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Phase 3A Sam Harper > Paediatrics 2 > Flashcards

Paediatrics 2 Flashcards

1
Q

Why is it important to investigate UTI’s thoroughly in children

A

Potential for structural abnormalities in the urinary tract and scarring of the kidneys if pyelonephritis develops

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2
Q

Common causative organisms for UTI

A

E.Coli, Klebsiella, Proteus, Pseudomonas

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3
Q

Clinical presentation of UTI

A

Infants: Fever, vomiting, lethary, poor feeding, jaundice, septicaemia, smelly urine and febrile convulsions

Older children: Dysuria, Abdo pain, fever, lethargy, D+V, haematuria, Smelly/cloudy urine

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4
Q

Ix for UTI

A

Clean catch urine sample
Older: midstream urine
USS KUB

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5
Q

Tx for UTI

A

Abx - IV for under 3mo e.g. Cefotaxime

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6
Q

What does an atypical UTI present with?

A

Seriously ill/septic, Poor urine flow, abdo mass, raised creatinine, Failure ot respond to Abx after 48 hours, Infection with non E.coli

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7
Q

Ix for atypical UTI

A

US for abnormalities, potential DMSA and MCUG to look for scarring and vesicoureteric reflux

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8
Q

What is vesicoureteric reflux

A

Developmental abnormality where the ureters are displaced and enter directly into the bladder rather than at an angle causing reflux of urine into the renal pelvis which can cause scarring with a UTI

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9
Q

UTI prevention

A

High fluid intake, Regular voiding, complete emptying, Prevention/treatment of constipation, prophylactic ABx

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10
Q

Causes of nocturnal eneuresis

A

Genetic delay in sphincter competence, stress are secondary

Underlying disorders: UTI, Faecal retention, Polyuria from osmotic diuresis

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11
Q

Management of nocturnal eneuresis

A

Explain that its common and beyond conscious control
Star charts
Eneuresis alarm which sounds when bed is wet to awaken child
Desmopressing to provide short term relief

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12
Q

Nephrotic syndrome diagnostic criteria

A

Oedema
Hypoalbuminaemia <25g/l
Proteinuria with 3+/4+ on dip or a urine protein:creatinine ratio of >200mmg/mol

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13
Q

Aetiology of Nephrotic

A

Primary: Idiopathic e.g. minimal change disease
Secondary: HSP, SLE

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14
Q

Clinical presentation of nephrotic

A

Periorbital oedema
Scrotal, vulval, leg and ankle oedema
Ascited
SOB due to effusion and abdo distension

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15
Q

Ix for nephrotic

A

Urine dip
Urine protein:creat
Urine micro
Urine cultures
Bloods - FBC, U+E, albumin and bone profile

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16
Q

Management of nephrotic syndrome

A

Corticosteroids - Pred and reduce over time
Diueretics - furosemide
Diet with reduced salt
Pneumococcal immunisation

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17
Q

Explain steroid resistant nephrotic

A

Common in asian boys
Can lead to hypovolaemia, thrombosis, infection and hypercholesterolaemia
Can progress to renal failure
Some respond to cyclophosphamide, tacrolimus or rituximab
Causes include focal segmental glomerulosclerosis and membranous nephropathy

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18
Q

Triad of Sx in Nephritic syndrome

A

Reduced kidney function, Haematuria and Proteinuria

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19
Q

Post strep glomerulonephritis patho

A

Occurs 1-3 weeks after B-haem strep infection such as tonsilitis

Immune complexes made up of strep antigens, antibodies and complement proteins lodged in glomeruli then cause inflam and AKI

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20
Q

IgA Nephropathy Patho

A

Related to HSP, IgA deposits in nephrons cause inflam

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21
Q

Ix for Nephritic

A

Urine micro
Protein and calcium excretion
KUB US
Bloods: FBC, U+E and Creatinine

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22
Q

Management of nephritic

A

Supportive
Diuretics and antihypertensives
Immunosuppressant meds such as steroids

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23
Q

What is Hypospadias

A

Condition affecting males where the urethral meatus us abnormally displaced to underside of penis towards scrotum

