q

What is the difference in management between viral induced wheeze and suspected asthma in under 5s

A

Only difference is that the benefits of ICS is not as good for VIW as it is in asthma, and that you start VIW children on LTRA before ICS.
VIW: SABA + LTRA (only high dose ICS if at all, low dose not effective)
Asthma: SABA + ICS + LTRA

191
Q

What syndrome is polydactyl common in (extra digits)

A

Pataus

192
Q

What is the second line test for newborns after the newborn hearing test

A

Auditory brainstem response as a newborn/ infant

193
Q

What types of rash is characteristic in JIA

A

Salmon pink rash

194
Q

What is perthes disease

A

Perthes’ disease occurs in a part of the hip joint called the femoral head. This is the rounded top of the thigh bone (femur) which sits inside the hip socket (acetabulum). Something happens to the small blood vessels which supply the femoral head with blood. So, parts of the femoral head lose their blood supply. As a result, the bone cells in the affected area die, the bone softens and the bone can fracture or become distorted. The amount of bone damage can vary from mild to severe.

195
Q

Describe the presentation of squint

A

Deviation of the eyes

May be conversion squint

196
Q

What are the causes of visual impairment in children

A

Genetic - cataracts, albinism, retinal dystrophy, retinoblastoma
Perinatal - infection, retinopathy of prematurity, HIE, cerebral abnormalities
Postnatal - trauma, infection, JIA

197
Q

What are the risk factors for severe visual impairment in children

A 
Family history (retinoblastoma, autosomal dominant)
Developmental delay
Prematurity
198
Q

Why is it important to have eye checks and correct refractive error defects in children

A

To prevent amblyopia - permanent inability to correct refractive error ‘lazy eye’
If dont treat before the age of 7 the eye never learns to focus correctly and ability to do this can be permanently lost

199
Q

List some signs of visual impairment in babies and children

A

Loss of red light reflex
White reflex - retinoblastoma, cataract, retinopathy of prematurity
Red light reflex not in same position
Not smiling by 6 weeks
No fix and follow by 6 weeks
Random eye movements
Squint (sudden on set - paralysis or concomitant)

200
Q

What light reflex would you see in a child with cataract, retinoblastoma or ROP

A

loss of red light reflex or white reflex (think pink/ white is an early sign)

201
Q

What reflexes should be tested as part of the newborn exam

A

Moro’s reflex
Suck reflex
Grasp reflex - stroke babies hand and should grasp

202
Q

What are the causes of motor delay in children

A

Central motor deficit - cerebral palsy
Spinal lesion - spina bifida, neuroblastoma
Muscle - congenital myopathy/ primary muscle disease
Global developmental delay - genetic, perinatal, postnatal

203
Q

What Is a neuroblastoma

A

Embryonal malignancy
Malignancy of sympathetic peripheral nervous system
Starts in kidney, can metastasise to spinal cord, chest and neck.
Usually presents under 5, peak at 20 months
Most commonly sporadic
1-2% familial

204
Q

Broadly what are the causes for developmental delay

A

Genetic - chromosomal abnormalities
Metabolic - thyroid, liver (bilirubin)
Antenatal - alcohol, hypoxia, nutritional growth retardation
Perinatal - infection (TORCH), traumatic birth - HIE, asphyxia, haemorrhage, prematurity, hypoxia
Post-natal - infection (meningitis, encephalitis), trauma/ injury (bleed), impoverished environment

Specifics - CMV sensorineural hearing loss, hyperbilirubinaemia - sensorineural hearing loss
Prematurity - retinopathy

205
Q

What are the long term consequences of kernicterus

A

athetoid movements, deafness, and reduced IQ (intellectual disability). Preventable by phototherapy +- exchange transfusion

206
Q

What are risk factors for autism

A

Gender (boys > girls)
Famiily history
Prematurity
Parental age >35 years

207
Q

Give some examples of disordered speech in autism

A

Ecolalia (repetition of what is said to child)
Monotonous, pedantic speech
Lack of gestures/ non verbal communication

208
Q

Give some examples of impaired social interaction in autism

A

does not seek comfort/ affection, or affection on own terms
would not hug if parents asked for a hug
no parallel play
Does not appreciate social cues
Has difficulty dressing themselves/ dislikes getting dressed/ always scruffy
Does not help with dressing
Delayed toilet training
Delayed finger food, use of spoon, feeding themselves

209
Q

Give some examples of impaired imaginiation in autism

A 
No imaginative play - role play, turn taking
Only plays with same toys 
Obsessions / rituals / fixations
Not interested in stories 
Distressed by change
210
Q

List some causes of tip toe walking in children

A

Cerebral palsy
Autism
Other antenatal/ perinatal hypoxic injury

211
Q

What comorbidities exist with autism

A 
Learning difficulties (2/3)
Seizures (1/4)
212
Q

Define seizure

A

A sudden disturbance in neurological function associated with a surge/ increase in synchronised neuronal discharge

213
Q

What are the causes of basal ganglia disorders in children

A 
Acquired brain injury (hypoxic, ischemia, post cardiopulmonary bypass chorea)
Post-strep chorea - rheumatic fever
Mitochondrial cytopathies
Wilsons disease
Huntington disease
214
Q

What are the causes of cerebellar disorders in children

A

Medication and drugs including alcohol and solvent abuse
Post-viral, particularly varicella infection
Posterior fossa lesions or tumours eg medulloblastoma
Genetic and degenerative eg ataxic cerebral palsy
Friedreich ataxia and ataxia telangiesctasia

215
Q

What is the age of onset for friedreichs ataxia

What is friedreichs ataxia

A

10-15 years
Genetic (autosomal recessive) disease - mutation of FXN gene that is involved in maintaining mitochondria of highly active cells. Get degeneration of dorsal root ganglia, which then damages dorsal colums and input to cerebellum. Also get cardio problems, and DM.

216
Q

What vitamin deficiency can cause ataxia

A

Vitamin E - usually presents between ages 5 - 15 years

Need life long injections of vitamin E for management

217
Q

What is charcot marie tooth disease, how is it inherited

A

It is a disease that affects the sensory and motor peripheral nerves. Genetic disease associated with damaged to peripheral myelin. Depending on gene involved can be inherited autosomal recessive, dominant or x linked.

218
Q

What should you rule out in a child with bells palsy

A

involvement of VIII CN (cerebellopontine angle mass)

hypertension - coaractation of aorta

219
Q

what investigations should you do in a child with suspected myopathy

A

creatine phosphokinase - elevated in Duchenne and Becker muscular dystrophy
Muscle biopsy
DNA testing
USS and MRI muscles - used to monitor progress

220
Q

What is the inheritance pattern of Duchenne

A

X linked recessive

221
Q

What is the function of creatine

A

Recycles ADP to ATP - needed a lot in muscles and nerve tissue

222
Q

What are the signs of hydrocephalus in a baby
What are the causes
What is the management

A

Increase in head circumference
Separation of skull sutures
Bulging of anterior fontanelle
Distension of scalp veins, sun setting of eyes - late signs
Causes: communicating, non-communicating
Communicating - SAH, meningitis, pneumococcal, TB
Non-communicating - aqueduct stenosis, atresia of outflow foramina, chiari malformation
Treat with a ventriculoperitoneal shunt

223
Q

What is a chiari malformation

A

When the cerebellar tonsils push down on foramen magnum

Can be a cause of obstructive hydrocephalus

224
Q

What are the neurocutaenous syndromes

A

Neurofibromitosis T1 and 2 - dominant inheritance
Tuberous Sclerosis - dominant inheritance - benign multi organ tumours - hamartomas - MRI
Sturge-Weber - sporadic, MRI,

