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AA ST2 > Paeds > Flashcards

Paeds Flashcards

1
Q

When does clincial concern beign for scoliosis?

A

lateral curvature exceeds 10 degrees
pain
not fully corrected

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2
Q

what type of radiographs for scoliosis

A

standing PA and lateral
all of the iliac crests included

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3
Q

what is the Risser staging?

A

assess skeletal maturity on the iliac crests

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4
Q

what can cause scoliosis that should be reviewed for?

A

malignancny and abscess paraspinally.

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5
Q

MRi in scoliosis is reserved for who?

A

pain
neuro deficit

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6
Q

MRI in scoliosis
what protocol

A

Sag T1 and T2 of whole spine
Coronal T2 to look at bones
Axial of abnormal area and the conus (for tethered cord)

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7
Q

Scoliosis what angle is used?

A

Cobb angle

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8
Q

Most common type of scoliosis

A

Idiopathic

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9
Q

Other types of scoliosis

A

Idiopathic

nerumuscula
congenital
developmental
tumour
miscellaneous

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10
Q

Congenital Vertebral Anomalies:Types of Anomalies

A

Unilateral.
Bilateral (balanced defect)
Incarcerated

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11
Q

associated abnormalities with congenital vertebral anomalies

A

urinary tract
congenital heart disease
undescended scalulae
diastematomyelia

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12
Q

which scoliotic defect causes loss of longitudinal growth?

A

hemivertebrae

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13
Q

what are the management options for scoliosis?v

A

Observe, if no disability and not beyond 25 degrees.

Bracing - for growing child, prevent progression

Surgery - fusion - hold progression

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14
Q

What time frame of onset in scolioisis is a definite indication for MRI

A

eary onset (<10yrs)

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15
Q

Child back pain - reasons to CT

A

?osseous tumour
sondylolysis
history of truama
focal back pain

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16
Q

Spondylolysis - what is it?

A

Spondylolysis is a defect in the pars interarticularis,

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17
Q

difference between facet joint and spondylolyis

A

facet smooth
spndylo rough

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18
Q

MRI changes in a Pars defect

A

On MRI, there will be altered signal in the pars interarticularis (high signal on T2-weighted images and low signal on T1-weighted images) in pars defect.

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19
Q

Discitis is characterised by …..

A

disc space narrowing with end-plate irregularity and sclerosis.

may take two weeks to show on radiographs

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20
Q

OSteoid osteoma appears as what on radiographs/v

A

central lucent nidus surrounded by sclerotic bone

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21
Q

cause of back pain and is typically worse at night, exacerbated by alcohol and relieved by non-steroidal anti-inflammatory drugs

A

OSteoid osteoma

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22
Q

Osteoblastoma is what kind of tumour

what does it produce

A

is a benign osseous tumour that produces osteoid and wormian bone.

slow growing

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23
Q

Appearance of Osteoblastoma on MRI

A

low T1 and intermediate to high T2.

Signal void on all sequences related to matrix calcification

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24
Q

what can Langerhand cells histiocytosis cause in the spine

A

complete collapse of the vertebral body

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25
Q

Metastatic disease in the spine can be caused by what conditions in paeds

A

lymphoma, leukaemia, neuroblastoma, Ewing’s sarcoma and rhabdomyosarcoma.

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26
Q

Kyphosis with anterior wedging and end-plate irregularity are typical findings in XXXX

A

Scheuermann’s disease.

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27
Q

In infancy, torticollis is usually due to a

A

benign sternomastoid tumour (fibromatosis colli)

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28
Q

rotatory atlantoaxial fixation - what is it?

A

C1 is rotated and fixed.
Out of alignment, not symmetrical

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29
Q

atlantoaxial dislocation - what is it

A

complete disruptin of the articular mechanism.

likely truama but also congential segmentation of spine.

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30
Q

Torticollis and atlantoaxial subluxation may be secondary to retropharyngeal infection.

what is the syndrome called

A

This is known as Griesel’s syndrome.

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31
Q

Sandifer syndrome

A

Severe gastro-oesophageal reflux can cause abnormal posturing of the head and neck which may resemble torticollis.

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32
Q

Note the herniation of elongated cerebellar tonsils through the foramen magnum - what could be the problem?

A

Chiari 1 malformation

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33
Q

The hallmark of DDH is

A

acetabular dysplasia resulting in a shallow or dysmorphic socket for the femoral head

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34
Q

Is DDH present at birth?

A

No, only after first few months

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35
Q

early DDH treatment

A

abduction device
short treatment (2-4 months)
Normal or near normal hip likely

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36
Q

late DDH diagnosis considered when

A

4 months

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37
Q

complications of DDH

A

Osteoarthritis

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38
Q

Ortolani ad Barlow manoevres - WHEN?

A

DONE AT 6 WEEKS and birth

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39
Q

Ortolani and Barlow are done when

A

birth and 6 weeks

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40
Q

Ortolani and Barlow - which is which

A

Ortolani isto reduce the hip

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41
Q

what imaging is used for DDH based on patients age?

A

under 1 - US

over 1 - CT or MRI

Need to see the floor of acetabulum and cant if ossified

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42
Q

DDH US need to show

A

Labrum, coronol plane
lower limb of the ilium

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43
Q

DDH Graf types of hip

A

4 types
T1 and 2 - centred hips

Types 3 and 4, decentred

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44
Q

biggest cause of intusseption

A

idiopathic

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45
Q

complications of intussepction

A

obstruction and ischmaeia

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46
Q

intussuseption associations

A

coeliac
cystic fibrosis

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47
Q

why does intusseption present with rectal bleeding?

A

meckels

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48
Q

underlying causes of intussuseption?

A

meckels
duplication
polyp or lymphoma

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49
Q

plain film in intusseption?

A

can appear normal

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50
Q

What blood vessels to chekc in US scan of intusseption?

A

Always check the superior mesenteric artery (SMA)/superior mesenteric vein (SMV) orientation, if you can, during your ultrasound.

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51
Q

Factors contributing to the likely successful reduciton of intussuseptio

A

acute onset and scanning

Vascular flow within the intussuseptio

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52
Q

which side of intussuseption is harder to reduce

A

left sided more difficult

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53
Q

prior to intersusseption suflation - what needs to be checked locally?

A

surgeons and anaesthetist available to do procedure and happy to

IV access is a must

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54
Q

insufflation pressures

A

80 to 120mmHg

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55
Q

conditions that may cause intussuseption>

A

meckels
peutz jeghers
Henoch- Schoenlein

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56
Q

Cuases of acute abdo pain are categorised as what

A

surgical and non surgical

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57
Q

examples of non surgical casues of abdo pain

A

Gastroenteritis
Diabetic Ketoacidosis
Pneumonia / pharyngitis

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58
Q

aim of imaging in abdominal pain?

A

to work out who needs abx or surgery?