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24
Q

Management of hypospadias

A

Surgery at 3-4 mo to correct position

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25
Q

Aetiology of AKI

A

Prerenal: most common cause in children, hypovolaemia caused by infection such as gastroent, burn, sepsis, haemorrhage or nephritic

Renal: HUS, vasculitis, renal vein thrombosis, acute tubular necrosis, glomerulonephritis, pyelonephritis

Post-renal: Obstructions such as posterior urethral valves, blocker catheters

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26
Q

Management of AKI

A

Regular monitoring of fluid balance and circulation

US to find obstruction

Treatment depending on cause e.g. fluid replace, asses site of obstruction, renal biopsy

Dialysis in severe cases

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27
Q

Triad in HUS

A

Acute renal failure, microangiopathic anaemia, thrombocytopenia

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28
Q

HUS cause

A

Secondary to GI infection, contact with farm animals or eating uncooked beef

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29
Q

Pathophysiology of HUS

A

Toxin enter HI mucosa and localises to the endotheliak cells in the kidney causing activation of clotting cascade and consumption of platelets. Anaemia is caused by damage to RBC as they circulate

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30
Q

Clinical presentation of HUS

A

Reduced urine, Haematuria, Abdo pain, Lethary and irritable, Confused, Oedema, HTN

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31
Q

Management of HUS

A

Early supportive therapy including dialysis, Anti hypertensives, Carely fluid balance, blood transfusion

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32
Q

How is CKD defined

A

eGFR of < 15ml/min

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33
Q

Aetiology of CKD

A

Structural Malformations, glomerulonephritis, hereditary nephropathies, systemic disease

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34
Q

Clinical presentation of CKD

A

Anorexia and lethargy, Polydip and polyuria, Faltering growth, HTN, Acute-on-chronic renal failure, Incidental proteinuria

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35
Q

Management of CKD

A

Feed, Phosphate restrict and activated Vit D, Bicarb, EPO, Growth hormone, Dialysis and transplant if needed

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36
Q

What is Leukaemia

A

Cancer of the stem cells in the bone marrow

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37
Q
A
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38
Q

What are the most common types of Leukaemia in children and what ages are affected

A

ALL - Most common in children - peaks ages 2-3
AML - next most common - peaks aged 2 years and under
CML - very rare

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39
Q

RF for Leukaemia

A

Downs, Kleinfelters, Radiation exposure during pregnancy, Noonans

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40
Q

Clinical presentation of Leukaemia

A

Fatigue, unexplained fever, faltering growth, Weight loss, night sweats, anaemia, Petechiae and abnormal bruising, Abdo pain, Generalised lymphadenopathy, Hepatosplenomegaly

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41
Q

Ix for Leukaemia

A

NICE: any child with unexplained Petechiae or hepatomegaly be referred

FBC: Anaemia, Leukopenia, thrombocytopenia

Blood film: blast cells

Bone marrow biopsy is definitive

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42
Q

Tx for Leukaemia

A

Chemo, potential radiotherapy and bone marrow transplant

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43
Q

What is the leading cause of childhood cancer deaths in the UK

A

Brain tumours, they are almost always primary

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44
Q

Explain the five types of brain tumours that present in children

A

Astrocytoma - varies from malignant to benign
Medulloblastoma - arises in the midline of the posterior fossa and may seed through the CNS via the CSF giving spinal mets
Ependymoma - mostly in posterior fossa where it behaves like a medulloblastoma
Brainstem glioma
Craniopharyngioma - developmental tumour arising from an embryological remnant

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45
Q

Clinical presentation of brain tumours

A

Raised ICP - Headache worse on waking, coughing, straining and bending forward and papilloedema
Focal neuro signs
Back pain, peri weakness, bladder/bowel dysfunction

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46
Q

Ix for brain tumour

A

MRI

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47
Q

Tx for Brain tumour

A

Surgery
Chemo and radio depending on type and age

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48
Q

What is a neuroblastoma

A

Tumour arising from neural crest tissue in the adrenal medulla and sym nervous system

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49
Q

Neuroblastoma epidemiology and prognosis

A

Occurs before age 5
very good prognosis - over 80% are cured

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50
Q

Clinical presentation of Neuroblastoma

A

Abdo mass, Pallor, Weight loss, Hepatomegaly, Bone pain, Limp, Cervical lymphadenopathy, Periorbital bruising, Skin nodules

