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Step 2 Pediatrics > URx 4 > Flashcards

URx 4 Flashcards

1
Q

High fever and sore throat in the absence of respiratory symptoms should raise suspicion for _____.

A

Group A streptococcal (GAS) infection

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2
Q

A _____ score of 2 or higher should prompt a pharyngeal swab for rapid antigen testing or bacterial culture in suspected cases of Group A streptococcal (GAS) sore throat.

A

Centor Score:
assigns 1 point for each of the following s/s:
-fever,
-absence of cough,
-presence of tonsillar exudates,
-swollen, tender anterior cervical nodes, and
-Age 3-14 years (1 point); 15-44 years (0 points); ≥45 years (-1 point).

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3
Q

Initiation of treatment for group A streptococcal pharyngitis is indicated in patients with a Centor score of ____ while awaiting culture results if rapid testing is not available.

A

Centor score of 3 or higher

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4
Q

A Centor score of ____ indicates that viral pharyngitis is more likely the cause of sore throat in a patient.

A

viral

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5
Q

_____ is used to establish the diagnosis in a suspected case of Meckel diverticulum.

A

Technetium 99m scan aka “Meckel scan” (identifies gastric mucosa in the small bowel).

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6
Q

In suspected case of meningitis, _____ before lumbar puncture (diagnostic) must be done to exclude a _____ and _____.

A

to exclude a
-mass lesion or
-increased intracranial pressure esp. if a patient has one or more of the following risk factors:
-Immuno-compromised state c/by HIV or medications.
-h/o of CNS disease such as stroke, masses.
-New onset seizure
-Papilledema
-Altered level of consciousness
-Focal neurologic deficit

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7
Q

A skeletal survey is mandatory for all patients younger than ____ age in whom physical abuse is suspected.

A

younger than 20 months

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8
Q

The differential diagnosis for conjugated hyperbilirubinemia in a newborn includes ____ conditions.

A

-obstructive abnormalities: biliary atresia or choledochal cysts,
-neonatal or infectious hepatitis,
-metabolic enzyme defects, and
-α1-antitrypsin deficiency.

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9
Q

What is the next step in the diagnostic evaluation of a neonate with conjugated hyperbilirubinemia, and whose ultrasound is suggestive of biliary atresia?

A

liver biopsy followed by an intra-operative cholangiogram (gold standard).

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10
Q

Varicella zoster viral (VZV) infection aka ______, is usually more severe in patients of ____ age group, with potential for _______ complications.

A

aka chicken pox;

more severe in patients aged 13 years or older;

potential complications include pneumonia, meningo-encephalitis, and hepatitis.

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11
Q

Treatment with Acyclovir within 24-72 hours of rash onset is specifically indicated for _____ patients with chicken pox.

A

-patients > 13 years of age,
-children > 12 months with complicating conditions, and
-any patients with severe/disseminated infection.

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12
Q

In addition to giving PGE1 to keep the ductus arteriosus open in neonates with moderate-severe CoA may also be administered other supportive treatments (in addition to PGE1 to keep the ductus open) such as _____ and _____to improve cardiac contractility and accompanying heart failure.

A

IV inotropes (e.g. milrinone or dopamine)

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13
Q

______ is a validated screening tool used to screen for the risk of undiagnosed mental health conditions in children as young as 4 years old.

A

The Pediatric Symptom Checklist (PSC)-17 (https://depts.washington.edu/dbpeds/Screening%20Tools/PSC-17.pdf)

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14
Q

______ aka allergic acute interstitial nephritis, is the most common cause of acute interstitial nephritis (AIN) in developed countries, accounting for an estimated ____ % of cases.

A

Drug-induced acute interstitial nephritis (DI-AIN) aka allergic acute interstitial nephritis;

accounting for an estimated 70-75% of cases.

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15
Q

_____ drugs are the most common cause of drug-induced acute interstitial nephritis (DI-AIN), accounting for approx. ____ % cases followed closely by ___ drugs.

A

NSAIDs ~ 44% of cases;

Antibiotics ~ for 33% of cases.

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16
Q

Glomerulonephritis (GN) especially PSGN could be differentiated from acute interstitial nephritis (AIN) based on _____ clinical and lab criteria.

