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C TO REVISE - PHASE 3A > PAEDS - NEURO AND RENAL > Flashcards

PAEDS - NEURO AND RENAL Flashcards

1
Q

CEREBRAL PALSY
What is cerebral palsy?
How does it progress?

A
  • Permanent disorder of movement + posture due to a non-progressive lesion of motor pathways in the developing brain
  • Sx develop over time as the brain starts to develop
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2
Q

CEREBRAL PALSY
What are some early features of cerebral palsy?

A
  • Abnormal limb/trunk tone + posture with delayed motor milestones
  • Feeding issues > oromotor incoordination, slow feeding, gagging + vomiting
  • Abnormal gait when walking achieved
  • Hand preference before 12m + primitive reflexes after 6m
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3
Q

CEREBRAL PALSY
What are the 4 broad types of cerebral palsy?

A
  • Spastic (pyramidal, 70%)
  • Ataxic (10%)
  • Dyskinetic (athetoid, 10%)
  • Mixed (10%)
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4
Q

CEREBRAL PALSY
What is affected in spastic cerebral palsy?

A
  • UMN pathways damaged (pyramidal or corticospinal) so UMN signs
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5
Q

CEREBRAL PALSY
What is dyskinetic cerebral palsy?

A
  • Intellect unimpaired as basal ganglia affected (extra-pyramidal)
  • Associated with kernicterus + HIE
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6
Q

CEREBRAL PALSY
What are the investigations of cerebral palsy?

A
  • Clinical Dx (assess posture, pattern of tone, hand function + gait)
  • Functional ability judged by Gross Motor Function Classification System
  • MRI head to identify cause but not necessary for Dx
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7
Q

CEREBRAL PALSY
What are the stages of the Gross Motor Function Classification System?

A
  • I = walks without limitation
  • II = with limitation
  • III = handheld mobility device
  • IV = III with limitation
  • V = wheelchair
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8
Q

VISION
What are some causes of severe visual impairment?

A

Genetic –

  • Congenital cataracts
  • Albinism
  • Retinal dystrophy
  • Retinoblastoma
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9
Q

STRABISMUS
What is the pathophysiology of strabismus?

A
  • When eyes not aligned the images on retina do not match + pt will experience diplopia
  • When this occurs in paeds, before the eyes have fully established their connections within the brain, the brain will cope by reducing the signal from the less dominant eye
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10
Q

STRABISMUS
What causes strabismus?

A
  • Multifactorial (combination of hereditary + refractive errors)
  • Idiopathic
  • Secondary to vision loss
  • Higher incidence in cerebral palsy
  • SOL (retinoblastoma) rare but suspect if sudden onset + other neurology
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11
Q

STRABISMUS
What are some investigations for strabismus?

A
  • (Single) cover test for manifest/tropias
  • Cover-uncover (alternate cover) test for latent/phorias
  • Corneal light reflex test (Hirschberg’s test)
  • Important to assess visual acuity + ocular movements to exclude paralytic
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12
Q

STRABISMUS
What medical treatment can be given in strabismus?

A
  • Botox injections = paralyse the muscle that is pulling the eye in a certain direction
  • Esotropia = MR, exotropia = LR
  • May need repeat injections as effects wear off, ketamine anaesthesia
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13
Q

HEARING
What are some causes of sensorineural hearing loss?

A
  • Genetic or syndromes
  • Perinatal (trauma, infection, hypoxia)
  • Congenital infections (rubella, CMV)
  • Meningitis (pneumococcus can cause ossification of cochlear)
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14
Q

HEARING
What are some risk factors for conductive hearing loss?

A
  • Down’s syndrome,
  • craniofacial syndromes
  • cleft palate
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15
Q

HEARING
What is evoked otoacoustic emission?
What are the pros?
What are the cons?

A
  • Earphone produces sound which evokes an echo from ear if cochlear function normal
  • Simple + quick
  • Misses auditory neuropathy, cochlear test not hearing, high false +ve in first 24h
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16
Q

HEARING
What is auditory brainstem response audiometry?
What are the pros?
What are the cons?

