All right. Well, good morning, everyone. We're going to get started in just a little bit.
If you don't mind, if you're just joining us, going ahead and opening up your chat box and saying hello. Would love to know where everybody is from. I'm just going to change the chat box setting so that you all can interact and engage with me.
Excellent. Wonderful. We have so many people logging in. We have Ahmad from Texas, Anna from New York, Tulwani from Nigeria, Stephanie from New York, Carolyn from Naples. Thank you all so much for joining.
We'll get started in just a little bit. And please note that. today's session is a very special session because it's going to be a nice preview to my comprehensive pediatrics rapid review webinar for shelf and step 2ck. I'm going to be going into detail as to what that course entails, but I did want to put the link to sign up if you're interested.
And if you want to preview the curriculum, feel free to scroll down on the page. And that's going to be in mid-May where we're going to be going through. pediatrics in a more comprehensive manner. But we're going to get started in just a few minutes. I'm so glad you are here.
And if you're just joining us, if you don't mind opening up your chat box, saying hello, where you're logging in from, that would be absolutely awesome. Wonderful. Christine from Connecticut, Mabel from North Carolina, Ty from Vietnam.
I love how we have a global audience today. This is great. Francis from Philippines, Maria from New York. Excellent.
get started in just about a minute or so. And to my YouTube family, thank you guys for tuning in on YouTube. If you're just joining on YouTube, feel free to say hello into the chat box. We have a full house classroom.
Appreciate you guys joining as well. And again, if you are just joining, welcome to today's session. I'm very excited to get started in just about a minute or so, but if you don't mind going ahead. and saying hello in the chat box and where you're logging in from.
That would be awesome. Please keep your chat box open throughout the duration of today's session, because my goal is to make you guys very active and engaged as you all are going to be preparing with me. Wonderful.
Jacqueline from Pittsburgh's here, Vaishnavi, Cedric. Excellent. All right. Well, let's go ahead and get started with today's session.
Welcome to each and every one of you. Today, we are going to be covering a topic that is near and dear to my heart, a topic that I am a little bit biased to that is probably the best topic out there, and that is going through the top NBME. shelf concepts for pediatrics. This session is going to be very high yield.
If you're preparing for your M3 clerkship exams, if you're in dedicated study or preparing for USMLE Step 2 CK, or even your comp or CBS essays, I am very excited to go through pediatrics with you today in an active recall and integrated manner. If this is your first session with HiGuru and joining one of my YouTube lives, I just want to give you a warm welcome to all of you who have been to prior sessions. Welcome back.
My name is Rahul. I'm currently a practicing pediatric critical care physician, very interested in medical education. And particularly, I have developed a passion for USMLE step one and step two CK preparation.
There's my email if you need to reach me, I will try to do my best to get back. to you, but just wanted to introduce myself. So I did want to spend just a few minutes telling you why my project, HiGuru, is just super unique.
HiGuru is a very strategic, active learning approach to USMLE Step 2CK. And when it comes to USMLE Step 2CK, here are the pillars that I really base my content and sessions on. Number one, I really focus on active recall and vignette-focused learning. Secondarily, I focus on integrating amongst different organ systems, and you will see that today. The other pillar that I really like to focus on is test-taking strategy.
I am going to highlight some of the key test-taking strategies today as it relates to pediatrics. And what I want you all to do is take those test-taking strategies and keep those in mind as you're going through your question banks. as well as practice and BMEs. And then finally, as you can see, I'm super pumped and excited and so should you.
But more importantly, I like to create this safe learning environment. And as you progress in your education, I like to make sure that you have peak test-taking psychology so you can perform on test day and beyond. Most importantly, and I am so grateful to have so many of you joining me today, Thai Guru has... really become over the past five years, a lifelong community of learners. And I'm excited that, you know, we were able to go through a lot of step one content this year and these next couple months, I'm going to be focusing on step two CK.
And eventually I'll be trying to get through all of the relevant content that you need to know for your exams, as well as becoming a developing clinician in whichever field you go into. Here's just a little bit of a snapshot of some of the students who I've worked with in the last year or so. Very proud and, you know, again, very excited that you are joining me today.
As I'm ramping into the Step 2 CK sessions, I did want to highlight first what I find as the key differences between Step 1 and Step 2. You know, Step 1 is all about mechanisms, mechanisms of disease, mechanisms of normal homeostasis. Step 1 questions. usually are going to be diagnosis focused as well as mechanisms.
And they will really assess your understanding as to what's the underlying etiology that kind of triggers the whole pathophysiologic cascade. Step two CK, as you all know, is a little bit more clinical. And it focuses on questions such as what is the most likely diagnosis? What is the next best step in management? And what are the underlying risk factors that are going to be behind?
this patient's condition. Now, what I want to really emphasize is that The way I teach Step 2CK is it's actually a build on the Step 1 material. And what you'll see is you'll see a lot of basic science integrations. And one of the key integrations that I'm going to really emphasize is symptomatology to basic science mechanism.
Because once you understand how a symptom relates to the why, the physiology behind it, so to say, then you are able to really capture diagnostics, as well as therapeutics. I do want to start out with a little bit of a inspirational boost and want to let you know that my goal today is to take you from the learning zone and push you just a little bit so that you are able to grow in your content knowledge, in your integration, in your study practice, et cetera. Because remember that we are all going to have ups and downs throughout our lives, throughout. our careers in medicine and in studying.
And the definition of grit is going challenge to challenge without losing any enthusiasm. All right. I do want to let you all know that today is a free preview session.
It is going to be covering concepts in a more high level manner. And we are going to be going through all of the comprehensive concepts and in a little bit more depth with an emphasis on test taking and vignettes. on May 13th, where I'll be hosting my comprehensive rapid review USMLE Step 2CK Pediatrics review. I'm going to go ahead and put the link in the description and I'll answer any questions you may have at the end of today's session, but feel free to check out the curriculum, which I drafted. And as soon as you register, you'll get a detailed curriculum as well as a handout shortly before the session.
But I am excited for us to get started. without any further ado. So if you are ready to get started, go ahead and type in yes into the chat box.
All right. Hey, Emma. Hey, Ridley. Hey, Cedric. Excellent.
Everybody is pumped and ready to get started. I do want to let you all know that over the next hour, hour and 15 minutes, I would highly encourage you to put away any distractions, make sure you are staying active and engaged. I want you all to interact with me in the chat box, answer some of the questions, and I will be doing a live Q&A at the end.
So feel free to write down any questions you may have as we go through this presentation. Just as a big picture, as we are reviewing pediatrics, one of the key test-taking strategies, high level for pediatrics, is that Pediatric questions frequently test congenital, whether it's embryologic or metabolic abnormalities that affect multiple organ systems. So it is not uncommon for you to get a vignette with symptomatology from many different organ systems.
So I'm going to build on that in this slide. So anytime in a USMLE vignette, you see multi-organ involvement, you want to really categorize that. for pediatrics as either a congenital condition or a syndromic condition.