A

Unlike AIN
GN/PSGN: nephritic urine (hematuria, proteinuria, and RBC casts); No Rash.

versus

AIN: fever, rash, s/s of AKI, HTN
HALLMARK: Eosinophilia with AKI (elevated creatinine) with WBCs & WBC casts, proteins in urine following h/o antibiotic consumption.

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17
Q

AIN is defined as ____.

A

an increase of 0.5 mg/dL or 50% in sr. creatinine over a 24 to 72-hour period, starting 24 - 48 hours after exposure to a potential triggering medication.

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18
Q

The clinical triad of ___, ___, and ____ along with elevated creatinine, proteinuria, and WBC/WBC casts in urine is the classic characteristic clinical presentation in patients with AIN.

A

fever, rash, and eosinophilia (+/-eosinophiluria)
+
elevated creatinine, proteinuria, and WBC/WBC casts.

NOTE: The classic triad of fever, rash, and eosinophilia/eosinophiluria is not seen in all patients of AIN.

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19
Q

The classic clinical triad of fever, rash, and eosinophilia along with elevated creatinine, proteinuria, and WBC/WBC casts in urine in AIN is most commonly seen in patients with ____ drug exposure, and least common with ___ use.

A

most common with Beta-lactam antibiotics esp. methicillin use;

least common with the use of NSAIDs (which are the most common cause of AIN).

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20
Q

Other than NSAIDs and Beta-lactam antibiotics, what drugs including antibiotics can cause AIN?

A

Other antibiotics include
-rifampin
-sulfonamides
-ciprofloxacin

-Other drugs:
Sulfa drugs (loop diuretics)
-PPIs
-Immune checkpoint inhibitors (monoclonal antibodies).
-tyrosine kinase inhibitors,
-antiepileptics (phenytoin),
-antivirals, and
-histamine-2 antagonists.

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21
Q

The underlying pathophysiology of DI-AIN is thought to be a _____.

A

Type IV idiosyncratic T-cell–mediated delayed hypersensitivity reaction.

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22
Q

In patients with AIN, if the withdrawal of the offending drug does not result in improvement in renal function after 5 to 7 days, _____ treatment may be started.

A

corticosteroids;

Note: Short-term dialysis is often needed in ~ 30 -69 % of patients with DI-AIN, regardless of initial treatment.

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23
Q

___ medications are most commonly implicated in the development of drug-induced lupus.

A

-Hydralazine,
-Procainamide, and
-Isoniazid.

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24
Q

_____ aka _____ manifests with weight loss, hypoglycemia, hypotension, hyponatremia, hyperkalemia, skin hyperpigmentation, and sexual immaturity in adolescents d/t reduction in the adrenal cortical hormones.

A

Primary adrenal insufficiency aka Addison disease;

cortisol deficiency -> weight loss, hypoglycemia, hypotension, orthostasis, hyperpigmentation (d/t high ACTH/MSH levels as secondary response in PAI).

Aldosterone (Mineralocorticoid) deficiency -> hypotension, orthostasis, hypoNa+, hyperK+.

Androgen deficiency -> sexual immaturity (e.g. scant pubic and axillary hair), loss of libido.

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25
Q

The only glucocorticoid with sufficient mineralocorticoid activity so that it can be used as a monotherapy in the treatment of Addison disease is ______.

A

hydrocortisone.

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26
Q

Addison disease versus SIADH?

A

Addison Disease:
-hyponatremic hyperkalemic hypovolemia (kidneys unable to reabsorb Na+ & H2O d/t ↓↓↓ aldosterone).
-metabolic acidosis
-hypoglycemia (d/t ↓↓↓ cortisol).

SIADH:
-Euvolemic hyponatremia d/t excessive H2O retention by the renal collecting tubules (no loss of volume, BP is normal).
-Normal sr. K+ levels.

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27
Q
A
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28
Q

Steroids such as dexamethasone and prednisolone that lack mineralocorticoid properties can be used in combination ____ with sufficient mineralocorticoid activity in the treatment of patients with PAI.

A

fludrocortisone, as it can provide sufficient mineralocorticoid coverage that dexamethasone and prednisolone lack.

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29
Q

Non-GI symptoms in patients with celiac sprue (aka celiac disease or gluten-sensitive enteropathy) include _____s/s.

A

-arthritis or arthralgia,
-anemia, and
-skin rashes.