A
  • Computer analysis of EEG waveforms evoked in response to auditory stimuli
  • Screens hearing pathway ear>brainstem, low false +ve rate
  • Affected by movement (time consuming), electrodes on infant’s head, complex computerised gear
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17
Q

HEARING
What testing might be done in children 6–9m?

A
  • Distraction testing
  • Relies on baby locating + turning appropriately to high + low frequency sounds out of field of vision
  • 2x trained staff
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18
Q

HEARING
What testing might be done in children 10–18m?

A
  • Visual reinforcement audiometry
  • Hearing thresholds are established using visual rewards (illumination of toys) to reinforce the child’s head turn to stimuli of different frequencies
  • First test that does single ear measures
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19
Q

HEARING
What hearing tests are done at…

i) >2y?
ii) >2.5y?
iii) 4y?

A

i) Performance testing = child performs an action when hear a noise
ii) Speech discrimination tests (McCormick toy test)
iii) Pure tone audiometry at school entry = child responds to pure tone stimulus with headphones

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20
Q

HEARING
What are 3 main investigations in hearing?

A
  • Rinne’s test (mastoid then external acoustic meatus)
  • Weber’s (forehead in midline)
  • Audiograms
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21
Q

HEARING
What does Rinne’s test show you?

A
  • Normal = louder at EAM
  • Conductive = louder on mastoid
  • Sensorineural = both decreased
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22
Q

HEARING
What does Weber’s test show you?

A
  • Normal = vibrations equal in both ears
  • Conductive = louder in abnormal ear
  • Sensorineural = louder in normal ear
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23
Q

FEBRILE CONVULSIONS
What is the management of febrile convulsions?

A
  • Period of observation, paeds referral if first seizure or complex
  • Antipyretics have NOT shown to reduce risk of recurrence
  • Education = stay with them, ensure safe, nothing in mouth, call 999 if lasts >5m, teach how to use PR diazepam or buccal midazolam if Hx of prolonged seizures (>5m)
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24
Q

EPILEPSY
What are 4 epilepsy syndromes seen in children?

A
  • Infantile spasms (West’s syndrome)
  • Lennox-Gastaut syndrome
  • Juvenile myoclonic epilepsy
  • Benign Rolandic epilepsy = M>F, paraesthesia (unilateral face, tongue, twitching) during sleep, EEG shows centrotemporal focal spike waves
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25
Q

EPILEPSY
Who is affected by infantile spasms?

A
  • Early life (4-6m), M>F, often secondary to serious neuro abnormality (tuberous sclerosis, encephalitis, birth asphyxia)
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26
Q

EPILEPSY
What are the 3 components to infantile spasms?

A
  • Violent flexor spasms of head, trunk + limbs followed by extension of arms (salaam spasms) for 1-2s, can repeat up to 50 times
  • Progressive mental handicap
  • EEG shows hypsarrhythmia
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27
Q

EPILEPSY
What is Lennox-Gastaut syndrome?
How does it present?
Management?

A
  • Can be extension of infantile spasms, 1-5y
  • Atypical absences, falls, jerks + 90% have mod-severe mental handicap
  • EEG shows slow spike, ketogenic diet may help
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28
Q

EPILEPSY
Who is juvenile myoclonic epilepsy more common in?
How does it present?
Management?

A
  • Teens, F>M
  • Infrequent generalised seizures (often morning), daytime absences, sudden shock-like myoclonic seizures (can happen before seizures)
  • Good response to valproate
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29
Q

EPILEPSY
What is the management of tonic clonic seizures?

A

male = sodium valproate

female = lamotrigine / levetiracetam

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30
Q

EPILEPSY
What is the management of focal seizures?

A

1st line = lamotrigine/levetiracetam

2nd line = carbamazepine

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31
Q

EPILEPSY
What is the management of absence seizures?

A

1st line = ethosuximide

2nd line =
- male = sodium valproate
- female = lamotrigine/levetiracetam

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32
Q

EPILEPSY
What is the management of myoclonic seizures?

