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Pediatrics > Falcon Review Pediatrics 4 > Flashcards

Falcon Review Pediatrics 4 Flashcards

1
Q

What is enuresis

A

The involuntary passage of urine in a child who should be toilet trained

Usually by five years of age

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2
Q

What are the causes of enuresis

A

Primary which is 90% of time: patient has never been dry

Secondary 10 %: previously continent child becomes acontinent usually associated with emotional difficulty

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3
Q

What is the treatment for enuresis

A

Limiting water and take at night
Buzzer
Imipramine
DDAVP

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4
Q

What should be considered for a febrile UTI child less than three

A

Pyelonephritis

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5
Q

What causes a UTI

A 
Usually they sending infection from:
Proteus
E. coli
Enterococcus
Klebsiella
Staph saprophyticus
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6
Q

What are the signs and symptoms of a UTI

A

Lower tract signs: dysuria, polyfrequency

Upper tract signs: fever, flank pain, chills

Nonspecific signs infants (fussiness, lethargic, vomiting)

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7
Q

What is the gold standard for diagnosing UTI

A

Urine culture

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8
Q

What will a urinalysis demonstrate for UTI

A

Greater than five white blood cells per high-powered field
Positive for nitrites
Leukocyte esterase

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9
Q

What imaging can be done for UTI

A

Consider renal ultrasound for first UTI

VCUG abnormal renal ultrasound or recurrent febrile UTI

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10
Q

What is a vesicoureteral reflux

A

abnormal backflow of urine from the bladder to the kidney cased by congenital
incompitence of the vesicoureteral junctions

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11
Q

What are the classifications of a vesicoureteral reflux

A

Grade I-ureter only
Grade II-without dilation of kidney
Grade III-mild to moderately dilated ureter
Grade IV-moderately dilated ureter pelvis and calyces
Grade V- this massive reflux

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12
Q

What is the diagnostic test of choice for vesicoureteral reflux

A

VCUG

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13
Q

What is the treatment for vesicoureteral reflux

A

Surgical repair for grade 4 or 5 reflux

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14
Q

What are the complications of this vesicoureteral reflux

A

Pyelonephritis
Real scarring
Reflux nephropathy
Hypertension

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15
Q

What is required to diagnose acute poststreptococcal glomerulonephritis

A

Evidence of an antecedent strep infection

Low C3 and low CH 50 returns to normal in about eight weeks (in MPGN and lupus nephritis (SLE), the C3 level remains low)

C4 typically normal

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16
Q

What is the Pathophysiology of acute poststreptococcal glomerulonephritis

A

Immune-complex depositional glomerular basement membrane

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17
Q

What is the treatment for acute streptococcal glomerulonephritis

A

Consider anabiotic’s of untreated step (does not modify renal disease)
Treat hypertension, support real failure

95% will have complete recovery

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18
Q

What is the most common cause of chronic hematuria worldwide

A

IgA nephropathy

Bergers nephropathy

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19
Q

What are the signs symptoms of IgA nephropathy

A

Acute onset gross hematuria following a respiratory illness

Persistent microscopic hematuria

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20
Q

What is the treatment for IgA nephropathy

A

Steroids

ACE inhibitor

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21
Q

Discuss hemolytic uremic syndrome

A

Exposure to E. coli 0157:H7 is produces a shiga-like toxin causes microangiopathic hemolytic anemia, acute renal failure and thrombocytopenia

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22
Q

What are the risk factors for E. coli 0157:H7

A

Undercooked meat
Inadequately wash fruits
Vegetables exposed to manure

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23
Q

What are the signs and symptoms of hemolytic uremic syndrome

A

Approximately one week after acute onset of abdominal pain, nausea vomiting and bloody diarrhea the patient will develop oliguria, pallor, weakness, lethargic, petechiae

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24
Q

What is diagnostic for hemolytic uremic syndrome

A

Anemia with hemolysis on smear (schistocytes)
Decreased platelets
Hematuria/protein urea, renal insufficiency (uremia)

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25
Q

What is nephrotic syndrome

A

Glomerular disorder characterized by proteinuria, hypoalbuminemia, edema and hyperlipidemia

90% are idiopathic, of those, 85% are minimal change

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26
Q

What are the signs and symptoms of nephrotic syndrome

A

PeriOrbital edema, abdominal pain and fatigue
Usually follows a viral upper respiratory infection
Hypertension is uncommon

