Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

PAEDS - NEURO AND RENAL Flashcards

(119 cards)

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

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

A
  • Spastic (pyramidal, 70%)
  • Ataxic (10%)
  • Dyskinetic (athetoid, 10%)
  • Mixed (10%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CEREBRAL PALSY
What is affected in spastic cerebral palsy?

A
  • UMN pathways damaged (pyramidal or corticospinal) so UMN signs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

CEREBRAL PALSY
What is dyskinetic cerebral palsy?

A
  • Intellect unimpaired as basal ganglia affected (extra-pyramidal)
  • Associated with kernicterus + HIE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

VISION
What are some causes of severe visual impairment?

A

Genetic –

  • Congenital cataracts
  • Albinism
  • Retinal dystrophy
  • Retinoblastoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

HEARING
What are some risk factors for conductive hearing loss?

A
  • Down’s syndrome,
  • craniofacial syndromes
  • cleft palate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

HEARING
What does Rinne’s test show you?

A
  • Normal = louder at EAM
  • Conductive = louder on mastoid
  • Sensorineural = both decreased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
EPILEPSY Who is affected by infantile spasms?
- Early life (4-6m), M>F, often secondary to serious neuro abnormality (tuberous sclerosis, encephalitis, birth asphyxia)
26
EPILEPSY What are the 3 components to infantile spasms?
- 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
27
EPILEPSY What is Lennox-Gastaut syndrome? How does it present? Management?
- 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
28
EPILEPSY Who is juvenile myoclonic epilepsy more common in? How does it present? Management?
- Teens, F>M - Infrequent generalised seizures (often morning), daytime absences, sudden shock-like myoclonic seizures (can happen before seizures) - Good response to valproate
29
EPILEPSY What is the management of tonic clonic seizures?
male = sodium valproate female = lamotrigine / levetiracetam
30
EPILEPSY What is the management of focal seizures?
1st line = lamotrigine/levetiracetam 2nd line = carbamazepine
31
EPILEPSY What is the management of absence seizures?
1st line = ethosuximide 2nd line = - male = sodium valproate - female = lamotrigine/levetiracetam
32
EPILEPSY What is the management of myoclonic seizures?
male = sodium valproate female = levetiracetam
33
EPILEPSY What is the management of tonic/atonic seizures?
male = sodium valproate female = lamotrigine
34
EPILEPSY What is a note about treatment with carbamazepine?
- Can exacerbate absent + myoclonic seizures
35
'FUNNY TURNS' What are some other causes of 'funny turns'?
- Syncope - Migraine - Benign paroxysmal vertigo - Cardiac arrhythmias - NEAD - Fabricated by parent or child
36
TUBEROUS SCLEROSIS What are some other features of tuberous sclerosis?
- Neuro = epilepsy (infantile spasms or partial), developmental delay + intellectual impairment - Retinal hamartomas, - polycystic kidneys, - rhabdomyomata of heart
37
NEURAL TUBE DEFECTS What are 5 different types of neural tube defects?
- Spina bifida occulta (#1) - Meningocele - Myelomeningocele (most severe) - Anencephaly - Encephalocele
38
NEURAL TUBE DEFECTS What is spina bifida occulta?
- Failure of fusion of the vertebral arch, often incidental XR finding
39
NEURAL TUBE DEFECTS What is meningocele?
- Sac of fluid protruding spinal canal (without neural tissue), not exposed
40
NEURAL TUBE DEFECTS What is a myelomeningocele?
- Sac of fluid protruding spinal canal (with neural tissue), open lesion
41
NEURAL TUBE DEFECTS How does Chiari malformation lead to hydrocephalus?
- Herniation of cerebellar tonsils + brainstem > foramen magnum = disrupt CSF flow
42
NEURAL TUBE DEFECTS What is encephalocele?
- Brain + meninges extrude through midline skull defect
43
OTITIS MEDIA What are the viral causes of otitis media?