A

male = sodium valproate

female = levetiracetam

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33
Q

EPILEPSY
What is the management of tonic/atonic seizures?

A

male = sodium valproate

female = lamotrigine

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34
Q

EPILEPSY
What is a note about treatment with carbamazepine?

A
  • Can exacerbate absent + myoclonic seizures
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35
Q

‘FUNNY TURNS’
What are some other causes of ‘funny turns’?

A
  • Syncope
  • Migraine
  • Benign paroxysmal vertigo
  • Cardiac arrhythmias
  • NEAD
  • Fabricated by parent or child
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36
Q

TUBEROUS SCLEROSIS
What are some other features of tuberous sclerosis?

A
  • Neuro = epilepsy (infantile spasms or partial), developmental delay + intellectual impairment
  • Retinal hamartomas,
  • polycystic kidneys,
  • rhabdomyomata of heart
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37
Q

NEURAL TUBE DEFECTS
What are 5 different types of neural tube defects?

A
  • Spina bifida occulta (#1)
  • Meningocele
  • Myelomeningocele (most severe)
  • Anencephaly
  • Encephalocele
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38
Q

NEURAL TUBE DEFECTS
What is spina bifida occulta?

A
  • Failure of fusion of the vertebral arch, often incidental XR finding
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39
Q

NEURAL TUBE DEFECTS
What is meningocele?

A
  • Sac of fluid protruding spinal canal (without neural tissue), not exposed
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40
Q

NEURAL TUBE DEFECTS
What is a myelomeningocele?

A
  • Sac of fluid protruding spinal canal (with neural tissue), open lesion
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41
Q

NEURAL TUBE DEFECTS
How does Chiari malformation lead to hydrocephalus?

A
  • Herniation of cerebellar tonsils + brainstem > foramen magnum = disrupt CSF flow
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42
Q

NEURAL TUBE DEFECTS
What is encephalocele?

A
  • Brain + meninges extrude through midline skull defect
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43
Q

OTITIS MEDIA
What are the viral causes of otitis media?

A

RSV
rhinovirus
adenovirus
influenza virus

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44
Q

OTITIS MEDIA
What are the bacterial causes of otitis media?

A

S. Pneumoniae
H. Influenzae
M. Catarrhalis
S. Pyogenes

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45
Q

OTITIS MEDIA
What are some complications of otitis media?

A
  • Extracranial = mastoiditis, tympanic membrane perforation, glue ear
  • Intracranial = meningitis, abscess, venous sinus thrombosis
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46
Q

OTITIS MEDIA
What is the management of otitis media?

A
  • Regular pain relief (paracetamol, ibuprofen)
  • Most resolve spontaneously, may need amoxicillin/co-amoxiclav
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47
Q

OTITIS MEDIA
Which antibiotics are used?

A

1st line = amoxicillin
alternatives = erythromycin or clarithromycin

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48
Q

OTITIS MEDIA
What are the complications?

A

Otitis media with effusion
Hearing loss
Perforated eardrum
Recurrent infection
Mastoiditis
Abscess

49
Q

GLUE EAR
What is glue ear/otitis media with effusion (OME)?

A
  • Most common cause of conductive hearing loss in children
50
Q

GLUE EAR
What is the management?

A
  • Insertion of ventilation tubes (grommets) to drain excess fluid
  • Adenoidectomy as adenoids can harbour organisms + obstruct Eustachian tube so poor ventilation + drainage
51
Q

OTITIS MEDIA
Who is most at risk?

A

Younger children as Eustachian tubes short, horizontal + function poorly

52
Q

GLUE EAR
What investigations would you do?

A
  • Otoscopy (TM appears dull + retracted, often with visible fluid level)
  • Flat trace on tympanometry + evidence of conductive loss on pure tone audiometry (or reduced hearing on distraction test if younger)
53
Q

GROMMETS
what are grommets?

A

tiny tubes inserted into the tympanic membrane

they allow fluid to drain from the middle ear into the ear canal

54
Q

DEAFNESS
At what volume does deafness begin to cause problems with development?