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59
Q

age related diagnosis - Nenonatal abdominal pain

A

Intestinal obstruction
Malrotation with midgut volvulus
Meconium ileus
Hirschsprung’s disease
Bowel atresia
Necrotising enterocolitis

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60
Q

age related diagnosis - Toddler
abdominal pain

A

Malrotation +/- volvulus
Intussusception
Incarcerated hernia
Gastroenteritis
Haemolytic uraemic syndrome
Meckel’s diverticulum
Urinary tract infection
Constipation

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61
Q

age related diagnosis - Older school aged child

abdominal pain

A

Appendicitis
Mesenteric adenitis
Bowel obstruction
Inflammatory bowel disease
Henoch-Schönlein purpura
Urinary tract infection and obstruction
Cholecystitis and pancreatitis
Constipation
Primary peritonitis
Gynaecological causes
Non-abdominal causes such as pneumonia and diabetic ketoacidosis

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62
Q

Until proven otherwise bilious vomitting is considered as WHAT
until proven others

A

Surgical cause

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63
Q

Abdo pain and very high fevers (over 38.5) consider what

A

mesenteric adenitis over appendicitis

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64
Q

when should we do an abdominal radiograph in acute abdo pain

A

acute obstruction
renal colic
perforation

unclear following initial assessment

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65
Q

is intestinal perforation more or less common at neonatal age

A

more common.

as older child will have clear peritonitis with it

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66
Q

Psoas shadows and properitoneal fat stripes

their absence suggests

A

indicate retroperitoneal inflammation, acute appendicitis

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67
Q

How is obstruction classified

A

mechanical or functional

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68
Q

normal size of appendix

A

less than 6mm

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69
Q

appendicitis Peri appendicular fluid may be a sign of

A

imminent perforation.

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70
Q

what happens to the mesentry in mesenteric adentiis

A

very vascular

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71
Q

Meckel’s diverticulum is a true diverticulum arising from the

A

anti-mesenteric border of the distal ileum

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72
Q

Meckel’s diverticulum rule of 2’s

A

It occurs in 2% of the population
It is two times more common in males
It is 2 inches long
It rises 2 feet from ileocaecal valve
2% become symptomatic
Most patients present within the first 2 years of life
Two out of three cases have ectopic gastric or pancreatic tissue

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73
Q

most common complication from Meckel’s diverticulum is

A

GI haemorrhage

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74
Q

Meckels on US

A

incompressible, blind-ending tubular structure with hypervascularity on Doppler

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75
Q

Indications for a cranial USS

A

Prematurity

low birth weight
birth asphyxia
clotting disorders
seizures

congenital abnormality
large or small head circumference

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76
Q

Cranial US reviews what structures

A

Parenchyma
CSF spaces

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77
Q

cranial US - grey matter is hypo or hyper

A

hypo echoic

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78
Q

Over what times of gestation does sulci form ?

A

Sulcal development begins during the 5th month of gestation. Primary sulci are present by the 7th month. In the 8th and 9th months, there is bending and branching of the 1° sulci with the appearance of 2° and 3° sulci.

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79
Q

Brainstem echogenicity

A

anterior is echogenic

psoterior

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80
Q

what are the US cranial views needed

A

frontal lobes and then horns
munro and 3rd ventricle
bodies then trigone of lateral ventricles
occipital lobes

then sagittal - mid, lat ventricles then extreme lateral ventricles

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81
Q

what level is the US cranial ventricular index measures

A

level of foramen munro

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82
Q

if there is echogenic anterior to WHAT consider haemorrhage on paediatric ultrasound

A

Munro

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83
Q

In a term infant, a normal RI is

A

greater than 0.6.

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84
Q

UIS appearance of cerebral oedema

A

slit like ventricles
increased parenchymal echogenicity, poor definition of sulci and gyri, and decreased vascular pulsations.

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85
Q

cavum septum pallucidem at birth

A

normal finding.
50% of babies it.

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86
Q

Bilateral choroid plexus cysts indicate …..

A

trisomy

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87
Q

Pre term or term

Periventricular blush and asymmetry of lateral ventricles

A

Pre term more likely

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88
Q

most common US cranial pre term pathologies

A

intraventricular-germinal matrix haemorrhage (GMH)

periventricular leukomalacia (PVL)

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89
Q

GMH is also called

A

subependymal haemorrhage

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90
Q

neonates with IVH-GMH subsequently develop an associated parenchymal flare due to

A

venous infarction

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91
Q

What are the sequelae of Germinal matrix haemorrhage / IVH in the preterm neonate?

A

Hydrocephalus
Ventriculitis
Porencephalic cyst
Trapped fourth ventricle
Spinal canal dilatation

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92
Q

post hypoxic ischaemic neonatal brain injury how long for cysts to be made `

A

2 - 4 weeks

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93
Q

At what age in pre term does the water shed area move to the periphery of the brain

A

36 weeks

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94
Q

hydrocephalus vs dilatation from atrophy

hydrocaphalus features

A

temporal horns also dilated
4th centricle dilatation
cortical sulci effacement
raised iCP

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95
Q

causes of hydrocephalus

A

Congenital malformations, such as vein of Galen malformation or aqueduct stenosis

Rarely neoplasia, for example posterior fossa tumours or choroid plexus papilloma

Infection

Benign infantile hydrocephalus

Chiari malformation

Meningomyelocoele

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96
Q

causes of fetus meningioencephalitis infection

A

Cytomegalovirus (CMV)
Toxoplasma gondii
Rubella virus
Herpes simplex (HSV) type 2 virus (known as toxoplasmosis/rubella/cytomegalovirus/herpes simplex (TORCH) complex)

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97
Q

common infections for neonatal meningitis are…..

A

E Coli and Group B strep

or HiB for 2 months to 2 years

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98
Q

Congenital malformations that

Errors in histogenesis (development of tissues)

A

Vein of Galen malformation
Tuberous sclerosis
Sturge-Weber syndrome
Neurofibromatosis

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99
Q

Congenital malformations

Errors in organogenesis

A

Neural tube closure (3-4 weeks gestational age)
Diverticulation (5-10 weeks gestational age)
Neuronal proliferation (2-6 months gestational age)
Sulcation and migration (2-5 months gestational age)
Myelination (7 months in utero - 2 years)

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99
Q

Congenital malformations

Errors in organogenesis of brain

A

Neural tube closure (3-4 weeks gestational age)
Diverticulation (5-10 weeks gestational age)
Neuronal proliferation (2-6 months gestational age)
Sulcation and migration (2-5 months gestational age)
Myelination (7 months in utero - 2 years)

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100
Q

Features of Dandy walker complex

A

Large fluid filled posterior fossa cyst (dilated fourth ventricle)
Small or absent cerebellar vermis
Small cerebellar hemispheres displaced superiorly
Elevated tentorium
Lateral ventricles and third ventricle may be dilated

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101
Q

What are the common palpable masses in an neonate

A

Ovarian mass

hydronephrosis

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102
Q

what are the common cuases of a palpable abdominal mas in an infant

A

Pyloric tumour
constipation
hydronephrosis
intussusception
haptosplenomegaly

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103
Q

young female - abdo mass

first line investigation is

A

Ultrasound

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104
Q

paediatric hydronephrosis - next imaging step?