Major suggestive GI s/s include:
-poor weight gain and/or weight loss in the setting of persistent diarrhea, abdominal discomfort, pain, distension or bloating, constipation, and vomiting.

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30
Q

Management of celiac sprue entails ____ strategies.

A

-gluten-free diet
-correcting micronutrient deficiencies esp. folic acid, vitamins B6, B12, and D; zinc; iron; and copper.

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31
Q

In infants younger than age 6 months, _____ is the diagnostic tool to confirm Developmental Dysplasia of the Hip (DDH).

A

USG of the hip;
X-ray hip is not a test of choice as the femoral head and acetabulum are primarily cartilaginous at this age.

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32
Q

Screening tests for developmental dysplasia of the hip (DDH) include _____ and _____.

A

Ortolani maneuver and Barlow maneuver.
Refer to the link below for details
https://med.stanford.edu/newborns/clinical-rotations/residents/residents-newborn-exam/barlow-and-ortalani-manuevers.html

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33
Q

Developmental dysplasia of the hip (DDH) was previously known as ____.

A

congenital dislocation of the hip

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34
Q

Asymmetry in the hip position and the number of gluteal skin folds may suggest developmental _____.

A

Developmental dysplasia of the hip (DDH);

NOTE: asymmetry is also a normal finding in up to 27% of infants without DDH.

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35
Q

_____ sign compares the knee height while the hips and knees are flexed and the feet set flat on the table.

A

Galeazzi sign

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36
Q

In patients aged 1 to 6 months, ____ is the management for developmental dysplasia of the hip (DDH).

A

Abduction devices for “flexion-abduction orthosis” such as
-Pavlik harness (widely used)
-Von Rosen splint,
-Lausanne-developed abduction brace,
-Ilfeld orthosis (very successful in patients with failed Pavlik harness)
Frejka pillow.

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37
Q

Closed reduction with a hip spica cast under general anesthesia is the preferred treatment for developmental dysplasia of the hip (DDH) in patients aged ____.

A

6-18 months

Note; before 6 months, hip abduction devices are tried.

38
Q

When is open reduction indicated in the treatment of patients with developmental dysplasia of the hip (DDH)?

A

-in patients aged 18 months to 8 years.
-infants who have failed closed reduction.

39
Q

When is a major complication of open reduction in the treatment of developmental dysplasia of the hip (DDH)?

A

Avascular necrosis of the femoral head

40
Q

Risk factors for DDH include _____ (list most).

A

-female sex (4-times higher risk)
-breech positioning
-family history,
-tight swaddling
-space compromising conditions in-utero: multiple pregnancies
-oligohydramnios
-birth weight over 4 kg

41
Q

Congenital talipes equinovarus is commonly known as ____.

A

club foot;
presents as plantar flexed medially facing foot that resists repositioning.

42
Q

What are some intrinsic factors that increase the likelihood of a newborn p/w club foot?

A
  1. Spina bifida (most common).
  2. Trisomies
  3. Neuromuscular disorders such as meningomyelocele, myotonic dystrophy, and spinal muscular atrophy.
  4. Male sex
43
Q

Extrinsic factors associated with an increased likelihood of developing club foot include ______.

A

-multiple gestations
-breech presentation
-uterine abnormalities
-oligohydramnios.
-maternal obesity,
-maternal diabetes mellitus, and
-maternal/paternal tobacco use.

44
Q

______ is the most likely complication of club foot after treatment.

A

recurrence after treatment.

45
Q

What are the complications of untreated clubfoot?

A

-increased risk of
-arthritis, pain,
-impaired ambulation,
-infection.
-the affected foot will be smaller, and the affected calf will be underdeveloped.

46
Q

A young male presents with signs and symptoms consistent with meningococcemia. On exam, he is febrile, hypotensive with altered sensorium, generalized rash. Labs reveal hyponatremia, hyperkalemia, and metabolic acidosis. What is the most likely diagnosis?

A

Adrenal crisis caused by bilateral adrenal hemorrhagic necrosis
aka Waterhouse Friderichsen syndrome, a complication of meningococcal sepsis.

47
Q

______ physiologic process increases the intensity of cardiac right-sided murmurs (both systolic and diastolic) due to _____ mechanism.

A

Inspiration;
due to an increase in the venous return to the right heart upon inspiration.