A

hearing loss up to 20dB does not affect development

loss over 40dB affects speech and language development

55
Q

PERIORBITAL CELLULITIS
what are the causes?

A
  • following minor injury to the eye
  • following another infection such as cough or cold
56
Q

PERIORBITAL CELLULITIS
what are the investigations?

A
  • assessment of eye movements
  • visual acuity
  • assessment of cranial nerves + pupillary responses
  • CT sinus and orbits with contrast medium
  • bloods - WBC, blood cultures
57
Q

PERIORBITAL CELLULITIS
what is the management?

A

Mild = oral co-amoxiclav/cefuroxime + metronidazole for 7-10 days
Moderate-severe = immediate referral to hospital + IV cefotaxime/clindamycin

can also consider incision, drainage and culture of any abscesses

58
Q

PERIORBITAL CELLULITIS
what are the complications?

A

can progress to orbital cellulitis - infection involves the deeper tissues around the eye and the eyeball itself

59
Q

CEREBRAL PALSY
What are the main features of spastic cerebral palsy?

A
  • Limb tone persistently increased (spasticity, velocity-dependent)
  • Brisk deep tendon reflexes + extensor plantars (+ve Babinski)
  • Increased limb tone may suddenly yield under pressure (clasp knife)
60
Q

CEREBRAL PALSY
What are the features of dyskinetic cerebral palsy?

A
  • Intellect unimpaired as basal ganglia affected (extra-pyramidal)
  • Chorea, athetosis, dystonia
  • Muscle tone is variable (floppiness), involuntary movements, poor trunk control
  • Associated with kernicterus + HIE
61
Q

STRABISMUS
What are some causes of amblyopia?

A

Any interference with visual development > squint, refractive error, ptosis, cataracts

62
Q

HEARING
What are some risk factors for sensorineural hearing loss?

A
  • Premature,
  • FHx
  • consanguinity
63
Q

EPILEPSY
What are the investigations for absence seizures?

A

EEG = 3hz generalised spike, symmetrical

64
Q

EPILEPSY
What is the management of infantile spasms?

A

Vigabatrin or corticosteroids (poor prognosis)

65
Q

EPILEPSY
What is the management of myoclonic seizures?

A
  • 1st line = sodium valproate
  • 2nd line = clonazepam
66
Q

‘FUNNY TURNS’
What are the investigations for reflex anoxic seizures?

A
  • Ocular compression under controlled conditions often lead to asystole
  • paroxysmal slow-wave discharge on EEG
67
Q

‘FUNNY TURNS’
What are breath holding attacks associated with?

A

Linked with Fe anaemia so treating as such may minimise further ones

68
Q

TUBEROUS SCLEROSIS
What are the investigations?

A

CT/MRI will detect calcified subependymal nodules + tubers from 2nd year of life

69
Q

NEURAL TUBE DEFECTS
What is the presentation of spina bifida occulta?

A

Site may have identifiable birthmark, lipoma or hair patch (lumbar)

70
Q

NEURAL TUBE DEFECTS
What is the management of spina bifida occulta?

A

Neurosurgery

71
Q

NEURAL TUBE DEFECTS
How may a myelomeningocele present?

A
  • Paralysis of legs,
  • dislocation of hip + talipes,
  • sensory loss,
  • neuropathic bladder + bowel,
  • scoliosis
  • hydrocephalus from Chiari malformation
72
Q

NEURAL TUBE DEFECTS
What is the management of encephalocele?

A
  • Surgical correction but often underlying cerebral malformations
73
Q

PROTEINURIA
What are some causes of proteinuria?

A
  • Transient (febrile illness, after exercise = no investigation)
  • Nephrotic syndrome
  • HTN
  • Tubular proteinuria
  • Increased glomerular perfusion pressure
  • Reduced renal mass
74
Q

NEPHROTIC SYNDROME
What are some investigations for nephrotic syndrome?