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27
Q

What will be seen on electron microscopy for minimal change disease

A

Effacement of foot processes of renal epithelial cells

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28
Q

What are the signs and symptoms of Alport syndrome

A

Asymptomatic hematuria
Sensorineural hearing loss
Eye abnormalities

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29
Q

What will a renal biopsy demonstrate for patient with Alport syndrome

A

Glomerulosclerosis
Thickening basement membrane
Foam cells

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30
Q

What is the pathophysiology of Alport syndrome

A

Is the most common hereditary nephritis; X-linked

It’s a disorder of type IV collagen affecting basement membranes of kidney, eye and Ear

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31
Q

What is the most common cause of hydronephrosis in childhood

A

Uteropelvic junction obstruction

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32
Q

What are the causes of a uteropelvic junction obstruction

A

Intrinsic: ureteral hypoplasia, kinked ureter

Extrinsic causes: external compression by renal vessels

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33
Q

What is the most common cause of abdominal mass neonates

A

Hydronephrosis

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34
Q

How is a uteropelvic junction obstruction diagnosed

A

Intravenous pyelography, ultrasound

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35
Q

What is the treatment for utero pelvic Junction instruction

A

Surgery

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36
Q

What are the signs and symptoms of posterior urethral valve

A

Weak or dribbling urine streams
UTI
Leaflets in the prosthetic urethra causing partial bladder outlet obstruction only found in males

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37
Q

What is the treatment for posterior urethral valves

A

Transurethral ablation

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38
Q

What is hypospadias

A

Most common congenital anomaly of the penis in which to urethral meatus is malposition along the ventral surface of the penis

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39
Q

What is contraindicated with hypospadias

A

Circumcision.

The foreskin will be needed for surgical repair

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40
Q

What is cryptorchidism

A

Undescended testes that cannot be manipulated into the scrotum, retractable testes retracted back into the scrotum.

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41
Q

What arrests factors for cryptorchidism

A

Prematurity

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42
Q

What is the treatment for cryptorchidism

A

Surgical repair if testes have not descended by age 1

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43
Q

Or complications are associated with cryptorchidism

A

Torsion

Testicular cancer

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44
Q

What is a testicular torsion

A

Twisting of the sporadic cord with Strelach of the blood supply to the effect testicle; surgical emergency

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45
Q

What are the signs and symptoms of a testicular torsion

A

Acute onset of unilateral scrotal pain, nausea, vomiting, swollen exquisitely tender testes, scrotal edema and absence of cremasteric reflex

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46
Q

What is the hydrocele

A

Fluid filled sac of the scrotal cavity (remnant of tunica vaginalis).
Diagnosed by transillumination
Usually self resolving

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47
Q

What is a varicocele

A

Dialated testicular vein and enlarge pampiniform plexus results of absenting venous valve; presents in adolescents
“bag of words” on physical exam while standing and disappears in the supine position

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48
Q

What is achondroplasia

A

autosomal dominant condition (mutation in F GFR 3) resulting in disorder growth

signs and symptoms: short stature, large head, prominent for head, short limbs, lumbar lordosis, normal intelligence

prognosis: normal lifespan

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49
Q

What is osteogenesis imperfecta

A

Abnormal synthesis of type I collagen; most often autosomal dominant

signs and symptoms: brittle bones and blue sclera

multiple fractures

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50
Q

What is developmental dysplasia of the hip

A

Congenital hip dislocation that usually presents in the newborn. That may be detected as late as three years of age

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51
Q

Palace developmental dysplasia of the diagnosed

A

Barlow or Ortolani signs
ultrasounds (newborns)
“frog-leg” lateral x-ray (older infants/children)

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52
Q

What is Legg-Calve-Perthes

A

idiopathic avascular necrosis of the femoral head

20% of the cases arebilateral

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53
Q

What are the risk factors for Legg-Calve-Perthes

A

Ages 4 to 12 years

males 5 to 1

54
Q

What are the signs and symptoms of Legg-Calve-Perthes

A

Limping
initially painless but may become painful; worsened by activity and relieved by rest
as with all hip problems-referred knee pain

55
Q

What are the steps to diagnose Legg-Calve-Perthes

A

Plain radiograph reveals wide articular space, necrosis, and eventually a flat femoral head

56
Q

What is a slipped capital femoral epiphysis

A

SCFE

Displacement of the femoral head from the epiphysis

57
Q

what are the risk factors for a slipped capital femoral epiphysis

A

Obese adolescents

58
Q

what are the signs and symptoms of the slipped capital femoral epiphysis

A

Growing pain or knee pain, often after activity

limited internal rotation/abduction of the hip

59
Q

What are the steps to diagnose a slipped capital femoral epiphysis

A

Plain radiography reveals medial displacement of the epiphysis, bare upper femoral neck, wide growth plate