A

Bladder outlet obstruction must be excluded. The next stage is to proceed to a micturating cystourethrogram (MCUG) (after antibiotics).

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105
Q

Renal tumours

A

Wilms tumour
retroperitoneal adrenal neuroblastoma
pelvic rhabdomyosarcoma

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106
Q

Liver tumours

A

hepatoblastoma
HCC

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107
Q

the developing GI tract is divided into three parts: when

A

3 weeks

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108
Q

The ventral aspect of the foregut gives rise to the WHAT and its dorsal to the oesophagus.

A

respiratory primordium

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109
Q

Skin, central and peripheral nervous system is what embryonic layer

A

ECTOderm

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110
Q

GI and repsiraotry lining is what embryology layer

A

Endoderm
think endoscopic

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111
Q

Muskuloskeletal

A

mesoderm

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112
Q

diffrence between an enteric cyst and neuroenteric cyst

A

neuroenteric cyst involved the ectoderm
enteric only the endoderm

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113
Q

formes frustes TOF vs duplications

A

duplications are always posterior

TOF

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114
Q

Oesophageal lung

A

In this condition, the right main bronchus arises from the distal oesophagus. Patients present with recurrent chest infections.

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115
Q

double bubble sign

A

duodenal atresia

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116
Q

what are the VACTERL associations

A

V: vertebral defects
A: anal atresia
C: cardiac defects
TE: tracheoesophageal fistula
R: renal anomalies
L: limb abnormalities

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117
Q

what GI defects are ax with Downs syndrome

A

Duodenal atresia or stenosis
Annular pancreas
VACTERL
Hirschsprung’s disease
Small bowel malrotation

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118
Q

twisted ribbon sign

A

twisting of the mesentry around the SMA

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119
Q

Conditions with malrotation

A

exomphalos or gastroschisis

Congenital diaphragmatic hernia (often)

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120
Q

Hirshsprungs
Short vs long segment

A

Short - dilated normal bowel. Coned abnormal bowel .

Long - long affected length. Rare

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121
Q

inferior one-third of the anal canal is derived from the X

A

proctodaeum.

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122
Q

inferior one-third rectum is supplied by the:

A

Inferior rectal arteries
Branches of the pudendal artery

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123
Q

Imperforate anus and anorectal anomalies which include:

A

Anal atresia
Anal stenosis
Rectal atresia
Ectopic anus (‘fistula’)

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124
Q

Proliferation with hypertrophy of the mesenteric fat (fat wrapping) is a finding associated with

A

with inflamed bowel

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125
Q

Mucosal oedema, avid mucosal enhancement, mesenteric oedema and enhancing reactive lymph nodes are more commonly seen in ACUTE OR CHRONIC INFLAMMATION

A

ACUTE

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126
Q

Causes of abnormally shaped vertebral bodies

Conditions with normal bone density

A

Deficient ossification of vertebral bodies (hypoplasia with anterior wedging/kyphosis, coronal or sagittal clefting)

Hypoplastic peg

Deficient ossification of pedicles

Genetic, structural, congenital and acquired abnormalities of shape

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127
Q

Causes of abnormally shaped vertebral bodies include:

Conditions with reduced bone density and vertebral body collapse

A

Osteoporosis
Fracture

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128
Q

Odontoid hypoplasia is seen in

A

Achondroplasia
Diastrophic dysplasia
Metaphyseal chondrodysplasia (type McKusick)
Kniest dysplasia
Metatropic dysplasia
Mucolipidoses
Mucopolysaccharidoses (MPS)
Pseudoachondroplasia
Spondyloepiphyseal dysplasia congenita

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129
Q

Absent ossification of vertebral bodies

A

Achondrogenesis type I

Atelosteogenesis

Dyssegmental dysplasia

Hypochondrogenesis

Hypophosphatasia

Opsismodysplasia

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130
Q

Cervical kyphosis results from hypoplasia of the anterior parts of one or several vertebral bodies

seen in which conditions

A

telosteogenesis (Fig 1)
Campomelic dysplasia (Fig 2)
Chondrodysplasia punctata
Diastrophic dysplasia (Fig 3)
Kniest dysplasia
Larsen syndrome
Spondyloepiphyseal dysplasia congenita

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131
Q

Campomelic dysplasia means

A

(bent limbs)

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132
Q

Paeds vertebral body shape
Beaks:

A

MPS type IV (Morquio)

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133
Q

Paeds vertebral body shape
Bullets:

A

achondroplasia

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134
Q

Paeds vertebral body shape
Codfish:

A

osteogenesis imperfecta

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135
Q

Paeds vertebral body shape
Diamonds:

A

metatropic dysplasia

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136
Q

Paeds vertebral body shape
Hooks:

A

Hurler syndrome (MPS type IH)

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137
Q

Paeds vertebral body shape
Pears:

A

spondyloepiphyseal dysplasia congenita (SEDC)

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138
Q

Paeds vertebral body shape
Scalloped:

A

MPS, achondroplasia, neurofibromatosis

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139
Q

Paeds vertebral body shape
Wafers:

A

thanatophoric dysplasia

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140
Q

Ataxia and absent reflexes are the clinical signs of ….

A

Guillain–Barré syndrome

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141
Q

a solid tumour of the spine in paeds MRI will look like

A

hyperintense on T2W
hypointense on T1W imaging
Is a well-defined mass enhances gadolinium
associated with a tumoral cyst
May have a central area of necrosis, which has the MR characteristics of cyst formation

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142
Q

MRI haemorrhage does what intensities over time

A

Within several days of the haemorrhage, the state of oxygenation will change to deoxyhaemoglobin (which is hypointense on T1W and T2W imaging), and further to intracellular methaemoglobin, and the area of haemorrhage will become hyperintense on T1W and hypointense on T2W imaging.

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143
Q

Axial T1W imaging shows a flow void within the cord indicating the presence of a

A

blood vessel and an arteriovenous malformation.