A
  • Urinalysis (proteinuria + microscopic haematuria)
  • Urine MC&S (infection)
  • Renal function (U+Es, creatinine, albumin, urinary Na+ concentration)
  • Lipid profile
  • Systemic disease screen
  • Antistreptolysin O or anti-DNAse B titres + throat swab
  • Renal biopsy for histology if no steroid response
75
Q

NEPHROTIC SYNDROME
What are some complications of nephrotic syndrome?

A
  • Hypovolaemia as fluid leaks from intravascular to interstitial space
  • Thrombosis due to loss of antithrombin III
  • Infection due to leakage of immunoglobulins, weakening the immune system + exacerbated by Tx with steroids
76
Q

NEPHROTIC SYNDROME
What is the general management of nephrotic syndrome?

A
  • Strict fluid balance with restriction, no added salt
  • Tx hypovolaemia if present but albumin infusion is not routine
  • Diuretics if very oedematous + no evidence of hypovolaemia
  • Prophylactic PO penicillin V until oedema-free
  • PCV vaccine
77
Q

NEPHRITIC SYNDROME
What are some causes of nephritic syndrome?

A
  • Post-streptococcal glomerulonephritis
  • IgA nephropathy (Berger’s disease)
  • Vasculitis (HSP, SLE, Wegener’s, polyarteritis nodosa)
  • Goodpasture’s syndrome
  • Familial nephritis (Alport’s syndrome)
78
Q

NEPHRITIC SYNDROME
How does familial nephritis (Alport’s syndrome) present?

A
  • X-linked recessive
  • ESRF by early adult
  • Associated with nerve deafness + ocular defects
  • Mother may have haematuria
79
Q

NEPHRITIC SYNDROME
What is the clinical presentation of nephritic syndrome?

A
  • Haematuria (often macroscopic) + proteinuria of varying degree
  • Impaired GFR (rising creatinine), decreased urine output + volume overload
  • Salt + water retention > HTN (?seizures) + oedema (eyes)
80
Q

NEPHRITIC SYNDROME
What are some investigations for nephritic syndrome?

A
  • Urinalysis = haematuria, raised protein, (PCR, RBC casts on microscopy)
  • FBC, U+Es = raised urea) raised creatinine + hyperkalaemic acidosis
  • C3/4 may be low (post-strep, SLE)
  • Antistreptolysin O titre (may be raised), throat/skin swabs for strep
  • Renal biopsy
81
Q

NEPHRITIC SYNDROME
What is the general management of nephritic syndrome?

A
  • Fluid + electrolyte balance, monitor UO + creatinine
  • Treat HTN + oedema with antihypertensives ±diuretics (ACEi/ARB, furosemide or prednisolone)
  • Nephritis usually settles alone, may need steroids
82
Q

HSP
What is the clinical presentation of HSP?

A
  • Palpable purpuric rash affecting extensor surfaces of lower limbs + buttocks
  • Joint pain (knees + ankles, may be swollen + painful, reduced ROM)
  • Colicky abdo pain (GI haemorrhage > haematemesis + melaena, intussusception)
  • Renal involvement (IgA nephritis > haematuria + proteinuria)
83
Q

HSP
What are some investigations for HSP?

A
  • Exclude DDx of non-blanching rash
    – FBC + blood film (thrombocytopenia, sepsis + leukaemia), CRP, cultures, HSP = afebrile
  • Urinalysis for proteinuria + haematuria
  • PCR to quantify proteinuria
  • Renal biopsy if severe renal issues to determine if Tx
84
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the classic HUS triad?

A
  • Microangiopathic haemolytic anaemia (due to RBC destruction)
  • AKI (kidneys fail to excrete waste products like urea)
  • Thrombocytopenia
85
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the clinical presentation of HUS?

A
  • Prodrome of bloody diarrhoea
  • Urine > reduced output, haematuria or dark brown
  • Abdo pain, lethargy
  • Oedema, HTN, bruising
86
Q

HAEMOLYTIC URAEMIC SYNDROME
What are some investigations for HUS?

A
  • FBC (anaemia, thrombocytopenia), fragmented blood film
  • U+Es reveal AKI
  • Stool culture
87
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the management of HUS?