60
Q

What is the treatment for a slipped capital femoral epiphysis

A

Surgery: pending, external fixation, casting

61
Q

One of the types of Salter-Harris fractures

A

Type I: fracture through growth plate
type II: fracture through growth plate and metaphysics
type III: fracture through growth plate and epiphysis
type IV: fracture through both the metaphysis and epiphysis
type V: crushed growth plate

62
Q

What a scoliosis

A

Abnormal curvature of the spine caused by misalignment in the frontal plane

63
Q

What are the causes of scoliosis

A

Idiopathic
congenital: vertebralanomalies
neuromuscular

64
Q

What are the steps to diagnose scoliosis

A

Adams tests: forward bending with rib bump

x-ray

65
Q

What is the treatment for scoliosis

A

Mel curves needed therapy
bracing recommended to slow down progression
surgery required for severe greater than 45°; fusion, fixations rods

66
Q

What is talipes equinovarus

A

Clubfoot

causes:
sporadic and/or idiopathic
teratogenic
Oligohydramnios

signs and symptoms:
calcaneus and talus in plantar flexion (adduction); inability to bring foot to plantigrade position-tight Achilles
-forefoot and midfoot in adduction

67
Q

What is the treatment for talipes equinovarus

A

Stretching/manipulation initially with serial casting

surgery possible unfavorable response and for severe cases

68
Q

What is metatarsus adductus

A

Most common foot deformity in infants 2/1000

thought to be due to in utero positioning

Forefoot is adducted but hind foot is normal
“flexible”: forefoot can be brought to the neutral position

69
Q

What is the treatment for metatarsus adductus

A

Observation, passive range of motion for most flexible feet-90% result by age 4

casting/surgery for treatment failures and/or non flexible feet

most common cause of in-toeing less than 18 months

70
Q

What is a tibial torsion

A

Normal development: lateral rotation of tibia from 5° at birth to 15° of maturity so medial torsion improves with time

most common cause of in-toeing in children 18 months to three years

usually secondary to in utero positioning

almost always self resolving

71
Q

What is a femoral anteversion

A

Normal development: femoral anteversion of 40° in newborn, decreased to 10 to 15° by adolescence

most common cause of in-toeing in children older than three years, usually presents age 4 to 6

prefer the”W” position and cannot sit cross-legged

72
Q

What is a popliteal cyst

A

Baker’s cyst

arises from capsule or tendon sheath, sometimes as the result of an injury. Common in children between 4 and 7 years

signs and symptoms:
-painless, non-pulsatile swelling on posterior knee; more prominent with the extension

usually resolve spontaneously

73
Q

What is Osgood Schlatter disease

A

Traction apophysitis of the tibial tubercle caused by overuse

signs and symptoms:

  • localized tenderness/swelling of tubercle
  • pain worsened with activity; relieved by rest
  • seen during periods of rapid linear growth
74
Q

What is the treatment for Osgood Schlatter disease

A

NSAIDs and rest

usually self resolves over 12 to 24 months

75
Q

What is nursemaid’s elbow

A

Radial head subluxation

sudden traction of the arm of a child less than 4 years

signs and symptoms:
-sudden pain in refusal to use arm; arm held partially flexed elbow and pronated

76
Q

What is the treatment for nursemaid’s elbow

A

Reduction by gentle supination of hand in flexion at elbow with pressure over the radial head; click may be heard

77
Q

What are the types of juvenile rheumatoid arthritis

A

Pauciarticular
polyarthritis
systemic

78
Q

What are the general signs and symptoms of juvenile rheumatoid arthritis

A

Morning stiffness
joint pain
swelling
low-grade fever

79
Q

What are the features of pauciarticular JRA

A

55%

  • four or fewer joints involved
  • typically larger joints often asymmetric
  • may be ANA positive
  • maybe HLA B27 positive
    – majority or seronegative
    – increase risk of iritis
80
Q

what are the features of polyarticular JRA

A

35%

– five or more joints involved
– typically small joints, especially hands
– maybe RF positive
– maybe ANA positive

worse prognosis associated with older children

81
Q

What are the features of systemic JRA

A

10% (stills disease)

– initial extra articulate manifestations such as fever, rash, plueritis, pericarditis

82
Q

What arethe steps to diagnose JRA

A

– Elevated ESR, CRP, WBC, PLT
– x-ray: soft tissue swelling early, bone changes later
– ANA and haplotyping as indicated by clinical picture