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144
Q

Intramedullary masses have the following radiological features:

A

Enlargement of the spinal cord in all three planes
The spinal cord above and below the mass is positioned normally within the bony spinal canal
The margins of the mass may be well defined or poorly defined

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145
Q

Extramedullary masses have the following radiological features

A

The margins of the mass are always well defined
Small masses can be seen separated from the cord by CSF
Large masses will obliterate the space between the mass and the cord

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146
Q
  1. IntramedullarY - TUMOURS
A

pilocytic astrocytoma, ependymoma and ganglioglioma

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147
Q

Extramedullary CORD TUMOURS

A

neurofibroma, schwannoma and disseminated leptomeningeal metastases

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148
Q

The MR features of a discitis are

A

the same as in an adult. The disc space will be narrow and the disc will have both prolonged T2 (hyperintense on T2W images) and T1 (hypointense on T1W images) signals and will enhance

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149
Q

STAGE age t1 t2

DRAW THE TABLE FOR THESE ACROSS

HYPERACUTE

ACUTE
EARLY SUBACUTE

LATE SUBACUTE

CHRONIC

A

Hyperacute <24 h Isointense Mildly hyperintense

Acute 1-3 d Mildly hypointense Hypointense

Early subacute 3-7 d Hyperintense Hypointense

Late subacute 7-14 d Hyperintense Hyperintense

Chronic >14 d Hypointense Hypointense

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150
Q

ASSOCATION of NG2 and intramedullary tumours

A

pilocytic astrocytomas of the cord are seen in children with NF1 and ependymomas in children with NF

151
Q

Thoracic, lumbar locations; conus (especially myxopapillary)
Centra
Well-demarcated
Potential hemosiderin ‘cap sign’ on T2
Can have drop metastases

diagnosis

A

ependymoma

152
Q

Cervicomedullary junction
Eccentric
Can calcify
Heterogeneous T1
Little peritumoral oedema

diagnosis

A

gnagliiogllioma

153
Q

Well circumscribed
Cyst/slow voids
Can be haemorrhagic
Vigorous enhancement

diagnosis

A

haemangioblastoma

154
Q

Cervicothoracic junction
Eccentric
Cystic with enhancing nodule/infiltrative with irregular enhancement and ill-defined margins

diagnosis

A

astrocytoma

155
Q

round fusiform well-defined masses that can expand out of the neural foramen giving them a dumbbell appearance. They are usually isointense on TI and hyperintense on T2 with homogeneous enhancement post-contrast.

A

neurofibromas

156
Q

when does malrotation presentations normally occur

A

first month of life

157
Q

bile stained vomitting in a neonate is what until proven otherwsie

A

malrotation

158
Q

what does an abdominal radiograph offer in malrotation

A

nothing

159
Q

does US exclude malrotation?

A

no

thought the duodenum passing behind the sma is highly reassuring

160
Q

what is the relationship of the mesentry and DJ flexure to consider malrotation

A

should swing under. The DJ flexure should be at the same level as the duodenal cap

161
Q

commonest gastrointestinal emergency in neonates.

A

NEC

162
Q

when does NEC occur

A

second or third week of life

163
Q

what happens to bowel wall blood flow in NEC

A

more and more blood flow until sloughing leaving only the serosa intact

ischaemia wall becomes thin walled and no blood

164
Q

in NEC - what signs are there to look for

A

Pneumotosis intestinalis
portal venous gas
free intraperitoneal gas

165
Q

in neonatal abdo xr - bowel width can be compared to

A

widtth of L1

166
Q

how to differentiate intramural vs intraluminal gas in NEC on US

A

intramural gas is all the way around the bowel.
`
intraluminal rises to the top

167
Q

if on fluoro there is uncertainty of level or position of DJ flexure what can you do later?

A

abdo film to see if the caecum is seen in the righ tplace

168
Q

newborn with lung mass

differentials include

A

Congenital cystic adenomatoid malformation
Bronchopulmonary sequestration
Congenital diaphragmatic hernia
Lung filled with retained amniotic fluid secondary to a congenital lobar emphysema or bronchial atresia

169
Q

how to differentiate congenital cystic adnematoid malformation in the lung from sequestration

A

blood supply

Sequestration from the systemic

Also cysts in CCAM.

170
Q

what is Transient Respiratory Distress of the Newborn

A

delay in normal physiological clearance

171
Q

typical of meconium aspiration syndrome chest radiograph

A

Normal or slightly overinflated lungs
Extensive patchy lung shadowing with some peripheral overinflation
Often cardiac enlargement due to concomitant myocardial ischaemia

172
Q

differential for meconium aspiration

A

amniotic fluid apsiraiton

this clears more quickly and no complications such as pulmonary hypertension and secondary infection

173
Q

Overinflated lungs
Course reticular shadowing
‘Barrel’ shaped chest

chest radiograph

A

bronchopulmonary dysplasia

174
Q

patent ductus arteriosus causes what kind of shunting

A

left to righ

175
Q

why can the patent ductus arteriosus remain open in hypoxia ?

A

hypoxia which has led to higher pulmonary artery pressures due to failure of pulmonary artery resistance to fall after delivery

176
Q

Well-recognised but rare complication of surfactant treatment (due to capillary engorgement)

A

pulmonary haemorrhage

177
Q

features of pulmonary hypoplasia

A

Small volume chest
Hazy lungs due to associated pulmonary oedema
Clinical difficulty in ventilating (high pressures required) and poor oxygenation

178
Q

Common causes of pulmonary hypoplasia include

A

Oligohydramnios in pregnancy
Lung compression, e.g. by tumour or diaphragmatic hernia or effusion or large heart
Thoracic cage compression (e.g. bone dysplasia) or muscular disease (e.g. dystrophy)

179
Q

Unilateral Pulmonary Hypoplasia/Agenesis

features

A

Often asymptomatic
Can be discovered incidentally
May show associated rib or vertebral anomalies
association with oesophageal atresia and tracheal abnormalities

More serious if aplasia is right-sided (due to severity of associated cardiac anomalies)

180
Q

Features of pulmonary lymphangiectasia

A

Very rare condition
Intractable respiratory distress with cyanosis
Survival beyond neonatal period unlikely
May be isolated or associated with generalised lymphatic problems
Radiological appearances are a combination of distended lymphatics leading to streaky lung and chylous pleural effusion
Can be associated with Noonan’s syndrome and Turner’s syndrome

181
Q

right to left shunting through the patent ductus arteriosus - radiograph features

A

Right to left shunting
Poor lung vessel visualisation
Right heart enlargement (due to raised right heart pressures, tricuspid incompetence and myocardial dysfunction)

182
Q

at what time can bronchopulmonray dysplasia be diagnosed

A

at least 28 days of age

caused by surfactant deficinecy, prolonged ventilation and prematurity

183
Q

what are the surgical causes of neonatal respiratory distress

A

Oesophageal atresia and tracheo-oesophageal fistula
Congenital diaphragmatic hernia
Congenital cystic adenomatoid malformation of the lung
Pulmonary sequestration
Enteric duplication cysts
Diaphragmatic eventration
Bronchogenic cyst
Congenital lobar emphysema

184
Q

imaging post chest radiograph confirming oesophageal atresia

A

normally just an echo for sid eof aortic arch and cardiac anomalies ahead of surgery

185
Q

mediastinal mass which is displacing the trachea to the left

differentials

A

bronchogenic cyst
cystic hygroma
enlarged lymph nodes

186
Q

We must define where in the chest the abnormality exists. The fact that the lesion extends below the diaphragm means it must be XXXX

on chest XR

A

posteriorly situated

187
Q

if the chest drain is too medial it can damage what structure

A

phrenic nerve

188
Q

how to determine laterality of pathology on a unilateral hypodense lung

A

inspiratory vs expiratory film: no change is abnormal

dense normal vessels: normal

low vessels: abnormal

189
Q

Causes of a large hyperlucent hemithorax

A

Compensatory emphysema

Obstructive emphysema

Pneumothorax

190
Q

categories of obstructive emphysema

A

INtraluminal - mucus, foreign body

intramural - haemangioma, bronchomalaica

extraluminal - bronchogenic cyst, lymph

191
Q

hyperlucent hemithorax

primary abnormality of pulmonary blood flow

A

Pulmonary arterial hypoplasia
Unilateral pulmonary stenosis
Cardiac shunt procedure with unequal pulmonary blood flow
Pulmonary embolism (rare in children)

192
Q

The presence of the small lung, decreased pulmonary vascularity and evidence of bronchiolitis obliterans is often referred to as

A

McCleod’s or the Swyer-James syndrome.