RSV rhinovirus adenovirus influenza virus
44
OTITIS MEDIA What are the bacterial causes of otitis media?
S. Pneumoniae H. Influenzae M. Catarrhalis S. Pyogenes
45
OTITIS MEDIA What are some complications of otitis media?
- Extracranial = mastoiditis, tympanic membrane perforation, glue ear - Intracranial = meningitis, abscess, venous sinus thrombosis
46
OTITIS MEDIA What is the management of otitis media?
- Regular pain relief (paracetamol, ibuprofen) - Most resolve spontaneously, may need amoxicillin/co-amoxiclav
47
OTITIS MEDIA Which antibiotics are used?
1st line = amoxicillin alternatives = erythromycin or clarithromycin
48
OTITIS MEDIA What are the complications?
Otitis media with effusion Hearing loss Perforated eardrum Recurrent infection Mastoiditis Abscess
49
GLUE EAR What is glue ear/otitis media with effusion (OME)?
- Most common cause of conductive hearing loss in children
50
GLUE EAR What is the management?
- Insertion of ventilation tubes (grommets) to drain excess fluid - Adenoidectomy as adenoids can harbour organisms + obstruct Eustachian tube so poor ventilation + drainage
51
OTITIS MEDIA Who is most at risk?
Younger children as Eustachian tubes short, horizontal + function poorly
52
GLUE EAR What investigations would you do?
- 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
GROMMETS what are grommets?
tiny tubes inserted into the tympanic membrane they allow fluid to drain from the middle ear into the ear canal
54
DEAFNESS At what volume does deafness begin to cause problems with development?
hearing loss up to 20dB does not affect development loss over 40dB affects speech and language development
55
PERIORBITAL CELLULITIS what are the causes?
- following minor injury to the eye - following another infection such as cough or cold
56
PERIORBITAL CELLULITIS what are the investigations?
- assessment of eye movements - visual acuity - assessment of cranial nerves + pupillary responses - CT sinus and orbits with contrast medium - bloods - WBC, blood cultures
57
PERIORBITAL CELLULITIS what is the management?
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
PERIORBITAL CELLULITIS what are the complications?
can progress to orbital cellulitis - infection involves the deeper tissues around the eye and the eyeball itself
59
CEREBRAL PALSY What are the main features of spastic cerebral palsy?
- 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
CEREBRAL PALSY What are the features of dyskinetic cerebral palsy?
- 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
STRABISMUS What are some causes of amblyopia?
Any interference with visual development > squint, refractive error, ptosis, cataracts
62
HEARING What are some risk factors for sensorineural hearing loss?
- Premature, - FHx - consanguinity
63
EPILEPSY What are the investigations for absence seizures?
EEG = 3hz generalised spike, symmetrical
64
EPILEPSY What is the management of infantile spasms?
Vigabatrin or corticosteroids (poor prognosis)
65
EPILEPSY What is the management of myoclonic seizures?
- 1st line = sodium valproate - 2nd line = clonazepam
66
'FUNNY TURNS' What are the investigations for reflex anoxic seizures?
- Ocular compression under controlled conditions often lead to asystole - paroxysmal slow-wave discharge on EEG
67
'FUNNY TURNS' What are breath holding attacks associated with?
Linked with Fe anaemia so treating as such may minimise further ones
68
TUBEROUS SCLEROSIS What are the investigations?
CT/MRI will detect calcified subependymal nodules + tubers from 2nd year of life
69
NEURAL TUBE DEFECTS What is the presentation of spina bifida occulta?
Site may have identifiable birthmark, lipoma or hair patch (lumbar)
70
NEURAL TUBE DEFECTS What is the management of spina bifida occulta?
Neurosurgery
71
NEURAL TUBE DEFECTS How may a myelomeningocele present?
- Paralysis of legs, - dislocation of hip + talipes, - sensory loss, - neuropathic bladder + bowel, - scoliosis - hydrocephalus from Chiari malformation
72