And remember that whenever you see multi-organ involvement, when you have maybe an older child, you want to be thinking of systemic conditions, conditions that are going to pervade throughout all organ systems. For example, hematologic abnormalities, because blood flows through all organ systems. Infectious disease, remember you could get a question.
in a sickle cell patient who has fever, hypotension, tachycardia, multi-organ failure, high lactate, and you're worried about strep pneumosepsis. And then finally, you are going to be thinking about inflammation, autoimmune diseases. Those are going to be systemic pathologies that can give you multi-organ involvement in your vignette as well as in your labs.
So one of the key... Test-taking frameworks that I want to build on now is the fact that whenever you see a syndromic pathology, you want to pay particular attention to the growth percentiles in your USMLE vignette. Specifically, you want to identify when the child is not growing or when the child is having decreasing growth percentiles or is falling off the growth curve.
This indicates that there's a supply and demand issue when it comes to nutrients, as well as energy. Either the child is not taking too much in. Or there is some sort of syndromic condition in which the child is going to be burning so much that they are going to have failure to thrive. Something for you to really conceptualize in pediatrics, growth percentiles.
One of the most common chief complaints that you're going to be getting on your shelf, as well as Step 2CK, is going to be the cyanotic newborn. Now, when you're thinking about a cyanotic newborn, you got to put it into two buckets. The first bucket is going to be thinking about congenital heart disease, all of your T's. So for example, truncus arteriosus, transposition of the great vessels, tricuspid atresia, tetralogy of fallot, total anomalous pulmonary venous return. These neonates are going to particularly present in your question with central cyanosis.
Now, you may also have a child who has an underdeveloped left ventricle, and signs of poor perfusion systemically. And that is going to be known as hypoplastic left heart syndrome. We're going to be going into this in a little bit more depth in the subsequent slides, but this is just a big picture. The other big bucket that I would like for you to think of is going to be respiratory causes. Now, respiratory causes could be anything from parenchymal and surfactant issues, such as neonatal respiratory distress syndrome.
Watch for the gestational age being less than 35 weeks. It could be a fixed anatomic issue, such as tracheosophageal fistula. Watch for the patient who is having unable to pass the NG2. It could be some sort of pathophysiologic process, such as pulmonary hypertension.
The pulmonary vasculature doesn't relax, and the patients are going to look pretty sick on your exam with cyanosis. as blue blood shunts across the patent ductus arteriosus, or it could be some sort of infectious cause such as pneumonia. Remember, neonatal pneumonia is going to be due to three organisms just to tie in step one stuff, E.
coli, GBS, and listeria. One of the ways to differentiate these two buckets is to recognize that when you have cardiac pathologies that have right to left shunts, they are bypassing. the lung circulation. And as a result, intracardiac right to left shunts are typically going to be unresponsive to oxygen supplementation because the blood flow is not going through the lungs and there's no gas exchange at the alveolar capillary interface.
So with that, let's go ahead and go through our first question today. A three-month-old girl is brought to the emergency department due to episodic cyanosis. She becomes irritable and sweaty. while being fed, and her lips appear blue for a few minutes during feeding. Similar incidents have resolved quickly.
The patient was born at 38 weeks gestation, and weight gain has been slow. She's at the 10th percentile for weight. Her vital signs, temp of 37, blood pressure 78 over 48, heart rate of 155, and respiratory rate of 50. On examination, the infant appears unwell, agitated, cyanotic.
and tachypneic. Cardiac auscultation reveals a grade two out of six crescendo-de-crescendo systolic ejection murmur at the left upper sternal border and a single heart sound. The patient is promptly placed in a knee-to-chest position.
What is the mechanism by which this maneuver alleviates this patient's condition? Go ahead and put your answer into the chat box. A, decreases PDR. B, increases SVR.
C, decreases preload. D, increases preload. What do you think is the best answer here?
Wonderful. If you are thinking B, you're absolutely correct. Remember that this patient with episodic cyanosis is most likely going to have episodic decreases in pulmonary. blood flow because of tetralogy of Fallot.
So remember that the TETs in tetralogy of Fallot are going to be cyanosis during irritability, during feeding, signs of where you can have high pulmonary vascular resistance and obstruction to flow distally. Remember that when you put the patient in a knee to chest position, that is going to increase the systemic vascular resistance. It is going to take the...
right to left shunt and reverse it to left to right, and then optimize your pulmonary blood flow. Tetralogy of Fallot is probably one of the highest yield congenital heart diseases that is tested on your USMLE step two. Where do you think the murmur will be heard?
And that is going to be at the left second intercostal space. And that is going to be right at the pulmonic valve. Remember, one of the four pathologies that is in Tetralogy of Fallot is pulmonic stenosis. What you will also hear is a harsh holosystolic murmur at the parasternal border. Go ahead and try to identify those on your pericordium.
This is going to be representative of the VSD. And remember, the VSD in Tetralogy of Fallot is typically right to left. And that's why blue blood is going into the systemic circulation.
And Tetralogy of Fallot is thus a cyanotic heart disease. Now, in Tetralogy of Fallot, there is a characteristic. EKG and x-ray finding. The EKG finding is going to be the right axis deviation. And that's because you are going to have pulmonic stenosis that is going to cause right ventricular hypertrophy.
The right ventricle has to work so hard to get the blood across the stenotic pulmonary valve. So it's going to undergo hypertrophy and thus on your x-ray, because of that RVH, you are going to have a shift of the heart and On x-ray, you are going to see a boot-shaped heart, and that's a characteristic buzzword, so to say, for Step 2CK and Tetralogy of Fallot. So let's dive into this concept a little bit deeper. Remember that the four things in Tetralogy of Fallot, I like to remember the mnemonic P-R-O-V, pulmonic stenosis that causes the right ventricular hypertrophy.
You have a overriding aorta that is going to... expose a VSD. Now, because the right-sided pressures can be higher than the left-sided pressures, you're going to get right to left shunting.
So what is the mechanism by which squatting relieves the cyanosis? Just as a little bit of a space repetition, remember, it is going to increase your SVR, and that is going to cause you to have more left to right shunting. And as more blood is going to be in that right ventricle, hopefully you are going to get more blood flow.
to the pulmonic circulation, and subsequently you will have a relief of your cyanosis. All right, let's go ahead and go through our next question. A two-month-old girl presented with fair to thrive and decreased weight gain from the 50th to 10th percentile. The patient is exclusively breastfed, takes one hour to feed, and sweats during feeds. On physical exam, a grade three out of six systolic murmur is heard at the lower left sternal border and the liver edge is palpated five centimeters below the right costal margin.
What is the likely diagnosis? So as you can see, this patient is going to have failure to thrive. And with that murmur, you should be thinking, okay, it's fair to thrive due to most like some sort of congenital heart failure. And in this case, the heart failure is probably due to this systolic murmur that is heard right at the area of the VSD.