A hyperlucent small lung
In association with a previous history of pneumonia
It is not unusual to demonstrate abnormalities in the ‘normal’ lung on ventilation/perfusion imaging and CT scanning

193
Q

Increased translucency of both hemithoraces is commonly associated with hyperinflation of the lungs and may be related to

A

Exuberant inspiration
Hyperinflated lungs, which may be obstructive or non-obstructive
Decreased pulmonary blood flow (may be normal lung expansion)
Free intrathoracic air

194
Q

Non-obstructive hyperinflation

This is also referred to as physiological hyperinflation.

causes

A

acidosis and congential heart disease
mechanical ventilation
dehydration (through oligaemia)

195
Q

obstructive hyperinflation

Peripheral airway obstruction, such as

A

Meconium aspiration
Bronchiolitis
Asthma
Bronchopulmonary dysplasia
Cystic fibrosis (CF)
Immunologic deficiency

196
Q

obstructive hyperinflation

central airway obstruction

A

Tracheal foreign body
Tracheal compression
Tracheobronchomalacia

197
Q

Peribronchial cuffing is best seen in the

A

right middle lobe.

197
Q

Peribronchial cuffing is best seen in the

A

right middle lobe.

198
Q

oligaemia and boot shaped heart think

A

Tetrology of fallot

199
Q

Anterior tracheal and posterior oesophageal impressions, with bilateral lateral oesophageal impressions
Innominate artery with left aortic arch

what vascular anomaly is this?

A

double aortic arch

200
Q

Post oblique oesophageal impression and normal trachea

A

RSA with left aortic arch

201
Q

Post tracheal impression and anterior oesophageal impression

A

pulmonary artery sling

202
Q

Anterior tracheal impression and normal oesophagus

A

innominate artery with left aortic arch

203
Q

Anterior tracheal and posterior oblique oesophageal impressions

A

right aortic arch with lsa

204
Q

anatomy relations of the pulmonary artery bronchus and vein at the hilum on left and right

A

Note that the left pulmonary artery crosses over the left main bronchus becoming posterior to the left main bronchus. This is unlike the right pulmonary artery which passes anterior to the right main bronchus.

205
Q

Categories of enlarged lymph nodes

A

Infection: lower respiratory tract infection, mycoplasma, tuberculosis (TB), fungal

Neoplasm: lymphoma/leukaemia and secondary neoplasms such as osteosarcoma, Ewing’s, metastasis

Cystic fibrosis
Histiocytosis
Sarcoidosis

206
Q

Cold agglutinins are positive on blood testing

A

think mycoplasma

207
Q

unilateral hilar adenopathy +/- paratracheal adenopathy.

A

TB`

208
Q

pulmonary valve stenosis causes unilateral or bilateral hilar enlargement

A

bilateral

209
Q

what is cystic fibrosis - gene and how it transpires

A

Auto Recessive
mutation of fibrosis transmembrane conductance regulator gene

1 in 2500

210
Q

cystic fibrosis - associated abnormalities

A

Pancreatic insufficiency
Gastrointestinal and hepatobiliary disease
Nasal polyps
Sinusitis
Infertility

211
Q

Cystic fibrosis - pathogens for pneumonia

A

Staph aureus and pseudomonas

212
Q

most common presentation of gastro-intestinal disease in cystic fibrosis is with bowel obstruction in the newborn due to XXXX

A

meconium ileus

others

volvulus
fibrosing colonopathy
intussusception
Peptic ulcer
colitis
rectal prolapse

213
Q

complications of meconium ileus

A

occurs in 50% of infants

meconium peritonitis
ileal atresia
perforation
volvulus

214
Q

CT scan shows the liver has a lower attenuation than the spleen consistent with….

A

fatty liver

215
Q

if a patient has meconium ileus, 90% will have

A

Cystic fibrosis

216
Q

prtoprtion of paeds tumours are neuro?

A

15%

second commonest tumour

217
Q

supra vs infra tumours based on age

A

supra more comon in under 3
infra more common 4 to 10 and over 10 the same

218
Q

Raised ICP is a sign of aggreessive or insiduous brain tumours?

A

aggressive

219
Q

symptoms of cranial sutures unfused

A

Increasing head circumference
Nausea/vomiting
Irritability

220
Q

If sutures are fused brain malingnant features are

A

Headaches
Visual disturbances
Seizures and focal neurological signs and symptoms, such as ataxia and cranial nerve (CN) palsies

221
Q

cOMMONEST CHILDHOOD BRAIN TUMOURS

A

atrocytic tumours (50%)

then

primitive neurectoderman tumours
- infratentorial medulloblastoma
- supratentorail PNET

222
Q

Commonest adult brain tumours

A

high grade astrocytic tumours such as anaplastic astrocytoma

Glioblastoma multiforme

223
Q

Neonatal tumours are…

A

teratoma,
hypothalamic astrocytoma
choroid plexus papilloma and PNET.

224
Q

brain cancer - MRI sequence and protocol

A

bolus of paramagnetic contrast and should include post-contrast T1W images.
Coronal FLAIR
DWI and ADS

axial T1 T2

SPine
sag T1 (post gad)
ax T1

225
Q

Which imaging modality is the modality of choice when there is high suspicion of an intracranial tumour in a child and why?

A

MRI

226
Q

propensity to spread via the CSF -tumours will appear as

A

resulting in either multiple (usually) enhancing lesions in the subarachnoid space and/or diffuse smooth or nodular enhancement of the pia mater over the brain

227
Q

tumours have the propensity to spread via the CSF

A

Primitive neuroectodermal tumour e.g. medulloblastoma, supratentorial PNET, Pineoblastoma/pineocytoma

Supra and infratentorial ependymoma

Germ cell tumours

High grade astrocytic tumours e.g. anaplastic astrocytoma, glioblastoma multiforme (GBM)

Choroid plexus tumours e.g. papilloma and carcinoma

228
Q

common cerebellar tumours

A

Medulloblastoma
Astrocytoma - low grade (e.g. pilocytic astrocytoma) and high grade (e.g. anaplastic astrocytoma)
Ependymoma

229
Q

common brainstem tumours

A

Pontine glioma
Tectal plate glioma

230
Q

most common infratentorial paediatric brain tumour

A

medulloblastoma

231
Q

why does medulloblstoma have

solid CT apperaance
and cuase hydrocephalus

A

invasdes vermis and 4th ventricle.

made up of tightly compact round cells

232
Q

grades of astrocytoma

A

1 to 4

1 juvenil pilocytic astrocytoma

4 - anaplastic astrocytoma

233
Q

ASTROCYTOMA FOUND WHERE

A

MIDLINE STRUCTURE

234
Q

ASSOCIATIONS astrocytoma

A

NF1

235
Q

what are the three appearances of an astrocytoma?