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51
Q

Ix for Neuroblastoma

A

Raised urine catecholamine levels
Biopsy
Bone marrow sampling

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52
Q

Management of Neuroblastoma

A

Surgery
Metastatic - chemo, surgery and radiation

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53
Q

What is a Wilms tumour

A

Origin in embryonic tissue, most common renal tumour of childhood, presents before the age of 5

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54
Q

Clinical presentation of Wilms tumour

A

Large abdo mass, Abdo pain, Anorexia, Haematuria, HTN

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55
Q

Ix for Wilms tumour

A

CT/MRI show renal mass

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56
Q

Tx for Wilms tumour

A

Chemo followed by delayed nephrectomy

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57
Q

What are the two types of bone tumour seen in children

A

Ewings sarcoma and osteogenic sarcoma

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58
Q

Clinical presentation of bone tumours

A

Persistent, localised bone pain

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59
Q

Ix for bone tumours

A

Plain X-ray then an MRI and bone scan
Bone XR - destruction and variable periosteal new bone formation with Ewings and often substantial soft tissue mass (onion skin appearance)
CT - for lung mets

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60
Q

Tx for Bone cancer

A

Combo chemo and then surgery
Ewings - radio

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61
Q

What is retinoblasotma

A

Malignant tumour of retinal cells

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62
Q

Retinoblastoma heritability

A

Bilateral tumours are hereditary
Chromosome 13 with dominant inheritance

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63
Q

Clinical presentation of retinoblastoma

A

White pupillary reflex replaces the red one
Squint

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64
Q

Ix for Retinoblastoma

A

MRI and exam under anaesthetic

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65
Q

Tx for Retinoblasotma

A

Aim to cure but preserve vision
Chemo to shrink tumour and then local laser treatment
Most are cured but risk of visual impairment and secondary malignancy

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66
Q

Summarise hepatoblastoma

A

Primary malignant liver tumour

Abdo distension

Elevated a-fetoprotein

Tx: Chemo, surgery, Liver transplant

Prognosis: good

67
Q

ADHD pathophysiology

A

altered dopamine levels, structural and functional brain changes, genetic component

68
Q

Aetiology of ADHD

A

More common in boys
50% have a comorbid ASD, dyslexia or depression/anxiety

69
Q

Clinical presentation of ADHD

A

Inattention - Dont complete instruction, doesnt engage in intense tasks, easily distracted, difficulty organising, forgetful, loses things

Hyperactivity/Impulsivity - cannot play quietly, talks excessively, Doesn’t wait their turn, always on the go, interrupts others

70
Q

Ix for ADHD

A

Conners questionnaire, School observation, Home visit and info from relatives

71
Q

Tx for ADHD

A

Non-Medical - Care plans, CBT and Behavioural strategies

Medical - Methylphenidate
Lisdexafetamine
Dexamfetamine

72
Q

SE of Methylpenidate

A

Cardiotoxic so do an ECG

73
Q

What is autism spectrum disorder

A

Neurodevelopmental disorder that impacts social interaction, communication and behaviour

74
Q

Aetiology of ASD

A

Genetic with multi gene involvement, structural changes in brain

75
Q

Clinical presentation of ASD

A

Abnormal social interaction - Poor eye contact, play alone, uninterested in social interaction, difficulty forming close relationships

Impaired social communication - failure to develop spoken language, failure to initiate conversation, abnormal rhythm, pitch and tone

Repetitive ideas: need for routine, motor mannerisms: repetitive movements, sensory issues: only eat certain foods, don’t like loud noises

76
Q

Diagnosis of ASD

A

Lack of social attachments, abnormal/delayed expression, abnormal symbolic play

77
Q

Management of ASD

A

Education care plans, Applied behaviour analysis, Family support and MDT approach

78
Q

Kleinfelter syndrome genetics

A

Additional X chromosome for men making 47 XXY

79
Q

Clinical presentation of Klinefelters

A

Taller, Wide hips, Gynaecomastia, Weaker muscles, Small testicles, reduced libido, shyness, infertility, suble learning difficulties

80
Q

Tx for Klinefelters

A

Testosterone injections, Advanced IVF, Breast reduction surgery, MDT input for speech, language and muscles

