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Special Pops - Peds > Nephrology, Neuro, Ortho, Endo > Flashcards

Nephrology, Neuro, Ortho, Endo Flashcards

1
Q

What is antenatal hydronephrosis?

A
  • Congenital dilation of kidney

- Detected by prenatal routine US

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2
Q

Treatment of antenatal hydronephrosis

A

-Controversial

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3
Q

What is prenatal US most useful for?

A

Detection of obstructive uropathy - significant risk of neonatal demise due to pulmonary hypoplasia (Potter’s syndrome)

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4
Q

Describe Potter’s syndrome

A
  • Kidneys fail to develop (and they usually produce amniotic fluid)
  • Decreased fluid
  • Head collides with uterine wall
  • Facial features (flattened nose, recessed chin, prominent epicanthal folds, low set ears)
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5
Q

Clinical presentations of obstructive uropathy

A
  • UTIs

- Failure to thrive

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6
Q

Presence of hydronephrosis and presence of urinary obstruction

A

Hydronephrosis does NOT necessarily indicate presence of urinary obstruction

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7
Q

Post-natal management of obstructive uropathy

A
  • FU US

- Abx prophylaxis

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8
Q

Who is MC affected by primary nocturnal enuresis?

A

Strong family history

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9
Q

What is used as a justification for not treating primary enuresis?

A

Resolution rate is approx 15% per year

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10
Q

Labs for primary nocturnal enuresis

A
  • Morning U/A to eval concentration

- Urine culture and sensitivity if U/A suggests cystitis

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11
Q

How must the U/A be performed in evaluation of primary nocturnal enuresis?

A
  • On a concentrated urine specimen

- Dilute UA with SG under 1.010 might not reveal infection

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12
Q

Treatment of primary nocturnal enuresis

A
  • Behavioral
  • Alarm therapy
  • DDAVP, anticholinergics, tricyclics
  • ENT if signs of obstructive breathing
  • Ultimately, time
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13
Q

What is ultimately the best treatment of primary enuresis?

A

Time!

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14
Q

Clinical presentation of HUS

A
  • Prodromal gastroenteritis (83%)
  • Progressive renal failure a/w microangiopathology
  • Hemolytic anemia
  • Thrombocytopenia
  • HTN (47%)
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15
Q

Etiology of HUS

A

Predominantly occurs in infants/children after prodromal diarrhea (E coli infection MC)

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16
Q

Clinical presentation of Henoch Scholein Purpura

A
  • Prodrome: HA, anorexia, fever

- MC subsequent symptoms: rash (95-100% pts), abd pain and vomiting (35-85%), joint pain (60-84%)

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17
Q

What is West syndrome?

A
  • Severe epilepsy syndrome

- Consists of a triad: infantile spasms (Shalom), hypsarrhythmia EEG, mental retardation

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18
Q

What are Shalom seizures?

A
  • Infantile spasms
  • Part of West syndrome
  • Sudden, rapid, tonic contraction of trunk and limb musculature
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19
Q

Warning signs of pediatric brain tumor

A
  • HA that awakens child or worse in AM/night
  • NV
  • Changes in speech, vision, hearing
  • Problems w/balance
  • Changes in mood, personality or ability to concentrate
  • Problems with memory
  • Seizures
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20
Q

What is pseudotumor cerebri?

A

Idiopathic intracranial HTN (unknown etiology)

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21
Q

Possible causes of pseudotumor cerebri?

A
  • Exposure to or withdrawal from certain drugs (Vit A in infants)
  • Systemic diseases (e.g. Lyme)
  • Certain endocrine or metabolic diseases
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22
Q

Who is MC affected by pseudotumor cerebri?

