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1

Meckel diverticulum

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.

2

if suspect Meckel's diverticulum, what diagnostic tests?

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

3

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

anal fissures

4

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

myringotomy and placement of pressure equalization (PE) tubes

5

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

tympanometry

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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)

tympanocentesis

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most common bac OM pathogens

Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis

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other OM orgs seen in neonates and immunocompromised

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

9

Acute OM is diagnosed in a child with ?

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

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“watchful waiting” is appropriate in who with OM?

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

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1st line treatment for AOM

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

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

recurrent AOM unresponsive to amoxicillin or has concurrent purulent conjunctivitis

13

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

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

14

when to consider myringotomy with PE tubes

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

15

rare but serious AOM complications

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)

16

ddx asthma exacerbation

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

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classification of asthma severity

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

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asthma exacerbation triad

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

19

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

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

20

Airway inflammation in asthma (immediate and late)

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)

21

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

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

22

management of truncus arteriosis

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.

23

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

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

24

conotruncal heart defects

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.

25

Ductal-dependent heart lesions

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

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

right-to-left shunt across the ductus

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a single S2 occurs with ?

pulmonary valve atresia or truncus arteriosus

28

an early systolic ejection click is heard with ?

pulmonary stenosis or truncus arteriosus.

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

increased pulmonary vascularity and cardiomegaly

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cyanotic CHD with DECREASED pulmonary vascularity

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

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TOF on CXR

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

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D-TGA on CXR

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

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TAPVR on CXR

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

34

neonate EKG

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

35

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

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

36

treatment in cyanotic CHD

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

37

the most common fatal congenital heart defect

hypoplastic left heart syndrome (HLHS)

38

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

90%

39

more CXR findings with CHD

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

40

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

heart failure
diuretics and ACE inhibitors

41

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

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

42

macrocytic anemia with low reticulocyte count is typically associated with

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

43

what infants are at risk for a vitamin B12 deficiency?

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

44

juvenile pernicious anemia

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

45

other causes of B12 deficiency

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

46

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

atypical bone marrow pathology (such as leukemia or myelodysplasia)