7

Question 1

Meckel diverticulum

Answer 1

A 3- to 6-cm pouch off the ileum and is a remnant of the omphalomesenteric duct. It is often lined with an endothelium that can secrete acid similar to gastric mucosa, causing ulceration of the adjacent ileal mucosa. It causes half of the lower GI bleeds in children aged 2 years or older. It can have a chronic presentation with only occult blood detected in the stool by FOBT, or it can present with acute large volume hematochezia and a child in shock.

Question 2

if suspect Meckel’s diverticulum, what diagnostic tests?

Answer 2

Meckel radionucleotide scan, if negative and still suspect, diagnostic laparoscopy

Question 3

the most common cause of hematochezia in infants, children, and adolescents

Answer 3

anal fissures

Question 4

surgical procedure involving TM incision and placement of tubes to ventilate the middle ear and help prevent reaccumulation of middle ear fluid

Answer 4

myringotomy and placement of pressure equalization (PE) tubes

Question 5

An examination that measures the transfer of acoustic energy at varying levels of ear canal pressures, which will reflect TM mobility.

Answer 5

tympanometry

Question 6

A minor surgical procedure in which a small incision is made into the TM to drain pus and fluid from the middle ear space (typically done by a specialist)

Answer 6

tympanocentesis

Question 7

most common bac OM pathogens

Answer 7

Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis

Question 8

other OM orgs seen in neonates and immunocompromised

Answer 8

Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa

Question 9

Acute OM is diagnosed in a child with ?

Answer 9

fever (usually less than 104°F [40°C]), ear pain (often nocturnal, awakening child from sleep), and generalized malaise,
red, bulging TM with middle ear effusion and decreased mobility

Question 10

“watchful waiting” is appropriate in who with OM?

Answer 10

a child older than 6 months with mild symptoms (ie, mild otalgia for less than 48 hours, temperature less than 39°C)

Question 11

1st line treatment for AOM

Answer 11

amoxicillin at doses up to 80 to 90 mg/kg/d for 7 to 10 days

Question 12

when to add B-lactamase (i.e. augmentin) coverage for AOM

Answer 12

recurrent AOM unresponsive to amoxicillin or has concurrent purulent conjunctivitis

Question 13

In the AOM child begun on amoxicillin who demonstrates clinical failure after 3 treatment days, change to ?

Answer 13

amoxicillin-clavulanate, cefuroxime axetil, cefdinir, azithromycin, ceftriaxone, or tympanocentesis

Question 14

when to consider myringotomy with PE tubes

Answer 14

when the fluid does not resolve or recurrent episodes of AOM occur (3+ in the previous 6 months or 4+ in the previous year with 1 in the previous 6 months), especially if hearing loss is noted

Question 15

rare but serious AOM complications

Answer 15

mastoiditis, temporal bone osteomyelitis, facial nerve paralysis, epidural and subdural abscess formation, meningitis, lateral sinus thrombosis, and otitic hydrocephalus (evidence of increased intracranial pressure with OM)

Question 16

ddx asthma exacerbation

Answer 16

anaphylaxis, cystic fibrosis, foreign-body aspiration, and CHF

Question 17

classification of asthma severity

Answer 17

http://casefiles.mhmedical.com.mwu.idm.oclc.org/ViewLarge.aspx?figid=140631109&gbosContainerID=75&gbosid=219794

Question 18

asthma exacerbation triad

Answer 18

acute, progressively worsening bronchoconstriction, airway inflammation, and mucus plugging

Question 19

A variance of systolic BP greater than 10 mm Hg between inspiration and expiration (pulses paradoxus) suggests ?

Answer 19

severe obstructive airway disease, pericardial tamponade, or constrictive pericarditis.

Question 20

Airway inflammation in asthma (immediate and late)

Answer 20

immediate IgE response to environmental triggers occurs within 15 to 30, late-phase reaction (LPR) is characterized by infiltration of inflammatory cells into the airway parenchyma (2-4 hrs after allergen exposure, causes chronic inflammation)

Question 21

other long-term asthma medications (besides B-agonists, anticholinergics, steroids)

Answer 21

mast cell stabilizers (cromolyn, nedocromil) and leukotriene modifiers (montelukast), which act by reducing the immune response to allergen exposure. They become effective after 2 to 4 weeks of therapy

Question 22

management of truncus arteriosis

Answer 22

meds to reduce the CHF: digoxin, diuretics to reduce preload (furosemide, chlorothiazide), afterload reducers (ACE- inhibitors), and inotropes (dopamine, dobutamine). Ultimately surgical correction is needed.

Question 23

Clinically apparent cyanosis and heart failure from truncus arteriosus may not be present until after the first weeks of life, why?