A

Cyst with mural enhancing nodule: 50% (Fig 1)
Rim-enhancing mass with necrotic/cystic centre: 40-45% (Fig 2)
Non-necrotic solid mass

236
Q

astrocytoma enhance

A

YES

237
Q

what density is astrocytomas

A

can be low density most of th etime.
high grade can be isodense to grey matter though - increased cellularity

238
Q

what is the fluid in cystic astrocytomas like

A

slight denser than csf

239
Q

who gets affected by ependymoma?

A

kids 1 to 5
slightly more boys

240
Q

what disease is true (rare) and pseudo- (more common) perivascular rosettes,

A

Ependymomas

241
Q

why does ependymoma present with lower cranial nerve palsies ?

A

extension through the
Lushka and Magendie formaina

242
Q

appearance of infratnetorial ependymoma

A

clacification and small cysts
invades 4th ventricle and expands it

invades lushka and magendie
out through foramen magnum

enhances around necrotic areas

243
Q

Ependyomoma MRI features

A

predominantly iso to hypointense to GM on T1W

especially heterogeneous on T2W imaging

iso to hyperintense solid components, hyperintense intratumoural small cysts and hypointense areas due to calcification or blood products

Mild to moderate heterogeneous enhancement

244
Q

How to differentiate a medulloblastoma and ependymoma infratentorial lesion

A

Does it invade lusdka / magendie

245
Q

features of glioma to wathc out for

A

surround the bsailar artery

can compress the 4th ventricle

invades the pons, infiltartes

246
Q

Tectal plate gliomas are assocaited with

A

NF1

247
Q

Subependymal giant cell astroxytosis is only found in which disease

A

Tuberous sclerosis

248
Q

differentiate suependyaml astrocytoma and hamartoma that look similar

A

the subependymal astrocytoma will grow

249
Q

pyloric stenosis presents when

A

6 weeks

250
Q

where to find the pylorus on US

A

behind the gallbladder

251
Q

pylorus measurements taken in which plane

A

longitudinal

252
Q

Laryngitis causes can be divided by

A

Location of obstruction

253
Q

Supraglottic

A

Laryngomalacia
Epiglottitis
Foreign body
Trauma

254
Q

Glottic

A

Laryngeal web
vocal cord palsy
recurrent respiratory papillomata
foreign body
trauma

255
Q

Subglottic

A

Laryngo tracheo bronchitis
subglottic stenosis
tracheomalacia
haemangioma
abnormal vessels
complete tracheal ring
foreign body
truama

256
Q

acute epiglottitis is uncommon now due to

A

HiB vaccine

257
Q

tracheobroncholmalacia - hwat happens to the aireway in expiration

A

it collapses

258
Q

Risk factors for tracheobronchomalacia include

A

prematurity,
tracheo-oesophageal fistula,
vascular ring and congenital heart disease

259
Q

The laryngeal web is usually located

A

between the cords anteriorly.

260
Q

chest xr - posterior junctional line suggests what?

A

hyperinflated lungs present

261
Q

mbryologically thymus is derived from

A

the third pharyngeal pouch

262
Q

At what age won’t you see the thymus on a chest xr

A

6 plsus

often after 3 though

263
Q

thymus size will change acutely with

A

illness
reduces with endogenous steroids. Cna then get rebound much bigger

264
Q

22q11 deletion syndromes eg

A

DiGeorge/congenital thymic aplasia, velo-cardio-facial syndrome (VCFS) or Shprintzen syndrome

265
Q

22q11 deletion syndromes caused by what

A

failure of normal development of the third and fourth branchial arches

Absence of the thymus and parathyroids, congenital heart disease, oesophageal atresia and facial abnormalities

266
Q

5 normal features of cxr thymus

A

Widened superior mediastinum

Notch at the junction with the heart

Smooth, well-defined, convex lateral border

Scalloped/wavy left lateral border cause by indentation by the anterior rib ends

No mass effect or adjacent structure,

267
Q

which embryological layer gives rise to the kidneys

A

dorsal mesoderm

268
Q

What are the common kidney congenital abnormalities?

A

Autosomal recessive polycystic kidney disease (PCKD)
Autosomal dominant PCKD
Multicystic dysplastic kidneys (MCDK)
Potter syndrome
Duplication of the urinary collecting system
Nephroblastomatosis: persistence of undifferentiated metanephric blastema cells

Wilms’ associations
Ureterocoele

269
Q

What is the anatomical differnece between recessive and dominant polycystic kidney disease?

A

Recessive - collecting ducts

270
Q

how does wilms tumour come about?

A

nephric blastema remains undifferentiated

271
Q

syndromic associations of WIlms

A

Beckwith-Wiedemann syndrome and hemihypertrophy.

272
Q

nship of nephtogenic rests, Nephroblastomatosis and wilms

A

normal cells that involute.

nephroblastomatosis is benign involvement.

Wilms is malignant

273
Q

multiple arteries to a kidney due to

A

failure of resorptoin of vessles as the kidneys move higher up the abdomen

274
Q

what is crossed fused ectopia for a kidney

A

This variant results when one kidney crosses over and fuses with the contralateral kidney, and both ascend together to form a unilateral kidney.

275
Q

what classic feature distinguishes Wilms tumour from neuroblastoma?

A

Vascular invasion

276
Q

Under 6 months - freqwuency of uti to need an US scan

A

just the one

277
Q

filler bladder - normal wall thickness

A

up to 3mm

278
Q

what pathology is looked for on US bladder

A

Thickening of the bladder wall
Ureterocoele
Dilated distal ureter(s)
Pelvic masses

279
Q

Antenatal hydronephrosis

A

calyceal dilattion
parenchymal thinning
cortico-medullary differentitation
increased parenchymal echogenicity
renal cysts
ureteric dilatation
oligohydraminos

280
Q

Antenatal hydronephrosis - what are the markers of poor prognosis ?

A

renal dysplasia and oligohydramnios

281
Q

imaging options for suspected renal obstruction in postnatal baby

A

MAG3
MRI
IV U

282
Q

If vesicoureteric reflux is susspeced

A

direct imaging - fluro, radionuclide, cystosonography

indirect - voiding mag3

283
Q

what should be done ig posterior urethral valves are suspected?