225
Q

What is fanconis anameia

A

A genetic condition that causes bone marrow failure and aplastic anaemia

226
Q

What is diamond blackfan anaemia

A

A genetic condition that impairs ribosomes in the synthesis of RBCs - causes red cell aplasia. Have short stature and abnormal thumbs

227
Q

What are the differentials for red cell aplasia

A

Diamond blackfan anaemia
Parvovirus
Transient erythrobalstopenia of childhood
Rare: fanconis anaemia, aplastic anaemia, leukaemia

228
Q

What are the common causes of iron deficiency in children

A

Diet - under nutrition (especially if having cows milk feeds, as not much of this iron is absorbed, other periods where likely to happen is during weaning)
Malabsorption - eg coeliacs/ IBD
Less common - bleeding

229
Q

What is the treatment of iron deficiency anaemia in children

A

Oral iron supplements - continue until Hb is normal for 3 months
If not responding consider whether there could be a bleed - eg meckles diverticulum, or malabsoprtion

230
Q

is thalassamia dominant or recessive

A

recessive

231
Q

What blood markets should you check in a child that has anaemia

A

Reticulocytes (tells you about marrow function)

Bilirubin (tells you about haemolysis

232
Q

What are the causes of haemolytic anaemia

A 
Thalassaemia 
Sickle cell disease 
Hereditary spherocytosis
Glucose-6-phosphate dehydrogenase deficiency  
Do blood film with these
233
Q

What signs would you expect to see with haemolytic anaemia

A

Jaundice
Hepatomegaly
Splenomegaly

234
Q

What are the diagnostic clues of haemolytic anaemia

A

Raised unconjugated bilirubin
Increased urinary urobilinogen
Abnormal appearance of red cells on a blood film
Postitive direct antiglobulin test
Increased red blood cell precursors in marrow

235
Q

What is the worldwide commonest cause of haemolytic anaemia

A

G-6-PDD
Glucose-6-phosphate dehydrogenase deficiency
x-linked

236
Q

What is the diagnostic investigation for spherocytosis

A

Blood film

Can do osmotic fragility and dye binding but not usually needed

237
Q

What is the antenatal screening for sickle cells

A

Mothers at high risk are offered screening bloods

If they are a carrier, father is offered screening bloods

238
Q

When do children with sickle cell become symptomatic

A

Around 5 months

239
Q

What Hb protein does sickle cell affect how does this affect symptoms

A

Affects beta chain
This means they have some normal fetal Hb (alpha and gamma chains) but as it starts to be replaced, they develop symptoms as the beta chains of HbS are mutated

240
Q

What is the difference in management between major and minor beta-thalassaemia

A

Major is transfusion dependent
Minor is not necessarily transfusion dependent - non-transfusion-dependent thalassaemia - only get transfusions if they are ill or circumstance where anaemia is precipitated

241
Q

What monitoring should be done in all patients with beta thalassaemia receiving blood transfusions

A

Iron monitoring

242
Q

What is the management of sickle cell disease

A

Prevention - vaccination, avoid triggers (cold weather), folic acid
Management of crisis - analgesics, treat the cause (eg abx), exchange transfusion - acute chest syndrome
Management of chronic illness - hydroxycarbamide (promotes HbF), sometimes bone marrow transplant - only curative treatment

243
Q

What are the different types of alpha thalassaemia

What is the difference in presentation and management

A

Alpha thalassaemia - bart syndrome - no alpha chains - will present antenatally with hydrops fetalis. 4 alpha gene mutations
HbH disease - 3/4 mutations - mild-moderate haemolytic anaemia. Treatment mostly not needed other than monitoring bloods, usually quite well, will need transfusions if become unwell.
1/4 or 2/4 mutations - asymptomatic - carriers

244
Q

What are the constituents of fetal Hb

A

2 alpha globulins, 2 gamma gobulins
NB: Newborn 74% fetal, 25% adult
>1year 97% adult, 2% adult HbA2 - 2 alpha globulins, 2 delta globulins

245
Q

List some causes of blood loss in infants and children

A

Meckel diverticulum

Von Willebrand disease

246
Q

List some of the signs of beta thalassaemia in an infant/ children

A

Skull bossing
maxillary overgrowth
Splenomegaly
Hepatomegaly

247
Q

What are the causes of haemolytic anaemia

A

Immune (haemolytic disease of the newborn)
Red cell membrane disorders (spherocytosis)
Red cell enzyme disorders (glucose-6-phosphate dehydrogenase deficiency)
Abnormal Hb (alpha-thalassaemia major)

248
Q

What is the treatment of spherocytosis

A

Folic acid

Splenectomy if symptomatic

249
Q

Who is usually affected by G-6-PDD

A

Males - X-linked
Enzyme deficiency that can lease to oxidative haemolysis
May present with neonatal jaundice
Management is avoid foods/ triggers/ infection that can lead to haemolysis (nitro, broad beans, quinines)

250
Q

What can be the symptoms of beta and alpha thalassaemia traits

A

mild iron deficiency and confusion

251
Q

How would you diagnose diamond blackfan anaemia

A

Blood results - macrocytic anaemia, low reticulocytes
Can do genetic testing
Marrow biopsy

252
Q

What FBC results are a hallmark feature of HSP and why

A

Purpura with normal platelets - suggests a vasculitis instead of a sepsis or virus

253
Q

When does Fanconis anaemia usually present

A

Around 5-6 years

Can transform into leukaemia

254
Q

What is haemophillia, how is it inherited

A

It is an inherited deficiency in VIII (A) or IX (B) clotting factor
It is X-linked recessive, affects males

255
Q

What are the symptoms, investigations and management of haemophillia in children

A

Symptoms: MSK bleeding (arthritis), mucocutaenous bleeding, bruising, GI bleeds
Investigations: raised PATT (because VIII is part of intrinsic pathway), normal PT, vWF antigen -ve. Definitive test is DNA analysis.
Management: VIII recombinant replacement. Can give virally inactivate plasma-products if VIII unavailable. Will be given in hospital untill ~2-3 years, when parents can give it at home, then 7-8 years children can give themselves. Quantity - in general raise circulating blood level by 30%, up to 100% if surgery or life threatening bleed.
Prophylactic VIII given to all severe haemophillia.
Desmopressin can be used in mild haemophillia to stimulate clotting factor and vWF synthesis by liver.