NEURAL TUBE DEFECTS What is the management of encephalocele?
- Surgical correction but often underlying cerebral malformations
73
PROTEINURIA What are some causes of proteinuria?
- Transient (febrile illness, after exercise = no investigation) - Nephrotic syndrome - HTN - Tubular proteinuria - Increased glomerular perfusion pressure - Reduced renal mass
74
NEPHROTIC SYNDROME What are some investigations for nephrotic syndrome?
- 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
NEPHROTIC SYNDROME What are some complications of nephrotic syndrome?
- 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
NEPHROTIC SYNDROME What is the general management of nephrotic syndrome?
- 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
NEPHRITIC SYNDROME What are some causes of nephritic syndrome?
- Post-streptococcal glomerulonephritis - IgA nephropathy (Berger's disease) - Vasculitis (HSP, SLE, Wegener's, polyarteritis nodosa) - Goodpasture's syndrome - Familial nephritis (Alport's syndrome)
78
NEPHRITIC SYNDROME How does familial nephritis (Alport's syndrome) present?
- X-linked recessive - ESRF by early adult - Associated with nerve deafness + ocular defects - Mother may have haematuria
79
NEPHRITIC SYNDROME What is the clinical presentation of nephritic syndrome?
- Haematuria (often macroscopic) + proteinuria of varying degree - Impaired GFR (rising creatinine), decreased urine output + volume overload - Salt + water retention > HTN (?seizures) + oedema (eyes)
80
NEPHRITIC SYNDROME What are some investigations for nephritic syndrome?
- 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
NEPHRITIC SYNDROME What is the general management of nephritic syndrome?
- 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
HSP What is the clinical presentation of HSP?
- 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
HSP What are some investigations for HSP?
- 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
HAEMOLYTIC URAEMIC SYNDROME What is the classic HUS triad?
- Microangiopathic haemolytic anaemia (due to RBC destruction) - AKI (kidneys fail to excrete waste products like urea) - Thrombocytopenia
85
HAEMOLYTIC URAEMIC SYNDROME What is the clinical presentation of HUS?
- Prodrome of bloody diarrhoea - Urine > reduced output, haematuria or dark brown - Abdo pain, lethargy - Oedema, HTN, bruising
86
HAEMOLYTIC URAEMIC SYNDROME What are some investigations for HUS?
- FBC (anaemia, thrombocytopenia), fragmented blood film - U+Es reveal AKI - Stool culture
87
HAEMOLYTIC URAEMIC SYNDROME What is the management of HUS?
- 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
HAEMATURIA What investigations for haematuria should all patients get?
- Urinalysis + urine MC&S - FBC, platelets, clotting + sickle cell screen - U+Es, creatinine, albumin, Ca2+, phosphate - USS kidneys + urinary tract
89
HYPOSPADIAS What is the clinical presentation of hypospadias?
- Ventral urethral meatus - Hooded prepuce - Chordee (ventral or downwards curvature of the penis in more severe forms) - Usually identified during NIPE
90
UTI When is a UTI classified as atypical?
- Septicaemia - Poor urine flow - Non-E. Coli - Failure to respond
91
UTI What are some risk factors for UTI?
- Incomplete bladder emptying - Vesico-ureteric reflux - Structural abnormality (horseshoe kidney, ureteric strictures) - Inadequate toilet hygiene
92
UTI In terms of performing ultrasounds scans in UTI, what are the guidelines?
- USS within 6w if 1st UTI + <6m but responds well to Tx within 48h or during illness if recurrent or atypical bacteria
93
UTI What is the management of UTI for >3m with upper UTI?
?Admission for IV, if not PO co-amoxiclav for 7–10d
94
UT ABNORMALITIES Name 6 urinary tract abnormalities
- Renal agenesis - Multicystic dysplastic kidney - Polycystic kidney disease - Pelvic/horseshoe kidney - Posterior urethral valves - Prune-belly syndrome
95
ACUTE KIDNEY INJURY What is acute kidney injury (AKI)? What is it characterised by?