A
  • ABCDE as emergency
  • Often self-limiting so supportive > refer to paeds renal unit for ?dialysis
  • Anti-hypertensives, careful fluid balance, blood transfusions
  • Plasma exchange if severe + not associated with diarrhoea
88
Q

HAEMATURIA
What investigations for haematuria should all patients get?

A
  • Urinalysis + urine MC&S
  • FBC, platelets, clotting + sickle cell screen
  • U+Es, creatinine, albumin, Ca2+, phosphate
  • USS kidneys + urinary tract
89
Q

HYPOSPADIAS
What is the clinical presentation of hypospadias?

A
  • Ventral urethral meatus
  • Hooded prepuce
  • Chordee (ventral or downwards curvature of the penis in more severe forms)
  • Usually identified during NIPE
90
Q

UTI
When is a UTI classified as atypical?

A
  • Septicaemia
  • Poor urine flow
  • Non-E. Coli
  • Failure to respond
91
Q

UTI
What are some risk factors for UTI?

A
  • Incomplete bladder emptying
  • Vesico-ureteric reflux
  • Structural abnormality (horseshoe kidney, ureteric strictures)
  • Inadequate toilet hygiene
92
Q

UTI
In terms of performing ultrasounds scans in UTI, what are the guidelines?

A
  • USS within 6w if 1st UTI + <6m but responds well to Tx within 48h or during illness if recurrent or atypical bacteria
93
Q

UTI
What is the management of UTI for >3m with upper UTI?

A

?Admission for IV, if not PO co-amoxiclav for 7–10d

94
Q

UT ABNORMALITIES
Name 6 urinary tract abnormalities

A
  • Renal agenesis
  • Multicystic dysplastic kidney
  • Polycystic kidney disease
  • Pelvic/horseshoe kidney
  • Posterior urethral valves
  • Prune-belly syndrome
95
Q

ACUTE KIDNEY INJURY
What is acute kidney injury (AKI)?
What is it characterised by?

A
  • Spectrum of potentially reversible, reduction in renal function
  • Rapid rise in creatinine + development of oliguria (<0.5ml/kg/h)
96
Q

ACUTE KIDNEY INJURY
What are some renal causes of AKI?

A
  • Vascular = HUS, vasculitis, embolus)
  • Glomerular = glomerulonephritis
  • Interstitial = interstitial nephritis, pyelonephritis
  • Tubular = acute tubular necrosis
97
Q

ACUTE KIDNEY INJURY
What are some investigations for AKI?

A
  • FBC, U+Es (high urea), high creatinine, USS to identify if obstruction
  • Can have hyperkalaemia, hyperphosphataemia + metabolic acidosis
98
Q

ACUTE KIDNEY INJURY
What is the management of AKI?

A
  • Maintain strict fluid balance (IV fluids if hypovolaemic, restrict if overload)
  • If failure of conservative Mx, severe electrolyte disturbances or acidosis then ?dialysis
99
Q

CHRONIC KIDNEY DISEASE
What are some causes of chronic kidney disease (CKD)?

A
  • Structural malformations (congenital dysplastic kidney)
  • Glomerulonephritis
  • Hereditary nephropathies
  • Systemic diseases
100
Q

CHRONIC KIDNEY DISEASE
What is the clinical presentation of CKD?

A
  • Failure to thrive, anorexia + vomiting
  • HTN, acute-on-chronic renal failure, anaemia
  • Bony deformities from renal osteodystrophy
  • Incidental proteinuria, polydipsia + polyuria
101
Q

CHRONIC KIDNEY DISEASE
What are some investigations for CKD?

A
  • Monitor growth
  • FBC = anaemia due to reduced EPO
  • U+Es + electrolytes (Ca2+ low, phosphate high)
102
Q

CHRONIC KIDNEY DISEASE
What is the management of CKD?