48
Q

Ingestion of ____ mg/kg of elemental iron is a/w moderate toxicity; ingestion of more than ____ mg/kg of elemental iron is a/w severe systemic toxicity leading to severe morbidity and mortality.

A

ingestion of 20-60 mg/kg of elemental iron is a/w moderate toxicity;

Ingestion of > 60 mg/kg of elemental iron is a/w severe toxicity.

49
Q

Peak (4-6 hours post-ingestion) serum iron levels below ___ µg/dL are a/w minimal toxicity; levels between ____to ___ µg/dL are a/w moderate toxicity, and levels above ___µg/dL are a/w severe systemic toxicity.

A

Peak (4-6 hours post-ingestion) serum iron levels
-below 350 µg/dL -> minimal toxicity;

-between 350 to 500 µg/dL -> moderate toxicity;

-level > 500 µg/dL -> severe systemic toxicity.

50
Q

In patients with suspected/confirmed iron intoxication with regular supplement formulations, peak serum iron levels are tested at _____ hours after ingestion;

a second serum iron level is measured at ____ hours after ingestion if the patient has consumed sustained-release or enteric-coated formulations that are a/w erratic absorption patterns.

A

peak serum level measured as 4-6 hour post-ingestion;

If the patient has consumed sustained-release or enteric-coated formulations, a second serum iron level is measured at 6-8 hours after ingestion.

51
Q

True/False?
Plain radiographs may reveal iron in the GI tract, but many iron preparations are not radiopaque, and hence, normal radiographs do not exclude iron ingestion.

A

true.

52
Q

What measures can be taken to prevent the toxic effects of iron ingestion in patients who remain asymptomatic 4 - 6 hours after ingestion of elemental iron, or those who have not ingested a potentially toxic amount (ingestion of <20mg/kg of elemental iron)?

A

do not require any treatment for iron toxicity.

53
Q

_____ is the method of choice for GI decontamination in patients with iron overdose, if undissolved tablets are visible in the small intestine on x-ray.

A

Whole bowel irrigation through oral or nasogastric administration of polyethylene glycol solution.

54
Q

For most cases of iron intoxication, gastric lavage is not indicated as the risks of the procedure outweigh the benefits; however, gastric lavage with a large-bore orogastric tube is only indicated under ____scenario.

A

if abdominal x-ray demonstrates a large number of visible pills in the stomach.

55
Q

Activated charcoal is not indicated for GI decontamination in patients with iron intoxication d/t ___ reason.

A

d/t poor binding of activated charcoal with metals (such as iron).

56
Q

While mild hyperkalemia is usually asymptomatic, a rise (esp. dramatic) in serum K+ levels to higher than ____ mEq/L, is associated with life-threatening complications such as ___, _____, and ___.

A

Sr. K+ levels > 6.5- 7 mEq/L is a/w life-threatening
-cardiac arrhythmias,
-muscle weakness, or
-paralysis.

57
Q

The most common cause of hyperkalemia is ____, which can occur due to _____ reasons.

A

pseudohyperkalemia;

-most commonly d/t hemolysis of the sample esp. when a syringe is used to collect blood than a vacuum device, or use of tourniquets and excessive fist-pumping during the blood draw also increase the risk.
-leukocytosis or thrombocytosis are also frequently a/w falsely elevated serum K+ concentrations.

58
Q

What are the three main causes of hyperkalemia?

A
  1. Increased Potassium Intake:
    -Food (See footnote)
    -Iatrogenic: IV intake through TPN, medications with high K+ content.
    -massive blood transfusions.
  2. Intracellular (IC) Potassium Shifts:
    -Cellular injury releasing IC K+ into the extracellular (EC) space (ECS): rhabdomyolysis (crush injury, excessive exercise), hemolysis, tumor lysis syndrome,
    -Metabolic acidosis: IC K+ shift into the ECS; seen with hypovolemia, sepsis, or dehydration.
    -Insulin deficiency/DKA: dramatic EC shifts presenting as hyperK+ in the setting of whole-body K+ depletion.
    -Medications: digoxin, K+ sparing diuretics, NSAIDs, ACEIs, K+ penicillin, or succinylcholine.
    -Hyperkalemic periodic paralysis: rare, AD condition with impaired skeletal muscle Na+ channel (causes K+ to shift into the ECS).
  3. Impaired Potassium Excretion:
    -Acute or chronic kidney disease at GFR < 30 ml/min.
    -Aldosterone deficiency or insensitivity.
59
Q

List some food increased intake of which may lead to hyperkalemia esp. in patients with underlying renal pathology.