This is going to be a persistent VSD that is now causing over-circulation and signs of heart failure. Signs of heart failure in pediatrics, sweating with feeds, diuresis with feeds, slow to feed, tachypnea with feeding. as well as decreasing weight.
Now, when it comes to pediatric heart failure and over-circulation, the way to think about it is that you are going to get chronic left to right shunting. So blood is going to go from left ventricle into the right ventricle, and that is going to happen over time. Because now there's so much blood going to the right ventricle, there's going to be more blood that is going to go to the pulmonic circulation. And as a result, what can happen is you get increased pulmonary capillary hydrostatic pressure, and that can cause transudative effusions that are going to be going into the alveoli.
And you can also get rising pulmonary vascular resistance because of the increased flow. This is where over time, if you don't correct a VSD, for example, not only can you get heart failure, but you can get Eisenmenger syndrome, where you can... go from a left ventricle to right ventricle.
physiology and switch it to a right ventricle to left ventricle physiology. And this is primarily due to the fact that you have over-circulation and pulmonary hypertension that is acquired. Now, as you can see in this schematic, we see that in a VSD that is unrepaired, you are going to get left to right shunting over time. that is going to go directly into the pulmonary trunk. And eventually that can cause increased pulmonary capillary hydrostatic pressure and can cause you to have over-circulation that will manifest as both cardiac as well as pulmonary symptoms.
All right. So now what we're going to be doing is a quick little rapid review of the other cyanotic heart diseases. Let's go ahead and go through some.
key vignette features. And I want you to participate with me when I say to see what you think the diagnosis is. All right.
Infant born to gestational diabetic mom, there's a loud P2 and egg on string appearance on chest x-ray. What do you think is the best answer here? Go ahead and put it into the chat.
Excellent. If you're saying transposition of the great vessels, you're absolutely correct. Remember, this is where you are going to have the aorta come out of the right ventricle and the pulmonic veins, or excuse me, pulmonic arteries coming out of the left ventricle.
Decreased pulmonary blood flow, RV hypoplasia, right atrial dilation. This is going to be tricuspid atresia. Remember that an atretic tricuspid valve is going to cause you to have a backup into the right atrium. Hypocalcemia, absent thymic shadow, loud S2, and VSD murmur.
What do you think is the best answer here? Excellent. I did give a syndromic appearance here. As you can see, multiple organ systems, right? You see electrolytes, you see...
the immune system, cardiac. This is going to be your truncus arteriosus when you're thinking about the loud S2 and the VSD murmur and the syndrome that it's related to is 22Q11 deletion, which is degeorge. Pulmonary edema, respiratory failure, and the snowman sign. This is going to be your total anomalous pulmonary venous return. Now in total anomalous pulmonary venous return, The pulmonary veins have a mind of their own.
They are not going to be going into the back of the left atrium. Remember, normally pulmonary veins drain into the left atrium, but sometimes in total anomalous pulmonary venous return, the pulmonary veins go back to the cable circulation or the pulmonary veins go infra diaphragmatic into the hepatic circulation. All in all, this is a bad sign.
because all of that blood backs up into the lungs, you get engorgement, pulmonary edema, respiratory failure. And because of a backup of that blood, say in a supra diaphragmatic total anomalous pulmonary venous return, you are going to have the snowman sign, which is this bulge right above the left ventricle, left ventricular hypoplasia and poor systemic perfusion. This is going to be.
hypoplastic left heart syndrome. Typically in hypoplastic left heart, you have an underdeveloped left ventricle. You also may have mitral atresia where your mitral valve is not going to be forming correctly. And thus you are going to be in great need of an ASD as blood is going to go from right atrium to right ventricle through the pulmonic circulation, left atrium, but then it can't go down.
So what it's going to do is shunt across the ASD and then try to go systemically via the ductus arteriosus. This is going to be an example of the egg on a string heart that is characteristic of your transposition of the great vessels. This is going to be characteristic of the snowman sign when you're thinking about total anomalous pulmonary venous return. Now, if I asked you, here are the cyanotic heart disease, and you have a question of a one day old who presents with any of these, what would be your next best step in management?
Go ahead and put that into the chat. What would be your next best step in management for these cyanotic heart diseases? Excellent. You got it. If you said prostaglandin infusion, you're absolutely correct.
Remember, PGE2 keeps the ductus arteriosus open. And sometimes to optimize systemic blood flow, you are going to need... prostaglandins to keep that ductus arteriosus open.
All right, we're going to pivot and talk about bronchiolitis. Now, bronchiolitis, you want to think about a patient on your USMLE that is going to be an infant less than two years old that presents in the winter months with increased work of breathing and diffuse wheezing as well as runny nose. That is a classic illness script.
for bronchiolitis. And remember that these patients are going to have respiratory distress. How do you recognize respiratory distress in pediatrics?
You're going to have things such as nasal flaring, head bobbing, suprasternal retractions, belly breathing, intercostal retractions. These are all of the manifestations that they put in the vignette in the physical exam. So go ahead and type into the chat.
What is the morphology of the most common etiology behind bronchiolitis? What do you think? Yeah, exactly.
RSV. And RSV is going to be a paramyxovirus. And remember, RSV is an enveloped, linear, single-stranded negative RNA virus. Please note that bronchiolitis can be caused by many viral organisms.
RSV is the most common. And what you can get is a interstitial infiltrate with herihylar, heribronchial thickening, indicating that this is a viral interstitial process. Let's go ahead and go through this question.
A neonate is born at 28 weeks gestation. He is on home oxygen for chronic lung disease of prematurity. What preventative health measure would decrease hospitalization?
of bronchiolitis in this patient. And this is going to be administration of palovizumab. Now, palovizumab is going to be a monoclonal antibody against the F protein, which is a key virulence factor in RSV.
All right, let's get ready for our next question. An eight-year-old male presents with persistent cough for the past eight weeks. Mother states that he wakes up in the night with the dry cough.
He has been afebrile. There is a family history of seasonal allergies in the father. What are the pulmonary function tests likely to show? So this is going to be a patient who is going to have chronic cough and chronic cough with especially nighttime awakening.
and a family history of ATP should make you be thinking of asthma. And remember, I want to ask you two-step thinking questions. In asthma, you're going to be seeing an obstructive lung disease pattern on your PFTs. You're going to get a decreased FEV1 as the air cannot come out of the lungs, and you're going to get air trapping in obstructive lung disease. And that's why your total lung capacity is going to be elevated.
At times, to really diagnose asthma, you are going to trial albuterol and see if your PFTs are going to improve pre and post albuterol. So albuterol is prescribed. However, the patient continues to have activity limitation every week and persistent nighttime cough.
What is the next best step in management? Go ahead and put that into the chat box. What is the next best step in management here? Excellent.