81
Q

Complications of Klinefelters

A

Increased breast cancer risk, osteoporosis, diabetes and anxiety

82
Q

Turners syndrome genetics

A

When a female has a single X chromosome making them 45 XO

83
Q

Clinical presentation of Turners

A

Short, webbed neck, widely spaced nipples with broad chest, high arching palate, downward sloping with ptosis, underdeveloped ovaries with reduced function, late or incomplete puberty, most are infertile

84
Q

Conditions associated with Turners

A

Recurrent otitis media, Recurrent UTI, Hypothyroidism, Hypotension, Obesity, Diabetes

85
Q

Tx for Turners

A

Growth hormone therapy, Oestrogen and prog to help establish female sex characteristics, menstrual cycle and prevent osteoporosis

86
Q

Downs syndrome genetics

A

3 copies of chromosome 21 - trisomy 21

87
Q

Clinical presentation of Downs

A

Hypotonia, small head with flat back, short neck, short statute, flattened face and nose, low set ears, single palmar crease, Prominent epicanthic folds, upward sloping palpebral fissures

88
Q

Testing for Downs

A

Antenatal - offered as a screening where further tests take place if necessary

Combined test - 11-14 weeks of gestation and combines US results looking at thickness on the back of the neck of the foetus (thickened) and beta-HCG (raised) and PAPPA (reduced)

Triple test - 14-20 w and looks at beta-HCG (raised), AFP (low) and serum oestriol (low)

Quadruple test - same as triple test but includes Inhibin-A (high)

89
Q

Tx for Downs

A

MDT approach and regular screening includes echo, thyroid checks, eye checks and audiometry

90
Q

Complications of Downs

A

Learning disability, Recurrent otitis media, Deafness, Visual problems like strabismus, Hypothyroid, Cardiac defects e.g. ASD,VSD, Leukaemia, dementia

91
Q

What is Noonans

A

Autosomal genetic condition

92
Q

Clinical presentation of Noonans

A

Short, Broad forehead, Downward sloping eyes with ptosis, wide space between eyes, low set ears, webbed neck, wide spaced nipples

93
Q

Conditions associated with Noonans

A

Congenital heart disease (pul sten, hypertrophic cardiomyopathy, ADD), Undescended testes and infertility in males, learning disability, Bleeding disorders, Increased leukaemia risk

94
Q

Tx for Noonans

A

Supportive MDT care
Corrective heart surgery

95
Q

What mutation causes fragile X syndrome

A

Mutation in the FMR1 gene on the X chromosome which codes for fragile X mental retadation protein

96
Q

Inheritance pattern for fragile X

A

X linked

97
Q

Clinical presentation of fragile X syndrome

A

Delay in speech and language development, intellectual disability, long narrow face, large ears, large testicles, hypermobile joints, ADHD, autism, seizures

98
Q

Management of fragile X

A

Supportive, symptomatic tx and treat complications

99
Q

Prader willi mutations

A

loss of genes on proximal arm of chromosome 15

100
Q

Clinical presentation of prader willi

A

Constant insatiable hunger, hypotonia, learning disability, fairer softer skin that is prone to bruising, mental health issues, dysmorphic features, narrow forehead, almond shaped eyes, strabismus, thin upper lip, hypogonadism

101
Q

Management of prader willi

A

dietician for weight control, growth hormone, mental health input

102
Q

Angelman syndrome mutation

A

Loss of function of the UBE3A gene caused by deletion on chromosome 15

103
Q

Clinical presentation of Angelman syndrome

A

delayed development, absence of speech development, fascination with water, happy demeanour, wide spaced teeth, inappropriate laughter, abnormal sleep patterns, epilepsy, ADHD, Dysmorphic features, fair skin light hair blue eyes

104
Q

Management of Angelmans

A

MDT approach

105
Q

William syndrome mutation

A

Deletion of epigenetic material on one copy of chromosome 7

106
Q

Clinical presentation of William syndrome

A

Broad forehead, Starburst eyes, Flattened nasal bridge, very sociable, wide spaced teeth and mouth, small chin