256
Q

When do symptoms of haemophillia usually present

A

At around 1 year - when starting to walk, crawl, fall

40% in neonatal period - intracerebral haemorrhage

257
Q

What medications should you never in haemophillia

A

NSAIDs

Aspirin

258
Q

What is the inheritance of von willebrand disease

A

Autosomal dominant

259
Q

What is von willebrand disease

A

Inherited autosomal dominant disease - get either quantitative or qualitative problem with von willebrand factor
von willebrand factor is needed for platelet adhesion and it is a carrier protein for VIII so leads to problems in platelet plug and clotting

260
Q

What are the symptoms of von willebrand disease

When does it usually present

A

Can be a much milder disease than haemophillia - can present in puberty
Bruising (less so than Haemophillia)
Bleeding post surgery
Menorrhagia
Mucosal bleeds, epistaxis (acute bleed of the nostril)

261
Q

What is the treatment of von willebrands disease

A

Desmopression for mild disease - promotes von willebrand factor and VIII
Severe disease needs VIII replacement

262
Q

What is the intrinsic and extrinsic coagulation pathways
What factors are in each
How are they related to PT and APTT

A

Intrinsic - slower, longer production of thrombin. All others. Endothelial contact.
Extrinsic - fast, rapid production of thrombin - celluar injury. 10,7,2,5
PET = PT extrinsic
APITT = APTT intrinsic
Explains why haemophillia (VIII deficiency) only has prolonged APTT time and not PT, as VIII not part of extrinsic pathway
Warfarin inhibits extrinsic
Heparin inhibits instrinsic

263
Q

What is purpura fulminans

A

Thrombotic condition in children
Purpura originating from clots that starts to necrose
Life threatening

264
Q

What are the acquired causes of bleeding in children

A

Low vitamin K (diet, newborn, chronic disease)
Liver disease
ITP, causes below:
Immune thrombocytopenia (post viral, low platelets)
Leukaemia (marrow displasia) - know red flags - hepatosplenomegaly, need to do blood film, aplastic anaemia, chestxr for mediastinal lymph nodes, marrow biopsy confirms
DIC - from meningococcal disease/ sepsis - very low platelets, prolonged PT and APTT, raised fibrinogen
HSP - post upper respiratory infection (strep), joint swelling, haematuria - platelets normal

265
Q

What are the inherited causes of bleeding very low platelets

A

Wiskoff-alrich

Bernerd-soulier

266
Q

What is the typical presentation of immune thrombocytopenia

A

Recent upper viral infection
Wide spread petechiae and purpura
Brusising
Child well in themselves but will isolated low platelets
Must rule out leukaemia / marrow failure causes

267
Q

What is the most important differential of immune thrombocytopenia

A

Leukaemia

Congenital causes of thrombocytopenia (bernerd- soulier)

268
Q

What is the management of immune thrombocytopenia

What is the prognosis

A

80% resolve within 6-8 weeks
20% - chronic ITP - specialist management - need screening for SLE
No treatment unless significant bleeding - can give oral steroids (pred), anti-D, IvIG

269
Q

What are the causes of thrombosis in children

A 
Inherited:
Protein C deficiency 
Protein S deficiency 
(these are anti-thrombins)
Antithrombin deficiency 
Factor 5 leiden
Acquired:
Catheter thrombosis 
DIC
Hypernatraemia
Polycythaemia
Malignancy 
SLE
270
Q

What is pleocytosis and when would you expect to see it

A

presence of an abnormally large number of lymphocytes in the cerebrospinal fluid.
See this in leukaemia

271
Q

What is the presentation of leukaemia

A

Short hx - days to weeks
Marrow failure - anaemia (pallor, lethargy, fatigue)
Reticulo-endothelial - infection, hepatosplenomegaly, cervical lymphadenopathy
Metastasis - CN involvement (CN palsy, headaches), testes enlargement

272
Q

What is the presentation of NHL lymphoma

A

Can present similar to ALL - acute (tends to be T cell NHL)
B cell NHL - longer hx
Large, painless, rubbery lymph node - neck, head, abdomen, groin
Compression symptoms - abdominal obstruction

273
Q

What is the presentation of hogkins lymphoma

A

Long-ish hx - months
Enlarged painless lymph node
Possibly B symptoms (sweating, fever, itch) but uncommon

274
Q

What investigations should you do for leukaemia

A

Bloods - FBC + blood film (to look for blasts)
Pancytopenia, high or low WCC
Marrow biopsy - looks for % blast occupation in marrow
LP - look for CNS involvement - pleocytosis
Chest XR - mediastinal lymph node involvement
+/- imaging to stage - MRI, CT (eg brain imaging)
Blood tests for genetic risk factors (philidephia)

275
Q

List some risk factors for ALL

A 
2-6 years
Philadelphia chromosome 
Trisomy 21 - downs 
X ray exposure inutero 
Perinatal infection
276
Q

List good prognostic factors for ALL

A

Female
WCC <50
age 2-10
No CNS involvement

277
Q

What is the cure rate for ALL

A

80%

278
Q

What is the treatment for ALL

A

Manage risk, eg complications from marrow failure - blood/ platelet transfusions, hyperuricaemia - allopurinal
Chemo - 4 weeks (longer if have poor prognostic markers) IV and intra-thecal for CNS disease eradication, continuing chemo therapy 2 years female, 3 years male. May have Rx / surgery if CNS involvement

279
Q

What are the major complications of ALL treatment

A

Neutropenic sepsis
Growth failure (lots of GI problems with chemo)
Hyperuricaemia
Secondary tumours

280
Q

List some long term complications of ALL treatment

A 
Infertility 
Growth problems 
Endocrine dysfunction 
Psychological 
Secondary malignancy 
Intellectual impairment (surgery, CNS involvement)
281
Q

What investigations should be done for ?lymphoma

A 
Lymph node biopsy 
FBC + film (look for blasts + reed sternberg for HL)
Imaging - CT. MRI 
LP
CXR
282
Q

What is the management of lymphoma in children

A

Combination Chemotherapy

+ Rtx if needed

283
Q

What is the cure rate of HL and NHLymphoma in children

A

80%

284
Q

What syndrome causes resistance to growth hormone

A

Laron syndrome

285
Q

Which hormonal axes regulate growth

A 
Growth hormone axis, particularly GH and IGF-1 - stimulate epipyheseal growth plates -  via chondrogenesis 
Reproductive axis (HPG) - regulates puberty onset (stimulates second growth spurt) and completion (closes epiphyseal plates) 
HPA axis (adrenarche) - perhaps not a direct regulator but involved in puberty onset
286
Q

Summarise the physiology of normal bone development

A 
Endochondrial ossification (cartilage)
Intramembranous ossification (no cartilage)

Endochrondial - cartilage made up of chondrocytes. GH and IGF-1 stimulate chrondrogenesis (proliferation of chrondrocytes). Steps are proliferation, hypertrophy, degeneration, cavity. This process provides the scaffold for ossification, and possibly some of the bone matrix (calcium). After degeneration, vascularisation bringing osteoprogenerators that become osteoblasts start to secrete osteiod (organic matrix). Osteoblast then dies and regulates deposition of inorganic matrix (not sure how).

287
Q

What are the major influencers of growth during:
Neonatal/ infancy (18 months)
Mid-childhood
Puberty

A

Neonatal/ infancy (18 months) - nutrition, thyroid
Mid-childhood - psychosocial, nutrition, hormonal axis - growth, genes
Puberty - psychosocial, hormonal axis - growth and reporductive

288
Q

What stimulates puberty

A

Activation of the reproductive axis - HPG
Active antenatally - then shuts down untill puberty
Central mechanism of activation - unknown specifically what turns it on. It is preceded by adrenarche.