And the answer is going to be inhaled corticosteroids, which could be fluticasone, mometasone. Remember to note that there are questions where a child with asthma is going to have inhaled corticosteroids, and they love for you to know that it can cause a local immunosuppression as well as a hot, arid climate. in which they can get oral thrush secondary to candida.
So some of the preventative guidelines that we give patients who are on inhaled corticosteroids is to make sure they brush their teeth before and after. And if you do have thrush, the treatment of choice is going to be Nystatin in a swish and spit formulation. All right, let's go ahead and go through this vignette.
An eight-year-old male with persistent asthma on inhaled corticosteroids presents to the emergency department with acute exacerbation of symptoms of cough. shortness of breath, and chest tightness. Physical exam reveals wheezing and decreased breath sounds, and chest x-ray is negative for a focal infiltrate, which means the patient doesn't have a pneumonia.
What is the next best step in management? Well, before you manage a patient, you want to think of your working diagnosis, and this could be status asthmaticus. Remember that when it comes to acute asthma exacerbations, You want to relieve the bronchospasm.
That's the pathophysiology. So I actually like this mnemonic, asthma for acute asthma exacerbations. A is going to be standing for albuterol.
ST is going to be standing for steroids. Remember, these are going to be systemic steroids, not the inhaled steroids. H is humidified oxygen.
M is going to be magnesium. especially in severe cases, magnesium bronchorelaxis. And the last eight are anticholinergics like ipratropium.
Typically we give albuterol plus ipratropium in these acute flares. All right. Before going on to the next question, just want to ask you all, are you all learning something?
Go ahead and type in yes into the chat box. Everybody good? Excellent. You guys are doing wonderful.
I really appreciate your engagement. I mean, we have over 100 people here today and really grateful. Let's go ahead and dive in to our next vignette.
You all are doing wonderful. All right, here we go. A four-year-old boy with a history of asthma is brought to the clinic for persistent coughing and wheezing for the past seven days. It began at a friend's birthday party last Saturday. His mother states that initially his albuterol inhaler was helping.
However, now he persistently coughs with activity and at rest. He has no fever or upper respiratory infection symptoms. Exam notes end expiratory wheezing in the right middle lobe. Skin exam shows stable atopic dermatitis.
Chest x-ray is normal. Which of the following is the best next step in managing this patient? A, bronchoscopy, B, steroid course, C, increased inhaled corticosteroid, B, ipratropium combined with albuterol, or E, IV clindamycin. What do you think is the best answer here?
Excellent. If you're concerned about a foreign body, you're absolutely correct. Some of the key things to note is the fact that There may have been an acute trigger. The patient is persistently coughing and it's refractory to albuterol.
There is a lack of infectious symptoms. And if you had an asthma exacerbation, typically you'll have wheezing bilaterally, whereas here you have focal wheezing. Now, this patient has a normal chest x-ray, but remember that there are foreign bodies that are going to be radiolucent. And If your index of suspicion is still high, you want to proceed with bronchoscopy.
So A is going to be your best answer. Excellent. Very good.
The next topic that we're going to be diving deep into is foreign body ingestion. Now, when it comes to foreign body ingestion, you really want to be aggressive because these can be life-threatening. Let's go ahead and go through this vignette. A toddler presents with cough.
He is otherwise asymptomatic. A chest x-ray is shown. Examination shows stable vital signs with no difficulty in breathing.
So he's Jay Chillon. What is the next best step in management? Well, as you can see, here's a radio opaque foreign body, and it has two rings on it or a double halo.
And this is very concerning. for a button battery. And remember, for a button battery, you want to do emergent endoscopy, ASAP, and removal of the battery.
Why is that? Because the alkaline charge of the battery can cause esophageal erosion, ulceration, and so much inflammation that you can get fistulas with either the airway or even the aorta. So the key here is to recognize that the severe complication is esophageal erosion that can progress to a fistula and bronchoscopy is your next best step in management on your exam.
Whenever you have button battery ingestion, magnet, sharp item, even if the patient is asymptomatic, and that's very important for us to note. All right. So this whole concept of upper airway obstruction helps us integrate a very important physical exam finding, and that is going to be the approach to stridor. Now, when it comes to stridor, stridor is going to be. a sound primarily heard on inspiration and stridor is going to signify upper airway obstruction.
So the couple buckets that I want you to keep in mind here are congenital causes of stridor, acquired causes, and other. So congenital causes, you could get this vinyin, a six-month-old healthy male with stridor that is louder, supine, and softer when on the belly or prone. And this is going to be classic for laryngomalacia. These patients are going to have a squeaky, squeaky sound when they are going to be supine.
Management is growth. You could also get this congenital cause, a six-month-old male plus biphasic stridor plus a port wine stain in the trigeminal nerve distribution. This is going to be classic for Sturge-Weber syndrome. And this could be nevus flemmi that they are describing.
But at times when you have a vascular malformation on the face, you could have vascular malformations such as airway hemangiomas in the upper airway, and that can cause you to have stridor. Acquired causes are going to be the following. A six-month-old ex-preemie baby who is going to present.
With prolonged intubation in the NICU and now with stridor, prolonged intubation can give you subglottic stenosis. And that subglottic stenosis can cause you to have persistent stridor. A six-month-old male with URI symptoms, fever, barky, harsh cough, and stridor. What do you think is the likely diagnosis here?
Go ahead and put that in the chat. Excellent. That barky, harsh cough is going to be croup due to parainfluenza virus.
Now, the key here is to note that when you have stridor at rest with croup or laryngotracheal bronchitis, you want to give racemic epinephrine and corticosteroids such as dexamethasone. A six-year-old male with sore throat drooling, difficulty breathing, a recent strep infection, a muffled voice, and now stridor. This is going to be characteristic, especially with the recent strep infection of a peritonsillar abscess. These patients can also present with retropharyngeal abscess.
In a retropharyngeal abscess, the patient may even have a little bit of head extension. Speaking of acute causes of stridor, let's go ahead and go through this one. A six-year-old unimmunized male with sore throat, drooling, tripodding. This is going to be your, you got it, epiglottitis. And remember, epiglottitis, this is going to be a airway emergency.
So these patients need to be emergently taken to the OR and intubated. with anesthesia. And then you are going to have a two-year-old male with acute onset unilateral hyperinflation on chest x-ray. That is what we've talked about, and that is foreign body. Remember, foreign bodies can present with wheezing, can present with stridor.
The key here is to note the asymmetry and the acute onset of those respiratory symptoms in the absence of any upper respiratory. runny nose, cough, congestion type of things. Excellent. I hope that this was helpful. Again, this is a little snapshot of what we are going to be tackling in our May 13th webinar as well.
All right, let's go ahead and keep going. A two-year-old previously healthy male is brought to the emergency department due to sudden onset rhythmic movements in all four limbs. This lasted about three minutes. He was unresponsive during the event.
Upon initial evaluation to the ED, he was drowsy. The patient has had rhinorrhea for two days and fever since this morning. Immunizations are up to date and there's a family history of epilepsy.
