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Peds > BRS Ch. 11-15 > Flashcards

BRS Ch. 11-15 Flashcards

1
Q

How would a dehydrated child be rehydrated parenterally?

A

Two phases

  1. ) Emergency: restore volume to ensure perfusion. 20mL/kg of normal saline or Ringer’s
  2. ) Repletion: more gradual correction of water/electrolyte deficits (very slowly for hypernatremic state)
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2
Q

When evaluating a urine sample for hematuria, what can give a false-negative result?

A

Ascorbic acid (Vitamin C)

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3
Q

RBCs in the urine can be significant for many disorders. Wha does their shape tell you?

A

RBC casts = glomerulonephritis
Dysmorphic RBCs = glomerular process
Normal RBs = lower urinary tract

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4
Q

How many days after a GABHS infection will kidney symptoms occur?

A

In post-streptococcal glomerulonephritis, look for hematuria, proteinuria, and hypertension due to fluid overload within 8-10 days.
Dx: ASO titer, anti-DNAse B (ADB) titer

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5
Q

IgA nephropathy will classically present with gross hematuria after what pulmonary disease?

A

Respiratory infections

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6
Q

What IgA mediated vasculitis will present with palpable purpura on the buttocks and thighs?

A

HSP nephritis. Also look for ab pain, joint pain/swelling, hematuria

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7
Q

How will most children suffering from one of the three categories of nephrotic syndrome usually present?

A

Edema folowing an URI, and then heavy proteinuria. Note these patients are predisposed to thrombosis secondary to hypercoagulability (arises due to hypoproteinemia).

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8
Q

HUS is acute renal failure in the presence of microangiopathic hemolytic anemia and thrombocytopenia. What are the two subtypes of HUS?

A

Stx HUS: shiga-toxin (from GI infection from beef/milk) leads to endothelial injury and plt thrombi formation
Atypical: caused by drugs/genetics, same as above but w/o diarrhea

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9
Q

Patients with Alport’s syndrome have symptoms in which three systems of the body?

A

Renal (HTN/hematuria)
Hearing loss
Ocular abnormalities

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10
Q

What is the difference between ARPKD and ADPKD?

A

Autosomal recessive leads to childhood presentation with hx of oligohydramnios
Autosomal dominant presents in adults

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11
Q

How can the size of blood pressure cuff affect measured levels?

A

A cuff too small will give elevated BPs, whereas a cuff too big will give lower BPs

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12
Q

What BP measurements will a physician find in a patient with coarctation of the aorta?

A

Elevated in the R arm, lower BP in both legs

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13
Q

What are the fatal sequelae of congenital urologic structural abnormalities?

A

Congenital obstruction –> renal dysplasia –> oligohydramnios –> pulmonary hypoplasia

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14
Q

What is the most common abdominal mass found in newborns?

A

Multicystic dysplastic kidney secondary to urinary tract atresia

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15
Q

What is the most common etiology of vesicoureteral reflux in infants?

A

A short submucosal tunnel in the which the ureter inserts through the bladder wall.
VUR usually resolves on its own.
High comorbidity with UTIs, can eventually lead to reflux nephropathy

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16
Q

Furosemide can predispose newborns to what type of urolithiasis?

A

Furosemide leads to hypercalciuria.
Enteric malabsorption –> hyperoxaluria
Leukemia/lymphoma therapy –> hyperuricosuria
All children with urolithiasis should be evaluated for a metabolic disorder

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17
Q

How are UTIs diagnosed in children?

A

Culture. For newborns and infants, suprapubic aspiration is required. Children who can void on command can pee in a cup.
Treat UTI with bactrim or cephalexin while culture is running.

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18
Q

What is the difference between hypotonia and weakness?

A

Hypotonia is decreased resistance during passive stretching of muscles.
Weakness is decreased force generated during active contraction.

19
Q

How does the differential change between central and peripheral hypotonia?

A

Central: acquired (electrolytes, hypoxia, infection, trauma), congenital
Peripheral: spinal cord, peripheral nerve, NM junction, muscle dystrophy/myopathy

20
Q

What are recommended diagnostics with central and peripheral hypotonia?

A

Central: head CT, serum electrolytes, chromosome studies
Peripheral: serum creatinine kinase, DNA tests, EMG, muscle biopsy

21
Q

What are three peripheral hypotonic disorders?

A

Spinal muscular atrophy (SMA): anterior horn cell degeneration, mutation in SMN1 gene on Ch5, look for bell-shaped chest, frog-leg posture
Infantile botulism: no presynaptic release of Ach, constipation –> neuro sx –> descending paralysis
Comgenital muscular dystrophy: inability to relax contracted muscles. Trinucleotide repeat disorder. AD = mother will show hypotonia

22
Q

What are the three classes of spina bifida?

A

Myelomeningocele: herniation of the cord and the meninges, lots of neuro problems, fluctuant mass on spine
Meningocele: herniation of the meninges only
Occulta: no herniation of tissue at all
(often caused by maternal ingestion of FOLIC ACID)

23
Q

What should be assessed on the HEENT exam of a comatose patient?

A

Scalp injuries
Breath odors
Nuchal rigidity
CSF/blood draining

24
Q

What is the difference between decorticate and decerebrate posturing?