289
Q

What are the main causes of failure to thrive in infants

A
  1. Poor intake - insufficient diet (breast milk), poor feeding technique, GORD
  2. Malabsorption - IBD, Allergies -cows milk, gluten, fructose, lactose, Infection, Liver disease, Pancreas disease - CF
  3. Increased demand - urine infection, CHD, respiratory demand, renal disease
  4. Central defects - GH, thyroid, psychosocial
290
Q

What is the impact of an emotionally undernourised environment

A

Reduced GH

Down regulation of growth hormone axis

291
Q

What investigation can you do to determine true or psedu precocious puberty

A

GnRH test - this will tell you if HPG axis is turned on (and tf truely activated early, by a rise in FSH and LH), or if it is not turned on (pseudo - no rise in FSH or LH) and early puberty is being driven by something else - eg Adrenal hyperplasia

292
Q

What is the definition of short stature

A

Short stature - below <3 centile on height, should always consider <25th centile on velocity as abnormal as well

293
Q

What are the causes of short stature

A

Psychsocial deprivation - inhibits growth factor
Endocrine causes - panhypopituitary, hypothyroid, steroids (cushings), GH deficiency - these ones are associated with weight gain
Nutrition/ enteropathy - IBD, chrons etc - associated with being short and underweight
Genetic - downs, turners, noonans, laron syndrome
Familial/ constitutional

294
Q

What is the purpose of testing bone age via xray - what conditions does it distinguish

A

GH deficiency causes of short stature will have delayed bone age, these are: Endocrine causes, psychosocial, constitutional delay, Nutritional causes
Non GH deficiency causes of short stature will not cause delayed bone age: syndromes, familial short statute

295
Q

What should be considered as tailing growth in children

A

Crossing of 2 centiles

<25th centile for speed (velocity) of growth / height

296
Q

What is a synthetic GH you can prescibe

A

somatotropin

297
Q

What work up would you do in a child with short stature

A

Endocrine screen - TFT, test GH following a stimulus eg insulin, cushings syndrome - overnight dexamethasone suppression test, 24 urine cortisol
Nutrition - CRP, ESR, FBC, Anti-TTG, IgA, breath tests
Syndromes - genetic test s
Familial - calculate expected height based on parents height +/- 12.5 cm

298
Q

How long should you make allowances for prematurity for in growth and development

A

18 months

299
Q

List some of the causes of poor feeding in infants

A 
Breast-feeding poorly
Bottle feeds too dilute
Juice drinker
Exclusion diets
Cleft palate
Vomiting
300
Q

What is sandifers syndrome

A

Neck extension, arching of the back

Infants do this is response to GORD

301
Q

What test do you need to do for Giardia

A

ELISA

302
Q

List the malabsorption causes of failure to thrive in infants

A

Coeliacs - anti TTG - always check IgA
Lactose intolerance - lactose hydrogen breath test
Fructose intolerance - fructose hydrogen breath test
Cows milk protein allergy - IgE
IBD - CRP, ESR, FBC
Giardia
Todders diarrhoea

303
Q

What causes extreme short stature

A

Laron syndrome - complete insensitivity to growth hormone
Primordial dwarfism
Idiopathic short stature

304
Q

What is the SHOX gene, what are mutations linked to

A 
Important for skeletal growth 
Mutations or absence linked to short statute - turners (X,0)
Or replication (Kleinfelters, XXY) linked to increased growth
305
Q

What are the common genetic syndromes linked to short stature

A

Downs
Turners - responds to GH
Noonan - responds to GH. Signal transduction mutation.
Russell-Silver - responds to GH

306
Q

List some common dysmorphic features to look for on a newborn exam

A

Low set ears
Wide eyes (hypertelorism)
Epicanthal folds
Microganthia - short jaw

307
Q

What are some of the dysmorphic features of FASD

A

Low nasal ridge
Thin upper lip
smooth philtrum

308
Q

What are the dysmorphic features of turners syndrome

A

webbed neck
Wide spaced nipples
Microganthia - mandibular hypoplasia

309
Q

Which two syndromes affect chromosome 15

A

Prader-Willi

Anglemans - happy personality, microcephaly

310
Q

What factors affect the prognosis of neuroblastoma

A

Age of child - better prognosis the younger they are (usually better if <1 year)
Stage they present at - if it is isolated, may be resectable. Metastatic disease if likely to recur and poor prognosis.

311
Q

What is the common presentation of neuroblastoma

A 
Abdominal mass
Abdominal distension 
Difficulty walking (if near spinal cord)/ limp 
Pallor (anaemia if spread)
Weight loss
Hepatomegaly (spread)
Bone pain
312
Q

What investigation should be done for neuroblastoma

A 
Urinary catecholamines 
CT scan
Biopsy 
MIGB scan - maps metastatic spread 
Marrow sample
313
Q

What is the prognosis of neuroblastoma

A

30% cure

314
Q

What is the prognosis of Wilms tumour

A

80% cure

60% cure for those presenting with met disease

315
Q

How does Wilms tumour present

A 
abdominal mass
work up - USS/ CT/ MRI
-chemo
-nephrectomy 
-radiotx in advanced disease
316
Q

What is the usual treatment for hydrocephalus in infants

A

ventriculoperitoneal shunt

317
Q

What are the causes of hydrocephalus in children

A

Communicating - SAH, meningitis
Non-communicating (obstructive) - intraventricular haemorrhage, posterior fossa tumour, posterior fossa vascular malformation, chiari (cerebellar tonsil) malformation, aqueduct stenosis, atresia of outflow foramina of fourth ventricle (Dandy-walker syndrome)

318
Q

What are the features of hydrocephalus in children

A 
Excessive increase in head circumference
Bulging fontanelle 
Separation of skull sutures 
Distension of scalp veins 
Sun setting of the eyes
319
Q

What are the features of raised ICP in children

A 
Pressure headaches 
Bulging fontanelle 
Visual changes
Blurred vision 
Vomitting
320
Q

What are the different types of brain tumours that children get

A

Astrocytoma (most common) - grade 1 pilocytic astrocytoma common
Medulloblastoma - low to high grade. Posterior fossa
Ependymoma - similar to medulloblastoma
Brainstem glioma
Craniopharyngioma

321
Q

What is the treatment of short stature

A

If a growth hormone deficiency is found, treat with biosynthetic growth hormone. Sub cut injection.
Turners, Prader-Willi and SHOX deficiency and IUGR can also be treated with growth hormone.

322
Q

What investigations can you do for short stature

A

Calculate predicted height based on parents
Xray of wrist and hand - marked delay for hypothyroidism or growth hormone deficiency or other endocrine. Small delay for constitutional delay. No delay for familial.
FBC - anaemia, coeliacs, chrons
Creatinine and electrolytes - Cr raised in chronic renal failure
TFT (incl TSH) - primary hypothyroidism
Karyotype - Turners
Anti-TTG - coeliacs
IgA, CRP, ESR
Growth hormone provocation tests (insulin, glucagon, clonidine, arginine) - growth hormone deficiency
IGF-1 - disorders of growth hormone axis
Cortisol and dexamethasone suppression test - cushing
MRI scan if neuro symptoms - craniopharyngioma
Skeletal survey - skeletal dysplasia

323
Q

Why do children born with IUGR warrant GH treatment

A

1/3 of IUGR who were premature remain short. This is an indication for GH.

324
Q

what is achondroplasia

A

disproportionate dwafism

325
Q

causes of tall stature

A 
congenital adrenal hyperplasia 
kleinfelters 
marfan 
sotos syndrome
hyperthyroid (rare)
obesity - will be normal height just start growth spurt early
326
Q

What is the enzyme deficiency in congenital adrenal hyperplasia

A

21-hydroxylase deficiency

90% have this

327
Q

What test should you do for congenital adrenal hyperplasia

A

17-alpha-hydroxyprogesterone

328
Q

What is the difference in female and male presentation of congenital adrenal hyperplasia

A

Female - presents with virilisation of external genitalia - clitoral hypertrophy, fusion of labia
Male - enlarged penis, scrotal discoloured
Tall stature - precocious puberty, but short stature as adult. Salt loss.