Temperature is 40.3 centigrade. Physical exam shows a child with clear rhinorrhea. The neck is supple.
Labs show normal serum glucose and sodium. The rest of the exam is normal. Just want to highlight, these are called pertinent negatives.
This ruled out meningitis. This is not a metabolic etiology that's causing the seizure-like symptoms. And the rest of the exam is normal. After administering antipyretics, what is the next best step in management? A, non-contrast head CT.
B, lumbar puncture. C, reassurance. D, EEG. Or E, blood culture.
What do you think is the best answer here? Excellent. If you're saying reassurance for a simple febrile seizure, you are absolutely correct. All right. So let's go ahead and differentiate simple febrile seizure from something a little bit more scary, meningitis and encephalitis.
So with simple febrile seizures, typically you are going to have a patient who is going to be six months to five years of age in your vignette. They have a fever in the vital signs and the generalized tonic-clonic seizure was short-lived less than 15 minutes. Typically, it's a one-time event in the first 24 hours, and you are again going to have a symmetric and generalized tonic-clonic semiology. Now, if it's focal, if it's prolonged, if it's recurrent, if it's outside of this age range, you would be worried about a complex febrile seizure, and that may require further evaluation. Now, you may also get vignettes.
related to fever plus seizure, and they want you to go down the route of meningitis and encephalitis. So how do you differentiate? Well, first off, in the HPI, neonates typically are going to present with lethargy, poor feeding, and bulging fontanelle.
A child or adolescent may have the classic meningeal signs, such as neck stiffness. Now, when it comes to the diagnostics, you will see that these patients are going to have a lumbar puncture that has a positive gram stain, and they're going to have WBCs that are going to be elevated in the CSF. Now, if it's more neutrophils, think about bacterial meningitis. If it is going to be more lymphocytes, think about your viral encephalitis.
Remember that encephalitis is a little bit of a deeper inflammation or infection, and that's why encephalitis can have the neck stiffness stuff, but characteristically has altered mental status as well. as plus or minus seizures. Remember that there's a classic encephalitis vignette on HSV encephalitis, which is going to have a temporal lobe enhancement on your imaging. So here is the quick approach to seizures.
I like to break this down because this is a common chief complaint you may get on your pediatrics question. Think about febrile seizures, which we covered. Think about infections, which we also alluded to, metabolic etiologies, such as hyponatremia, hypoglycemia, vascular etiologies, such as any sort of hemorrhagic stroke, subdural, epidural, et cetera, traumatic causes.
And then finally, you are going to have structural causes, which are any congenital brain malformations, as well as even brain tumors. that can cause seizures. All in all, this is not an exhaustive list, but it helps you bring forth a differential so that then you can narrow down to a correct answer.
All right, let's keep going. A 14-day-old girl presented to the physician for a well-child exam with a five-day history of looking yellow. She was born at term.
and has been breastfeeding. And sorry, if I said 14-year-old, it's a 14-day-old. I apologize.
All right. So she is jaundiced and she's been breastfeeding. Her stools have been light brown per mother.
On physical exam, she has generalized tan skin and scleral icterus. Her total bilirubin is elevated at 13, direct component of 8.8, with an indirect component of 4.2. The urine analysis is negative. What is the next best step in management? So here you are going to have a patient who is going to have poor feeding and specifically is going to have jaundice.
Now, when it comes to jaundice and this clay colored stools, you want to pathophysiologically say that bile is not being excreted into the intestine. And this is very characteristic of. biliary atresia.
So you want to get an abdominal ultrasound, which will show in biliary atresia, absence of the gallbladder, and paucity of bile ducts. And remember that biliary atresia presents with a direct hyperbilirubinemia, and that is very key in exam questions. So here is a very good test-taking tip. If you see jaundice on your shelf, think about hepatobiliary causes as well as hemolysis, very high yield for you to know.
If you are going to have more hepatobiliary causes, you're going to be thinking about LFT as well as your bilirubin issues. And in hemolysis, it's primarily going to be an anemia, so low hemoglobin, and you could even have an indirect hyperbilirubinemia. So if you have not checked out my NBME labs breakdown video, it's on my YouTube channel.
I would... highly encourage you to take a look at it. What I want to go through are the gallbladder tree labs.
And what got us into this integration is the direct hyperbilirubinemia in our question. So there are three labs that say that the gallbladder is messed up, a high ALK-FOS, a high indirect bilirubin, or a high direct bilirubin. When you see a high ALK-FOS, not only should you think about the biliary tract.
but you should also be thinking about bone turnover. Indirect hyperbilirubinemia could be prehepatic, could be hemolysis, and could also be intrahepatic. Say that you're going to have a patient with cirrhosis, such as with alpha-1 antitrypsin deficiency or Krigler-Najjar syndrome, in which they can't conjugate the bilirubin.
And then also direct hyperbilirubinemia, you want to be thinking about some sort of obstruction, either post-hepatic There's some sort of cholestasis. Again, this is post-hepatocyte conjugation. Maybe there is going to be a stone in the common bile duct causing choledocholithiasis, or even pancreatitis as the stone is going to be dislodged right near the pancreatic duct.
What's very high yield for pediatrics is to note that direct hyperbilirubinemia could also be due to, again, congenital causes. Dubin-Johnson and Roter syndrome. are two causes of direct hyperbilirubinemia in neonates.
And remember that in Dubin-Johnson, you characteristically have a black liver on your gross appearance of the liver. Whereas in Rotor, that's how you differentiate it. There is no black liver.
All right. An 18-month-old female is brought to the office for routine examination. The child has been developing appropriately with adequate weight gain. Diet is consisting primarily of whole cow's milk, which is greater than 25 ounces per day, as well as cheese and yogurt. Immunizations are going to be up to date.
There is a family history of beta thalassemia. Mucus membranes on exam are pale and a flow murmur is appreciated across the percordium. Lab findings, hemoglobin is low. MCV is low, platelets and WBCs are normal. Given these findings, what is the likely lab abnormality to be seen in this patient?
All right, go ahead and put your answer into the chat box. Is it A, elevated indirect bilirubin? B, Coombs positive? C, schistocytes on smear? D, elevated RDW?
Or E, low haptic liven? So in this case, the patient has physical exam signs of anemia as well as a flow murmur. also has laboratory evidence of a microcytic anemia and excess amount of cow's milk. And with that, you want to be thinking of iron deficiency anemia, which characteristically gives you an elevated RDW. And that's kind of what differentiates it from thalassemia, the elevation in RDW.
So what is the pathophysiology of cow's milk causing iron deficiency anemia? Well, First off, a lot of cow's milk in children greater than one year of age can cause you to have irritation of the GI tract and a slow microscopic GI bleeding that can lead to your iron deficiency anemia. Cow's milk in and of itself is low in iron.
So if there is high dietary intake, you are predisposed to iron deficiency anemia. And then finally, Excess amount of calcium from the cow's milk. And again, these children are drinking so much milk that excess amount of calcium interferes with iron absorption. Speaking of nutrition, I'm going to be going through a quick little rapid fire of some of the breastfeeding vignettes you're going to see on your exam. Let's go through this.
A young infant with dry patches of skin in the flexural regions, spit ups. and painless bloody stools. So this patient has a little bit of ATP, is having feeding intolerance, painless bloody stools.
You're worried about food protein-induced proctocolitis. The management here is maternal diet modification. She may have to, if she's breastfeeding, abstain from any lactose or soy-containing foods. And the baby, if they're formula-fed, could be put on a very elemental or hydrolyzed formula.
What about this one? A one week old breastfed infant, poor feeding, delayed capillary refill time, jaundice, and brick red urate crystals in the diaper. So this is going to be very characteristic of breastfeeding jaundice.
And remember that your bile acids and bile salts are going to undergo increased enteroepatic circulation because of the poor feeding. And in breastfeeding jaundice, what you want to do is optimize breastfeeding. And if you are going to get a increased total hyperbilirubinemia, these children may need phototherapy while the lactation consultant is working with mom to optimize breastfeeding. A two-week-old breastfed infant with asymptomatic jaundice and a normal exam. Well, this is not breastfeeding jaundice.
This is breast milk jaundice. And the mechanism in breast milk jaundice is the beta glucuronidase in breast milk actually deconjugates intestinal bilirubin. You also have a little bit of enterohepatic circulation that is going to be behind the mechanism of breast milk jaundice.
So please note that the time period is really important to differentiate feeding versus milk jaundice. And I like to be thinking of this mnemonic. FM radio.
And so FM radio, that is going to tell us that feeding is first and then milk is second. What about this one? A breastfed infant with jaundice, hepatomegaly, cataracts, and gram negative sepsis or E. coli sepsis.
And this is going to be very characteristic against systemic pathology of galactosemia. In galactosemia, you have an aldolase B deficiency. So you can't break down glucose into galactose and excuse me, and glucose, but in particular, you can potentially break down the lactose.
But what is very challenging for these babies with the aldolase B deficiency is they cannot break down the galactose. And that's very high yield for you to note because the treatment is to reverse this pathology by having the child. not take any sort of lactose-containing products.
And in particular, there are very few contraindications to breastfeeding, but in terms of a metabolic contraindication to breastfeeding, you need to know that galactosemia is a contraindication. All right, let's go ahead and keep going on. A five-year-old girl is brought to the clinic for evaluation of fever and painful urination.
The fever started two days ago and she cried while urinating yesterday evening. Ibuprofen alleviated her fever and pain, but she began vomiting this morning. Her medical history includes a febrile urinary tract infection at 14 months, which resolved after antibiotic treatment. A renal and bladder ultrasound at that time was normal. Her temperature is 39.1.
Calpation reveals suprapubic and left CVA tenderness. Urine analysis. shows positive nitrites and leukesterase.
Urine culture, excuse me, grows gram-negative rod. A repeat renal bladder ultrasound is normal. Which of the following is the next best step in managing this patient? And I apologize for this typo here. A, CT of the abdomen pelvis, D, reassurance, C, daily antibiotic prophylactic therapy, or D.
a VCUG, which is a voiding systourethrogram. Excellent. If you're saying D, voiding systourethrogram, you are absolutely correct.
Please note that this patient has a recurrence febrile UTI. Even though... structurally, she has no signs of scarring. You have a high index of suspicion of what pathophysiologic mechanism. This is highly tested vesicle uretero reflux.
So what is that? This is where you are going to have P refluxing up to the kidney from the bladder. So from the bladder, vesicle uretero reflux.
The management is very important here. So let's say you have a vignette with a child less than two years of age who presents with the first febrile UTI. What is the next best step in management?
Well, this child is young, has a febrile UTI. You definitely want to get a renal ultrasound. And if that renal ultrasound shows any sort of abnormality, you're going to get a functional test, which is the voido voiding cystourethrogram to see how the P is traveling.
If The child is going to be greater than two kind of potty training age. You don't need to get imaging for febrile UTI. And remember, a big risk factor for children greater than two who present with UTIs, one of the risk factors is constipation, and that's high yield for you to know.
Now, say you have a recurrent febrile UTI, which was in our vignette. What is the next best step in diagnosis? And that is going to be ultrasound.
as well as VCUG. In your ultrasound, you want to look for hydronephrosis, a dilated ureter, any scarring of the kidney. And in a VCUG, you want to see whether or not there's retrograde reflux during micturition or peeing. With vesicouritorial reflux, yes, you may need surgical treatment, but these patients may be placed on long-term prophylactic antibiotic treatment with nitrofurantoin or amoxicillin.
So I did want to go through a quick little mechanism of disease and differentiate some vignettes. Remember that the first step when you're thinking about the urinary tract, the first pathophysiologic step to think about is colonization, in which maybe STI or gut bacteria that translocated to the urethra can cause you to have a urethritis, but then that can ascend into the bladder. Now, this whole concept of ascension is really important when you're talking about the urinary tract because it integrates a key basic science concept. And that is typically of E.
coli having that P. lie that is going to cause attachment and penetration and eventual ascend into the kidney. And in the kidney, once you have an infection there, you're going to have very systemic symptoms, fever, nausea, as well as costovertebral ankle tenderness. So in cystitis, you get suprapubic tenderness with a little less systemic symptoms, whereas in pylo, it's fever, nausea, and CVA tenderness, which is going to be with the palpation of the back.
A seven-year-old male with history of focal segmental glomerulosclerosis presents to the emergency department with acute onset, frothy, blood-tinged urine, swelling, and abdominal pain. Physical exam reveals bilateral lower extremity edema and abdominal distension. Laboratory studies show hypoalbuminemia, proteinuria, and elevated serum creatinine. The urine analysis is notable for hematuria and proteinuria.
Doppler ultrasound of the abdomen is ordered. What is the likely diagnosis? Go ahead and put that into the chat. A nephrotic syndrome patient with acute onset abdominal pain. What do you worry about?
Excellent. Wonderful. If you are going to be thinking about renal vein thrombosis, you're absolutely correct. And the USMLE loves to go for this because essentially what they want you to know is that when a patient has nephrotic syndrome.
they lose an endogenous anticoagulant, antithrombin 3, and that predisposes them to have hypercoagulability. So anytime you see acute symptoms with a patient who's going to have nephrotic syndrome, think about Virchow's triad, hypercoagulability, and in this case, renal vein thrombosis. So our patient had hematuria.
And what I want to do is I want to integrate a test-taking framework on... when you need to be thinking about glomerular causes of hematuria or non-glomerular causes. So glomerular causes, you're going to have microscopic hematuria, RBC cast, because they form with the tubule. What you want to integrate are pathologies such as PSGN or IgA nephropathy. In PSGN, electron microscopy shows subepithelial humps.
And because it's an immune complex deposition, C3 is low and immunofluorescence is positive. IgA nephropathy could have a prodrome of upper respiratory symptoms and sore throat, but typically within two weeks, they get hematuria and characteristically on labs, you have a normal C3 level. Now, basement membrane disease is also going to be a cause of glomerular hematuria, and that's Alport syndrome, where you have a basement membrane defect and these patients have hematuria as well as deafness. Now, non-glomerular causes, this is where you could have gross hematuria.
You may have normal appearing RBCs. You definitely won't have any casts. And in the case of nephrolithiasis, you may get dysmorphic RBCs. So what are some pediatric differentials? Well, you could be thinking of a kidney stone, polycystic kidneys, as well as a non-glomerular cause of hematuria could be renal papillary necrosis.
And this is typically going to be seen in sickle cell patients. as they are going to get sickling in the medulla of the kidney and sloughing off of that tissue. A 16-year-old female with a history of sickle cell disease presents with extremity pain. This is her fifth admission this year for this similar presentation.
She has a history of a blood culture that grew strep pneumonia, and she has admitted for management of her pain. On hospital day one, she now has inability to speak, and weakness in a right upper and lower extremity. The CT of the head is negative.
Which of the following is the best next step in management? Go ahead and put that into the chat. A, hydroxyurea, B, sumatriptan, C, morphine, D, blood culture and antibiotics, E, exchange transfusion, or F, IV anticoagulation. And I want everybody to participate.
You all are doing great. Please go ahead and put your answer into the chat box. Excellent.
Well, this patient, sickle cell plus focal neurological deficits. It's a medical emergency. This is a sickle cell stroke, sickling in the cerebral vasculature.
No bueno. So you want to get the bad sickle cells out and put good ones in. And so the answer is just going to be exchange transfusion.
So what are some indications of exchange transfusion? Well, we're going to get to that in just a little bit, but I did want to do a quick little systems-based integration of the complications of sickle cell disease. What's really high yield, and we're going to be covering this in our May 13th comprehensive review, are the systemic conditions, cystic fibrosis, sickle cell, lupus, Down syndrome, et cetera. So let's go through the sickle cell disease complications in a...
multi-system way. All right. CNS, sickle cell plus altered mental status.
We talked about sickle cell stroke. Respiratory-wise, these patients can have increased PVR due to sickling, pulmonary hypertension, which causes a high afterload to the right ventricle and signs of right heart failure or coropulmonoly. Say your sickle cell patient had fever and a new chest x-ray finding.
You're worried about acute chest syndrome. From a GI standpoint, these patients can have pigment gallstones because of the chronic hemolysis. From a renal standpoint, these children are going to have renal papillary necrosis as they're sickling in areas of the kidney that have low oxygen tension.
MSK wise, remember that if you have a sickle cell patient with bone pain and fever, think osteomyelitis due to salmonella. And then from an infectious disease standpoint, these patients are asplenic, and this is super high yield for you to know. And as these patients are anatomically or functional asplenic, they have increased risk.
of infection from encapsulated bacteria, such as strep pneumo, neisseria, hemophilus. So you definitely want to vaccinate these children with the PPSV23 and PCV13, which are the pneumococcal vaccines. So I'll do a quick little rapid review to solidify this.
Sickle cell plus extremity pain, that's going to be dactylitis. Sickle cell plus groin pain, remember, sickling. near the hip vasculature, you're going to be thinking about osteonecrosis of the femoral head.
Sickle cell plus echocardiogram showing tricuspid regurg. This is going to be the pulmonary hypertension. Remember, if you have high pulmonary vascular resistance, the blood can jet backwards from the right ventricle into the tricuspid, through the tricuspid. Fever plus new infiltrate on chest x-ray. That's your acute chest.
Fever. plus difficulty walking. That's your osteomyelitis fever plus hypotension plus tachycardia in your sickle cell patient. That's going to be strep pneumo sepsis. And then finally focal neurological deficit plus sickle cell.
That's your stroke. And that's where we talk about the indications of exchange transfusion. You're taking out the waste blood and you're putting in the donor blood. So what are indications for RBC exchange? Well, sickle cell stroke, acute chest syndrome with severe hypoxemia and respiratory distress, and then also priapism in a sickle cell patient, which presents as a painful erection.
All right, we're almost done. We're going to continue on going through this question. A one-day-old female neonate is brought to the pediatrician for evaluation of jaundice. The mother reports that the baby was born at 39 weeks gestation via spontaneous vaginal delivery without any complications.
The pregnancy was uneventful and prenatal care was adequate. Mother has blood type O, while the baby's is determined to be A positive. The neonates vital signs are stable.
Her weight is appropriate for her age and on physical exam, she is alert. active and is breastfeeding well. The neonate appears jaundiced, predominantly in her face and extending to the chest.
The remainder of the physical exam is unremarkable. Laboratory findings reveal the following, a low hemoglobin, a high indirect bilirubin, and a COOMS that is positive. What is the likely diagnosis? Go ahead and put that into the chat. A, RH incompatibility.
B. DIC, C, sickle cell trait, D, ABO incompatibility, E, cricular nechar, or F, hereditary spherocytosis. So the best answer here is going to be ABO incompatibility.
Please note that when the mom has blood type O and baby is A positive, you are going to really have a high index of suspicion that they're testing you. on ABO incompatibility. These patients usually have mild jaundice, but in severe cases, they may need RBC exchange.
This is an autoimmune process, so your COOMS is going to be positive. And remember, it's not RH incompatibility because that typically is going to be in an O negative mother. We're going to pivot and integrate a very important chief complaint in pediatrics, and that is ear pain or otalgia.
The two areas of focus in your diagnostic schema, it could be true ear pain or it could be referred pain from a non-ear cause. So let's go through this. Your ear pain could be due to foreign body, could be due to otitis media, or it could be due to otitis externa.
And we're going to differentiate that in just a sec. Your non-ear pain causes could be tooth pain, like for example, an abscess or maybe even teething. It could also be due to pharyngitis, such as from group A strep, or it could be in an older patient, TMJ.
Now, what is high yield for us to know is if they're going to test you on strep pharyngitis, they want you to really recognize that the absence of a cough really is an important criteria for group A strep pharyngitis. Also, on exam, you're going to have it. exudative tonsillitis, but I want you to recognize that if they have URI symptoms and they are going to have a cough, typically you're going to be dealing with a viral pharyngitis rather than a bacterial pharyngitis.
All right. So when it comes to otalgia, we want to differentiate otitis media with otitis external. So otitis media, fever, plus ear pain, you're going to have an ear exam that is going to show a bulging tympanic membrane, dull tympanic membrane, and limited movement on pneumatic otoscopy because behind the tympanic membrane, there's infection.