83
Q

What is the treatment for JRA

A

NSAIDs are first-line treatment
methotrexate
antimalarials
PT, ophthalmology follow-up – iritis

84
Q

What is Systemic Lupus Erythematosus

A

Autoimmune multisystem disease

primarily affecting females greater than 8 years of age

85
Q

What is the criteria to diagnose Systemic Lupus Erythematous

A 
Minimum of 4:
– malar rash
– serositis
– arthritis
– neurologic
– anti-nuclear antibody
– Renal
– discoid rash
–  oral ulcer
– photosensitivity
– hematologic
– immunologic
86
Q

What are the steps to diagnose SLE

A

ANA best screening test
double-stranded DNA antibodies
decreased C3/C4/C 50
anti-Smith antibodies

87
Q

What is the treatment for SLE

A

NSAIDs, steroids, cyclophosphamide

consider anticoagulants

88
Q

What are the complications of SLE

A

Nephritis
CNS complications
infection

89
Q

What is neonatal lupus

A

Newborns of mothers with Lupus
transfers of a IgG autoantibodies

signs and symptoms:
– congenital heart block (highly associated with anti-Ro positivity)
– other transient manifestations such as rash

90
Q

What is dermatomyositis

A

Inflammatory disease involving small vessels of skin, striated muscle, and occasionally the G.I. tract
usually presents around six years of age

typically will present as a girl having difficulty brushing her hair

91
Q

What are the signs and symptoms of dermatomyositis

A

Malaise, fatigue, weight loss, intermittent fever
progressive muscle weakness of pelvic and shoulder girdle muscle groups
Violaceuos dermatitis of the eyelids, hands, elbows, knees and ankles

– elevation of serum creatinine kinase
– Groyton papules
– 10% will progress to wheel chair dependence

92
Q

What is Kawasaki disease

A

Mucocutaneous lymph node syndrome

– most common cause of court heart disease in children

93
Q

What arethe signs and symptoms of Kawasaki disease

A

Fever lasting greater than 5 days and 4 of the 5 of the following:

  1. Conjunctivitis, limbic sparing
  2. Oral mucosal changes, strawberry tongue, cracked lips
  3. Rash, often perineal
  4. Extremity changes (erythema palms and soles, swelling of hands and feet)
  5. Cervical lymphadenopathy greater than 1.5 cm usually unilateral
94
Q

What are the complications associated with Kawasaki disease

A

Coronary artery aneurysms and 25% of untreated individuals

95
Q

What is the treatment for Kawasaki disease

A

IVIG and high-dose aspirin initially decreases incidence of late onset aneurysms

low-dose aspirin for 6 to 8 weeks until inflammatory markers normalize and eight-week echo shows no aneurysms

96
Q

What is Henloch Schonlein Purpura

A

IgA mediated vasculitis of small vessel; often follows viral URI

signs and symptoms:
colicky abdominal pain, palpable purpuric rash with normal platelets on buttocks, renal manifestations, edema, arthritis (classically knee)

– increased risk for developing intussusception

97
Q

What is the treatment Henloch Schonlein Purpura

A

Supportive
not indicated to Arthritis and other criteria present
consider corticosteroids for severe abdominal pain

98
Q

What is precocious puberty

A

Secondary sex characteristics present in female before age 8 or males before age 9, especially pubarche with virilization

99
Q

What are the causes of precocious puberty

A

Central (GnRH dependent)
– CNS lesions and idiopathic
– CNS lesions are more common in boys

peripheral (pseudo-precocious puberty: GnRH independent)
– exogenous sex hormones, CAH, adrenal tumors

100
Q

How are sex hormones stimulated

A

GnRH acting in pulsatile fashion stimulates LH/FSH

LH stimulates Leydig cells and granulosa cells

101
Q

What are the steps to diagnose precocious puberty

A
  1. Bone age
  2. LH – delineates Central from noncentral
  3. Hormone levels: testosterone, estrogen, DHEA S, 17 – 0H progesterone
  4. CNS imaging if young child or male
102
Q

What is premature thelarche

A

Isolated breast development

103
Q

what is premature adrenarche

A

Appearance of sexual hair

steps to diagnose:
– adrenal androgen’s are often slightly elevated for chronological age
– bone age is slightly advanced
– usually idiopathic and benign

104
Q

What is the treatment for central precocious puberty

A

Injections of long-acting GnRH-leuprolide-(interrupts pulsatile stimulation)