A 
Decerebrate = subcortical injury, arm/leg extension
Decorticate = bilateral cortical injury, arm/leg flexion
25
Q

How is status epilepticus defined and treated?

A

A seizure that lasts more than 30 minutes.

Tx: IV anticonvulsants (benzos, phenobarbital, phenytoin)

26
Q

What are different categories of seizures?

A

Febrile vs. afebrile
Partial (one hemisphere) vs. generalized (two hemispheres)
Simple vs. complex (loss of consciouness)

27
Q

How are febrile seizures identified and treated?

A

Dx: hx, normal neuro exam, exclusion of CNS infection
Tx: if frequent/recurrent, treat prophylactically with valproic acid or phenobarbital

28
Q

What are three common epileptic syndromes?

A

Infantile spasms: caused by tuberous sclerosis, brief myoclonic, hypsarrhythmia pattern on EEG
Absence epilepsy of childhood: AD, short, frequent absence seizures, 3-Hz spike and wave discharge on EEG
Benign rolandic epilepsy: nocturnal partial seizures w/ oral/buccal sx, spike and sharp wave disturbance

29
Q

What clinical information should be analyzed while evaluating childhood headaches?

A
  1. ) Pain quality: migraine = throbbing, tension = aching
  2. ) Site/radiation: migraine = unilateral, periorbital –> forehead/occiput, tension = generalized/temporal
  3. ) Onset: tension: end of the day, increased ICP = morning
  4. ) Duration: shorter = less serious
30
Q

What is the most common cause of headaches in children?

A

Migraines. Autosomal dominant. Increased 5-HT, sub. P –> changes in cerebral blood flow.
Tx: sumatriptan (5-HT agonist), propranolol

31
Q

What is the most common cause of ataxia in children?

A

Acute cerebellar ataxia. 2-3 weeks after viral infection. Truncal ataxia, slurred speech and nystagmus.

32
Q

What infectious agent usually causes Guillain-Barre syndrome?

A

Campylobacter. Causes demyelination due to cell-mediated immune response, look for ascending paralysis, areflexia and normal sensation.

33
Q

What is Sydenham chorea?

A

An autoimmune disorder associated with rheumatic fever that leads to restless proximal limb movement. Caused by GABHS Ab cross-reactivity that attacks the basal ganglia. Occurs 2-7 mos after infection.
Terms: chameleon hand, choreic hand, milkmaid’s grip

34
Q

What might you consider on the differential for tics?

A

Tourette’s, Wilson’s, Sydenham, PANDAS, partial seizures
Also consider simple habits, which are situation-dependent and under voluntary control
Tx: Pimozide, clonidine

35
Q

Why cause a dystrophin gene mutation lead to degeneration of muscle fibers?

A

Weakness and rupture of the muscle cell plasma membrane. Replacement of muscle with fibroblasts/lipid deposits.
DMD = early onset, BMD = late onset
Look for enlarged calf muscles in a young boy with muscle weakness

36
Q

To what membrane protein are antibodies directed in myasthenia gravis?

A

The AchR at NM junctions. Common in girls. Ptosis/diplopia –> increasing weakness.
Dx: Tensilon test (IV injection of edrophonium chloride, an Achase inhibitor)
Tx: Cholinesterase inhibitors

37
Q

How does IDA (a microcytic, hypochromic anema) arise in children?

A

Nutritional deficiency (9-24 mos or adolescent girls)
Occult blood loss (polyps, Meckel’s diverticulum, IBD, PUD, etc.)
Look for low serum ferritin, increased transferrin and decreased transferrin saturation

38
Q

How are the thalessemias (microcytic, hypochromic anemia) categorized?

A

alpha: defective alpha-chain synthesis. Minor –> Hbg H disease –> fetal hydrops
beta: defective beta-chain synthesis. Homozygous deletion = major (HSM, bone marrow hyperplasia, thalassemia facies, hemochromatosis). Hetero deletion = minor (sx similar to IDA)

39
Q

What are four signs of ataxia telengiectasia?

A

Combined immunodeficiency
Cerebellar ataxia
Oculocutaneous telengiectasias
Predisposition to malignancy

40
Q

What is the mnemonic for DiGeorge syndrome?

A

CATCH-22: cardiac defects, abnormal facies, thymic hypoplasia, cleft palate, hypocalcemia due to Ch.22q11 deletion

41
Q

What syndrome is a X-linked disorder characterized by 1.) combined immunodeficiency 2.) eczema and 3.) congenital thrombocytopenia?

A

Wiskott-Aldrich syndrome. Tx: HLA-matched BMT

Also, look for decreased IgM, thrombocytopenia, defective Ab response

42
Q

A mutation in the BTK gene on the X chromosome will lead to what syndrome?

A

X-linked agammaglobulinemia. All isotype-deficient, B cells absent BUT T cells wholly unaffected.

43
Q

How are the CGD disorders characterized?

A

Defective neutrophil oxidative metabolism (NADPH oxidase).

44
Q

What happens in deficiency of various stages of the complement system?

A
  • early: autoimmune like SLE
  • late: increased meningococcal and gonococcal
  • C1 esterase: hereditary angioedema

Peds (6 decks)

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