A
  • Diet + NG or gastrostomy feeding may be needed for normal growth
  • Phosphate restriction + activated vitamin D to prevent renal osteodystrophy
  • May need recombinant growth hormone
  • Recombinant erythropoietin to prevent anaemia
  • Dialysis + transplantation if in ESRF (GFR <15ml/min/1.73m^2)
103
Q

NEPHROTIC SYNDROME
what can cause minimal change disease?

A
  • NSAIDs,
  • Hodgkin’s lymphoma,
  • infectious mononucleosis
104
Q

HAEMATURIA
What are some non-glomerular causes of haematuria?

A
  • Wilm’s tumour,
  • trauma,
  • stones (esp if FHx),
  • sickle cell disease
  • other bleeding disorders
105
Q

UTI
What is the management of children under 3m in UTI?

A

ALL children <3m + fever get immediate IV cefuroxime + full septic screen (blood cultures, FBC, CRP lactate, LP etc)

106
Q

UTI
What is the management of UTI for >3m with lower UTI?

A

3d PO trimethoprim, nitrofurantoin, amoxicillin or cephalosporin with follow-up if still unwell after 24-48h

107
Q

UT ABNORMALITIES
What causes multicystic dysplastic kidney?

A

Failure of union of ureteric bud with nephrogenic mesenchyme

108
Q

UT ABNORMALITIES
What are the two types of polycystic kidney disease?

A
  • AD = HTN, haematuria in childhood with renal failure in adulthood
  • AR = defect on chromosome 6 that encodes fibrocystin, protein for normal renal tubule development
109
Q

UT ABNORMALITIES
What are some complications of autosomal recessive polycystic kidney disease?

A

Often liver involvement with portal + interlobular fibrosis

110
Q

NEPHROTIC SYNDROME
What is the pathophysiology of nephrotic syndrome?

A
  1. Inflammation – from immune cells (Ab’s, Ig’s - IgG), complement proteins, HTN, atherosclerosis, medications/immunisations, infection
  2. Damage to podocytes – protein leakage (albumin, Ab’s)
  3. Increased liver activity – to increase albumin, - Consequential increase in cholesterol + coagulation factors
  4. Reduced oncotic pressure – oedema - Consequential blood volume decrease, RAAS stimulation, exacerbation
111
Q

PYELONEPHRITIS
what are the risk factors?

A
  • vesicoureteral reflux (VUR) = most common + most important
  • previous history of UTI
  • siblings with a history of UTI
  • female sex
  • indwelling urinary catheter
  • intact prepuce in boys
  • structural abnormalities of the kidneys and lower urinary tract
112
Q

PYELONEPHRITIS
What are the investigations?

A
  • urine microscopy and culture
  • CT KUB with contrast
113
Q

NOCTURNAL ENURESIS
what are the causes?

A
  • not waking to bladder signals
  • inadequate levels of vasopressin (ADH)
  • overactive bladder
  • constipation
  • UTIs
  • Family history
  • Anxiety/stress
  • poor bedtime routines
114
Q

NOCTURNAL ENURESIS
what is the presentation of inadequate levels of vasopressin?

A
  • large volumes of urine passed at night
  • wet in the early part of the night
  • wet more than once per night
115
Q

NOCTURNAL ENURESIS
what is the presentation of an overactive bladder?

A
  • damp patches that occur at night also occur during the day
  • the volume of urine passed is variable
  • children often wake after wetting at night
116
Q

NOCTURNAL ENURESIS
what are the investigations?

A
  • physical examination (back, genitalia + lower limbs)
  • urinalysis + MS&C
  • bladder scan
  • uroflowmetry
  • ultrasound
117
Q

ALPORT SYNDROME
what is the clinical presentation?

A
  • haematuria
  • oedema
  • hypertension
  • loss of kidney function
  • progressive hearing loss
  • proteinuria
  • vision problems
118
Q

ALPORT SYNDROME
what is the management?

A

ACE inhibitors
dialysis
kidney transplant

119
Q

ALPORT SYNDROME
what are the investigations?

A
  • genetic testing
  • tissue biopsy
  • urinalysis
  • hearing tests

C TO REVISE - PHASE 3A (11 decks)

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