A

catheter
prophylactic abx
voiding cystourethrogram

284
Q

what is the Weigert-Meyer rule

A

up obstruct, low flow(reflux)

There is obstruction of the upper renal moiety and ureter by an ectopic ureterocele situated at an abnormal ureteric insertion, as illustrated: the dilated upper moiety pelvicalyceal system is associated with a tortuous, dilated ureter and an obstructing ureterocele
The lower moiety vesicoureteric junction is normally sited, superior and lateral to the upper moiety ureteric opening, but is prone to VUR

285
Q

how to differentiatie hydronephrosis from MCDK

A

MCDK has lots of cysts so the areas aren’t connected

286
Q

The most frequent cause for a solitary normal kidney which exhibits compensatory hypertrophy is ?

A

complete involution of a contralateral MCDK.

287
Q

commonest cause of haematuria in children

A

UTI
Calculi
Trauma

288
Q

Glomerular causes of haematuria: charachterised by what features

A

abnromal red cell morphology (distorted as traverse the basement membrane)
Proteinuria
red cell and tubular casts in urine
non-urological cause if most frequent
OFTEN MICROhaematuis

289
Q

non-Glomerular causes of haematuria: charachterised by what features

A

presence of intact red cells in the urine
urological cause is most frequent
macrohaematuria most common

290
Q

Cuases of microhaematuria

A

Glomerulonephritis (various types)
Familial nephritis (Alport’s disease)
IgA nephropathy
Poststreptococcal
Henoch-Schönlein purpura

291
Q

causes of macrohaematuria

A

Urinary tract infection
Trauma (including iatrogenic)
Calculi
Tumours
Vascular lesions, for example renal venous or arterial thrombosis and arteriovenous connection

292
Q

What is Henoch Schonlein purpura

A

acute vasculitis affecting small vessels in children. It is caused by a systemic allergic response, which may be caused by conditions such as infections, insect stings and drug reactions.

293
Q

UTI accounts for what proportion of macro haematuria in kids

A

25%

294
Q

7 types of calculi

A

rate, struvite, cystine, calcium oxalate, calcium phosphate, matrix (mucoprotein) and xanthene

295
Q

can tumours cause haematuria?

A

yes, but very rare. Wilms tumour. Rhabdomyosarcoma normally obstuction.
angiomyoliopomas, possible

296
Q

Renal vein thrombosis

risk factors in neonates

A

dehydrated and hypotension

297
Q

US fetures of renal vein thrombosis

A

Enlargement of one or both kidneys

Reduced echogenicity in the kidney owing to oedema, but echogenic intrarenal haemorrhage may be seen

Reduced/absent flow in the renal vein with or without thrombus

Diminished/reversed diastolic flow in the renal artery

298
Q

recommended scheme of investigation of an atypical UTI in a child aged <6 months is

A

Sonography
A DMSA scan (after 4-6 months for scarring)
An MCUG

299
Q

DMSA binds to what?

A

proximal tubular cells

300
Q

coloiform bacteria is typcial or atypcial for uti

A

atypical

301
Q

how is hypertension meausured in kids

A

x3 occasions where bp is greater than 95% percentile for age

302
Q

what is the main cause of hypertension in paeds

A

renal pathology - RAS, renovascular malformations.

neonate - occlusion from catheter
over 12 think drugs or renal parenchymal disease

303
Q

in US kidneys for hypertension what needs to be examined?

A

Renal size
The presence of parenchymal scarring`
The presence of collecting system dilatation
The presence of adrenal masses
Examination of the aorta

304
Q

In Renal US - if the RI is 0.5 (normal is 0.7) what are the thoughts on diagnosis.

A

more of a parvus et tardus waveform.
Upstream dilatation (could be in aorta) - no pulsitile waveform

305
Q

what is the difference between dimercaptosuccinic acid and mercaptoacetyltriglycine for renal studies.

A

DMSA stays in proximal convoluted tubules - can show defects like scarring.

Mercaptoacetyltriglycine - for dynamic studies of tubular secretion. Perfusion, transit and drainage

306
Q

most common renovascular disorder encountered in children is

A

fibromuscular dysplasia

307
Q

differnetials for FMD

A

Williams
NF1

308
Q

what takes up MIBG?

A

Neurblastoma
Haeo
Normal adrenal medulla
Ganglionneuroma

309
Q

why are first and second ribs spared in coarctation rib notching

A

supplkied by the sublcavians

310
Q

Renal cysts can be classified into which two groups?

A

Genetic disease and non genetic disease

311
Q

genetic causes of cystic kidneys

A

Autosomal recessive polycystic kidney disease (ARPKD)
Autosomal dominant polycystic kidney disease (ADPKD)

Tuberous sclerosis
Juvenile nephrophthisis
Glomerulocystic kidney disease
Cysts with multiple malformation syndromes

312
Q

non genetic causes of cystic kidney

A

simple
dysplastic kidney
Multilocular renal cysts
CKD
calyceal diverticulum
Medullary cystic kidney
medullary sponge kidney

313
Q

which imaging is used for renal cysts

A

US
MRI
NucMed

314
Q

extra renal cysts - look in which organs

A

pancreas, spleen and liveer

315
Q

The most important feature of ARPKD is that

A

both kidneys are enlarged and this diagnosis should never be made if the kidneys are normal or small in size.

316
Q

ARPKD - what happens to liver and biliary tree

A

hepatic fibrosis and cystic dilatation of the biliary tree

look for portal hypertension ect

317
Q

bone lesions - over 40 differential diagnosis includes

A

infective
mets
myeloma
lymphoma

318
Q

Types of matrix mineralisation

A

osseous
chondral ground glass

319
Q

Ground glass bone matrix mineralisation is what

A

‘Ground-glass’ density due to numerous fine spicules of bone is seen within the lesion. Punctate calcium is also possible.

320
Q

slow growing lesions are which

A

Cysts/geodes
Simple bone cysts (SBC)
Enchondroma
Resolving LCH
Brodie’s abscess

321
Q

types of cortical response to a tumour

A

Expanded =
scaplloped - Chondral and fibrous
trabeculated - cysts/GCT

322
Q

Types of periosteal reaction and their cancers

(solid/cortical thickening)
onion-skin
(spiculated)
Aneurysmal bone cyst (periosteal buttress)

A

Osteoid osteoma (solid/cortical thickening)
Ewing’s sarcoma (onion-skin)
Osteosarcoma (spiculated)
Aneurysmal bone cyst (periosteal buttress)

323
Q

types of spiculated bone for bone lesion

A

Perpednciular - reactive bone - ewings, mets,

divergent - sunburst. osteosarcoma.

velvet - disorgansied, ewings

324
Q

Typically, osteosarcoma will be found WHERE

A

metaphyseal in location, often found in the distal femur, proximal tibia or proximal humerus (Fig 3).

325
Q

OSteosarcoma - what age

A

adolescents

326
Q

Ewing s- age group

A

5 - 25

327
Q

In ARPKD what should the parents have?

A

Normal kidenys as it is recessive

328
Q

AD PKD manifests when?