A

Food:
-dried fruits, seaweed, nuts, molasses, avocados, lima beans;
-spinach, potatoes, tomatoes, broccoli, beets, carrots, and squash;
-kiwis, mangoes, oranges, bananas, and cantaloupe,
-red meat

60
Q

Inside the kidney, potassium excretion occurs in the ____ functional areas.

A

DCT and the cortical collecting ducts.

61
Q

Neuromuscular effects of hyperkalemia include ___ signs and symptoms.

A

tiredness, fatigue, muscle weakness, flaccid paralysis, or depressed DTRs.

62
Q

____ is the most lethal complication of hyperkalemia that can lead to sudden death.

A

cardiac arrhythmias

63
Q

Dose-dependent ECG changes with hyperkalemia include ____ changes.

A

Serum K+ level at
5.5 - 6.5 mEq/L: Tall, peaked T-waves.

6.5 - 7.5 mEq/L: Loss of P-waves

7 - 8 mEq/L: QRS widening.

8 - 10 mEq/L: sine-wave pattern, cardiac arrhythmias, and asystole.

64
Q

____ pancreatic hormone shifts K+ into the cells.

A

insulin

65
Q

Even though ______ does not alter the serum K+ levels, it is used as emergency first-line therapy to stabilize the impending life-threatening cardiac response to severe hyperkalemia.

A

Calcium as

-IV calcium gluconate (less irritant),
or
-IV calcium chloride (highly irritant to vessels; only given through central venous lines except in cardiac arrest where it can be given peripherally).

66
Q

What is the role of beta-2 adrenergic agonists such as albuterol in the emergency m/m of hyperkalemia?

A

Beta-2 adrenergic shift potassium into the intracellular compartment.

67
Q

Of the gastrointestinal cation exchangers, Patiromer and Sodium polystyrene sulfonate used in the m/m of hyperkalemia in a patient in whom hemodialysis cannot be immediately undertaken, ______ is a/w adverse effects such as bowel necrosis in elderly patients, especially if given with Sorbitol.

A

sodium polystyrene sulfonate;

is falling out of favor d/t the lack of effectiveness and adverse effects, particularly bowel necrosis in elderly patients; should not be given with sorbitol, which increases toxicity.

68
Q

True/False?
Hyperkalemia is an independent risk factor for death in hospitalized patients.

A

True

69
Q

True/False?

Sudden onset, extreme hyperkalemia can cause cardiac arrhythmias that can be lethal in up to two-thirds of cases if not rapidly treated.

A

True

70
Q

Temporary ___ type of hearing loss can occur in patients with Kawasaki disease (KD).

A

Sensorineural hearing loss (SNHL);

does not persist.

71
Q

Based on standard pediatric guidelines, a _____ test is indicated for a first-time febrile UTI in a child under 2 years of age; a voiding cystourethrogram (VCUG) is indicated under ____ three conditions.

A

renal USG for first-time UTI in a child < 2 yrs of age;

VCUG if there are:
(1) abnormalities on the first-time renal USG,
(2) recurrent febrile UTI, and/or
(3) atypical or complex clinical circumstances.

72
Q

_____ condition is characterized by atrialization of the right ventricle leading to right heart failure and tricuspid regurgitation.

A

Ebstein anomaly

73
Q

Although stool culture is the gold standard for diagnosis of campylobacter enteritis, it is often quickly diagnosed by darkfield microscopy of fresh stool or gram staining for ____ or _____ bacterial characteristics, respectively.

A

darkfield microscopy: bacilli with darting motility;

gram staining: gram-negative vibrioid bacilli.

74
Q

Antibiotic agent of ___ class is the first-line treatment for campylobacter enteritis.

A

Macrolide (eg, azithromycin or erythromycin);

Azithromycin (preferred) 500 mg daily for 3 days.

75
Q

Secondary sites of mumps infection include ____ sites.

A

-pancreas: mild/subclinical > severe pancreatitis.