107
Q

Management of William syndrome

A

MDT approach

108
Q

Complications of Williams

A

Supravalvular aortic stenosis, ADHD, HTN, Hypercalcaemia

109
Q

Edwards syndrome mutation

A

Trisomy 18

110
Q

Clinical presentation of Edwards syndrome

A

Low birthweight, small mouth and chin, short sternum, flexed overlapping fingers, rocker bottom feet, cardiac and renal malformation

111
Q

Patau syndrome mutation

A

Trisomy 13

112
Q

Clinical presentation of Pataus

A

Structural brain defects, scalp defects, eye defects, cleft lip and palate, polydactyly, cardiac and renal malformations

113
Q

Duchennes muscular dystrophy mutation

A

deletion on short arm of X

114
Q

Clinical presentation of Duchennes

A

Waddling gait, slow running, language delay, Gowers sign (need to turn prone to rise from floor), Pseudohypertrophy of the calves as the muscular tissue is replaced by fat/fibrous tissue, slower and clumsier, cant walk by 10-14 years of age

115
Q

Management of Duchennes

A

Exercise, night splints and passive stretching, Good sitting posture, Corticosteroids

116
Q

What is Becker Muscular Dystrophy

A

Some functional dystrophin is produced so its similar to DMD but progresses slower

117
Q

What is Osteogenesis Imperfecta

A

Autosomal dom condition that results in brittle bones, affects formation of collagen,

118
Q

Clinical presentation of osteogenesis imperfecta

A

Recurrent and inappropriate fractures, blue/grey sclera, hypermobile, triangular face, deafness from early adulthood, dental issues, bone deformaties

119
Q

Ix for Osteogenesis Imperfecta

A

Clinical, X rays are useful, genetic testing rarely

120
Q

Management of Osteogenesis Imperfecta

A

Bisphosphonates to increase bone density, Vit D supplementation, Physio and Occupational health support, manage fractures

121
Q

What is rickets

A

Condition where theres defective bone mineralisation causing soft and deformed bones

122
Q

Aetiology of rickets

A

vit D def, Calcium def, Hereditary hypophospatemic rickets

123
Q

Rf for rickets

A

Darker skin, low sunlight, colder climates, indoors

124
Q

Clinical presentation of rickets

A

Lethargy, bone pain, poor growth, dental issues, muscle weakness

125
Q

Bone deformities in rickets

A

Bowing of the legs, Knock knees, rachitic rosary (end of ribs expand at costochondral junctions causing lumps along chest), Craniotabes (soft skull delayed closure and frontal bossing), delayed teeth

126
Q

Ix for rickets

A

Serum 25-hydroxyvitamin D - <25 nmol/L

Xray, Serum cal and phos, Serum ALP and PTH (high), Full panel

127
Q

Tx for rickets

A

Prevention is best, Treat children with ergocalciferol, give vit d and calcium supplements

128
Q

What is transient synovitis

A

Irritable hip - most common cause of hip pain in children 3-10 yo

Temporary irritation and inflammation in the synovial membrane often associated with viral URTI

129
Q

Clinical presentation of Transient synovitis

A

Sx within a few weeks of viral infection, Limp, refusal to bear weight, groin or hip pain, mild low grade temp, otherwise well

130
Q

Tx for transient synovitis

A

Symptomatic, exclude other ddx particularly septic arthritis, good prognosis

131
Q

What is septic arthritis

A

Infection inside a joint - most common in under 4’s

132
Q

Septic arthritis causative organisms

A

S.aureus, Neisseria gonorrhoea, Group A strep, Hib, E.Coli

133
Q

Clinical presentation of septci arthritis

A

Admission to hospital with involvement of orthopaedics

Aspirate joint and do gram stain, crystal micro, MC&S

Empirical IV ABx followed by specific

Surgical drainage

134
Q

What is osteomyelitis

A

Infection of the bone and bone marrow - typically in the metaphysis of the long bones

135
Q

Osteomyelitis causative organism

A

S.Aureus

136
Q

RF for Osteomyelitis

A

Males under 10, Open bone fracture, Ortho surg, Immunocompromised, Sickle cell, HIV, TB

137
Q

Clinical presentation of OSteomyelitis

A

Fever, Refuse to weight bear, Pain, swelling, tender

138
Q

Ix for Osteomyelitis

A

XRay 1st line, MRI is gold, Bloods (CRP, ESR,WBC), Blood cultures, bone marrow aspirate