- Spectrum of potentially reversible, reduction in renal function - Rapid rise in creatinine + development of oliguria (<0.5ml/kg/h)
96
ACUTE KIDNEY INJURY What are some renal causes of AKI?
- Vascular = HUS, vasculitis, embolus) - Glomerular = glomerulonephritis - Interstitial = interstitial nephritis, pyelonephritis - Tubular = acute tubular necrosis
97
ACUTE KIDNEY INJURY What are some investigations for AKI?
- FBC, U+Es (high urea), high creatinine, USS to identify if obstruction - Can have hyperkalaemia, hyperphosphataemia + metabolic acidosis
98
ACUTE KIDNEY INJURY What is the management of AKI?
- Maintain strict fluid balance (IV fluids if hypovolaemic, restrict if overload) - If failure of conservative Mx, severe electrolyte disturbances or acidosis then ?dialysis
99
CHRONIC KIDNEY DISEASE What are some causes of chronic kidney disease (CKD)?
- Structural malformations (congenital dysplastic kidney) - Glomerulonephritis - Hereditary nephropathies - Systemic diseases
100
CHRONIC KIDNEY DISEASE What is the clinical presentation of CKD?
- Failure to thrive, anorexia + vomiting - HTN, acute-on-chronic renal failure, anaemia - Bony deformities from renal osteodystrophy - Incidental proteinuria, polydipsia + polyuria
101
CHRONIC KIDNEY DISEASE What are some investigations for CKD?
- Monitor growth - FBC = anaemia due to reduced EPO - U+Es + electrolytes (Ca2+ low, phosphate high)
102
CHRONIC KIDNEY DISEASE What is the management of CKD?
- 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
NEPHROTIC SYNDROME what can cause minimal change disease?
- NSAIDs, - Hodgkin's lymphoma, - infectious mononucleosis
104
HAEMATURIA What are some non-glomerular causes of haematuria?
- Wilm's tumour, - trauma, - stones (esp if FHx), - sickle cell disease - other bleeding disorders
105
UTI What is the management of children under 3m in UTI?
ALL children <3m + fever get immediate IV cefuroxime + full septic screen (blood cultures, FBC, CRP lactate, LP etc)
106
UTI What is the management of UTI for >3m with lower UTI?
3d PO trimethoprim, nitrofurantoin, amoxicillin or cephalosporin with follow-up if still unwell after 24-48h
107
UT ABNORMALITIES What causes multicystic dysplastic kidney?
Failure of union of ureteric bud with nephrogenic mesenchyme
108
UT ABNORMALITIES What are the two types of polycystic kidney disease?
- 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
UT ABNORMALITIES What are some complications of autosomal recessive polycystic kidney disease?
Often liver involvement with portal + interlobular fibrosis
110
NEPHROTIC SYNDROME What is the pathophysiology of nephrotic syndrome?
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
PYELONEPHRITIS what are the risk factors?
- 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
PYELONEPHRITIS What are the investigations?
- urine microscopy and culture - CT KUB with contrast
113
NOCTURNAL ENURESIS what are the causes?
- not waking to bladder signals - inadequate levels of vasopressin (ADH) - overactive bladder - constipation - UTIs - Family history - Anxiety/stress - poor bedtime routines
114
NOCTURNAL ENURESIS what is the presentation of inadequate levels of vasopressin?
- large volumes of urine passed at night - wet in the early part of the night - wet more than once per night
115
NOCTURNAL ENURESIS what is the presentation of an overactive bladder?
- 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
NOCTURNAL ENURESIS what are the investigations?
- physical examination (back, genitalia + lower limbs) - urinalysis + MS&C - bladder scan - uroflowmetry - ultrasound
117
ALPORT SYNDROME what is the clinical presentation?
- haematuria - oedema - hypertension - loss of kidney function - progressive hearing loss - proteinuria - vision problems
118
ALPORT SYNDROME what is the management?
ACE inhibitors dialysis kidney transplant
119
ALPORT SYNDROME what are the investigations?
- genetic testing - tissue biopsy - urinalysis - hearing tests

C TO REVISE - PHASE 3A (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions