The 2019 Pediatric Board Review Preview with Free Pediatric Board Review Questions and Mnemonics is now AVAILABLE.

2019 Pediatric Board Review Sneak Peek

2017 PEDIATRIC BOARD EXAM RESULTS ARE ENLIGHTENING

Your 2019 Pediatric Board Review PREVIEW (and Discounted PREORDER Code) Is Here!

2019 Pediatric Board Review Sneak Peek Publication Date

Best Pediatric Board Review Study GuideUnlike other board review courses, the PBR's Core Study Guide gets corrected and updated EVERY year. Many of the corrections and clarifications of the are made available to the PBR community (below) prior to the initial certification exam. This allows members to have a more secure pediatric board review experience, and more secure board exam experience. This is one of the many reasons why members recognize PBR as the best pediatric board review course in the industry.

For non-members who are trying to figure out how they will approach the board exam, or for anyone preparing for the MOC (or for MOCA-Peds), this is a great opportunity to essentially have a sneak peak into the 2019 edition.

In this article, you will:

  • Get a preview of the most EFFICIENT 2019 pediatric board review course available
  • Get a great review of several excellent and high-yield topics
  • Get a FREE MP3 Audio Chapter from PBR
  • Get 50 FREE High-Yield Images from PBR
  • Get a FREE Test-Taking Strategies Video Training Session
  • Get the opportunity to PREORDER the 2019 edition books for 50% off of the value of the Ultimate Bundle Pack or 85% OFF of the LIFETIME package called “PBR FOR LIFE!” Please note that the PBR FOR LIFE package is NOT typically available through the PBR catalog, so this is a SPECIAL opportunity!

A FEW WORDS OF THANKS TO THE PBR COMMUNITY

Every year I like to go through all PBR error submission and send corrections to PBR members before the initial certification exam. It’s an EXTREMELY time consuming task (takes several full days), but I believe it’s worth it.

If you have been following THE PBR EFFICIENCY BLUEPRINTthe information in this guide WILL NOT make or break your test-experience. Having said that, several test-takers have previously said that they enjoyed reading the clarifications, and that the review of the guide even helped them correctly answer several questions that came up on the exam.

THANKS TO YOU!

  1. Thank you to EVERYONE who submitted spelling errors, typographical errors, corrections or requests clarifications from within the PBR by visiting the ERROR page:

www.pediatricsboardreview.com/error

           For everyone who provided a page number, a clear question and a reference – oh my goodness… you rock!

  1. Thank you to EVERYONE who submitted broken links from within the PBR and the PBR Picture Atlas by visiting the BAD LINK page:

www.pediatricsboardreview.com/badlink

  1. An absolutely MASSIVE THANKS TO DR. JOHN COLE! John is a PBR alum, he’s been an OVC Summertime Q&A Webinar panelist and now he’s taken on the role of being PBR’s editor! He has a HUGE heart, and he does this to help you and the PBR community.

NOW… WHAT IS THIS THING?

I like to address as many concerns about the PBR content BEFORE the initial certification boards in October so this guide was specifically created and distributed to our members prior to the board exam

IN ORDER OF PRIORITY, MY FOCUS HAS BEEN….

  1. Addressing error submissions from the PBR Error portal (www.pediatricsboardreview.com/error). Basically, stuff where folks are saying,“Ashish… I think (or I know) that this is wrong. You should fix it in the book and let folks  know about it because it’s more than just a spelling or grammar issue.”
  2. Addressing possible errors/concerns mentioned in our private members' only forum (the PBR Facebook CREW)! Yes… I kind of “stalk” the group and if I see something comes up that might warrant a correction in the PBR. I set it aside for this time of year to review.
  3. Requests for content clarification through the portal or “The CREW”.

The “PBR Facebook CREW!” is meant to help you get the help you need to understand a topic. BUT, if I see that there’s a topic that could be explained better based on CREW conversation, I make a note of it and try to polish it up for the next edition and address the issue in this guide.

Because the PBR membership continues to grow, there has been EXCELLENT chatter in “The PBR Facebook CREW.”

PEARL: If you are a member of the “The PBR Facebook CREW” but you have NOT been seeing all of the posts, please visit the private group and make sure that your NOTIFICATION SETTINGS ARE SET TO ALL POSTS. This is critical!

ARE YOU NERVOUS BECAUSE THERE ARE “CORRECTIONS” FOR THE PBR CONTENT?

ALL study guides have errors!

I’m simply the only author who is crazy enough, and passionate enough, to take on something like this prior the boards every year so that you can rest EASY. And instead of just giving you a one page errata sheet based on error submissions, we try to go much deeper in our explanations and we also SEEK OUT areas of improvement to share with you.

For some people, though, the idea that the PBR has errors can be anxiety provoking.

If you’re one of those members, please keep in mind that there are OVER 2000 topics within the PBR, and each topic has MANY salient points associated with it. There are probably over 10,000 individual pieces of information in the PBR. Therefore, the number of corrections below is relatively TINY.

So you should rest easy knowing that there is MORE THAN ENOUGH excellent content within your PBR to get you your PASS! The PBR CERTIFICATION SYSTEM has helped pediatricians get ABOVE the national average score after MULTIPLE years of failing… so you’ll be fine!

WHAT ABOUT IMAGE LINK CORRECTIONS?

We have a very innovative system that allows you to view approximately 400 high-yield images across the web. Since the images that we refer you to are not owned by PBR, your timely submission of any broken links have helped us keep over 97% of our image links updated. Thank you!

If you happen to still find a broken link, please notify us immediately by visiting: www.pediatricsboardreview.com/badlink

The EASIEST way to go through all of these images is by using the online picture atlas created by Team PBR (called the Virtual Atlas of Pediatric Pictures). The VAPP gives you a SUPER fast and high-yield review of board-relevant images.

You can watch the video below to see how it works:

vapp-video

www.PediatricsBoardReview.com/vapp

GET 50 FREE IMAGES BY CLICKING THE IMAGE BELOW!

DOWNLOAD 50 HIGH-YIELD IMAGES FOR REVIEW NOW!

FREQUENTLY ASKED QUESTIONS

“Is this a complete list of everything that’s changing for the new edition?”

 NO! The new edition will have MORE additions and modifications. This Corrections & Clarifications Guide includes:

  1. A set of absolute notifications because they were true errors that we verified.
  2. Several clarifications and discussion around confusing stuff.

“If I have the old book… Should I keep that one or get the new one?”

If you have a 2017 Edition, it DOES HAVE enough information in it to help you pass the initial certification exam or the recertification exam. But, we tend to add new information and sometimes even new chapters when we release a new edition.

Here are the 6 main reasons to get the new edition if you still have an old one:

  1. SAVE AND MAXIMIZE YOUR TIME 
    • If you have an older version of the book and you are taking the boards several months from now, then this is NOT the time to spending your energy cross checking everything in this guide against your older version of the PBR. Please understand that your time is PRECIOUS and needs to be spent EFFICIENTLY and effectively. Plus, there is ALWAYS new content in a new release.
    • Start with a fresh book, transfer any notes/drawings from your previous hardcopy to the new edition as you read through it the first time, and then use the new one as your bible!
  2. COST  (No… I’m not just talking about money!)
    • By cost, I mean money and opportunity cost. The cost of a new book is minimal compared to the hard financial cost and the opportunity cost of FAILING the boards. The financial cost of FAILING includes over $2000 for your board fees, plus the cost of taking time off of work to study again next year (THOUSANDS of dollars of lost income). You also must include the stress and the time away from loved ones as a tremendous unmeasurable cost.
    • If you have some OTHER reason to keep studying from an older edition, so be it… but if it’s due to financial concerns, that’s actually pretty silly. Sorry… this is the one place in this guide where I need to blunt (for your sake). I have such a passion for efficiency and QUALITY USE OF TIME that it pains me to hear about physicians that are trying to go back and forth between the corrections guide and their old study guide in order to save a few bucks.
  3. REFERENCES TO PBR IN THE CREW!
    • The PBR Facebook CREW comes alive with discussion as the boards approach. Many PBR alumni have said that the Facebook CREW heavily contributed to their success on the boards. When your peers in “The CREW” are referring to a topic on a certain page, do you really want to (again) waste your precious time fumbling around and trying to find the topic they’re referring to because your pages don't match up with theirs?
  4. UPGRADED FORMATS: Every edition is MUCH better than the previous.
  5. NEW CORRECTIONS: There WILL be other corrections that will make their way into the new edition. MANY of the corrections below were included in this guide because of help from the PBR community, and many were done on my own. But there are more that need further investigation before the next edition is released.
  6. NEW CLARIFICATIONS: Again, there was ACTIVE discussion within the members’ only PBR Facebook CREW! about board review topics that I THOUGHT were explained well within the PBR. Those discussion have allow us to create EVEN CLEARER topic explanations in our new editions.

DISCLAIMERS/WARNINGS – PLEASE READ THIS BEFORE YOU GET STARTED

  • The page numbers in this guide refer to the 2018 Editions of the Pediatrics Board Review books (covers shown below).

2018 Pediatrics Board Review Core Study Guide and Q&A Book Corrections & Clarifications

  • DEAR NON-PBR MEMBERSthe PBR Facebook CREW! is a private, members-only area for anyone who has signed up for a qualifying product. YOUR REQUEST TO JOIN WILL BE DENIED if you have only signed up to get free info from PBR (free GI & DERM study guides, free emails about new PBR web article, free Q&A discounts, free MP3, etc). We cross-check all requests before clicking the APPROVE button. This is done in order to keep it a spam-free, private and intimate area.
  • Reminder… I LOVE being told I’m wrong (sort of), so keep the comments coming! Just keep in mind that the best place to submit error submissions, corrections, requests for clarifications, etc. is here:

Use PROMO CODE “PREORDER” and PREORDER the 2019 Edition of the PBR at 50% OFF the Value

Our goal is to release the 9th Edition of the PBR between December 15th and January 1st.

  1. Lock in current pricing for either of these memberships:
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  3. Get immediate online access to the online and mobile versions of the PBR Core Study Guide and Q&A Book!
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PBR 12-MONTH ALL ACCESS PASS + BONUSES
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During our 2019 PREORDER Window, PBR is Offering the
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===


LET’S GET STARTED WITH THE CORRECTIONS FIRST!

OKAY…. This first section is going to cover TRUE ERRORS that were in the PBR and possibly some clarifications that are going to result in CHANGES for the next edition.

Got more errors to submit? Send them over!
www.pediatricsboardreview.com/ERROR


ADOLESCENT MEDICINE

On page 66 of the 8th edition in adolescent medicine, although this is a minor point, please update the ASCUS section. It is wrong.

Thank you, this will be updated in the next edition of the book.

For a young patient from 21-24 with ASCUS, the current guidelines are NOT to do colposcopy in 6 months. Updated sections are below!

PAP SMEARS

The first PAP smear should be performed at age 21 regardless of other risk factors. Women between the ages of 21-30 years old should have a PAP smear every 2 years. If a patient presents with a known (or likely) STD, it is okay to do a PELVIC EXAM. But, you should hold off on doing a PAP SMEAR of the cervix because the inflammatory changes can result in a false positive! Thin vaginal discharge is not a contraindication. Mucopurulent discharge suggesting an STD is a contraindication. If the patient is on her period, don’t do a pap smear.

ASCUS (ATYPICAL SQUAMOUS CELLS OF UNDETERMINED SIGNIFICANCE)

In general, pap smears are being performed less frequently in young adults. If a pap reveals ASCUS in a woman under age 24, then repeat a PAP smear in 1 year. If the second PAP smear also shows ASCUS, then consider a colposcopy.


ENDOCRINOLOGY

re: 21-OH Deficiency on page 82, PRB book says “oral Dexamethasone should be given to the pregnant mother until the sex of the baby can be determined..” etc.

This is actually very controversial in the Endocrine community, as the risks associated with giving high-steroids to the mother are high. I would say that prenatal Dexa CAN be given to the mother, however it is not considered standard of care.

We agree that oral dexamethasone given to the mother should only be given after careful consideration by the parent. See corrected text below.

21-HYDROXYLASE DEFICIENCY

21-Hydroxylase Deficiency is the autosomal recessive disorder that’s usually responsible for Congenital Adrenal Hyperplasia on the pediatric boards. During pregnancy, if either parent is a known carrier (or has the disorder), oral Dexamethasone CAN be given to the pregnant mother (after careful consideration of the risks/benefits) until the sex of the baby can be determined (checked by amniocentesis or chorionic villus sampling). If the baby is male, treatment may stop (even if the baby has the disorder) because an excess build-up of androgens during pregnancy has no major side effects on males. After birth, the baby will need steroid treatment. If the baby is found to be female and has the disorder on genetic testing, maternal treatment should continue. This is extremely important and is done to prevent female virilization. Due to lack of aldosterone, this is a SALT WASTING CAH, resulting in Hyponatremia and hypERkalemia. There is NO hypertension. On labs, expect 17-HYDROXY­PRO­GES­TE­­RONE to be high.


Clarification request: We had a few lecturers during residency who mentioned that the missed menstrual cycles are no longer a diagnostic criteria for anorexia.

You are correct, the DSM-5 has changed the criteria to remove amenorrhea from the diagnostic criteria of anorexia.  We will remove the statement on page 64 titled “anorexia as a cause of amenorrhea.” See updated section below:

ANOREXIA

In patients with anorexia, look for laxative abuse, diuretic abuse (supportive labs include hypOkalemia, alkalosis, and HIGH FeNa!), emesis, bradycardia, ST depression, prolonged QT, Ventricular Tachycardia (V-tach), hypothermia, orthostasis. The patient’s history must include a restriction of energy intake, an intense fear of gaining weight, and body image disturbance. There are two subtypes: restricting type and binge-eating/purging type per the DSM-V.

MNEMONIC: ProLONGed QT and ST Depression = “A LONG-faced anorexic QT/Cutie is a little too Skinny/Thin… Even so, she still can’t stop being DEPRESSED because her body just doesn’t look right when she looks in the mirror!”

MNEMONIC: Bradycardia and Hypothermia = Just imagine that the super skinny anorexic girl’s body is so STARVED, that her heart beats slow and her body produces LESS HEAT ENERGY (to go into a calorie conservation mode).

https://www.aafp.org/afp/2015/0101/p46.html


OB/GYN and some STD’s

Hi, I just had a case of a newborn born to mom who was RPR + but unsure if she was adequately treated. Looking at the PBR on page 89 it states: If a mom was RPR+ but the FTA was not done, obtain the FTA in the baby. However both UptoDate and the CDC seem to say: All neonates born to mothers who have reactive nontreponemal and treponemal test results should be evaluated with a quantitative nontreponemal serologic test (RPR or VDRL) performed on the neonate’s serum, because umbilical cord blood can become contaminated with maternal blood and yield a false-positive result, and Wharton’s jelly within the umbilical cord can yield a false-negative result. Conducting a treponemal test (i.e., TP-PA, FTA-ABS, EIA, or CIA) on neonatal serum is not recommended because it is difficult to interpret. Any idea what to go with on the test?

Yes, you are correct!  Good catch. According to the red book, CDC, and UpToDate: “All neonates born to mothers who have reactive nontreponemal and treponemal test results should be evaluated with a quantitative nontreponemal serologic test (RPR or VDRL) performed on the neonate’s serum.”  The text will be updated as below:

(DOUBLE TAKE) SYPHILIS

Syphilis is caused by TREPONEMA PALLIDUM. Non-treponemal tests (RPR or VDRL) can be FALSE positives, so you need to do a confirmatory treponemal test (FTA). While the FTA does not correlate with disease activity, the non-treponemal tests do. Also, the non-treponemal tests may eventually disappear with decreased disease activity. So once disease presence is confirmed with FTA, look at disease activity with non-treponemal titers to help guide management. Neonates born to a mother with a reactive nontreponemal (RPR or VDRL) or treponemal (TP-PA, FTA-ABS, EIA, or CIA) test result should have a quantitative nontreponemal serologic test (RPR or VDRL) performed on the infant’s serum. Treponemal serologic tests on a baby are difficult to interpret so are not recommended. An immunoglobulin (IgM) test is also not currently available. If the mom was treated and the baby’s titers are lower than hers, it’s safe to assume that those are just the mom’s IgGs that crossed the placenta and that there is NO NEED TO TREAT (just follow the titers). If the mom was treated < 1 month ago, TREAT. If the mom was given Erythromycin, TREAT because it doesn’t cross the placenta.

https://www.cdc.gov/std/tg2015/congenital.html


ALLERGY AND IMMUNOLOGY

I’m confused bout the definition of anaphylaxis, as well as the exception to the usual rule of requiring two separate systems in order to diagnose anaphylaxis. Can you help?

Please see updated material below that will be in the 2019 edition of the PBR Core Study Guide.

ANAPHYLAXIS

Anaphylaxis is a serious allergic reaction that is rapid in onset and may cause death according to the NIH and the Food Allergy & Anaphylaxis Network. The criteria generally require TWO systems to be affected in order to qualify for the definition of anaphylaxis. The one exception is when there is acute hypotension (may be evidenced by hypotonia or syncope), in which case the single finding can be used to define anaphylaxis. The four systems that can be affected minutes to hours after exposure to a suspected allergen include:

  • Skin or mucosal involvement: Considered one system. Look for hives, itching, flushing or edema.
  • Respiratory system: Look for wheezing, stridor, hyposemia or coughing.
  • Continued GI symptoms: Look for vomiting or abdominal pain.)
  • Circulatory system compromise: Look for hypotension as evidenced by hypotonia, syncope or a drop in systolic blood pressure of > 30% (or a systolic blood pressure that is below the 70 mmHg + the child’s age in years).

The following is a review of some common issues to be aware of in case a child presents with anaphylaxis:

*  FOOD EXPOSURE: Watch for four hours before discharging from the ER.

*  RSEVERE RESPIRATORY COMPROMISE: Intubate and quickly secure the airway first. THEN give EPInephrine (1:1000, “3 zeroes for 3 letters of EPI”), diphenhydramine, IVF, and steroids.

*  BETA BLOCKERS: They blunt the response to EPInephrine. Give glucagon to reverse the beta blocker effect and then give EPInephrine (again).

*  ANAPHYLACTOID REACTIONS result from mast cell degranulation. These are not true IgE mediated reactions. They may be seen with the use of NSAIDS, Opiates, Vancomycin, and Contrast. Pretreat with steroids and diphenhydramine.


CARDIOLOGY

pg 132, hypertension screening in children. AAP says to start screenings at age 3 years during preventative visits.

Yes, you are correct.  See updated content below:

*  Obtain routine blood pressure measurements at annual preventive care visits starting at 3 years of age.


Is there a good mnemonic for heart murmurs? I always get them mixed up!
and good resources for EKG reading?

As for heart murmurs, the book has excellent content and mnemonics in the cardiology chapter. We will also add two new mnemonics to the next edition thanks to A.K. which are:

PASS = pulmonary/aortic stenosis is systolic

PAID = pulmonary/aortic insufficiency is diastolic

Opposite is true for mitral/tricuspid valves

Normal sinus rhythm

Sinus tachycardia

Sinus bradycardia

Supraventricular tachycardia (SVT)

Wide-complex tachycardia; presumed ventricular tachycardia (monomorphic)

Ventricular fibrillation (VF)

Asystole

Pulseless electrical activity (PEA)

SVT converting to sinus rhythm with adenosine administration

Wide-complex tachycardia (in a child with known aberrant intraventricular conduction; this is SVT with aberrant conduction)

First-degree AV block

Torsades de pointes (polymorphic ventricular tachycardia)

VF converted to organized rhythm after successful shock delivery (defibrillation)


Thank you to the Live Test-Taking Strategies Course members who contributed to these new mnemonics to help remember the meds that close, or keep patent, a PDA:

  • MNEMONIC: “IN-DOOR”-Methicin. Come IN and CLOSE the DOOR. Meaning, indomethacin CLOSES the PDA.
  • MNEMONIC: PPP = Prostaglandin keeps the PDA Patent

Where are you getting to obtain routine blood pressure measurements at annual preventive care visits starting at 1 year of age? I think the age is incorrect.

You are correct, that is a typo, see update material below on page 132.

PEDIATRIC BLOOD PRESSURE GUIDELINES

Hypertension affects 3.5% of all children and adolescents and many of these kids go undiagnosed and untreated. Therefore, the most recent guidelines released by the AAP simplify the identification and treatment of high blood pressure in children.

Obtain routine blood pressure measurements at annual preventive care visits starting at 3 years of age.

http://pediatrics.aappublications.org/content/early/2017/08/21/peds.2017-1904#T41


DERMATOLOGY

No Corrections! But the 2019 Pediatrics Board Review Study Guides May Have New Content (Or Corrections).


NEONATOLOGY

Can you clarify what we should consider full term when estimating gestational age? Page 157 says full term is 39 to 40 6/7 weeks but pg 163 says full term is 37-42 weeks. pages per 2017 Thanks!

Great catch! Anything before 37 weeks is preterm and anything after 41 + 6/7 weeks is post-term. The book will be updated as below on page 163.


MISCELLANEOUS

FULL TERM

For the boards, assume 37 – 41 + 6/7 weeks gestation is full-term, prior to 37 weeks is preterm and 42 weeks or later is considered post-term.

NEONATE

The term “neonate” applies from birth to 1 month of age.

INFANT

The term “infant” applies from 1 month to 12 months of age.


DEVELOPMENTAL MILESTONES

No Corrections! But the 2019 Pediatrics Board Review Study Guides May Have New Content (Or Corrections).


EMERGENCY MEDICINE AND TOXICOLOGY

In page 190, under Clonidine and phenothiazines overdose: it says clonidine can also produce some anticholinergic effects such as muscle rigidity and dystonic reaction? …. It should be cholinergic effect not anticholinergic effect, that is the way clonidine works! is that right?

The book is correct, although I can see your confusion. Please read carefully and note the word “some anticholinergic effects” in the text. Clonidine is an alpha-2 agonist and toxic exposure can be associated with some adverse ANTIcholinergic effects, including dry mouth, constipation, and CNS depression. Cholinergic effects such as diarrhea, increased urination, bronchospasm, and emesis do not typically occur. Note that miosis OR mydriasis, and hypotension OR hypertension and bradycardia OR tachycardia can occur with clonidine overdose. So, it is not useful to use these symptoms for differentiation. Hypothermia has been reported, but is usually mild.

  • Addition to the 2019 book will read:

On p. 185’s toxidrome chart, I think the sympathomimetic effect on bowel sounds should be “up” instead of “down”.

Yes, you are correct. Similar to the anticholinergic toxidrome but distinguished by hyperactive bowel sounds and sweating. Will be updated as shown below.

TOXIDROMES

Toxidrome BP HR RR Temp Pupils Bowel Sounds Diaphoresis
Anticholinergics ~ Up ~ Up Large Down Down
Cholinergics ~ ~ ~ ~ Small Up Up
Opioids Down Down Down Down Small Down Down
Sympathomimetics Up Up Up Up Large Up Up
Sedative-hypnotics Down Down Down Down ~Small Down Down

 


VITAMINS AND NUTRITIONAL DISORDERS

No Corrections! But the 2019 Pediatrics Board Review Study Guides May Have New Content (Or Corrections).


GASTROENTEROLOGY

Page 209. Dubin Johnson Syndrome is a benign direct hyperbilirubinemia. But how do you know on the test if the level of direct hyperbilirubinemia is due to this vs biliary atresia or other diseases with an elevated the conjugated bilirubin?

Updates in the book with include the following:

DUBIN JOHNSON SYNDROME

In Dubin Johnson Syndrome, there is a DIRECT hyperbilirubinemia. It is benign and relapsing. Most common in the teenage years presenting as nonpruritic jaundice without any other significant symptoms or pathology.

MNEMONIC: DuBin Johnson = D for Direct, B for Benign.

BILIARY ATRESIA

In cases of biliary atresia, initially look for an elevation in the direct bilirubin (AKA conjugated bilirubin) in a neonate. If found, obtain an abdominal ultrasound followed by a HIDA scan. If left untreated, this can result in liver failure. Until the liver fails, conjugation of bilirubin continues. KERNICTERUS only occurs once the liver fails and indirect bilirubin (AKA unconjugated bilirubin) can no longer be conjugated (only unconjugated bilirubin can cross the blood-brain barrier). Later in the course of the disease, indirect bilirubin (AKA unconjugated bilirubin) will also be elevated if left untreated.


Pages 211 and 215 state different ages that GERD should resolve by. The first page says by 12 months and the second mention of it by 2 years. Which is it?

Neonatal GERD should resolve by 18 months. The 2 areas in the book will be updated in the next edition of PBR.

https://www.mayoclinic.org/diseases-conditions/infant-acid-reflux/symptoms-causes/syc-20351408


Does Biliary Atresia present with elevated Direct or indirect hyperbilirubinemia or both are elevated?

Both, but the classic finding is a conjugated hyperbilirubinemia. This will be updated in the next edition of PBR.

BILIARY ATRESIA

In cases of biliary atresia, initially look for an elevation in the direct bilirubin (AKA conjugated bilirubin) in a neonate. If found, obtain an abdominal ultrasound followed by a HIDA scan. If left untreated, this can result in liver failure. Until the liver fails, conjugation of bilirubin continues. KERNICTERUS only occurs once the liver fails and indirect bilirubin (AKA unconjugated bilirubin) can no longer be conjugated (only unconjugated bilirubin can cross the blood-brain barrier). Later in the course of the disease, indirect bilirubin (AKA unconjugated bilirubin) will also be elevated if left untreated.


1) Under food protein induced ENTEROPATHY, you mention that “Protein induced ENTEROCOLITIS typically resolves once the GI tract matures.” Was this a typo, or was that sentence meant for the food protein induced ENTEROCOLITIS syndrome (FPIES) section?

2) For the diagnosis of food protein induced enteropathy (vs. proctitis/colitis), the book says flexible sigmoidoscopy with biopsy. But, wouldn't it be EGD with biopsy of the small intestine?

1) Typo for enteropathy, but the content is still correct.  Food induced intolerance conditions are typically temporary diseases, however some enteropathies can present in adulthood.

2) Yes, you can do either, but the primary diagnosis is usually made by history. Allergy skin tests don’t typically detect this type of food reaction.

New content will be as seen below in the next edition of the book.

(DOUBLE TAKE) FOOD PROTEIN INDUCED ENTEROPATHY

Food Protein Induced Enteropathy is NOT IgE mediated. It can cause problems from birth, but often presents as FAILURE TO THRIVE (FTT) after months of already being on cow’s milk formula, or less commonly from exposure to other allergenic foods. Celiac disease is a member of this group. SYMPTOMS include diarrhea ± emesis, malabsorption, anemia and failure to thrive while on formula, but not on clears or non-whole-protein-containing formulas. This CAN occur in breastfed babies, but only if enough whole protein from the mom’s diet enters the breast milk. It usually presents after switching from breastfeeding to formula. Forty percent of children are also sensitive to soy.

*  MNEMONIC: It’s so much easier if you just call it “FORMULA INDUCED Enteropathy.”  SYMPTOMS include diarrhea ± emesis and possibly BLOODY stool or flecks while on formula, but not on clears or non-whole-protein-containing formulas.

* PEARL: Less severe than Food Protein Induced Enterocolitis (FPIES). Children with Food Protein Enteropathy usually have less vomiting, no bloody diarrhea and less severe reactions to the problem foods.

*  DIAGNOSIS: Usually made by history, however for celiac disease get an upper endoscopy and duodenal biopsy showing villous atrophy. Allergy skin tests don’t typically detect this type of food

*  TREATMENT: If the mom is breastfeeding, try asking mom to stop drinking milk products. If that doesn’t work, change to HYDROLYSATE formula (formula containing HYDROLYZED cow’s milk proteins) or to an AMI­NO ACID DERIVED FORMULA. Typically resolves once the GI tract matures, although some food sensitivities may remain.

(DOUBLE TAKE) FOOD PROTEIN INDUCED PROCTITIS/COLITIS

Food Protein Induced Proctitis/Colitis is another disorder that is NOT IgE mediated so does not need allergy testing. It occurs in the lower GI tract and the main sign is blood in the stools.

  •      More common in breastfed infants due to cow’s milk protein in the mother’s diet
  •      Babies are usually well other than having blood in the stools

*  TREATMENT: Same as for food protein induced enteropathy. Even small amounts of milk protein in mom’s diet can cause problems, so have her check the contents of everything she eats. If eliminating milk doesn’t work, try eliminating eggs, soy, then consult a gastroenterologist. Typically resolves once the GI tract matures, although some food sensitivities may remain.

(DOUBLE TAKE) FOOD PROTEIN INDUCED ENTEROCOLITIS SYNDROME (FPIES)

Food Protein Induced Enterocolitis Syndrome (FPIES) is the other non-IgE mediated food intolerance in infants. Its chronic form is similar to food protein induced enteropathy, with vomiting, diarrhea, and malabsorption. The acute form, however, is more dramatic, with severe vomiting ± diarrhea, often leading to lethargy and a shock-like state. Occurs 1–3 hours after ingestion of offending food. Cow’s milk and soy are the most common triggers but solids, especially RICE, are also frequent. Typically resolves once the GI tract matures, although some food sensitivities may remain.

https://allerg.qc.ca/Information_allergique/3_5_enteropathies_en.html

https://emedicine.medscape.com/article/931548-followup#e5


Page 210: Charcot's triad is fever, jaundice, and RUQ pain. The book lists it as fever, RUQ pain, and leukocytosis.

Correct, the book will now read: …with Charcot’s triad of fever, RUQ pain, and jaundice from an infection in the biliary tract.

Acute Cholangitis Clinical Presentation: History, Physical Examinationhttps://emedicine.medscape.com/article/774245-clinical


Isn't C.diff treatment, metro PO, metro PO and then PO vanc?

No, but thanks for bringing this up. It looks like there has been a good bit of research in adults, but not as much in children. Even so, here are the most up to date recommendations that will be driving some changes to the 2019 edition of the Pediatrics Board Review Core Study Guide:

  • Nonsevere Disease: Use metronidazole or oral vancomycin.
  • Severe Disease: Use oral vancomycin
  • First Recurrence: Retreat with the same medication
  • Second Recurrence: Use oral vancomycin

PHARMACOLOGY AND DRUG PEARLS

No Corrections! But the 2019 Pediatrics Board Review Study Guides May Have New Content (Or Corrections).


OPHTHALMOLOGY

No Corrections! But the 2019 Pediatrics Board Review Study Guides May Have New Content (Or Corrections).


GENETICS

Hasn’t the terminology around Asperger’s (page 247) changed to the new terminology?

Yes, please see the updated section that will be in the new 2019 edition of the book.

AUTISM SPECTRUM DISORDER

Children with autism have delayed language, serious social impairment, and compulsive and repetitive behaviors. This is a CLINICAL diagnosis and is based on observations of the behavior of a child. At least one of the mentioned impairments must have been prior to the age of 3.

PEARL: For autism or any clinical suspicion of a language/mental delay, start your workup with a HEARING TEST.

PEARL: The outdated term ASPERGER SYNDROME (AKA ASPERGER’S SYNDROME) is a milder form of autism. Patients have impaired social interactions and repetitive stereotypical behavior, but there is NO delay in language or cognitive development.

IMAGE: www.pbrlinks.com/AUTISM1


On page 239, could you please clarify trisomy 21 and translocation Down's. In the book, on same page, line 2 of the “DOWN SYNDROME” paragraph, the statement “TRISOMY 21 versus a Translocation Down's (due to a nondisjunction during gametogenesis)” conflicts with the TRISOMY 21 DOWN's paragraph where that is said to be due to nondisjunction.

Thanks for bringing this to our attention. Please have a look at the image below and move the parenthesis over to after the word DOWN’s.

 


HEMATOLOGY AND ONCOLOGY

I believe you have an error on page 267 of the 2018 Core Study Guide. Maternal ITP is not the same thing as NAIT. When there is suspicion for NAIT in a neonate, you test the mother's platelet count first- if it is low, it is maternal ITP, if mom's platelet count is normal, that is consistent with NAIT. NAIT is an allo-immune (nAIt) response of the mom's immune system to an antigen on the baby's platelets (HPA1a), as opposed to maternal ITP where there is an auto-immune response to the mother's (and baby's) platelets. The vast majority of people (>95%) have the HPA-1a antigen, so if mom is HPA-1b/1b and dad is HPA-1a/1a or 1a/1b and passes 1a onto the baby, then the mother will mount a response to the fetal platelets expressing HPA-1a.

Excellent point. We created a NEW topic called NEONATAL ALLOIMMUNE THROMBOCYTOPENIA (NAIT) that is listed below.

MATERNAL IMMUNE (OR IDIOPATHIC) THROMBOCYTOPENIC PURPURA (ITP)

In Maternal Immune Thrombocytopenic Purpura (ITP), the mother carries antibodies that affect her own platelet count as well as the platelet count of the neonate. The neonatal thrombocytopenia can last for weeks and can cause severe, and even fatal, bleeds. The key to finding the diagnosis is the presence of the thrombocytopenia in the baby and the mother.

NEONATAL ALLOIMMUNE THROMBOCYTOPENIA (NAIT)

In Neonatal Alloimmune Thrombocytopenia (NAIT), the mother forms antibodies against fetal platelet antigens. These antigens are often inherited from the father and are absent in the mother in much the same way as in Rh disease. Thrombocytopenia is present in the neonate and is a leading cause of intracranial hemorrhage in full-term infants. There is a high risk of NAIT recurring in subsequent pregnancies.


On page 270 (and in the video lecture) it lists Factor VIII concentrate incorrectly. The actual medication is Humate-P.

Thank you! The corrected version is below:

VON WILLEBRAND DISEASE (AKA VON WILLEBRAND FACTOR DEFICIENCY)

Von Willebrand disease (AKA von Willebrand factor deficiency) is an autosomal dominant disorder. Both factor VIII and platelets depend on the vW factor (vWF), so there is an elevated PTT and a prolonged BLEEDING TIME. Measure VIII and IX (to rule out hemophilia) and the vWF (to confirm that it is low). Keep in mind that factor VIII can be slightly low. No treatment is needed for minor bleeding, but DDAVP can be used to increase plasma vWF and Factor VIII. For EXTREME bleeding, GIVE FACTOR VIII CONCENTRATE (AKA HUMATE-P). Cryoprecipitate can be used as a last resort (it has Fibrinogen, VIII, vWF). Aminocaproic acid is used sometimes for mucosal bleeds since it helps inhibit fibrinolysis.


In the book on page 256, it states that the fetal hemoglobin structure is made of 2 alpha chains and 2 gamma chains, each with 2 alleles. Don't the ALPHA chains have 4 alleles?

Good eye! Yes, fetal hemoglobin is composed of two α (alpha) subunits and two γ (gamma) subunits, and is commonly denoted as α2γ2. The alpha chains have 4 alleles and the gamma chains have 2 alleles. The book will now read as follows:

FETAL & ADULT HEMOGLOBIN STRUCTURE

  • FETAL HEMOGLOBIN structure is made of 2 alpha chains and 2 gamma chains, denoted as α2γ2. The alpha chains have 4 alleles and the gamma chains have 2 alleles. Fetal hemoglobin is referred to as Hemoglobin F (Hgb F).
  • NEWBORNS: 50-80% of the circulating hemoglobin is fetal hemoglobin (Hgb F).
  • 6 MONTHS: 10% of the circulating hemoglobin is fetal hemoglobin (Hgb F).
  • 12 MONTHS: < 2% of the circulating hemoglobin is fetal hemoglobin (Hgb F).

INFECTIOUS DISEASES

On page 285, for RSV it says, “albuterol may or MAY NOT help. Consider steroids for severe case.” According to the updated 2014 AAP bronchiolitis guidelines, you are not supposed to give albuterol and you are not supposed to give steroids.

Yes, you are correct! See the revised text below:

RESPIRATORY SYNCYTIAL VIRUS (RSV)

The chest X-ray of RESPIRATORY SYNCYTIAL VIRUS (RSV) BRONCHIOLITIS will show HYPER­IN­FLATED LUNGS and DIFFUSE infiltrates. Diagnose with PCR or direct immunofluorescence testing on naso­pha­ryn­geal aspirates. Routine use of albuterol should be avoided as the wheezing is related to mucous plugging of the bronchioles and not bronchoconstriction caused by asthma in most cases. Nebulized hypertonic saline can be used in patients that are hospitalized, but is not recommended for the emergency room setting. Avoid the use of racemic epinephrine, systemic steroids, chest physiotherapy, and continuous oxygen monitoring in patients hospitalized for RSV. Patients frequently need hospitalization due to the severity of symptoms, comorbidities such as dehydration, and possibly their social situation (family reliability).

*  SEVERE BRONCHIOLITIS: Refers to pO2 < 65 on ABG, pCO2 > 40 on ABG, respiratory rate > 70 or pulse oximetry with saturations < 95%. This is associated with future asthma in about half of patients.

*   PEARL: RSV is NOT the only bug to cause bronchiolitis! Paramyxovirus is second in line.

http://pediatrics.aappublications.org/content/134/5/e1474


I think the test of choice to diagnose pertussis is now PCR, please clarify.

You are correct, nasal pharyngeal cultures are no longer routinely performed. See corrected text on page 281 below:

  • BORDETELLA PERTUSSIS (AKA WHOOPING COUGH)

Bordetella pertussis (AKA whooping cough) patients are described as having bursts, or “paroxysms,” of coughing. They cough so much they can’t breathe, then they inspire deeply, causing a WHOOP! Patients may have a HIGH WBC (lymphocytosis) of > 20,000. Diagnosis is made by PCR with a nasopharyngeal swab. Erythro­mycin, clarithromycin, and azithromycin are all acceptable agents. Use azithromycin for children under one month of age due to concerns about erythromycin-induced pyloric stenosis. Any macrolide should be okay for after one month of age. Bactrim is an alternative for children older than one month. All contacts (even if immunized) need to be given prophylaxis since immunity of the vaccination wanes.

PEARLS: Consider this diagnosis in any patient with a chronic cough. Antibiotic treatment shortens the early stage of pertussis in which the patient is infectious and has URI-type symptoms (known as the catarrhal stage). It does NOT decrease the “whooping,” or paroxysmal stage. Also, because of FDA regulations and much uncertainty as to exactly which macrolide “should” be used in infants, you will NOT be expected to choose one macrolide over another for infants > 1 month of age.


We have a new mnemonic for babesiosis on page 291!

  • MNEMONIC: Imagine a “babe” with a CROSS on her chest which represents the “Maltese cross.”

Please update the section on HUS and EHEC as the new term for shiga-toxin is STEC on page 301.

Thanks! Updated material is shown below:

*  ENTEROHEMORRHAGIC E. COLI (EHEC): As the word “hemorrhagic” suggests, look for BLOODY diarrhea caused by a Shiga-toxin producing E. Coli such as O157:H7 or O103:H4. These are also known as Shiga-toxin producing Escherichia coli (STEC). Also look for renal dysfunction and signs of hemolysis because this can cause Hemolytic Uremic Syndrome (HUS). Do NOT give antibiotics because that makes this worse!

(DOUBLE TAKE) PEARL: There are 3 types of HUS that affect children. Shiga-toxin producing Escherichia coli (STEC) accounts for > 90% of cases and results in abdominal pain, vomiting and bloody diarrhea, followed by Pneumococcal-associated HUS in young children with pneumonia, and lastly complement-mediated HUS due to mutations in genes for complement proteins.

(DOUBLE TAKE) MNEMONIC: The mnemonic for HUS is simply HAT. Hemolytic anemia, Acute renal failure, and Thrombocytopenia


Is there a risk of rheumatic fever after GAS scarlet fever? The book seems to say only after pharyngitis but I remember learning in the past it was also after scarlet fever. Can you look into this?

Yes, there is a risk of rheumatic fever after Scarlet fever. Scarlet fever causing rheumatic fever is FAR less common than pharyngitis causing rheumatic fever, but it is possible, so we will update the Core Study Guide. Thanks!

VACCINES, IMMUNIZATIONS AND CONTRAINDICATIONS

For meningococcal disease, page 313 at the top say we will give prophylaxis to close “intimate” contacts including nursery school, but not elementary school classmates or healthcare workers. I will underscore healthcare workers. According to the CDC, prophylaxis should still be given to anyone exposed to oral secretions (example: anesthesiologist/ER staff/or whoever intubating a patent who has N. Meningitidis). In this case a healthcare worker would get prophylaxis. Is this correct?

  • Good catch! You are correct. Per PBR on page 313 à Close “intimate” contact includes nursery school, but not elementary school classmates or healthcare providers
  • Will change in the 2019 edition of the PBR:
    • Close “intimate” contacts include household members, child-care center contacts (not elementary school classmates), and persons directly exposed to the patient’s oral secretions (e.g. kissing or endotracheal intubation/management)
  • Per CDC àClose contacts of a patient who has meningococcal disease include:
    • 1) household members
    • 2) child-care center contacts
    • 3) persons directly exposed to the patient's oral secretions (e.g., by kissing, mouth-to-mouth resuscitation, endotracheal intubation, or endotracheal tube management).

https://www.cdc.gov/mmwr/preview/mmwrhtml/rr5407a1.htm


On page 315, under the catch up immunization pearls, it states that Hib's last dose is given at 4 years. I think it’s actually given between 12 and 15 months. Right?

Hib only has 3-4 doses depending on the manufacturer, so see the revised statement under the mnemonic 5-4-3-2-1 on page 315 that will now read:

  • MNEMONIC: 5-4-3-2-1 – Use this to help you remember the number of times various vaccinations are administered.
    • 5 = Total of 5 DTaP doses (last one at 5 years of age)
    • 4 = P (and it kind of looks like an H) = Pneumococcal, IPV and Hib = 4eumococcal, I4V and 4 For 4neumococcal, there are a total of 4 doses with last dose given at 12-15 months of age. For I4V, there are a total of 4 doses with last dose given at 4 years of age. For 4ib, there are a total of 3-4 doses (this depends on the manufacturer), with last dose being given at 12-15 months of age. Since there can be 3 OR 4 doses for Hib, the 4ib mnemonic is kind of a fib for Hib. Ha!
    • 3 = Total of 3 Hepatitis B doses (last at 5–6 months)
    • 2 = MMR, VZV, and Hepatitis A
    • 1 = Rhymes with NONE

https://www.cdc.gov/vaccines/hcp/vis/vis-statements/hib.html


On page 314 in the “vaccine schedule reminders” section between 12 and 5 months, the second bullet should also mention “except IPV.” It should also INCLUDE Hib#4 towards the end of the sentence.

Yes, the text and mnemonic are updated as below:

*  BETWEEN 12 and 15 MONTHS: These do NOT need to be given all at the same time and there are different schedules and regimens available for working them into two well-child visits.

  •      The one-year virus shots: the live viruses plus Hepatitis A, so MMR #1, Varicella #1, and Hepatitis A #1
  •      Another dose of all the vaccines of the first year except Hepatitis B, IPV, and Rotavirus, so DTaP #4, Hib #4, and Pneumococcus #4 are given around the beginning of the second year.

INBORN ERRORS OF METABOLISM

Under galactosemia it says, “untreated galactosemia will result in cataracts.” How long does this take for patients to develop cataracts?

According to the American Academy of Ophthalmology, it can present within 2-3 weeks. See the updated section below.

GALACTOSEMIA (AKA GALACTOSE-1-PHOSPHATE URIDYLTRANSFERASE DEFICIENCY or GALT DEFICIENCY)

  • Galactosemia is caused by galactose-1-phosphate uridyltransferase deficiency, or GALT deficiency. It can look like an early version of lactase deficiency and can present with vomiting and diarrhea. The more serious symptoms include lethargy, hepatomegaly, jaundice, hypoglycemia, and seizures. Also, patients often PRESENT with gram-negative rod sepsis or meningitis (especially E. coli) before the diagnosis is even made. As a reminder, lactose breaks down into glucose and gaLactose. Due to the enzyme deficiency mentioned, galactose-1-phosphate cannot be broken down. Lactose is in breast milk and formulas, so this presents EARLY (within the first week). Test for an elevated galactose-1-phosphate level in the serum or tissues (builds up in the liver, kidney, and brain). You can also test for decreased GALT activity in RBCs. You can also test for non-glucose reducing substances in the urine. Treat with a LACTOSE- and gaLACTOSE-free diet, such as SOY MILK (the primary carbohydrate in soy milk is sucrose or corn syrup). Untreated galactosemia will result in CATARACTS (can presents within 2-3 weeks), severe cognitive defects/mental retardation, and liver disease.

Isn't MSUD considered an organic acidemia?

Sadly not. It’s an aminoacidopathy, but it can look like an organic acidemia, an it is listed in some areas as an organic acidURIA. Very confusing, and it would’ve been great if we could’ve just put it in the organic acidemia row!

https://www.ucsfbenioffchildrens.org/pdf/manuals/53_Metabolism.pdf

https://www.ncbi.nlm.nih.gov/pubmed/29094226

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210240/


The Inborn Errors of Metabolism summary chart mentions tyrosinemia. But, it is not mentioned much in the text. Is this important?

Thanks for pointing that out. We’re going to add the topic to the Core Study Guide, and you get to see it here first!

Tyrosinemia (type I)

Tyrosinemia is an aminoacidopathy that is caused by an inability to effectively break down the amino acid tyrosine. It results in liver and kidney disturbances and intellectual disability. Symptoms start in the first few months of life with failure to thrive. There can be liver failure (jaundice) and renal failure (oliguria). Other symptoms include nausea, vomiting, and frequent nosebleeds. The skin and urine can have a “cabbage-like odor.” There is a high risk of liver tumors (hepatoblastoma early in life and hepatocellular carcinoma in late childhood). Treat with a low-tyrosine and low phenylalanine diet. Monitor for kidney and liver damage.


ACID-BASE DISORDERS

No Corrections! But the 2019 Pediatrics Board Review Study Guides May Have New Content (Or Corrections).


FLUIDS AND ELECTROLYTES

Your video course mentioned that your shortcut to calculate maintenance IV fluids works for patients > 20 kg. But, page 340 says that it works for patients that are > 40 kg. It seems to work out for both. Can you clarify?

We were right the first time in the Online Video Course and will make sure that it’s consistent across all resources to show that it works for patient that weigh 20 kg or more. Thanks for having us triple-check this! The book will now read…

  • SHORTCUT: For patients > 20 kg, the hourly IV fluid rate = 40 + WEIGHT IN KG. For a 20 kg patient, the hourly rate is 60 ml/hour when using the 4/2/1 formula, and it’s also 60 ml/hour when we add 40 + 20 kg! For a 50 kg patient, the hourly rate is 90 ml/hour using the 4/2/1 formula, and it’s the same when we add 40 + 50 kg!

NEPHROLOGY

We no longer obtain a VCUG or ultrasound after first time febrile UTI, is that correct? Page 350 in the book says that we still do this, but I think the AAP released a policy on this in the past few years.

Good catch! This will be updated in the new edition of the book. Since there is still ongoing debate between pediatric urologist, as of this time, it is not recommended to obtain VCUG or U/S after 1st febrile UTI.


Please clarify the section on HUS and TTP on page 351.

Updated material to show that HUS and TTP have similar symptoms, but neurologic symptoms are more common in TTP.

HEMOLYTIC UREMIC SYNDROME (HUS)

Hemolytic uremic syndrome (HUS) can be associated with DIARRHEA caused by Shiga-toxin producing Escherichia coli (STEC). Symptoms include fever, hemolytic anemia, thrombocytopenia, renal failure, and neurologic symptoms. Look for schistocytes, burr cells or helmet cells, uremia + thrombocytopenia + purpura or ecchymoses, hematuria, oliguria, elevated creatinine, altered mentation, seizures, lethargy, coma, or hypertension (HTN). The hemolysis is Coombs negative, and the complement levels are normal. Hemolysis is caused by verotoxin (Synsorb can be given to bind it – low yield). The bug may have been contracted from bad meat or milk ingestion.

(DOUBLE TAKE) PEARL: There are 3 types of HUS that affect children. Shiga-toxin producing Escherichia coli (STEC) accounts for > 90% of cases and results in abdominal pain, vomiting and bloody diarrhea. Pneumococcal-associated HUS can occur in young children with pneumonia. Lastly, complement-mediated HUS can occur due to mutations in genes for complement proteins. The HUS associated with STEC is most widely tested on the boards and it typically occurs in children less than 5 years of age. This is unlike Thrombotic thrombocytopenic purpura (TTP), which can have a very similar appearing clinical syndrome, but it’s more common in teenagers.

(DOUBLE TAKE) MNEMONIC: The mnemonic for HUS is simply “HAT.” Hemolytic anemia, Acute renal failure, and Thrombocytopenia.

PEARL: Thrombotic thrombocytopenic purpura (TTP) is often indistinguishable from HUS, except that neurologic symptoms are much more severe and the child is usually a teen.

MNEMONIC: TTP = Teen = Top of head. Meaning, TTP occurs in adolescents and results in neurological symptoms that are more severe than those of HUS.

MNEMONIC: Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic Uremic Syndrome (HUS) can be recalled by using the mnemonic FAT RN. Fever, Anemia, Thrombocytopenia, Renal Failure, and Neurologic Symptoms.


STATISTICS

No Corrections! But the 2019 Pediatrics Board Review Study Guides May Have New Content (Or Corrections).


NEUROLOGY

No Corrections! But the 2019 Pediatrics Board Review Study Guides May Have New Content (Or Corrections).


ORTHOPEDICS AND SPORT MEDICINE

Osgood-Schlatter disease: PBR book says rest for a few weeks. Just did a Pedialink question where that was one of the answers, but so was “modify activity and wear patellar strap”. That ended up being the right answer. I know AAP isn't ABP, but what should I take as definitive?

Thanks for having us look this up. We’ll be updating this as shown below:

OSGOOD SCHLATTER DISEASE

Osgood Schlatter disease usually presents in active children around the time of adolescence, or a growth spurt, with pain below the knee. It occurs due to traction at the tibial tubercle by the patellar tendon at the point of insertion. Treatment is dependent on severity with the most severe cases requiring rest from the sport for a few weeks. Other treatment modalities include NSAIDS to reduce swelling and pain, a patellar tendon strap to help with pain, a knee pad to help protect the area from direct trauma, and stretching of the hamstrings and quadriceps muscles. A mild prominence may be noted into adulthood.

PEARL: This is typically a UNILATERAL problem, though it can occur on the other side later. Diagnosis can be clinical. If asked what imaging study to get, obtain a lateral X-ray.


For Salter Harris Fractures, it might be helpful to use the name as the mnemonic.

Great suggestion, thanks M.E. See updated section below with the new mnemonic.

SALTER HARRIS FRACTURES

There are five types of Salter Harris fractures (I, II, III, IV, and V) we’ll discuss. As a quick summary, they basically go through the growth plate, through the growth plate + metaphysis, through the growth plate + epiphysis, through the metaphysis + growth plate + epiphysis, or involve a crush injury in which the epiphysis is pushed towards the metaphysis, therefore crushing the growth plate and narrowing that space.

IMAGE: www.pbrlinks.com/SALTER1

IMAGE: www.pbrlinks.com/SALTER2

  • TYPE I: SEPARATED or SLIPPED. The fracture is through the growth plate, and the epiphysis has just slipped a little. Look for tenderness to palpation at or near the growth plate and a negative X-ray. Treat with casting for 2 weeks.
  • TYPE II: Growth Plate + Metaphysis. Most common. You may do a closed reduction and cast for 4 weeks.
  • TYPE III: Growth Plate + Epiphysis. This one is BAD because the fracture goes through the epiphysis and into the growth plate. May require an OPEN reduction and often results in poor bone growth after the injury.
  • TYPE IV: THROUGH all three layers. Epiphysis + Growth Plate + Metaphysis. This definitely requires open reduction to preserve the growth plate.
  • TYPE V: SMASHED. Crush injury in which the epiphysis is pushed towards the metaphysis, therefore crushing the growth plate and narrowing that space. Can result in poor growth after the injury. The X-ray may essentially look negative, or may show a POSTERIOR FAT PAD. This has the worst prognosis.

IMAGE: This shows the presence of an anterior and a posterior fat pad in an unrelated injury. www.pbrlinks.com/SALTERHARRIS3

  • MNEMONIC: S-a-l-T-S can help you remember SEPARATED, THROUGH and SMASHED for Types I, IV, and V. A different well-known mnemonic uses SALTR. It conflicts with the mnemonic used in the terminology section, though. Feel free to look it up if you’re struggling with these.
  • If you draw the bottom half of a long bone with the epiphysis on the bottom: S = Straight (across growth plate); A = Above the growth plate (metaphysis); L = Lower than growth plate (epiphysis); T = Through (metaphysis through to epiphysis); E = Everything/Everywhere (crushed, everything is messed up). If you use the same bone drawing to show the various segments of the bone (diaphysis, metaphysis, physis, epiphysis), it will lessen confusion and help build on knowledge.

RHEUMATOLOGY

How can you tell the difference between LUPUS CEREBRITIS and STEROID PSYCHOSIS?

We are going to assume that you’re ONLY talking about differentiating the two entities in a patient with KNOWN systemic lupus erythematosus (SLE). Differentiating the two can sometimes be challenging but keep these things in mind.

Steroid psychosis would only be found in a patient on steroids, usually after on them for a prolonged period of time. Symptoms would include more of the “psychiatric” flavor, and would usually include mania, hypomania or psychosis.

Lupus cerebritis can result in neuropsychiatric manifestations from lupus itself. Psychosis and other psychiatric manifestations CAN occur, so there’s overlap which can be difficult to tease out. Psychologic testing can sometimes help. Unlike steroid psychosis, though, CT and MRI imaging may reveal CNS lesions, EEG may be abnormal, CSF findings may be present, and the purely neurologic findings (stroke, seizures, meningitis, optic neuritis, etc.) would only be found in lupus cerebritis.

The 2019 PBR text will be updated on page 385 as shown below:

LUPUS CEREBRITIS: Associated with microischemia, cerebrovascular disease, seizures and can result in neuropsychiatric manifestations from lupus itself. Psychologic testing can sometimes help. Unlike steroid psychosis, though, CT and MRI imaging may reveal CNS lesions, EEG may be abnormal, CSF findings may be present, and the pure neurologic findings (stroke, seizures, meningitis, optic neuritis, etc.) would only be found in lupus cerebritis.

  • PEARL: Patients usually have steroid psychosis after being on steroids for a prolonged period of time. Symptoms would include more of the “psychiatric” flavor, and would usually include mania, hypomania or psychosis. Do not confuse that with cerebritis.

The board seems to be using “reactive arthritis” instead of “JUVENILE REITER SYNDROME” on most of the PREP questions and MOCA practice questions.

Will update in the next edition of the book on page 390. Thanks!

REACTIVE ARTHRITIS (AKA JUVENILE REITER’S SYNDROME)

Reactive arthritis (AKA juvenile Reiter’s syndrome) is a seronegative spondyloarthropathy (negative rheumatologic markers) that includes symptoms of iritis (look for pain and trouble with vision), urethritis, and arthritis.

PEARL: This is often preceded by an infection! Look for a recent infectious picture due to enteric bugs in young children (Salmonella, Shigella, Yersinia) and Chlamydia in older/adolescent children (nongonococcal urethritis).

MNEMONIC: Can’t SEE, can’t PEE, and can’t CLIMB A TREE. Refers to iritis or uveitis, urethritis, and arthritis.


PULMONOLOGY

In the pulmonary section on page 398, you mention bronchiolitis obilterans with organizing pneumonia (BOOP). BOOP is now considered an outdated term and cryptogenic organizing pneumonia (COP) is being used instead.

Good catch, it is now updated in the book.

Cryptogenic Organizing Pneumonia (COP, formerly bronchiolitis obilterans with organizing pneumonia)

Cryptogenic organizing pneumonia (COP) is associated with recurrent pneumonias that improve a little with antibiotics. Bronchoscopy will show grossly purulent material in the airways, but when the material is cultured it is negative for any growth! An open lung biopsy shows thickened alveolar septa and cell hyperplasia. This usually requires steroids but tends to eventually resolve for most patients. Etiology is unknown, but it’s often found in patients with chronic inflammatory diseases.


PSYCHIATRY AND SOME SOCIAL ISSUES

I think the AAP actually is okay with kids with single kidneys being involved in contact sports. They revamped that guideline back in 2012, so there are less restrictions on kids playing sports.

Good catch!  See updated content below:

CONTACT SPORTS PARTICIPATION

Contact sports participation should be avoided in children with hepatosplenomegaly and those who have had repeated concussions. Those with a single kidney, eye, or single testicle can participate given proper protection of the remaining organ. A single ovary is not a contraindication to contact sports, though the issue is somewhat controversial (thus probably won’t be tested!).

https://www.aap.org/en-us/about-the-aap/aap-press-room/pages/Young-Athletes-Unlikely-to-Injure-Kidney-Playing-Contact-Sports.aspx


ETHICS

Can non-emancipated minors <18 consent to procedures?

This content will be added to the PBR in the next edition.

For emergencies, there is implied consent and the procedure may move forward. If it’s not an emergency, then a non-emancipated minor needs parental consent. Certain situations can lead to emancipation, including getting married (state dependent) and enlisting in the military. Children can also seek emancipation through the courts.


PATIENT SAFETY AND QUALITY IMPROVEMENT

What is a diagnostic error?

What is considered medical negligence?

What is a sentinel error?

This content is still being developed but a version of it will be added to the PBR in the next edition within the Patient Safety/QI definitions chapter:

  • MEDICAL ERROR

Harm caused to the patient that results from the failure of a planned action to be completed as intended, or the use of a wrong plan to achieve an aim.

  • NEAR MISS (AKA CLOSE CALL)

Potential adverse event or an error that could have caused harm but did not, either by chance or by someone or something intervening to prevent the error. Close calls and near misses provide opportunities for the healthcare team to develop preventative plans and actions.

  • SENTINEL EVENT

An occurrence that signals the need for immediate investigation and response by the healthcare team. The Joint Commission defines a sentinel event as “an unexpected occurrence involving death or serious physical or psychological injury, or the risk thereof.” “Serious injury” specifically includes loss of limb or function. The phrase “or the risk thereof” includes any process variation for which a recurrence would carry a significant chance of a serious adverse outcome.

  • PREVENTABLE ADVERSE EVENT

Any preventable event that may cause or lead to inappropriate medication use or patient harm while the medication is in the control of the health care professional, patient, or consumer. Such events may be related to professional practice, healthcare products, procedures, and systems, including prescribing; order communication; product labeling, packaging, and nomenclature; compounding; dispensing; distribution; administration; education; monitoring, and use.

  • NON-PREVENTABLE ADVERSE EVENT

Directly related to the natural course of the patient’s illness or underlying condition, for example, terminal illness present at the time of presentation.


Pediatric Lab Values

What defines a “conjugated hyperbilirubinemia”?

  • A conjugated hyperbilirubinemia is defined as greater than 2mg/dL, or more than 20% of the total bilirubin.

http://pedsinreview.aappublications.org/content/28/3/83

  • See updated content below:

DIRECT BILIRUBIN (AKA CONJUGATED BILIRUBIN)

This is defined as having a direct bilirubin level that is > 2mg/dL, or a level that is > 20% of the total bilirubin (even in a newborn). Most common newborn jaundice issues are due to an indirect hyperbilirubinemia.


Pediatric Vital Signs

What would you consider to be hypotension for a neonate, infant and an older child?

  • A slightly low blood pressure should not be concerning if the clinical picture is otherwise normal and the patient doesn’t have any clinical signs hypotension.
  • Additional material will be added to the PBR in the next edition.

Term neonates: < 60 systolic BP (mmHg)

Infants: < 70, systolic BP (mmHg)

Children 1-10 years: < 70 + (age in years x 2), systolic BP (mmHg)

Children > 10 years: < 90, systolic BP (mmHg)

 

STRONG WORK EVERYONE!

THANK YOU SO MUCH FOR CALLING US OUT!

NOW LET’S GO OVER THE CLARIFICATION REQUESTS!

Again… we’ve tried to be as concise as we can because we know your time is short.

This section is going to cover CLARIFICATION REQUESTS from members, as well as anything that we felt might warrant a clearer explanation.

 


“Do you think we should study tympanograms?”

> Please avoid straying too far off of the PROVEN PBR PATH right now. It’s possible you’ll get ONE question on this. That’s too low yield for you to pursue studying now. Focus on the rest of PBR, which covers ALL of the very LOW HANGING AND HIGH-YIELD FRUIT!… AND SO MUCH MORE!


“I've seen a couple of practice questions about XXXXXXX and about XXXXXXX. I think you should consider maybe including these topics in the PBR.”

Thanks so much for ALL of your submissions, but 9 out of 10 times we will not tend up adding new topics to the PBR. Trust me when I say that it’s VERY possible to pass the exam with a first edition of the PBR from 2011. PBR will NEVER be a mini-Nelsons. Meaning, it’ll NEVER be a book where you can turn to for every pediatric diagnosis known to man. The PBR Certification System was not create to help you become the most well-rounded and knowledgeable pediatrician in the world. It is meant to give you MORE than what you need to pass the boards with a score that is ABOVE the national mean! Know it inside and out… and ignore everything else. Otherwise, you’ll find that there’s ALWAYS going to be more information that you could potentially chase. It’ll lead you down a rabbit hole… or the BLACK HOLE of Google Search.


ADOLESCENT MEDICINE

For a child that has GH deficiency vs. a child with constitutional growth delay, what would the growth curves look like?

  • A child with GHD will have a growth curve that will cross lines because of the deficiency. Kids with CGD tend to follow a smaller, more petite curve but not at 3% or lower. Technically, their growth RATE is usually normal. Eventually, the kids with CGD will reach a normal adult height because they’ll simply continue to follow that curve. You also have to always look at the mid-parental height to see if this child’s predicted adult height falls with within the range for the MPH.

ENDOCRINOLOGY

How can you differentiate between the elevated ADH as a result of Addison's disease versus SIADH (ref. p77)?

  • An ADH level doesn’t define either of these conditions. You’ll need to look at the other clinical signs, symptoms and lab values. In Addison’s look for signs of adrenal insufficiency.

How do we define being “overweight” versus being “obese”?

  • For kids > 2 yo, if BMI % is up to 94.99 = overweight. If 95% or above, then it’s called obesity. Use the CDC growth charts.
  • For kids < 2 yo, use WHO growth charts.

Page 78 states that Primary Addison's Disease is the most common reason for adrenal insufficiency in children. UpToDate reports that CAH is the most common cause of primary adrenal insufficiency. Does this need clarification?

  • The most common cause of adrenal insufficiency in infants is classic congenital adrenal hyperplasia, however the most common cause of adrenal insufficiency in children is Primary Addison’s Disease.

https://www.uptodate.com/contents/diagnosis-of-adrenal-insufficiency-in-children


“Excessive vomiting, laxatives, diuretics = hypokalemic, hypochloremic metabolic alkalosis” on page 69. My question is that laxatives cause a non-anion gap metabolic ACIDosis, right?

  • No, the book is correct. Laxative abuse can result in either a non-anion gap metabolic acidosis (similar to patients with chronic diarrhea) OR a hypochloremic metabolic alkalosis (from hypokalemia, increased renal bicarbonate reabsorption, and volume contraction due to profound loss of sodium and water in the stool).

For a female patient with 21-hydroxylase deficiency in CAH that is CONFIRMED, would she be treated with Hydrocortisone or Dexamethasone for life in order to prevent female virilization?

  • It depends – is the patient a fetus or a newborn? If the patient is a female fetus, dexamethasone will prevent female virilization, but if the patient is a newborn or infant, hydrocortisone is given for hormone replacement due to the fact most patients have adrenal insufficiency due to CAH by 21 hydroxylase deficiency, or to prevent further virilization (if the female patient was born with virilization) or to decrease further adrenarche (if patient has the non-salt wasting form with just premature adrenarche and advanced bone age presentation).

Are the exact same complications found in an Infant of a Diabetic Mother (IDM) as well as an infant of a mother with Gestational Diabetes?

  • Yes, both have the same complications due to the high blood glucose levels from themother and high insulin levels in the

https://www.stanfordchildrens.org/en/topic/default?id=infant-of-diabetic-mother-90-P02354


OB/GYN AND SOME STDs

No Clarifications! But the 2019 Pediatrics Board Review Study Guides Will Likely Have New Content (Or Clarifications).


ALLERGY AND IMMUNOLOGY

  1. 94: “If urticaria is noted as an isolated skin manifestation (with or without angioedema), you do NOT have to administer epinephrine.” With angioedema, wouldn't you want to give Epi, for fear of progression to upper airway swelling?
  • If urticaria is present without any airway involvement, you do not have to use epinephrine. If the patient is having chronic symptoms that are coming and going, this is not considered anaphylaxis, and you would simply give antihistamines. Again, no epinephrine. If the patient qualifies for the definition of anaphylaxis (typically requiring at least 2 systems), the FIRST thing you typically do is give epinephrine. If there’s airway compromise that raises concerns around the patient’s inability to keep their airway open, then intubate. ABCs! Acuity matters a lot on board questions!

  1. 99: The table lists hyper IGM as having nodes, but the memory aid states that the kid SCIDS and wipes out his nodes. This seems a bit contradictory. Can you clarify?
  • A child with SCID does NOT have palpable lymph nodes and that’s why the portion of the mnemonic that states that he SCIDS and destroys his NAD/NODES refers to a child with SCID who LACKS nodes.

PEARLS/MNEMONICS FOR BRUTON’S, SCID, AND HYPER-IGM

* PEARL: This table summarizes a few KEY findings from some of the disorders you’re about to see.

  LAD/TONSILS PCP PNA LYMPHOPENIA
Bruton’s NO NO  
SCID NO YES YES
Hyper-IgM PRESENT YES  
DiGeorge     YES

* MNEMONICS: The disorders will be discussed in more detail. Memorize the following mnemonic in the meantime. ABSENT NODES/SMALL TONSILS: “SMOOTH neck/face and oropharynx without any bumps.” The smooth neck/face represents a LACK OF LYMPHADENOPATHY on exam. The “oropharynx without any bumps” represents a LACK OF TONSILS.

  • BRUTON’S: “Use BRUT aftershave so you can have a SMOOTH face/neck!” Now imagine the most muscular man you know using BRUT aftershave. He has a SMOOTH face/neck (no LAD or tonsils on exam), but he also cut himself. He’s bleeding and starts to cry because he’s been too macho to establish care with a PCP. HE DOES NOT HAVE A PCP = PCP pneumonia is NOT seen in Bruton’s Agammaglobulinemia.
  • SEVERE COMBINED IMMUNODEFICIENCY = SCID: “You can SCID across SMOOTH surfaces, like a curvy and SMOOTH NECK.”

PNEUMOCYSTIS CARINII PNEUMONIA (PCP)

PNEUMOCYSTIS CARINII PNEUMONIA (PCP) = PNEUMOCYSTIS JAROVECI PNEUMONIA = FOUND IN Hyper IgM and SCID (but not BRUTons).

MNEMONIC: Imagine a super HYPER naked preschooler running all over the gravel schoolyard. He’s being chased by the teacher when he SCIDS. He does a running split and destroys his NADS/NODES. His mommy has to come and take him to his established PCP to get checked out…and maybe to rule out ADHD. J The destruction of the NADS kind of represents a LACK of lymph NODES (goNADS or goNODES or noNODES). This child DOES have a PCP, which means he IS susceptible to getting PCP/PJP.


What is the reference range for CH50?

  • The reference range of serum CH50 levels in persons older than 16 years is 30-75 U/mL.  There is no agreed upon reference range for children < 16 years old.

https://emedicine.medscape.com/article/2086931-overview

CARDIOLOGY

Much of this is over our heads, but thank goodness we had the help of a great pediatric cardiologist from our Online Video Course!


Can you clarify when we should give oxygen alone, versus Lasix alone, versus Lasix and oxygen for things like congestive heart failure versus Cardiogenic shock? And what about congenital heart disease patients (un repaired or repaired)? Would giving them oxygen make things worse?

  • On the boards, it’s likely going to be very clear what they want you to do. So this is more of a practical question in tricky situations rather than a situation in which a child clearly has pulmonary edema on CXR, in which case they need diuresis. If the child has low saturations and the lungs are clear, give O2. Or, if there’s pulm edema and low sats, give O2 and lasix. For the L to R shunts, there will be edema. DO give diuretics but do NOT give O2 because it’s a dilator and increases blood flow and will increase edema.

What is precordial catch syndrome?

  • We cover this in the CHEST PAIN section, but this is a vaguely defined condition. Happens in the growing years. Can complain of stabbing pain, possibly increased with breathing or moving. It’s musculoskeletal in nature and we don’t know the pathology. Patients are w/o symptoms before and after. Usually about a minute. No radiation. Comes and goes spontaneously.

Can you please explain the murmur of pulmonary stenosis.

  • Anything that leads to prolongation of blood flow through the pulmonic valve (e.g. that slows things down). Typically, ejection systolic murmur. There will be a wide split, but not a wide FIXED split. A wide FIXED split S2 is ONLY going to be found in an ASD for the boards.

Is the T wave upright/positive in newborns in the first week of life?

  • Yes. It’s upright as mentioned in the 2018 edition of the PBR, but then it changes to negative afterwards.

After the diagnosis of stage 1 HTN, will medications be started immediately, or do we just refer after the 24 hr ABPM?

  • This is very dependent upon risk factors such as obesity, family history, etc. Also, all of these patients typically have regular echocardiograms every 6 months. If there is ANY change in the LV size, then it’s an indication to start medication. So +risk factors or +end organ damage.

What anticonvulsants are associated with hyperlipidemia?

  • Phenytoin and carbamazepine have some association with an increase in LDL, but it’s not well-established.

p122 says truncus arteriosus has a bidirectional shunt vs p125 (table) says the shunt is R to L…I'm not sure which is correct?

  • Truncus arteriosus (TA) can have bidirectional flow across the VSD but the net shunt at the VSD level is from right to left. Patients with TA have univentricular physiology which is complex. In TA the VSD is the only outlet for the RV, hence all right sided (systemic) blood is shunted to the left side into the aorta. From Aorta there is left to right shunt into the pulmonary arteries.

DERMATOLOGY

Newborn Rashes (pg 152) discusses sebaceous hyperplasia as benign – but with Tuberous Sclerosis, sebaceous hyperplasia is another name for angiofibroma – how do these differ? just location. TS sebaceous hyperplasia spares the forehead and newborn sebaceous hyperplasia only occurs on nose?

  • These are the same thing, however in TS the patient would have at least 1 other feature such as an Ash leaf spot, a Shagreen patch, periventricular/cortical tubers, cardiac rhabdomyomas, or renal angiomyolipoma.

TUBEROUS SCLEROSIS

Tuberous sclerosis is AUTOSOMAL DOMINANT. Look for at least 2 of the following features:

* ASH LEAF SPOTS: These are hypOpigmented lesions, which can be seen with a Woods Lamp. You need at least 3 on the body to help make the diagnosis.

* SHAGREEN PATCH (hypERpigmented plaque that can be rough/thick and papular)

* ANGIOFIBROMAS (AKA ADENOMA SEBACEUM or SEBACEOUS HYPERPLASIA)

* PERIVENTRICULAR OR CORTICAL TUBERS: Usually associated with INFANTILE SPASMS or seizures

* CARDIAC RHABDOMYOMAS: Look for a kid with arrhythmias!

* RENAL ANGIOMYOLIPOMA

MANAGEMENTOF TUBEROUS SCLEROSIS: Most of the management has to do with seizures/infantile spasms and cardiac arrhythmias


In Dermatology Chapter, page 150, it says in the pearl, if an African American child is pictured it is not lice. Just wanted to ask why that is the case? Thank you!

  • Just a tip, not a rule.
  • There are several theories as to why African American children are less likely to get lice (type of hair, oils, sheens, etc.). What’s important to know is that African American children are less likely to get lice, and are therefore less likely to be shown in a picture of a child with a lice infestation.

Are HSV, Mycoplasma, and Syphilis associated with Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)?

  • They can be, but drugs are the most common cause. “Drugs were determined to be the causative agent in 94.8% of the severe cutaneous reactions followed by infectious agents at 5.2%, principally HIV, herpes simplex virus 1, and mycoplasma”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5457308/


In PBR, neonatal acne is listed as “aka neonatal cephalic pustulosis.” I had learned that these are two separate diagnoses that present at the same time. Neonatal acne are inflammatory papules/ pustules without comedones which doesn't require treatment while neonatal cephalic pustulosis are similar but responds to topical antifungals. Both occur during the same period. Am I misunderstanding something, is one a type of the other?

  • Neonatal cephalic pustulosis is a variant of neonatal acne. It is a pustular eruption on the face and/or scalp of newborn babies that unlike neonatal acne does not have comedones (blackheads, whiteheads). It generally resolves without treatment, however if appearance is unsightly topical antifungals can be used.

https://www.dermnetnz.org/topics/neonatal-cephalic-pustulosis/


Neonatal Lupus: regarding diagnosis: who do you send ant-rho or ant-la antibodies on? Mom or baby? If you could explain why as well that would be great! Thanks.

  • Confirm the diagnosis of neonatal lupus by obtaining anti-Ro or anti-La antibodies in the newborn. Another clue to the diagnosis is congenital heart block (which is associated with neonatal lupus) which can be detected at birth or prenatally.

https://rarediseases.org/rare-diseases/neonatal-lupus/


NEONATOLOGY

p160- Hemolytic disease can be prevented by Vitamin E? Is this suppose to be vitamin K? If not, why Vitamin E?

  • Vitamin E prevents oxidative stress on erythrocytes. Studies were previously done which suggested that Vitamin E reduces fragility of erythrocytes. More recent studies don’t support this so it’s falling out of favor and we’ll be removing it from the PBR Core Study Guide. Great question. Thanks!

From the discussion on Breastfeeding Jaundice and Human milk jaundice on page 161, how can we differentiate very well, in a board question, which jaundice it could be as they both can present in few days, 3 days.

  • If the question is talking about ANY issue with the feeding, think technique around BREASTFEEDING. Also, this usually presents around 1 week or less.
  • Human Milk Jaundice usually presents around 2 weeks.

DEVELOPMENTAL MILESTONES

I think the shapes section is off by one – I think 4yo can make squares – Looked on AAP. Can you clarify?

  • Great question. There’s a lot of variability out there between different sources. If you look at the DENVER II, you’ll see that the age ranges for the circle, cross and square actually line up with PBR fairly nicely. And if you do an online search for milestones, you’ll see that they are extremely variable depending on where you go. Our chapter in PBR, as is, has served the author (Ashish), editor (John), and MANY PBR alumni VERY well. Their scores in that section have SKYROCKETED. My recommendation is that you use ONE resource for this section (PBR’s) and know it inside and out!
  • Last, PUT NELSON’S DOWN! Do not use it to study. Bad, bad, bad idea. It’s overwhelming and not high-yield. My hope is that you used it for just a few minutes as a reference (if at all).
  • New visual mnemonic that Dr. John Cole came up with:

  • The head is the circle (3), squiggly lines for hair on top of head (2), necklace is a cross (4), body is a square (5), dress is a triangle (6) and the legs are diamonds (7).

Hi – I had a question… we get many practice questions with answer choices of 3 months, 5 months as answer choices etc thus the PBR only gives us milestones for 2,4,6 etc months … do we need to know milestones for ages in between for the boards?

  • I wouldn’t recommend that at all. Focus on the months that you would see a child for a well-child visit.

The book and videos say that kids can walk backwards at 2 yrs but then it says it again at 5-6 yrs – which is it?

  • 2-year-old = walks backwards (feet apart)
  • 5-year-old = walks backwards (heel to toe)

EMERGENCY MEDICINE AND TOXICOLOGY

No Clarifications! But the 2019 Pediatrics Board Review Study Guides Will Likely Have New Content (Or Clarifications).


VITAMIN AND NUTRITIONAL DISORDERS

What is the difference between zinc deficiency and acrodermatitis enteropathica?

  • Great question. It turns out that there are two forms of “acrodermatitis enteropathica.” There is an inherited acrodermatitis enteropathica and an acquired acrodermatitis enteropathica. The inherited form is due to a mutation in a zinc transporter gene. The acquired form is due to zinc deficiency due to other causes (diet, Crohn’s, etc.). The inherited form is rare and may present earlier in life (infancy). Findings may be similar in both forms since the findings are due to zinc deficiency.

I understand that calcium is the main electrolyte that affects PTH levels. But, do phosphorus levels affect PTH secretion?

  • For the purposes of the boards, the answer is “no.” In researching this question, it seems that high phosphorus levels may bind calcium and essentially make it invisible to the parathyroid hormone. This can result in the unexpected RELEASE of more PTH even when total body calcium levels are normal, but that’s way too much for you guys to have to know.

How would you distinguish Hartnup disease (aka pellagra-like dermatosis) from pellagra?

  • The key difference is that Hartnup disease is NOT a vitamin deficiency. It is a disorder of neutral amino acid transport and absorption. Look for someone with a normal, well-balanced diet. Pellagra, on the other hand, is a Niacin (Vitamin B3) deficiency that results from the lack of a well-balanced diet. E.g. The condition is often found in communities in which corn is a cornerstone of the diet.

GASTROENTEROLOGY

What is the treatment for Typhlitis?

  • Typhlitis (also called neutropenic enterocolitis) is usually found in patients that are hospitalized and neutropenic from chemotherapy. Usually, you would start with bowel rest, broad spectrum antibiotics (which may or may not include antifungals) and GCSF may also be given to correct the neutropenia.

I have seen a few questions asking for the difference in vs meconium ileus in NBs that don’t pass meconium. Some have just presented abdominal radiographs without physical examination findings. Do you think this topic is high yield?

How do you differentiate between Hirschsprung’s disease and meconium ileus?

What will the imaging look like to distinguish the two?

  • Meconium ileus is a problem of the small bowel. It can be found in association with various disorders, though its association with cystic fibrosis is commonly tested.
  • In Hirschsprung’s, they may not pass meconium, but on exam there is a tight rectum because the nerves are not there to allow relaxation. There can also be an “explosion” of stool when the finger is removed as the digital rectal exam completes.

What imaging would you get for Hirschsprung’s disease?

  • Barium enema

What is Paget's Disease? I found it mentioned on page 206 but not anywhere else in PBR

  • Paget’s Disease is mentioned in the Core Study Guide in one area, but it’s typically an adult problem. We’ll be removing it from the Core Study Guide.

I had learned that with bilious emesis in a newborn you need to do a STAT upper GI to look for malrotation. Is that correct because the book on page 217 just mentions KUB

  • You would do a KUB first (fast, quick, safe and easily done in patients of all ages) and then likely go to an UGI series.

Can you go over what the correct answer would be if you have a child you are concerned about celiac disease – do you do a test like colonoscopy or do you trial the gluten free diet or do you do serology

  • Serology first, then EGD with biopsy (not a colonoscopy) to confirm, and then withdrawal of gluten.

Page 212.  IBS pearl last sentence says: labs then fiber trial then EGD. Please clarify it. I know its under debate in Peds GI but what is the prevailing/accepted algorithm currently.

  • It’s a diagnosis of exclusion. So, do a basic workup. If there are no alarming findings and the patient is healthy appearing, then you could do a trial of fiber. If there are still problems, you could move on to an EGD.

What type of hyperbilirubinemia is found with Reye's Syndrome, Wilson's Disease, and Cholecystitis? They are in the section of causes of Jaundice but PBR does not mention in their descriptions what kind of bilirubin is elevated.

  • If you have an obstruction, then it is a conjugated (direct) hyperbilirubinemia:

Reye’s – drastic increase in transaminases, but not a proportionate elevation of bilirubin. So it looks like hepatic failure, but the bilirubin is not typically very high. It’s possible that this will be moved to a different section of the CSG, or that the section will be renamed.

Wilson’s Disease – can cause liver failure and have conjugated (direct) hyperbilirubinemia, but the bili is not elevated they go into liver failure.

Cholecystitis – obstruction so a conjugated (direct) hyperbilirubinemia.


Page 215 says to treat if apnea is present. So if an infant comes in with a BRUE is then found to really have reflux, do those patients should be treated? I thought treatment for GERD should only be if there is poor weight gain. Please advise.

  • TREAT if there is concerning pathology that may be associated with GERD.

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

Compared to pyloric stenosis, patients with gastroesophageal reflux disease (GERD) have vomiting that seems effortless. If the child is healthy, no need to treat. It will likely resolve by two years of age. Always consider overfeeding as a possible etiology. If there is apnea, signs of esophagitis (posturing), or poor weight gain, start a workup and also treat. A GI pH probe may help diagnose. Biopsy is unlikely to be an option, but choose GERD if eosinophils are noted on biopsy. You may treat with an H2 blocker (cimetidine, nizatidine, or ranitidine) or with a proton pump inhibitor (PPI), such as omeprazole.

PEARL: Metoclopramide and sitting upright during feeds have not been shown to decrease reflux.


PHARMACOLOGY AND DRUG PEARLS

Can you summarize what it means to have a medication that is a hepatic inducer versus a hepatic inhibitor?

  • The PBR has a very good section on this, but a hepatic inducer is a medication that speeds up the metabolism of a medication. That could be problematic because the patient may not have the medication effect desired because it’s cleared prematurely.
  • A hepatic inhibitor will slow down the metabolism and clearance of medications that are metabolized in the liver. As such, you may have HIGHER levels of medications than what are needed or desired. This can cause toxicity and side effects.

OPHTHALMOLOGY

No Clarifications! But the 2019 Pediatrics Board Review Study Guides Will Likely Have New Content (Or Clarifications).


GENETICS

Does the statement on page 235 in the Alport Syndrome section, “X-linked disorder will be present in 100% of the daughters of an affected MALE and NONE of his sons” specifically talk about children of affected male?

  • Yes. The affected father doesn’t pass on his X, so none of his sons are affected. But for an X-linked dominant disorder, all of his daughters will get his affected X chromosome.

Does the statement under Alport Syndrome – “more severe in males” pertains to affected children in general, and not necessarily children of affected males?

  • It’s generally more severe in males. The only children of affected males that will have the syndrome will be females.

What is the inheritance pattern for Rett Syndrome?

  • Rett syndrome occurs almost exclusively in females. More than 99% of cases are due to sporadic mutations in the X chromosome. Most of those mutations occur in the X chromosome that was inherited from a non-affected father. Due to this condition’s severe manifestations, the women who have this disorder do not typically reproduce.

HEMATOLOGY AND ONCOLOGY

For the Beta Thalassemia Major topic, the PEARL states the following:

“PEARLS: If tested on a thalassemia, it will likely be beta thalassemia major. If you are provided with an MCV that is low (60-70) and “out of proportion” with the fairly mild anemia, pick a thalassemia (but not beta thalassemia major).”

In terms of picking a thalassemia – which one should we pick?

  • For a generally healthy-looking patient with a very low MCV as compared to their mild and asymptomatic anemia, the answer will likely be alpha thalassemia minima or minor.

INFECTIOUS DISEASE

  1. 287 indicates if needle stick occurs with risk for HIV need to take 2 drugs. which are they?  also then indicates something about D drugs. Ddl or ddc? what does that mean?

If someone has cochlear implants, is this an indication for PCV 23 vaccine? What if someone has previously had meningitis?

  • Great question. We’ll likely update the Core Study Guide after doing a little more research, but this is almost verbatim from the CDC:
  • The CDC recommends pneumococcal conjugate vaccine (AKA PCV13 or Prevnar13®) for people who have cochlear implants (they are at higher risk for bacterial meningitis) or are candidates for cochlear implants. The CDC also recommends pneumococcal polysaccharide vaccine (AKA PPSV23 or Pneumovax23®) for people 2 years and older who have or are candidates for cochlear implants. Administer all recommended doses of PCV13 first and then administer PPSV23 according to the routine childhood and adolescent immunizations schedule.

What is the diagnostic test of choice for disseminated gonococcal arthritis?

  • Blood cultures (at least 2 sets)

https://www.uptodate.com/contents/disseminated-gonococcal-infection


P. 283, TB, when do we give triple versus quadruple therapy?

  • If it’s a smear-negative pulmonary TB that does not have extrapulmonary manifestations, or if it’s a “less severe” form of extrapulmonary TB, then use 3 drugs. For smear-positive pulmonary TB, or for severe extrapulmonary disease, use 4 drugs.

https://www.uptodate.com/contents/image?imageKey=ID%2F50271


Sorry just wanted to clarify vancomycin PO for staph, I remember PO vancomycin is given for c. diff infection since it stays in the GI tract, does it also work for staph skin infections? Thank you!

  • According to the PDR, PO vancomycin is only indicated for C.diff/enterocolitis.  All other infections require IV Vancomycin.

http://www.pdr.net/drug-summary/Vancocin-vancomycin-hydrochloride-802


Does giving MMR or Varicella to an HIV patient depend on viral load?

  • The CDC recommends MMR vaccination for all HIV-infected adults with CD4 counts of >200 cells/µL who lack evidence of measles immunity.
    • Ref: National Center for Immunization and Respiratory Diseases. General recommendations on immunization — recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2011 Jan;60(2):1-64.
  • The ACIP currently recommends primary varicella vaccination for HIV-infected children with CD4 percentages of ≥15%.
    • Ref: Marin  M, Güris  D, Chaves  SS, Schmid  S, Seward  JF; Advisory Committee on Immunization Practices, Centers for Disease Control and Prevention (CDC) and Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2007 Jun;56(RR-4):1-40.

VACCINES, IMMUNIZATIONS, AND CONTRAINDICATIONS

Hi. I have a super late question about DTaP. On p 314 it says that progressive neurological disorders are relatively contraindicated. Can you give an example of the type of diseases? Are we talking like an SMA or a muscular dystrophy or something more central?

  • Progressive neurological disorders are only a relative contraindication for DTaP and if the neurologic disorder has been stabilized or is no longer progressive, then you may give DTaP.
  • Progressive neurologic disorders are conditions with progressive deterioration in functioning. It can be gradual over years to decades or rapidly over weeks to months. These disorders affect an individual for the rest of their life.
  • Some examples are listed below and can be broken up into two major groups:
    • Acquired causes include: infectious (progressive Rubella syndrome, Chronic HIV, SSPE), metabolic causes (chronic lead poisoning, hypothyroidism, Vit B12 and E deficiency, and anticonvulsant drugs) and demyelinating (multiple sclerosis, Wilson’s disease, Huntington’s disease, Friedrich’s ataxia, and ataxia telangiectasia), ect.
    • Inherited causes include: Niemann pick disease, Gaucher disease, Rett Syndrome, Menke’s kinky hair disease, maple syrup urine disease, leukodystrophies (Krabbe disease, Adrenoleukodystrophy), etc.

Please discuss catch up vaccinations with age requirements (ie age last dose can be given, how many total vaccines in a series, and if time frame for subsequent vaccines is important. Thank you!

  • Just be aware that there is a catch-up vaccine schedule and the different types of vaccines included in it. It’s highly unlikely that you would be expect you to have this memorized.
  • Know general parameters surrounding catch-up vaccines such as:
    • No PCV-13 or Hib after 5 years old
    • No Rotavirus after 15 weeks old and hasn’t received the 1st dose.

Can you clarify what to do in a Hep A exposure? Getting lots of questions on when to give Hep A immunoglobin vs vaccine vs both. Thanks.

  • From PBR on page 313 -> HEPATITIS A: Give Hepatitis A immunoglobulin to the unimmunized family members only.
  • From the CDC -> “When administered within 2 weeks of last exposure, IG is 80%–90% effective in preventing clinical hepatitis A.”
    • Advisory Committee on Immunization Practices (ACIP) recommends IG exclusively for post exposure use due to limited data and studies.
    • Hepatitis A vaccine, if recommended for other reasons, could be given at the same time.
    • https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5641a3.htm

INBORN ERRORS OF METABOLISM

What is a good way to differentiate glycogen storage disorders (particularly type 1 or von Gierke) and organic acidemias? Esp. if the ammonia levels are elevated in both… would they tell us about organomegaly, and would that be a distinguishing factor between the two? And is the age of presentation the same for both disorders?

  • Using the age at presentation to differentiate is critical in this case. OA’s present EARLY. GSD 1 usually presents later. Also, keep in mind that GSD 1 will present when there’s STARVATION/FASTING.

What will a question typically say to clue us to Maple Syrup Urine Disease (MSUD) vs. Organic Academia (OA) since their labs are the same?

  • DOL 2 or earlier should increase your suspicion for an OA, though it doesn’t exclude MSUD because that can present within the first week of life. As a point of test-taking strategy, it would be very unusual for a question about Maple Syrup Urine Disease (MSUD) to have absolutely no mention an odor to the urine.

ACID-BASE DISORDERS

No Clarifications! But the 2019 Pediatrics Board Review Study Guides Will Likely Have New Content (Or Clarifications).


FLUIDS AND ELECTROLYTES

Is there an age when you would want to use 1/2 NS vs. 0.2NS? For example I remember in residency using 0.2NS for little babies but 1/2NS for older toddlers and if no renal problems and urinating would add 20KCL. I’m not sure why though. On the test would they be this specific?

  • It’s often a matter of preference. In general, isotonic fluid is almost never wrong for a regular child. If they have electrolyte abnormalities, that will change things. Also, if a patient has renal issues, you would likely avoid potassium. Lastly, NEVER bolus with fluid that is not isotonic. So ONLY bolus with lactated ringers or normal saline.

Are we expected to know and choose fluids to correct hyponatremia based on dehydration? I find this confusing and it really isn’t discussed in the chapter.

  • There’s a great SHORTCUT in the PBR that gives you the MAX amount of sodium that you would want to give a child (10 x their weight in KG) to raise their sodium by 12 meq over 24 hours. That’s the MAX that you would ever want to raise the sodium level. If you take that number, and your knowledge about how much sodium is in different kinds of IV fluids, and your knowledge about fluid resuscitation, then you should be able to quickly zero in on the answer.

NEPHROLOGY

Urology, Obstructions and Masses (pbr 2017 pg 347, bottom of page). “After postnatal ultrasound to confirm the findings, a VOIDING CYSTOURETHOGRAM (VCUG) should be done to rule out other anomalies and to look for reflux from the bladder into the renal pelvis due to POSTERIOR URETHRAL VALVES”.

Can you explain why a VCUG would show reflux from bladder into renal pelvis due to Posterior Urethral Valves. If the problem is in the URETHRA why would there be reflux in the bladder?

  • While the problem is in the urethra, everything is connected. If the urine flow out of the bladder is impeded, there can be filling of the bladder and then reverse flow into the ureters and renal pelvises.

Pg. 348 (pbr 2017): Vesicoureteral reflux: VUR. “It can be diagnosed by VOIDING CYSTOURETHROGRAM (VCUG) by showing reflux of contrast from the bladder into the ureter +/- renal calyx”. Is the sentence under UPJ (pg. 347 “after postnatal u/s to confirm the findings, a VCUG should be done to look for reflux from the bladder into renal pelvis due to Posterior urethral valves”) supposed to say VUR instead of posterior urethral valves? Or can PUV cause reflux from the bladder into the renal pelvis as well and if so – please explain how.

  • As mentioned above, PUV can cause reverse flow into the ureters.

On page 353, you mention that a patient with nephrotic syndrome can have hyponatremia. How is that so, and is that common?

  • For efficiency’s sake, it’s probably best to go ahead and just take our word for the fact that hyponatremia can definitely be present for patients with nephrotic syndrome. The proposed mechanism is a little complex, but you can see a great image and algorithm on the following page to better understand the mechanism:

https://www.researchgate.net/figure/The-Underfilling-theory-of-sodium-retention-in-the-nephrotic-syndrome-AVP-Arginine_fig1_256290368


Do we need to be able to identify grades of reflux on a VCUG?

  • You will not have to identify the grade of reflux on VCUG image/test.

STATISTICS

There is nothing in the book about confidence intervals and their significance. Worth a review? Do yall have a way to remember this that is not complicated? The way I have it now is that:

CI = 1- p value, so the larger it is the more significance is there?

  • The CI = 1 – p-value. The confidence interval is a range of values that is expected to contain your results (usually a mean or average). However, a “larger” CI is not necessarily “more significant.”
    • If the p-value is 0.05, then the CI is 95%, meaning that there is a 95% that your results (from your research) lie within the rangeof the CI.
    • If the p-value is 0.01, then the CI is 99%, etc . . .
  • In this way, the higher percentage means that you can be more confidentthat your results are within that interval (range of numbers).
  • In order to interpret a CI for statistical significance, you must understand the type of statistics that are being used (for example, an odds ratio).
  • The boards will not ask you how to do a statistical calculation of the Confidence Interval. They might expect you to know that the CI and the p-value need to add up to 100%.

NEUROLOGY

Can you clarify the difference between congenital and transient myasthenia gravis?

  1. Congenital MG– this is a very rare non-immune form of MG that is inherited as an autosomal recessive disease. This means that both males and females are equally affected and that two copies of the gene, one inherited from each parent, are necessary to have the condition. Symptoms of congenital MG usually begin in the baby's first year and are life-long.
  2. Transient neonatal MG– between 10 and 25 percent of babies born to mothers with MG may have a temporary form of MG. This occurs when antibodies common in MG cross the placenta to the developing fetus. Neonatal MG usually lasts only a few weeks, and babies are not at greater risk for developing MG later in life.
  3. Juvenile MG– this auto-immune disorder develops typically in female adolescents – especially Caucasian females. It is a life-long condition that may go in and out of remission. About 20 percent of MG cases are juvenile-onset.
  • The following are the most common symptoms of myasthenia gravis. However, each child may experience symptoms differently. Symptoms may include:
  1. Babies with neonatal MG may be weak, with a poor suck, and may have respiratory difficulty. A few babies may need the help of a mechanical breathing machine if their respiratory muscles are too weak to breathe on their own. Symptoms go away as the maternal antibodies disappear over time.
  2. Congenital MG symptoms may begin in the first year, with generalized weakness in the arms and legs, and delays in motor skills such as crawling, sitting, and walking. Babies may have difficulty feeding and may have weak eyelids and poor head control.
  3. Juvenile MG symptoms may begin gradually over weeks or months. The child may become excessively tired after very little activity and begin to have problems chewing and swallowing. Drooping eyelids may be so severe that the child cannot see.”

For ataxia telangiectasia, where do the telangiectasias typically present?

  • Usually begin in the eyes between three and six years of age and may spread to the eyelids, face, ears, roof of the mouth and possibly other areas of the body.

https://rarediseases.org/rare-diseases/ataxia-telangiectasia/


How can you differentiate between tick paralysis and Guillain-Barré Syndrome (GBS)?

  • Some of this may be differentiated in the interview by understanding what preceded the neurologic symptoms. For example, GBS may be preceded by a viral prodrome and tick paralysis may be preceded by an outdoor excursion. The timeline of symptoms is also very important. Tick paralysis can present within hours to days of the tick bite, while GBS may not present for weeks after the prodrome.

ORTHOPEDICS AND SPORTS MEDICINE

pg 378 – There is a sentence “This could be the farthest away from your joint” in regards to the epiphysis – I think it means to say “closest” to your joint.

  • The Epiphysis is the end of the bone so it can be either the closest or furthest away from the joint in question.

https://medical-dictionary.thefreedictionary.com/epiphysis


RHEUMATOLOGY

No Clarifications! But the 2019 Pediatrics Board Review Study Guides Will Likely Have New Content (Or Clarifications).


PULMONOLOGY

On the test – how can I differentiate between ABPA and Staph pneumonia in a CF pt if both look nodular on xray? I feel like the patients will present the same way??? Would the CF pts also worsen despite appropriate treatment like the asthmatics?

  • To clarify, in ABPA, you’re dealing with Aspergillosis, which is a FUNGAL infection. Staph will give you a bacterial pneumonia. ABPA will not respond to antibacterials. ABPA will also ONLY have nodular opacities in an immunocompromised Staph pneumonia typically does not have a nodular appearance. Hopefully the above helps.

PBR’s 2017 edition states that meconium aspiration can result in patchy areas of diffuse atelectasis. It says:

“Do not intubate and suction below the cords in a baby that is non-vigorous. Instead, warm, dry, stimulate and provide respiratory support if needed. The most common complication is persistent pulmonary hypertension.”

Does the above statement mean that you should NOT intubate and that you should NOT suction below the chords? Or, does it mean that you should not intubate and but that you should suction below the chords?

  • Great question. The guidelines have changed, as have the recommendations in the latest edition of the Pediatrics Board Review Core Study Guide. Please see the NEW recommendation below on page 401 of PBR, 2018 edition! But, in short, suctioning has not shown any benefit, and you should only intubate if there’s respiratory distress.

(DOUBLE TAKE) MECONIUM ASPIRATION SYNDROME (MAS): Meconium is rarely passed in utero before 34 weeks. Do not intubate and suction reflexively if there is Meconium Stained Amniotic Fluid (MSAF). Suctioning has not proven to provide any benefit. Intubation should be reserved for those showing signs and symptoms related to respiratory distress (labored breathing, hypoxia and bradycardia). Newborns showing evidence of respiratory distress within 15 minutes of birth, or those with APGAR scores of < 8, are at greatest risk for developing Meconium Aspiration Syndrome (MAS) requiring ventilatory support. The most common complication of MAS is persistent pulmonary hypertension. Vigorous newborns with APGAR scores > 9 rarely require ventilatory support (warm, dry and stimulate if needed).


On page 276 it says for a patient with CF that most common pneumonia pathogens are S. aureus or Pseudomonas which has been my clinic experience. However, on the OVC the speaker says it’s still pneumococcal pneumonia. Any consensus on which is correct?

  • The 2018 PBR book is correct on this point. Staph or pseudomonas are the most common cause of pneumonia in patients with Cystic Fibrosis. The role of Strep pneumoniae in Cystic Fibrosis children is debatable as it is not usually a colonizer. Therefore, in children with Cystic Fibrosis the correct answer would be given to you by paying close attention to the specifics in the vignette as either Pseudomonas (lung abscess) or Staph (nodular pneumonia).

PEARL: The answer may be revealed on an X-ray they show you. Read carefully and make sure that you correctly answer the question that they are asking. This is a common pitfall for people taking the pediatric boards.


PSYCHIATRY AND SOCIAL ISSUES

No Clarifications! But the 2019 Pediatrics Board Review Study Guides Will Likely Have New Content (Or Clarifications).


ETHICS

No Clarifications! But the 2019 Pediatrics Board Review Study Guides Will Likely Have New Content (Or Clarifications).


PATIENT SAFETY AND QUALITY IMPROVEMENT

No Clarifications! But the 2019 Pediatrics Board Review Study Guides Will Likely Have New Content (Or Clarifications).

AWESOME! YOU’RE DONE! – WHAT NOW?

  1. Read the PBR “Exam Day” article. It’s a MUST read. It will give you a great deal of insight into your exam day. I’ll list the link at the end of the document.
  2. Go back to your core PBR study material! At the end of the day, THAT is what will help you pass the boards.
  3. If you’re not a PBR member yet, this is a GREAT time to join!
  4. If you’re feeling pretty good about your pediatric KNOWLEDGE/CONTENT, then work on your TEST-TAKING STRATEGY by going through the CRASH COURSE on Test-Taking Strategies (it has been a HUGE HIT)!

IF YOU ARE NOT A PBR MEMBER, YOU SHOULD BE!

PBR has had streaks as long as 3 years in a row of 100% pass rates for general pediatricians who are first-time test-takers of the ABP recertification exam.

PBR also has an estimated pass rate of well over 95% for first-time test takers of the ABP initial certification exam (based on the insanely low number of requests we get for the 100% Money Back First-Time Pass Guarantee that we offer).

Also, the “PBR Certification System” has helped pediatricians pass the boards after they had FAILED UP TO SIX TIMES using other resources. That means they failed SIX times, and then passed on their LAST possible chance because they finally decided to use the PBR!

So What Are YOU Waiting For?

All Access Pass

Pediatrics Board Review…

YOUR RESOURCE FOR EFFICIENCY IN STUDYING…
ESPECIALLY DURING CRUNCH TIME!

As the final days of preparing for the initial certification exam come up, there’s often a sense of PANIC. Please BREATHE! If you’ve been studying the PBR thoroughly and you have a fair handle on your test-taking skills, you should be in GREAT shape!

What can you do to MAXIMIZE your remaining study time? Go over your PBR over and over again. Focus on the areas that you still need to master and SKIP the areas that you know well.

Get the DOWNLOADABLE MP3 audio course from PBR so that you can eat, sleep and breathe PBR no matter where you are. Yes… even between seeing patients!

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You can also WATCH 31 videos that cover ALL of the PBR through PBR’s Online Video Course, Conference & Live Webinars in a single day!

Pediatrics Board Review Online Video Course - Like a DVD Course

www.PediatricsBoardReview.com/VIDEOS

You’ll get chapter videos PLUS our webinar replays for the 2017 Summertime Q&A Webinars.

For the Acid Base chapter, I’ve even included a short impromptu practice question session as well as additional practice questions for our Online Video Course and All Access Pass members to enjoy. The Acid Base discussions and resources show how confused pediatricians are about the delta delta, when to check for compensation, Winter’s formula, etc… but by these talks and practice sessions, we get comments like, “This is so much easier!… The light bulb just went off!”

www.PediatricsBoardReview.com/VIDEOS

And if you want to CRANK THROUGH the videos and webinars in just 12-14 hours, you can do so at different speeds by clicking on the gear icon at the bottom of the video and increase the speed up to 2X!

Okay! That’s it!

Now go study in whatever way is going to give you the MOST REPETITION AND LEARNING. If that’s simply reading over and over again, GREAT!


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===


HAVE YOU FAILED?

If you have failed while feeling as though you had a strong handle on the content, it’s likely that you have a test-taking technique issue. Reach out to us and ask about our Test-Taking Strategies course which covers test-taking skills, test-day planning, anxiety management, diet and much more. We also offer LIVE coaching courses

www.PediatricsBoardReview.com/STRATEGIES

Lastly, don’t forget to read some excellent information about your exam and how you should structure your big day. The article below is a MUST read, so please click the link below and take 5 minutes to read it:

www.PediatricsBoardReview.com/EXAMDAY

Alright guys… Team PBR has worked VERY HARD this year to help you with the tools and guidance you needed to prepare for the boards. If you followed our lead, then I’m sure you’re going to rock your exam! Trust me, if I can do it… so can you!

Best of luck on your board exam.

Sincerely,

Ashish & Team PBR

2017 PEDIATRIC BOARD EXAM RESULTS ARE ENLIGHTENING
Ashish Goyal, M.D.
 

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