Answer 23

pulmonary vascular resistance is high after birth but drops to normal levels by 2 to 6 months of age. when it drops below systemic pressure, more blood flows to the pulm. system, leading to pulmonary congestion, increased myocardial work, and subsequent heart failure

Question 24

conotruncal heart defects

Answer 24

Malformations of the cardiac outflow tracts (aorta and main pulmonary artery).

• truncus arteriosus, tetralogy of Fallot (TOF), pulmonary atresia, and interrupted aortic arch
• commonly seen in chromosome 22q11.2 deletions such as DiGeorge syndrome.

Question 25

Ductal-dependent heart lesions

Answer 25

tricuspid atresia, pulmonary valve atresia, severe pulmonary valve stenosis, TOF if the accompanying pulmonary stenosis is severe, and TGA without ventricular inversion (D-TGA)

Question 26

if a difference of more than 3% to 5% between pre- and post-ductal O2 sats is found, then a ? may be present

Answer 26

right-to-left shunt across the ductus

Question 27

a single S2 occurs with ?

Answer 27

pulmonary valve atresia or truncus arteriosus

Question 28

an early systolic ejection click is heard with ?

Answer 28

pulmonary stenosis or truncus arteriosus.

Question 29

most cyanotic CHD (congenital heart disease) will show ? on CXR

Answer 29

increased pulmonary vascularity and cardiomegaly

Question 30

cyanotic CHD with DECREASED pulmonary vascularity

Answer 30

atretic tricuspid valve, atretic pulmonary valve, or TOF with its pulmonic valve stenosis (lack of flow to pulmonary circulation)

Question 31

TOF on CXR

Answer 31

RVH causes the apical shadow of the heart to point upward, creating a “boot” or “wooden shoe” shape to the heart

Question 32

D-TGA on CXR

Answer 32

“an egg of a string” because the reversed pulmonary artery and aorta give a narrow mediastinal vascular shadow

Question 33

TAPVR on CXR

Answer 33

a “snowman,” which is created by the round supracardiac shadow of a dilated innominate vein and vena cava that are receiving venous blood flow from the body as well as from the pulmonary veins

Question 34

neonate EKG

Answer 34

RVH can be normal for a neonate and biventricular hypertrophy may accompany a VSD

Question 35

tricuspid valve atresia may be distinguished by EKG because of its ?

Answer 35

left axis deviation, biatrial enlargement, and absent right ventricle markings (ie, no R waves in leads V1-V3)

Question 36

treatment in cyanotic CHD

Answer 36

PGE1 if ductal dependent
creating an atrial septum via cardiac catheterization (atrial septostomy), used for TGA before definitive surgery
creation of an aortic pulmonary shunt for tricuspid atresia or TOF

Question 37

the most common fatal congenital heart defect

Answer 37

hypoplastic left heart syndrome (HLHS)

Question 38

After complete surgical repair, ? of patients with TOF survive to adulthood

Answer 38

90%

Question 39

more CXR findings with CHD

Answer 39

http://casefiles.mhmedical.com.mwu.idm.oclc.org/ViewLarge.aspx?figid=105346789&gbosContainerID=75&gbosid=219797

Question 40

Truncus arteriosus presents with ? and requires stabilization with ? prior to undergoing surgical repair

Answer 40

heart failure

diuretics and ACE inhibitors

Question 41

A 2-year-old former premature infant with history of NEC and intestinal resection (including ileocecal valve) presenting with pallor and anemia, think?

Answer 41

Vitamin B12 deficiency secondary to terminal ileal resection and compromised intestinal absorption

Question 42

macrocytic anemia with low reticulocyte count is typically associated with

Answer 42

Hypothyroidism, trisomy 21, vitamin B12 deficiency, and folate deficiency

Question 43

what infants are at risk for a vitamin B12 deficiency?

Answer 43

Breast-fed infants of mothers who adhere to a strict vegan diet
otherwise vitamin B12 def. is rare; malabsorption can occur when the terminal ileum is absent, or when infectious or inflammatory conditions compromise intestinal function

Question 44

juvenile pernicious anemia

Answer 44

unable to secrete IF and become vit B12 deficient between the ages of 1-2 years, when the supply of vitamin B12 passed transplacentally from mother to child is exhausted
-at risk for permanent neurologic damage resulting from spinal cord demyelinization

Question 45

other causes of B12 deficiency

Answer 45

fish tapeworm Diphyllobothrium latum (uses vitamin B12), parasitic infection, IBD, exclusively fed on goat’s milk (also lacking folate and iron)

Question 46

For patients with macrocytosis but normal B12 and folate levels, consider ?

Answer 46

atypical bone marrow pathology (such as leukemia or myelodysplasia)