329
Q

What is the management of congenital adrenal hyperplasia

A

Life long glucocorticoids (to try and inhibit the axis)
Mineralocorticoids/ sodium chloride for salt loss
Monitor growth, skeletal maturity, plasma androgens, and 17-alpha hydroxyprogesterone

330
Q

How should you manage a salt loss adrenal crisis

A

Hydrocortisone

Saline and glucose IV

331
Q

What is the pathophysiology of congenital adrenal hyperplasia

A

Deficient in 21-hydroxylase needed in biosynthesis of mineralocorticoids and glucocorticoids. Deficient circulating cortisol, stimulates pituitary to release more ACTH - this causes even more progesterone that can only be metabolised by 17hydroxyprogesterone into testosterone.
Increased sex steroids causes stimulation of secondary sex characteristics, eg hypertrophy of external genitalia
Lack of circulating aldosterone leads to salt loss, hyperkalaemia, raised urea and decreased bicarb.

332
Q

What are the different childhood brain tumours

A

Astrocytoma - 40% - most common pilocystic astrocytoma - Grade 1
Medulloblastoma - Grade 1-IV - posterior fossa
Ependymoma - similar to medulloblastoma
Brainstem glioma
Craniopharyngioma

333
Q

What is the presentation of brain tumours in children

A

Raised ICP - bulging fontanelle, vomiting, visual changes, blurred vision
Any focal neurology - ataxia, personality/ mood changes/ changes at school, stumbling
Sometimes headache

334
Q

What investigations should be done for ?brain tumour in children

A

MRI
Biopsy if can get to location
Surgical resection

335
Q

What first line investigations should be done for a female with precocious or delayed puberty

A

LH/ FSH test - will tell you if axis is working at all
USS uterus and ovaries - will tell you if prepubertal (no puberty) or pubertal (early puberty)
Can do GnRH test to see if axis if turned on

336
Q

What is the normal sequence of puberty in girls and boys

A

Girls - breast buds, pubic hair, growth spurt, menarche

Boys - testicular enlargement >4ml, pubic hair, growth spurt

337
Q

What is the definition of precocious puberty

A 
Development of secondary sex characteristic plus Growth spurt before the age of 8 in girls or 9 in boys
Isolated thelarche (breast buds) or pubarche without growth not precocious puberty but still warrants investigation for causes like CAH
338
Q

What are the causes of precocious puberty in males and females

A

Females - likely to be true precocious puberty. Idiopathic and just premature onset of normal puberty. Other causes are CAH (isolated pubarache), neurofibromatosis . Flags for organic causes in girls are: dissonance in sequence, isolated pubarache, rapid onset, neuro signs.
Males - more likely to be pseudo and have an organic secondary cause.
Treatment for true PP is GnRH analogues if patient wants this - consider issues with growth with PP
Treatment for pseudo is identify the cause and treat eg androgen/ oestrogen inhibitors

339
Q

What genetic syndrome tends to only be noticeable after puberty and why

A

Fragile X - FMR-1 gene
Most common cause of inherited intellectual disability in males
Unsure why they have early puberty - axis just turns on earlier but end up as short adult because of closure of growth plate.
Girls in particular may be asymptomatic other than early puberty. Other manifestations in girls include some intellectual disability (30%) and cerebellar ataxia

340
Q

List some dysmorphic features of fragile x

A

Long and narrow face
Hypermobile joints
Prominant forehead
Large everted ears

341
Q

What is the normal range for plasma glucose

A

3.5 - 5.6 fasting

<7.8 post meal

342
Q

How do you diagnose diabetes

A

Fasting >7.0
OGTT (post meal) >11.1
HbA1C >48 (6.5%)

normal
Fasting 3.5 -5.6
OGTT <7.8
HbA1C <42 (4-5.6%)

prediabetes in between

343
Q

What are the symptoms of diabetes in children, what is the most common cause, what are your differentials

A 
Polyuria, polydipsia, weight loss, *enuresis, abd pain, concurrent infection, delayed growth, delayed puberty 
Commonest T1DM (97%)
differentials: T2DM, MODYs - can confirm modys w genetic tests - usually post puberty
344
Q

What are some symptoms of diabetes that you see in children and not in adults

A

Abdominal pain
Enuresis - especially at night
Delayed growth
Delayed puberty

345
Q

List some risk factors for T2DM

A

Asian, FHx (75% risk if mother and father), 15% individually, overweight

346
Q

How do you confirm a diagnosis of T1DM in children

A
  1. Symptoms of hyperglycaemia
  2. Venous blood glucose raised - either fasting or OGTT
    OR if no symptoms, raised blood glucose on two occasions
    >11.1 random/ post meal, >7 fasting
347
Q

What investigations should you do for a child with suspected diabetes

A

Venous blood glucose
Autoantibody profile - anti insulin, islet cell etc
Screen for other autoimmune diseases - TFT, Coeliacs

348
Q

What is the management of children with diabetes

A

T1DM - insulin dependent

T2DM - metformin and/or diet and exercise, may also need insulin

349
Q

What monitoring needs to take place in children with diabetes

A

HbA1c - every 3 months target <48

Eye, foot, U&Es/ renal, BP, injection sites

350
Q

What are the micro and macro vascular complications of diabetes in children
What are specific issues with children

A

Micro - retinopathy (ischemia and leakage), nephropathy, neuropathy
Macro - stroke, PVD, CVD
Childhood issues - growth, puberty, alcohol, drugs, transition

351
Q

What is the management of a hypo in a diabetic child

A

Mild-moderate:
Check blood glucose
Fast oral glucose - tablets, fizzy drink, lucozade
Wait 10 mins - check sugars
FU: Long acting oral glucose - bread, biscuit
Check BG after 15 mins
Severe - unconscious - subcut or IM glucagon
When conscious oral

352
Q

What are the symptoms of a hypo

A

Autonomic - palpitations, sweaty, irritable, pallor, anxious

Neuroglycaemia - dizzy, poor concentration, headache, visual changes, LOC, slurred speech, hearing loss

353
Q

What is the management of DKA

A

1.Resuscitate - 0.9% NaCl
2.Confirm diagnosis and investigate - blood sugar, ketones, urine ketones and glucose, Ca2+, ECG monitoring, blood gas
3.Start fluids - 0.9% NaCl + 20 mmol KCl
When BG <14 0.9% NaCl + 20 mml KCl + 5% glucose
After 12 hrs 0.45% NaCl + 20 + 5%
4. Start insulin. After 1 hr of fluids start insulin infusion. 0.1 unit/ kg/ hr. Only step down to 0.05 units once ph >7.3 and ketones are low.
5. Stop insulin. Once ph and ketones in range and child can eat, give subcut insulin, feed, and stop IV insulin 1 hr after feed.
6. Monitoring - CNS, blood glucose = hourly. UE and blood gas 2 hourly. ECG continuous monitoring. Fluid balance hourly.