A

Obese women of child bearing age

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23
Q

Clinical presentation of pseudotumor cerebri

A
  • Papilledema
  • HAs
  • Diplopia
  • Pulsatile tinnitus
  • Radicular pain
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24
Q

Treatment of pseudotumor cerebri

A
  • Pharm (acetazolamide, furosemide, HA proph, steroids)
  • Optic nerve sheath fenestration (decompression)
  • CSF diversion via shunt
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25
Q

Clinical presentation of NF-1

A
  • Cafe au lait lesions

- Gliomas, spinal cord tumors, vascular lesions, long bone abnormalities

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26
Q

Clinical presentation of NF-2

A
  • Minimal cutaneous findings

- Relative high incidence of meningiomas and acoustic neuromas

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27
Q

Which type of NF presents with cafe au lait lesions?

A

NF-1

28
Q

Diagnosis of NF-1

A

2 of 7 required and many may not appear until childhood/adolescence

  • 6 or more cafe au lait spots
  • Axillary or inguinal freckles
  • 2 or more neurofibromas (or 1 plexiform neurofibroma)
  • Optic nerve glioma
  • 2 Lisch nodules (iris hamartomas)
  • Long bone abnormalities
  • First degree relative with NF-1
29
Q

Diagnosis of NF-2

A
  • Bilateral vestibular schwannomas
  • First degree relative
  • Any 2 of: neurofibroma, meningioma, glioma, schwannoma
30
Q

Describe cutaneous manifestations of NF-2

A
  • Less common than NF-1
  • Plexiform neurofibromas are UNUSUAL
  • Cafe au lait spots tend to be fewer and lighter
  • Axillary and inguinal freckling is not present
  • Schwannomas occur on peripheral nerves (palpable spherical nodules)
31
Q

What is Von Hippel-Lindau disease?

A
  • Autosomal dominant neurocutaneous dysplasia complex

- Symptoms begin in 2-3 decades of life

32
Q

Clinical presentation of Von Hippel-Lindau disease

A
  • Ocular signs d/t retinal hemorrhage, detachment, glaucoma, uveitis
  • HAs, ataxia, blindness
  • Hemangioblastomas
33
Q

What is tuberous sclerosis?

A
  • Autosomal dominant disorder

- Non-malignant tumors form in many different organs

34
Q

How does tuberous sclerosis present?

A

Multi-systemic

  • Cutaneous: ash leaf spots, Shagreen patch, angiofibromas
  • Neuro: seizures, intracranial calcifications
  • Retinal, renal, pulm, MSK manifestations
35
Q

What are ash leaf spots and what are they a/w?

A
  • Congenital hypopigmental macules

- Tuberous sclerosis (87% have lesions at birth)

36
Q

What is Shagreen patch and what is it a/w?

A
  • CT nevus most often in lumbosacral region or trunk

- Diagnostic for Tuberous sclerosis

37
Q

What are angiofibromas and what are they a/w?

A
  • Firm, smooth, red to pink papules consisting of hyperplastic blood vessels and collagen
  • Occur on nasolabial folds, cheeks, chin
  • Diagnostic for tuberous sclerosis (usually appear by 4-10 yo)
38
Q

What is often the first presenting sign of tuberous sclerosis?

A

Seizures (focal or generalized including infantile spasms)

39
Q

What are cortical tubers?

A
  • Potatolike nodules of glial proliferation occurring anywhere in cortex, ganglia, ventricle walls
  • Characteristic for tuberous sclerosis
40
Q

What are infants with a white forelock often later diagnosed with?

A

Tuberous sclerosis

41
Q

What is Sturge-Weber syndrome?

A

Disorder characterized by facial port-wine stains and leptomeningeal vascular angiomatosis

42
Q

What is a/w port-wine stains?

A

Sturge-Weber syndrome

-Usually involves V1 and V2 divisions of trigeminal nerve

43
Q

Size of port-wine stain?

A

Does NOT predict neuro sequelae

44
Q

Neuro complications of Sturge-Weber syndrome

A
  • Can begin as early as 5 mo with partial motor seizures

- Most appear later in childhood and are CONTRALATERAL to the nevus

45
Q

What do skull radiographs show in Sturge-Weber syndrome?

A

Classic tram-track calcification (curved double outlines of parieto-occipital cortex)

46
Q

Treatment of Sturge-Weber syndrome

A
  • V1 port wine stain leads to ophtho complications (refer)
  • Laser treatment to avoid soft tissue swelling and hypertrophy
  • Antiepileptics for seizures
  • Surgery for pts w/medically refractory epilepsy
47
Q

What is ataxia-telangiectasia?

A
  • Autosomal recessive disorder

- Progressive cerebellar ataxia, oculocutaneous telangiectasia, recurrent viral/bacterial infections

48
Q

Cutaneous manifestations of ataxia-telangiectasia

A
  • Telangiectasias first develop on bulbar conjunctiva and ears around 3-6 yo
  • Later on, they appear on flexor surface of arms, eyelids, malar area of face, upper chest
49
Q

Neuro manifestations of ataxia-telangiectasia

A
  • Cerebellar ataxia
  • Choreic and athetoid movements
  • Progressive nystagmus
  • Intelligence may be normal early on but progressively deteriorates
50
Q

What is Rendu-Osler-Weber syndrome?

A
  • Autosomal dominant d/o involving mucus membranes
  • Tendency for bleeding
  • 20% pts unaware of family history bc lesions may be minimal and may have no episodes of bleeding
51
Q

Clinical presentation of Rendu-Osler-Weber syndrome

A
  • Spontaneous, recurrent epistaxis (90%)
  • Skin telangiectases (75%)
  • Hepatic or pulm involvement (AVMs, 30%)
  • GI bleeding (15%)
  • CNS lesions (8-12%)
52
Q

Causes of limp in toddlers (1-3 yo)

A
  • Infectious/inflammatory
  • Trauma
  • Developmental dysplasia of the hips
  • Cerebral palsy and congenital hypotonia
  • Abuse
53
Q

Causes of limp in children 4-10 yo

A
  • High energy injuries (fx, dislocations, ligamentous)
  • Infections
  • Rheumatoid conditions
  • Neoplastic lesions
54
Q

Causes of limp in adolescents 11 or older

A
  • Slipped capital femoral
  • Arthritis
  • STIs
  • Trauma
55
Q

Sequences of birth defects

A
  • Malformation (intrinsic malformation exists in embryo)
  • Deformation (abnormal external mechanical or structural force)
  • Disruption (healthy embryo is subjected to tissue breakdown or injury)
56
Q

Describe vascular/avascular bone cysts

A
  • Benign osteoblastic tumor

- Osteoid rich origin (unmineralized, organic portion of bone matrix)

57
Q

Where do vascular/avascular bone cysts occur?

A

Cortex of long bone shafts (80-90% cases)

58
Q

Treatment of vascular/avascular bone cysts

A
  • NSAIDs

- Surgery (9-28% recurrence)

59
Q

What is a unicameral bone cyst?

A

Common, benign, fluid-filled lesion almost exclusively in children

60
Q

Presentation of unicameral bone cyst

A
  • Most present after sustaining a pathologic fracture

- UE (lower stress) vs LE (higher stress)

61
Q

Treatment of unicameral bone cyst

A
  • Asymp lesion w/satisfactory cortical thickness may require only observation
  • Cortical thinning may require surgery
  • Younger children are more amenable to cast immobilization
62
Q

Prevalence rates of JRA

A
  • Oligoarticular (30%)

- Polyarticular RF negative (20%)

63
Q

Prognosis of JRA

A
  • Improved over last 20 yrs d/t early use of intra-articular steroids, MTX, biologics
  • Polyarticular disease may have problems w/active disease throughout adulthood
64
Q

What is mucopolysaccharidosis?

A
  • Defective activity of lysosomal enzymes
  • Blocks breakdown of mucopolysaccharides
  • Leads to abnormal accumulations
65
Q

Clinical presentation of mucopolysaccharidosis

A
  • CNS disease
  • CV (angina, valve dysfunction, HTN, CHF)
  • Pulm (airway obstruction)
  • Optho (corneal clouding, glaucoma)
  • Hearing impairment
  • MSK (short, joint stiffness)

Special Pops - Peds (10 decks)

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