105
Q

What is the reason to treat for central precocious puberty

A
  1. Social

2. Early puberty equals premature closure of growth plate

106
Q

What definesshort stature

A

Height below the 3rd percentile

107
Q

How short stature diagnosed

A

Growth curve
family history and Hts.
wrist film for bone age

108
Q

What are the causes of diabetes mellitus type I

A

Deficiency of insulin
autoimmune
possible viral trigger

109
Q

What are the steps to diagnose diabetes mellitus

A

Random glucose > 200
fasting glucose > 126
two hour glucose tolerance test >200

110
Q

What arethe complications associated with diabetes mellitus

A

Retinopathy
nephropathy
neuropathy

111
Q

What is diabetes insipidus

A

Loss of ADH secretion and inability to concentrate the urine
– maybe central or nephrogenic

Central: lack of ADH secretion
nephrogenic: kidneys do not respond ADH

112
Q

What are the signs and symptoms of diabetes insipidus

A

Polyuria
polydipsia
dehydration with dilute urine

113
Q

What is the most common cause of congenital hypothyroidism

A

Idiopathic thyroid dysgeneisis

114
Q

What are the signs and symptoms of congenital hypothyroidism

A 
Jaundice
poor feeding
large tongue
constipation
umbilical hernia
wide fontanelle
hypotonia
developmental delay
115
Q

What are the signs and symptoms of acquired hypothyroidism

A 
Growth deceleration
constipation
cold intolerance
decreased energy
goiter
116
Q

What is the most common cause of hyperthyroidism

A

Graves’ disease (toxic quarter associated with HLA-B8, HLA-DR 3)

117
Q

What causes neonatal hyperthyroidism ininfants

A

Infants born to mothers with Graves’ disease. Maternal antibody’s my cross placenta and induce hyperthyroidism

118
Q

What are the signs and symptoms of hyperthyroidism

A 
Hyperactivity
increased appetite
emotional disturbance
exophthalmos
sweating
tachycardia
palpitations
119
Q

What is the treatment for hyperthyroidism

A

propylthiouracil, methimazole
propanolol for symptoms
surgery or radio ablation

120
Q

What is congenital adrenal hyperplasia (CAH)

A

Disorder of steroid biosynthesis resulting in cortisol deficiency in androgen overproduction

21-hydroxylase deficiency is the most common cause
– salt was: hyponatremia, hypokalemia, hyperkalemia, elevated renin, decreased aldosterone

121
Q

Is 11 B hydroxylase deficiency associated with salt wasting

A

No, they are not so losing

122
Q

How is congenital adrenal hyperplasia diagnosed

A

ACTH challenge test for diagnosis
check levels of steroids for the precursors (17-OH progesterone levels)
in 21-OH deficiency: decreased cortisol and aldosterone, increased ACTH in 17 OH progesterone levels

123
Q

What is the treatment for congenital adrenal hyperplasia

A 
Glucocorticoids (increased doses during stress)
mineralocorticoid's
sodium replacement (salt losers)
124
Q

What is Cushing’s syndrome

A

High cortisol level
– exogenous corticosteroids
– endogenous overproduction (pituitary adenoma, bilateral adrenal hyperplasia, adrenal tumor)

signs and symptoms:
– Moon feces
– truncal obesity
– abdominal striae
– Buffalo hump
– hypertension
– muscle weakness
125
Q

How is Cushing’s syndrome diagnosed

A

Elevated serum cortisol level and increased 24-hour urine free course all tests

if cortisol elevated, dexamethasone suppression test

look for pituitary adenoma, adrenal tumor

126
Q

What is Addisondisease

A

Adrenal insufficiency resulting in low production of cortisol, two types:

  1. Primary adrenal insufficiency
  2. Secondary adrenal insufficiency
127
Q

What are the causes of primary adrenal insufficiency Addison’s disease

A

Autoimmune
congenital
ACTH unresponsiveness
infarct hemorrhage

associated with adrenoleukodystrophy

128
Q

What are the causes of secondary adrenal insufficiency Addison’s disease

A

ACTH deficiency

129
Q

What arethe signs and symptoms of Addison’s disease

A 
Weakness
vomiting
weight loss
salt craving
increased pigmentation (increased ACTH)
130
Q

What will the labs demonstrate for Addison’s disease

A

Hyponatremia
hyperkalemia
low serum cortisol level unresponsive to injection of ACTH

131
Q

What is the treatment of Addison’s disease

A

Maintenance oral glucocorticoids and mineralocorticoid’s

Adrenal crisis-life-threatening
– D5 normal saline and stress dose steroids

Pediatrics (8 decks)

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