354
Q

What fluid considerations need to made in DKA

A

Bolus - dont use, or if have to, use lower dose - 10 ml/kg NaCl
Maintenance - use lower mls per weight adjusted for DKA
Deficit - calculate as normal
Resus fluids - make sure these are subtracted from overall fluid calculations

355
Q

When should the ductus arteriosus close, what is the mechanism

A

Should close in first 1-2 days
Mechanism is a decrease in oxygen that causes vasoconstriction
Remains open often in prem babies

356
Q

Outline the circulatory changes that happen at birth

Consider - foramen ovale, ductus arteriosus, umbilical cord

A

First breath
Fall in thoracic volume = increase pulmonary flow
Flow return from lungs = increase pressure in LA with falling RA pressure = foramen ovale flap pushed closed
Arterial circuit now carries oxygenated blood (vasoconstriction of umbilical arteries)
Decreased flow through placenta = umbilical vein closure
Deoxygenated flow through pulmonary artery = ductus arteriosus closure

357
Q

List some of the causes of congenital cardiac disease

A

Maternal disorders - rubella, SLE, DM
Maternal drugs - warfarin, FAlcohol syndrome
Chromosomal abnormality - Downs, edwards, pataus, tuners, williams, noonans, chromosome 22q11.2 deletion

358
Q

When should the intraventricular foramen close

A

Week 7 gestation

359
Q

What are the causes of left to right shunts in babies

What is main presenting symptom

A

VSD, ASD, PDA

Breathlessness - main symptom because of life sided blood loss to right side

360
Q

What are the causes of right to left shunt in babies

What is the main presenting symptom

A

Tetrology of fallot
Transposition of great vessels
Cyanosis (blue) - main presenting symptom

361
Q

What are the symptoms of a large VSD in a baby

A

Murmurs: 1. Pansystolic loud (harsh) systolic murmur - day 1, may shorten and soften/ disappear as days go on
2. Apical mid-diastolic murmur (increased flow across mitral valve from increased pulmonary flow)
Symptoms:
Breathlessness
Failure to thrive - after 1 week
Heart failure features - tachypnea, tachycardia, pallor, difficulty feeding, breathless with activities (eg feeding), hepatomegaly
Active precordium

362
Q

What investigations would you do for a child with ?VSD

What is the management

A 
Chest XR - HF features
ECG - biventricular hypertrophy 
Echo
Diuretics 
Captopril - ACE inhibitor
Surgery at 3-6 months - want to prevent permanent damage to pulmonary vasculature
363
Q

List some of the XRay features of heart failure in a baby with VSD

A

Cardiomegaly
Enlarged pulmonary arteries
Increased pulmonary vascular markings
Pulmonary odema

364
Q

What are the symptoms of a small VSD, what is the management

A

Murmur: loud pansystolic murmur. No diastolic murmur. No associated features.
Symptoms: None.
ECG - normal
Chest XR - normal
Echo - will show defect
Monitoring to make sure hole closes = will be confirmed with echo. Still need information about endocarditis.

365
Q

What is the presentation of an atrial septal defect

A

Murmur: 1.Left upper sternal edge. Systolic murmur. 2.Splitting of HS II - fixed split. Sounds are from increased flow across pulmonary valve and increased stroke volume. (?may radiate to back)
Symptoms: None. Doesnt tend to cause HF in infancy but if hole is large enough my in later life.
Recurrent chest infections/ wheeze.
Arrhythmias (from 4 years onwards)

366
Q

How is an ASD investigated and managed

A

Chest XR: cardiomegaly, enlarged pulmonary arteries, increased pulmonary vascular markings (not sure why this isnt considered HF?)
ECG: Secumdum ASD - right bundle branch block, right axis deviation due to right ventricular enlargement
AVSD - ‘superior’ QRS (negative in avF).
Echo: shows anatomy, will confirm diagnosis.
Management: Only treat if it is large, as there is a risk of right ventricular hypertrophy and HF. Surgical closure of septum secundum.
Surgery usually happens around 3-5 years to prevent HF and arrhythmias.

367
Q

What is different about the management of patent ductus arteriosus in premature vs term infants

A

In prem you can leave it if it is asymptomatic and it should close on its own (roughly by 1 month post 37 weeks). If prem baby becomes symptomatic - do medical management first - NSAID. If still persists, treat as term baby and do occlusion (transcatheter) or surgical ligation. Lifetime risk of endocarditis is an issue with an open PDA.
Term - NSAIDs dont help to close duct. If still open at 1 month and asymptomatic, monitor and consider occlusion at 1 year. If symptomatic, consider surgery at any age.

368
Q

What is the medical management of PDA in premature babies

A

NSAID
indomethacin - most common
ibruprofen

369
Q

What is the management of a small VSD

A

Monitoring to check it closes

Endocarditis info

370
Q

What are the symptoms of ASD

What is the risk of not treating a symptomatic ASD

A

Small - none
Large - wheeze, recurrent chest infection, if really bad HF
Risk of HF and arrhythmias

371
Q

What are the CXR features of tetrology of fallot

A

Upwards apex

Convex shape where PA should be on the Left

372
Q

What are the CXR features of patent ductus arteriosus

A

Enlarged pulmonary arteries
May have pulmonary vascular markings
Cardiomegaly

373
Q

What are the common cardiac arrthymias in children

A

SVTs, Long QT - accessory pathways or inherited channelopathies
AV nodal re-entry tachy f>m, ring conducting pathway in AV node, re-entrant loops to atria cause p wave before and after QRS, QRS is normal.
AV reciprocating tachy, extra pathway between atria and ventricles. Eg WPW. Get short PR and delta wave.
Can get congenital complete heart block -rare, anti-Ro and anti-Lo related

374
Q

What is the most common cause of heart block in children

A

Cardiomyopathy, eg R ventricular enlargement as seen in ASD - it takes longer for right bundle to conduct

375
Q

What is administered to an unwell child with SVT

A

ABC - fluids
Vagal stimulation - eg carotid massage
Adenosine - slows down AV node, re-establishes sinus rhythm
Electrical (cardioversion) conversion with DC shock if adenosine fails

376
Q

What is the major complication of long QT in children

A

Ventricular tachycardia and sudden death
LOC during exercise, stress etc are the symptoms
Is associated with erythromycin
Associated with specific gene mutation - anybody with a FHx of syncope on exertion should be assessed

377
Q

When are AF, flutter, VT and VF seen in children (rare)

A

After cardiovascular surgery. Otherwise rare.

378
Q

What are the causes of syncope in children

A 
Neurocardiogenic - prolonged standing 
Situation - defecation, urination, cough 
Orthostatic - BP falls >20 mmHg after 3 mins
Ischemic
Arrhythmia - heart block, SVT, VT
Features associated with children are:
Associated with exercise
Family hx
palpitations
379
Q

What organism causes rheumatic fever
When does it present
What are the symptoms

A 
Group A (beta-haemolytic) streptococcus 
2-6 weeks following pharyngitis 
Joints (arthralgia, swelling), chorea, carditis, fever, malaise
380
Q

Which valve is most affected by rheumatic fever

A

Mitral

381
Q

What criteria is used to diagnose rheumatic fever, what does it involve

A

Jones criteria
Two major, or one major and two minor criteria, plus supportive evidence of a preceding GAS infection
Major:
Carditis - endo, myocarditis, pericarditis
Polyarthritis - ankles, knewws, tender, redness, swelling
Chorea - 2-6 months after strep infection, involuntary movements
Erythema marginatum - map like rash on trunk and limbs
Subcutaneous nodules (rare)
Minor:
Fever, polyarthralgia, Hx of rhematic fever, raised ESR, CRP, WCC, prolonged PR on ECG

382
Q

What is the management of rheumatic fever

A

No treatments affect the outcome of acute rheumatic fever. While treatment can shorten the acute inflammation, all of the various manifestations will resolve spontaneously, except for carditis. The degree of valvular regurgitation usually improves but may occasionally progress in the months following a diagnosis of rheumatic fever. No treatment used in the acute phase is effective at modifying the acute course of carditis, and good adherence with secondary prophylaxis is the only treatment known to improve the long-term progression of rheumatic heart disease and prevent rheumatic fever recurrences
Bed rest
Analgesics for arthralgia - anti-inflammatory, aspirin
ACE inhibitors and diuretics for carditis
Possibly surgery for carditis
IVIg may help with chorea but not first line at moment

383
Q

What follow up management does a child with rheumatic fever need

A

Secondary prophylaxis with IM penicillin to prevent the development of rheumatic heart disease - this is long term damage from scarring and fibrosis of heart valve tissue. Usually mitral valve, but any valve can be affected. If child has had repeated attacks of rheumatic fever, this can develop as early as 20s.