-inner ear (cochlea): SNHL (permanent)

-heart

-CNS: aseptic meningitis -> meningoencephalitis

-Kidneys: Nephritis, and

-Gonads: Epididymo-orchitis in post-pubertal age.

76
Q

Mumps-related Epididymo-orchitis is commonly seen in ___ age groups.

A

postpubertal male adolescents;

rare before puberty

77
Q

Mumps-related Epididymo-orchitis typically p/w ___ suggestive s/s.

A

development of high fever with chills, headache, vomiting, testicular pain with enlarged, warm, and tender testicles with erythema of the scrotum within the first days of parotitis in a postpubertal male.

78
Q

______ presenting with severe epigastric pain and tenderness with fever, nausea, and vomiting is an uncommon complication of mumps.

A

acute pancreatitis;

*mild or subclinical infection of the pancreas is more frequent than severe pancreatitis.

79
Q

____ is the most common complication, occurring in about 1-10 % of pre-adolescent patients with mumps parotitis.

A

Aseptic meningitis

80
Q

______ is an overgrowth syndrome caused most commonly by a spontaneous mutation affecting DNA methylation that p/w omphalocele (common) and characteristic features such as macrosomia, macroglossia, organomegaly, microcephaly, and ear creases/pits along with an increased risk of certain malignancies.

A

Beckwith-Wiedemann syndrome (BWS)

Memory Aid:
Think Wiedemann (wide man), think macrosomia, macroglossia, organomegaly!

81
Q

Beckwith-Wiedemann syndrome (BWS) is a/w increased risk of ___ malignancies within the first 8 years of life.

A

embryonal tumors such as
-Nephroblastoma (Wilms tumor) (most common)
-Hepatoblastoma (most common)

-Neuroblastoma
-Adrenocortical carcinoma,
-Rhabdomyosarcoma
-Some benign tumors.

82
Q

Bullous impetigo is caused by ____.

A

exfoliative toxin (usually exfoliative toxin A) producing strains of staphylococcus aureus that damage desmoglein1 (adhesion molecule) -> development of fragile fluid-filled vesicles -> erupt to form crusted lesions with a rim of scale (from rood of the bulla).

83
Q

Bullous impetigo versus allergic contact dermatitis, immunobullous diseases like linear IgA bullous dermatosis (LABD)?

A

bullous impetigo: fragile bullae random distribution.

allergic contact dermatitis: “tense” bullae and erythematous papules, often arranged linearly.

immunobullous diseases (e.g. LABD): “tense” bullae arranged in rings.

84
Q

The most common pathogen responsible for otitis media is _____.

A

S pneumoniae

Other common pathogens include
-H influenzae,
-Moraxella catarrhalis,
-Rhinovirus, Coronaviruses, and RSV.

85
Q

_____ is the most common posterior fossa anomaly characterized by (1) agenesis or hypoplasia of the cerebellar vermis, (2) cystic enlargement of the 4th ventricle with communication to a large cystic dilated posterior fossa, (3) upward displacement of tentorium and torcula, and (4) enlargement of the posterior fossa, commonly presenting with s/s of hydrocephalus.

A

Dandy-walker malformation/syndrome

86
Q

Children with short stature and poor growth are defined as ____.

A

Children crossing 2 or more percentiles on the growth chart and growing less than 4 cm between 4 and 6 years of age.

87
Q

Children with short stature and poor growth (crossed 2 or more percentiles and growing < 4 cm between 4 and 6 years old) should have a complete evaluation to rule out underlying causes such as _____ (list all).

A

-celiac disease,
-hypothyroidism,
-GH deficiency,
-IBD,
-CKD,
-genetic conditions a/w short stature.

88
Q

_____ tests are indicated in suspected cases of growth hormone deficiency.

A

serum levels of
-insulin-like growth factor binding protein 3 (IGF-BP3), and
-insulin-like growth factor 1 (IGF-1).

89
Q

____ (? IGF-BP3, IGF-1) is more reliable for the assessment of growth hormone deficiency in children less than 10 years of age.

A

insulin-like growth factor binding protein 3 (IGF-BP3).

90
Q

When is the growth hormone (GH) stimulation test indicated in the diagnostic evaluation of growth hormone deficiency?

A

to confirm after GH deficiency is identified through IGF-BP3 and/or IGF-1 tests.

91
Q
A

Step 2 Pediatrics (17 decks)

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