139
Q

Tx for Osteomyelitis

A

Extensive and prolonged Abx, Surgery for drainage and debridement

140
Q

What is Perthes disease

A

Disruption of the blood flow to the femoral head causing avascular necrosis of the bone - affects epiphysis of the femur

141
Q

Perthes epidemiology

A

5-8 yo boys

142
Q

Clinical presentation of Perthes

A

Slow onset pain in hip or groin, limp, restricted hip movement, referred pain to the knee, no hx of trauma

143
Q

Ix for Perthes

A

XR (can be normal), Bloods, technetium bone scan, MRI

144
Q

Tx for Perthes

A

Conservative (bed rest, traction, analgesia and crutches), Physio, Regular XR, Surgery in severe cases

145
Q

What is a slipped femoral epiphysis

A

Head of femur is displaced along the growth plate, More common in males aged 8-15, more common in obese children

146
Q

Clinical presentation of slipped femoral epiphysis

A

Adolescent obese male undergoing growth spurt, Hx of minor trauma, Hip groin or knee pain, restricted ROM hip, Painful limp, wanting to keep hip in external rotation

147
Q

Ix for slipped femoral epiphysis

A

XR, Blood test, CT/MRI

148
Q

Tx for slipped femoral epiphysis

A

Surgery to return femoral head to the right position

149
Q

What is osgood-schlatter disease

A

Inflammation of the tibial tuberosity where the patellar ligament inserts, common cause of anterior knee pain

150
Q

Clinical presentation of osgood-schlatter disease

A

Gradual onset, visible or palpable hard and tender lump at tibial tuberosity, pain in anterior aspect of knee, pain is worse with exercise, kneeling or extension

151
Q

Tx for osgood-schlatter

A

Reduce physical activity, Ice, Nsaids, Stretching physio

152
Q

What is developmental dysplasia of the hip

A

Structural abnormality in the hips caused by abnormal development of the foetal bones leading to instability and tendency for dislocation

153
Q

RF for developmental dysplasia of the hip

A

FHx, Breech presentation from 36 w onwards, breech at birth if 28 w onwards, multiparity

154
Q

Screening for dev dysplasia of the jip

A

NIPE exam:
different leg lengths
restricted hip abduction on one side
significant bilateral restriction in abduction
Difference in knee level when hips are flexed
clunking of the hips on special tests (Ortolani and barlow)

155
Q

Ix for dev dysplasia of the hip

A

US
XR

156
Q

Tx for dev dysplasia of the hip

A

Pavlik harness is less than 6 mo old
surgery

157
Q

What is juvenile idiopathic arthritis

A

Autoimmune inflammation in the joints, arthritis without other known cause under 16 yo

158
Q

Clinical presentation of Systemic JIA

A

Subtle salmon-pink rash, high swinging fever, lymph swelling, weight loss, joint pain and inflam, splenomegaly, muscle pain

159
Q

Ix for Systemic JIA

A

ANA and RF -ve, Raised CRP, ESR, platelets and serum ferritin

160
Q

Explain polyarticular JIA

A

Idiopathic inflam arthritis in 5 joints or more, tends to be symmetrical and can affect small or large joints

Minimal systemic sx

Most will be RF -ve

161
Q

Explain Oligoarticluar JIA

A

4 joints or less, often single joint

more common in girls under 6

Anterior uveitis (refer to optho)

No systemic sx, inflam markers normal or mildly elevated, ANA +ve but RF -ve

162
Q

Explain Ethesitis-related arthritis

A

More common in males over 6

Paeds version of seronegative spondyloarthropathies

Inflam where muscle inserts to bone

Majority have HLA-B27 gene

may have Sx of psoriasis or IBD

Prone to anterior uveitis

163
Q

What is Juvenile psoriatic arthritis

A

Seronegative inflam arthritis associated with psoriasis

Can be symmetrical affecting the small joints or asymmetrical affecting large joints in LL

May have nail pitting, dactylitis, enthesitis, plaques of psoriasis on the skin

164
Q

Tx for JIA

A

NSAID’s, Steroids, DMARDS, Biologics such as inflix/adalimumab

Phase 3A Sam Harper (4 decks)

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