384
Q

Which children are at risk of infective endocarditis

A

Any child with congenital heart disease - with the exception of septum secundum ASDs

385
Q

What are the signs of endocarditis in children

A

Infection (fever
Blood (its haemolytic bc if infective infarcts - anaemia, splinter haemorrhages, necrotic skin lesions, splenomegaly, retinal infarcts, haematuria)
Kidneys - haematuria - microscopic
Heart - clubbing, changing cardiac signs
Brain - CNS signs from infarction

386
Q

How is infective endocarditis diagnosed in children

A

Blood cultures, echo (can confirm but not exclude)
Common organism alpha-haemolytic strep - strep viridans
Usually treated with 6 weeks of penicilling + aminoglycoside (eg gentamicin)
Consider surgery
Prophylaxis - dental hygiene

387
Q

What age range of children does Kawasaki disease affect

A

6 months - 5 years
Need to do echo to look at myocardial (contractility), endocardial (valves), pericardial and coronary disease. Will need angiography or MRI if dilated coronary vessels.
Treatment: single infusion IVIG (need to give within 10 days), and aspirin (initially high then continued at low dose for 6 weeks until echo confirmed no coronary dilation/ aneurysm). Second dose if necessary, If IVIG resistant can try corticosteroids, infliximab or ciclosporin.

388
Q

List the features of kawasakis disease

A 
Young infants
Fever >5 days + 4 other features:
Non-purulent conjunctivitis 
Red mucous membranes
Cervical lymphadenopathy 
Rash 
Red and odematous palms 
Sores on palms, fingers, toes  
Peeling palms, fingers, toes
389
Q

What are the causes of pulmonary hypertension in children

A

Untreated congenital heart disease - left to right shunts
VSD, AVSD, PDA, Large ASD
Right to left shunts as well - but these should be treated in days to months as not compatible with life

390
Q

What is the presentation of osteomyelitis in children

A

Fever, painful, immobile limb, swelling, extreme tenderness, especially on moving the limb

391
Q

What investigations should you do for osteomyelitis in children

A

Bloods - inflammatory markers, FBC, CRP, ESR, LFT (albumin acute phase reactant), cultures, U&E (sepsis)
Imaging - MRI (X ray will be normal untill there is now bone deposition 7-10 days after infection). MRI will show soft tissue swelling in the periosteum.

392
Q

What is the treatment of osteomyelitis in children

A

Long course of antibiotics
Immediate IV abx untill acute phase reactants have come down and symptomatically improved, then oral abx for several weeks.
Aspiration or surgical decompression if not responding to abx treatment,

393
Q

What are the most common organisms of osteomyelitis in children

A

Staph aureus
If not vaccinated strep and H influenzae
Sickle cell prone to different organisms - including salmonella

394
Q

What is the definitive investigation for septic arthritis in children

A

USS guided joint aspiration for culture

395
Q

What is the management of septic arthritis in children

A

Long course of abx
Initially IV then oral
Joint may need wash out or surgical draining if abx dont work
Joint initially immobilised in functional position then must be mobilised to prevent deformity.

396
Q

What is the potential complication if septic arthritis and osteomyelitis in children

A

Joint / deformity problems

Destruction of articular cartilage and bone in joint

397
Q

At what age of a child should you always report sexual activity to social services/ safeguarding/ parents

A

You should usually share information about sexual activity involving children under 13, who are considered in law to be unable to consent.

398
Q

From what gestation week should you correct development age from

A

40

399
Q

List some causes of neonatal hypotonia

A 
Causes of neonatal hypotonia include:
neonatal sepsis
Werdnig-Hoffman disease (spinal muscular atrophy type 1)
hypothyroidism
Prader-Willi

Maternal causes
maternal drugs e.g. benzodiazepines
maternal myasthenia gravi

400
Q

Can x-linked conditions be past male to male

A

No

401
Q

Which children does intussusception affect most

A

Intussusception usually affects infants between 6-18 months old. Boys are affected twice as often as girls

402
Q

What is the diagnostic test for Hirschsprungs

A

Rectal biopsy

403
Q

How can androgen insensitivity present

A 
Female with delayed puberty 
Inguinal masses (testes)
404
Q

What is the exam definition of a PDA

A

Machinery murmur

ULSE

405
Q

What virus causes roseola

A

HHV-6
Starts on trunk
Spots on uvula

406
Q

What are some of the complications of JIA

A 
Chronic anterior uveitis
Flexion contractures
Growth failure 
Constitutional problems - anaemia, delayed puberty 
Osteoporosis 
Amyloidosis
407
Q

What is the management of JIA

A

Acute: Lifestyle modifications - exercise, keeping mobile, physiotherapy + NSAIDS
Long term:
1.methotrexate (if have bad polyarticular JIA may start this straight away) - movement to medicines depends on disease severity
2.Steroids
3.Biologics - anti-TNF

408
Q

What supplement needs to be given alongside methotrexate

A

Folic acid

409
Q

What are the different types of JIA

A

Polyarticular (>4 joints involved in first 6 months) - symmetrical, hand involvement
Oligoarticular (<4 joints) - asymmetrical large and small
Systemic - rash - salmon pink, macular
Psoriatic - dactylitis
Enthesitis (HLA B27)

410
Q

What are first line investigations for JIA

A

Inflammatory bloods + Autoimmune markers
FBC (WCC)
CRP, ESR
ANA, RF, HLAB27
2nd line USS - can be helpful for giving intraarticular steroid injections

411
Q

What demographics of children does JIA affect

A

Overall F>M
other than enthesitis - M>F HLA B27
Psoriatic and systemic 1:1

412
Q

What is the presentation of systemic JIA

A

Acute systemic illness + rash - salmon pink, macular
Think - liver, spleen, malaise, myalgia, arthralgia
Does not have to be joint swelling

413
Q

What investigations would you do for Septic arthritis and osteomyelitis in children

A

SA: Inflammatory plus joint aspirate culture, ESR, XR, USS

Osteomyelitis - inflammatory markers plus blood cultures, MRI

414
Q

What are the common causes of reactive arthritis

A 
GI infection (camylobacter, salmonella etc)
STI (older children)
415
Q

What is the most common cardiomyopathy in turners

A

Bicuspid aortic valve

416
Q

What is the cause of erythema multiforme

A

hypersensitivity reaction in response to herpes 7 virus

417
Q

When should children be able to achieve day an dnight time continence

A

3-4 years

418
Q

Where does scarlet fever ‘spare’

A

Face, palms, soles

419
Q

What bisphosphonate is used to treat osteogenesis imperfecta

A

Pamidronate

420
Q

What are the risk factors for vitamin D deficiency in children (i.e. risk of rickets)

A

Evidence of maternal vitamin D insufficiency
Lack of child’s exposure to sunlight
Lack of vitamin D in diet
Prolonged unsupplemented breast feeding