A

third decade of life

half patients are spontaenous mutations, no fam histroy

329
Q

what is the main dangerous assocation with AD PKD

A

subarachnoid haemorrhage

330
Q

AD PKD needs to be differentiated form which condition ?

A

Tuberous sclerosis

331
Q

What are some of the other manifestations of TSC that one might look for?

A

Rhabdomyelomas cardiac

Corticol tubers in brain

332
Q

The renal abnormalities associated with TSC include:

A

Cysts
Angiomyolipomas
Angiomyolipomas and cysts

333
Q

What is Multicystic dysplastic kidneys

A

non hereditory.
Failure of that kidney.

wide spectrum
non functioning on Nuc Med
sponatenous involution

334
Q

Medullary sponge kidney is a rare diagnosis to make in children, and must be characterised by:

A

Haematuria
Nephrolithiasis
Infection

NOT enlarged

335
Q

investigation algorithm for unliateral cysts

A

MCDK - MAG3
Simple cysts - IVU
Multilocular cystic nephroma- cross section

336
Q

investigat algorithm for bilateral cysts

A

Genetic - TSC, ARPKD, ADPKD
Dysplasia - MCU / MAg3

337
Q

VACTERL stands for

A

vertebral defects, anal atresia, cardiac defects, tracheo-esophageal fistula, renal anomalies, and limb abnormalities

338
Q

Autosomal recessive polycystic kidney disease. This condition describes

A

very large kidneys with small cysts, which result in a large bright kidney appearance

339
Q

Autosomal dominant polycystic kidney disease is a common condition that starts in childhood. The kidneys vary from

A

normal to enlarged, and there are a variable number of large cysts on each kidney. Renal involvement is often not bilaterally symmetrical

340
Q

In TSC, the kidneys may contain

A

angiomyolipomas and/or large cysts. There may be a family history of TSC, or the condition might have arisen as a new mutation

341
Q

how bright is the kidney in neonates to 6 months

A

should be brighter than the liver

The reasons for this difference are the relatively large volume of glomeruli versus medullary pyramids and the lack of echogenic sinus fat in the neonate.

342
Q

Pre renal causes of AKI

A

hypovolaemia
hypotension
hypoxia

343
Q

Renal causes of aki

A

Glomerulonephritis
Intravascular coagulation
ATN
AIN
Tumours
Developmental
Hereditary nephritis

344
Q

Post renal causes of AK I

A

Obstructive uropathy
Vesicoureteral reflux
Acquired - stones

345
Q

The renal medullae appear hypoechoic and prominent on normal ultrasonographic examination of the neonate

why?

A

lack of echogenic sinus fat

346
Q

How to commnet on kidneys in US

A

size, morphology, echotexture, pelvicalyceal dilatation and perfusion

347
Q

what is the cut off of difference between kidneys that raises suspicion?

A

over 10% concern for scarring

348
Q

demonstrating pelvicalyceal dilatation. The possibility of false positives should be borne in mind; for example,

A

extrarenal pelvis,
large major calyx,
recent obstruction or infection, clubbed calyces,
secondary to reflux or papillary necrosis.

349
Q

Renal venous thrombosis leads to diminished venous signals and produces characteristic changes in the waveforms of the main renal artery and its branches with….

A

sharp systolic peaks and reversed diastolic flow.

350
Q

What are the differentials for

echogenic kidneys with loss of corticomedullary differentiation

A

Unwell baby
- Asymmetrical, renal vein thrombosis
- symmetrical, ATN

Well baby
- Enalarged, ARPCKD
- Small, dysplastic kidneys

351
Q

What are the main causes of CKD in kids under 5

A

anatomical abnormalities
- hypoplasia, dysplasia, obstruciton, malformation

352
Q

What are the main causes of CKD in kids over 5

A

Acquired glomerular disease and herediatary
- HUS
- Alport
- Cystic disease
- Glomerulonephritis

353
Q

Lentiform nucleus + caudate nucleus =

A

basal ganglia

354
Q

Putamen + globus pallidus =

A

lentiform nucleus

355
Q

Putamen + head of caudate nucleus =

A

corpus striatum

356
Q

what is Periventricular Nodular Heterotopia

A

neurons develop in the germinal matrix and do not migrate

bumbpy inner ventricle lining

357
Q

what is focal heterotopia?

A

Groups of neurons may start to migrate but not reach the surface.

These can be recognised as a clump of tissue of grey matter intensity lying within the brain substance.

358
Q

what is classical lissencephaly

A

disorder of neuronal migration in which the cortex is abnormally organised and thicker than usua

359
Q

Types of classical lissenencephaly

A

agyira

pachy gyria
SBG

360
Q

how to differentiate between polymicrogyria and pachygyria

A

polymicrogyria are small so interdigitate with the wqhite matter - so no boundary is seen

361
Q

abnormal grey matter is what on T2W

A

high signal

362
Q

Grey matter - corpus striatum (head of caudate and putamen) are affected

what are the differentials ?

A

Mitochondrial disorders

Leighs, MELAS, hypoglycaemia

363
Q

Grey matter - mainly globus pallidus is affected with high signal T2

what are the differentials?

A

Methylmalonic acidaemia
L-2 hydroxyglutaric acidaemia
CO poisoning
Kernicterus
NG1

364
Q

Grey matter - mainly globus pallidus is affected with high signal T2

what are the differentials?

A

Methylmalonic acidaemia
L-2 hydroxyglutaric acidaemia
CO poisoning
Kernicterus
NF1

365
Q

Grey matter
Mainly thlamic involvement

what differentials

A

Krabbes disease
Gangliosidoses
Wilsons

366
Q

Bilateral proptosis in early infancy is often due to a

A

developmental bone abnormality.

367
Q

Unilateral proptosis is usually due to

A

an orbital mass.

368
Q

Rapidly progressive proptosis suggests an aggressive neoplasm such as

A

rhabdomyosarcoma

369
Q

main causes of proptosis in children?

A

Haemangioma
Venous lymphatic malformation
Dermoid cyst
Sinusitis and orbital cellulitis
Optic nerve glioma
Rhabdomyosarcoma
Neuroblastoma
Langerhans’ cell histiocytosis
Bone dysplasias (e.g. fibrous dysplasia, osteopetrosis, craniofacial abnormalities)

370
Q

Causes of periosteal reaction in children ?

A

Physiological
Trauma
Infection
Tumour
Metabolic
Chronic disease
Inherited conditions
Caffey disease
Iatrogenic

371
Q

sickle cell osteomyelitis is what organism?

A

Sallmonella

372
Q

chronic relapsing mutifocal ostemyelitis typcially involves what bones?

A

medial clavicle

373
Q

Physiological peri osteal reaction is allowed to be how deep

A

2mm

374
Q

Leukaemia and metastatic neuroblastoma may both give rise to periosteal reactions with…. what

A

lucent metaphyseal bands

375
Q
A

AA ST2 (14 decks)

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