421
Q

How is vitamin D linked to calcium

A

Is required for calcium absorption from the gut

And calcium release from bones

422
Q

What is the presentation of rickets

A 
Clinically
Metaphyseal swellings
Bowing deformities
Slowing of linear growth
Motor delay
Hypotonia
Fractures
Respiratory distress
Pathologically
Failure to mineralise new bone
423
Q

What tests should you do if you suspect rickets

A

Biochem - Calcium, vitamin D, PTH

X-ray

424
Q

What are the radiological features of rickets

A

Bowed legs
Splayed metaphyses
Frayed metaphyses

425
Q

What is the difference between rickets and osteogenesis imperfecta

A 
OI is archetypal osteoporotic condition
MDT input
Bisphosphonates
Rickets cases have undermineralised bones
Usually due to vitamin D deficiency
Both result in bone weakness
426
Q

What vitamin D is produced after metabolism by the kidneys

A

1,25 OH vitamin D

427
Q

Which osteogenesis imperfecta can be picked up antenatally

A

II - fractures on 20 week scan - lethal form

428
Q

Which children have automatic MSU and no dipstick

A

Those <3 months

429
Q

What percentage of children with UTI have VUR

A

35%

430
Q

What are the indications for DMSA (renography)

A

Recurrent UTI
FHx of GU disease
Infants

431
Q

What is the treatment of UTI <3 months

A

IV amoxicillin + gent (or IV cephalosporin and ampicillin to cover listeria)

432
Q

What is the treatment of a UTI in >3 months

A

Uncomplicated:
3 day course of trimethoprim PO, nitro or amoxicillin/ co-amoxiclav.
Avoid constipation, increase oral fluids, encourage full voiding, repeat MSU.
Complicated: ill child, pyelonephritis, septicaemia
IV gent

433
Q

What is a benign cause of proteinuria in children

A

Orthostatic proteinuria

434
Q

Define nephrotic syndrome

A

Proteinuria >3
Hypoalbuminaemia (20g/L
oedema

435
Q

What is the most common biopsy finding in nephrotic syndrome

A

Minimal change disease - podocyte change

436
Q

What are the causes of nephrotic syndrome in children

A 
90% unknown 
10%
HSP (post strep)
Allergies
Hep B, C
Viruses
Malignancy 
Toxins 
SLE
437
Q

What is the presentation of nephrotic syndrome

What is the diagnostic criteria

A 
Odema - periorbital, vulval, scrotal 
Ascites 
Breathlessness - pleural effusions 
Diagnosis:
Proteinuria >3+
Hypoalbuminamia (urine albumin:cr ratio >200+)
Odema
438
Q

What investigations should you do for nephrotic syndrome

A

Urine sample - dipstick (protein), MSU - MCS, Na+ levels

Bloods - FBC, U&E, ESR, Anti-SLO, Hep B/C, Calcium, VZV

439
Q

What is the management of nephrotic syndrome

A

Prednisolone 4 weeks, 60mg/kg then drop down dose
Relapse, consider cyclophosphamide
Dependent, ciclosporin - monitor BP
Steroid resistant - renal biopsy
Additional management, Fluid and Na+ restrict, diuretics, albumin infusion sometimes

440
Q

What are the complications of nephrotic syndrome

A

Hypovolemia
Hypercholestrolaemia
Infection - peritonitis
Thrombosis

441
Q

When should a child be dry by day and dry by night

A

Day - 3 -5 years

Night - 5 girls. 6 boys

442
Q

What are the causes of day or night enuresis

A 
GINS-P
GU/GI - tract abnormality/ constipation 
Infection - UTI
Neuro - neurogenic bladder, spina bifida
Sugars - diabetes 
Psychogeneic - lack of attention to bladder sensation
443
Q

What first line investigations should you do in a child with bed wetting/ not dry during the day

A

Examine for any possible neuro causes - enlarged bladder
Urine sample - MSU, MCS, glucose
Consider follow up USS, Spinal XRay, MRI if suspect
structural abnormality
Once ruled out neuro/ GU causes offer bladder training strategies, pelvis floor exercise, can use medications for overactive bladder - oxybutynin

444
Q

What are the most common causes of secondary bed wetting

A

Psychological/ emotional upset

Diabetes

445
Q

What is the triad of HUS

A

Haemolytic anaemia
Thrombocytopenia
Acute renal failure

446
Q

What is the management of acute nephritis in children

A

Fluid and electrolyte management

Monitor kidney function

447
Q

Is HSP more likely to cause nephritis or nephrotic syndrome

A

Nephritis - 80% mild and make a full recovery

If severe proteinuria, may develop nephrotic syndrome, which steroids are used for.

448
Q

Causes of acute nephritis in children

A

Infectious (post strep)
Vasculitis (HSP, SLE, Wegners)
IgA nephropathy

449
Q

What is the first line treatment for glomerulonephritis

A

Mild disease (preserved eGFR, mild proteinuria) Supportive - Na restriction, fluid restrict, monitor U&E/ electrolytes. Likely abx (benpen) if poststrep
Moderate (falling eGFR, moderate proteinuria).
ACE inhibitors - for proteinuria, diuretics for volume overload, consider abx if post strep.
Severe (rapid eGFR deterioration, heavy proteinuria).
Consider corticosteroids (prednisolone), immunosuppressants, plasma exchange, plus all other supportive measures.

450
Q

What rash is common with rheumatic fever

A

erythema marginatum

451
Q

What is the management of whooping cough

A

Clarithromycin

452
Q

What is the escalation for red, amber, green features in the fever under 5 tool

A

Red - if life threatening, ambulance to hospital, non-life threatening, urgent paediatric referral
Amber - consider paediatric referral, or GP management with safety netting in writing, arrange follow up
Green - home treatment with safety netting

453
Q

What should be given to all children with a suspicion of meningococcal disease in GP

A

Give parenteral antibiotics to children with suspected meningococcal disease at the earliest opportunity (either benzylpenicillin or a third-generation cephalosporin)

454
Q

What investigations should be done in GP for any child <5 scoring amber

A

Urinalysis - clean catch dipstick (except <3 months)
Do not prescribe antibiotics without a source.
Throat infection - consider Rapid GAS antigen test and throat swab and abx
If suspect pneumonia - need to either refer to paediatrics (if red flags) or if amber or green treat with abx as viral and bacterial cant be dissociated. Treat with amoxicillin, second line co-amoxiclav, or macrolide erythromycin, clarithromycin, azithromycin.

455
Q

What are the symptoms of bronchiolitis
What are the investigations
What is the management

A

Wheeze <1 year, coryza, cough, fever (sometimes), inspiratory crackles (widespread), intercostal recession, apnoea, cyanosis.
Tests: PCR/ fluorescent antibody tests - nasopharyngeal aspirate rapid test
Management:
Conservative
Oxygen
NIV - cPAP
NG feeds
IV fluids
Ribavarin - antiviral - immunocomp’d, CHD
Vaccine - palivizumab

456
Q

What is the management of an asthma attack in children

A 
Oxygen 
Salbutamol 5mg neb + ipratropium bromide 
Hydrocortisone IV, or pred sol
Magnesium sulfate IV
Aminophylline IV
457
Q

What are the different types of asthma attack in children

A

Life-threatening - peak flow <33%, silent chest, sats <92%
Acute/ severe - peak flow 33-55%, inability to complete sentences
Moderate exacerbation - 50-70%, normal speech,

458
Q

What do you need to monitor during an asthma attack

A 
Hypokalaemia (Salbutamol)
Blood sugars  
ABG - respiratory failure 
Oxygen sats 
Peak flow

Phase 3a (9 decks)

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