Complications could include mastoiditis, watch for on your exam, protrusion of the ear and painful posterior auricular tenderness. You could also have conductive hearing loss and that is an important complication with recurrent otitis media. Management for otitis media is you want to cover strep pneumo, non-typable H flu, and moroxella. So you're going to be using Amox, or if you're worried about resistance, you are going to be thinking of combining it with a beta-lactamase inhibitor, which is Amox clav.
Otitis externa, you want to think about the risk factors. Diabetics. Those who are immunosuppressed, maybe children who are going to be swimming. Remember, this is primarily due to pseudomonas. And you're going to have in severe cases, pain on manipulation of the tragus.
And that is very characteristic along with an occlusion of the ear canal because it's the external part. And so sometimes there could be so much edema there. And at times what you'll have to do is not only treat with ciprofloxacin drops, but you may have to put a wick in or some cotton in.
to get that antibiotic into that external ear canal. All right. We're going to close today by going through a systems-based integration of the neonate. This is one of my favorite ways to teach. And that is taking the neonate, for example, remember less than 28 days and going through all of the exam questions that could be related to the neonate.
All right. Are you guys ready to do this? Go ahead and type in yes into the chat box. Everybody pumped to get this done with today?
All right. You guys are doing wonderful, awesome, and amazing. Keep up the great work, and I'm so glad that you are interacting.
Active learning is so important, and we have gone through a lot of questions so far, so this is great. All right, here we go. So neonate with the red eye.
You want to be thinking, especially if it's within a week, with purulent discharge, gonococcal conjunctivitis. The treatment is going to be systemic ceftriaxone. And remember, we prevent gonococcal conjunctivitis with erythromycin eye drops. If it's later on, say seven to 14 days, and you have watery mucopurulent discharge, you want to be thinking about chlamydial infection of the eye. So I remember the mnemonic GC, that gonococcal comes before chlamydial.
And the treatment is going to be a macrolide systemically. Now, say you have a neonate who failed the hearing test on your vignette. You're going to be thinking about torch infections, CMV.
These patients may have microcephaly as well as periventricular calcifications, rubella, syphilis, as well as HSV. Metabolic abnormalities, they can say that the patient has a pending newborn screen. or a newborn screen that is abnormal.
And what you want to be really looking at is the blood gas. Because these children may actually have a underlying metabolic acidosis or some sort of metabolic derangement. So these are usually your biochemical enzyme deficiencies.
So think about if the child is going to have hypotension, hyperkalemia, ambiguous genitalia, elevated 17-hydroxyprogesterone. You're going to be worried about congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Hypoglycemia. with no ketones, this could be a fatty acid oxidation defect, a medium chain acyl dehydrogenase deficiency. Now, remember, an absence of ketones means that you don't have good counter-regulatory response, which means you're not probably breaking down fatty acids, and thus you don't have ketones.
Finally, if you're going to have a child with poor growth, recurrent infections, and decreased T receptor excision circles on your newborn screen, That means they don't have good T cells. So you may be worried about SCID. And remember, these patients could have bacterial, fungal, and viral infections.
What do you think about with lethargy and bulging fontanelle? Well, if they have a bulging fontanelle, I think of increased intracranial pressure. Could that be due to a hemorrhage? Remember, a premature baby with a hemorrhage, you should be thinking about germinal matrix hemorrhage. Could it be due to a vitamin K deficiency?
Say that they said that the baby was born at home, for example, so didn't get vitamin K. Remember, then your clotting factors are not there. And as a result, you are predisposed to bleeding and hemorrhage. Finally, you're going to be thinking about infectious etiologies.
Remember to cover those children for E. coli, GBS, and listeria with ampicillin and cefotaxime or ampicillin and gentamicin. All right.
let's go ahead and go through this. Neonate with jaundice. Remember that jaundice within the first 24 hours is always pathologic.
You want to be thinking of Krigler-Najjar. You want to be thinking about RH incompatibility or some severe form of hemolysis. If it's going to be within the first week and the baby is asymptomatic, think about physiologic jaundice. And then we go into our breastfeeding and breast milk jaundice.
which we did cover and time period is so important. The hip abnormalities, you're going to be thinking about a baby who was breached and maybe they had a C-section because of breach positioning. But then on physical exam, you see positive Ortolani as you manipulate the hip and asymmetric creases in the inguinal region.
In this case, you want to be worried about congenital dysplasia of the hip. And what you want to do is recognize that under four months, you're going to do a hip ultrasound, whereas greater than four months, you have better ossification. So to assess, you need an x-ray. So think of the four-month cutoff and then ultrasound younger and older x-ray.
Let's say that they give you a neonate who was just born. This may even be on your OB shelf. You're going to be thinking about your APGARs, which are...
the scores that you are going to calculate right after the baby is born based on appearance, pulse, their grimace, their appearance and activity, as well as their respirations. Now, what is important for us to note is that Apgars are not prognostic. They are going to require, or they are going to, excuse me, guide your next best step in resuscitation.
What do you need to do? If the Apgar is poor, say that the baby has bradycardia or is not breathing as well. You want to do positive pressure ventilation, get them to breathe more.
And if their heart rate is still less than 60, you may even have to do compressions. But an Apgar less than seven typically guides your next best step in management. What are some of the conditions that you are going to be thinking of reassurance? Reassurance?
Well, any time a newborn is born, we expect that their weight is going to add decline from their birth weight, typically in the first 10 days, no more than 10%. So in that situation, you would reassure. You would reassure if the baby is losing weight and then regains it back at two weeks of life. And you would reassure if there is a newborn girl on your exam that presents with mucoid vaginal discharge. And this is high yield for you to know, because what they want you to know is that the maternal estrogen after birth is kind of declining and withdrawing.
So they could have a physiologic period. The neonate could have some sort of bleeding from the vaginal canal. All right, what about eye abnormalities?
Well, if you see decreased light reflex, you're worried about things such as cataracts. So what are some pathologies that can cause cataracts? Well, you're gonna be thinking about rubella. We talked about galactosemia. You can also get leukochoria, which is indicative of an oncological lesion known as retinoblastoma.
Also remember that children who are going to be premature and who are going to be in the NICU with high oxygen for their lungs, they can get neovascularization of their eye and retinopathy of prematurity. Now, one of the other neonatal conditions that you want to be thinking of is the failure to pass an NG tube, so a nasogastric tube. And in this situation, if you have difficulty passing a nasogastric tube, you may be thinking, could there be coanal atresia or a membrane? behind the nose that is causing difficulty to pass it? Could it be due to a tracheoesophageal fistula where you are going to have esophageal atresia and you are going to have coiling in the mid thorax?
You could also have an NG tube that then loops into the left side of the neonate's chest. And that is going to be characteristic of congenital diaphragmatic hernia. And the USMLE would look like this.
wants you to know that these patients could have pulmonary hypoplasia. Now, failure to pass meconium is another important question that they give you or a thought process that they assess. And that means that the baby is not pooping within the first two days.
This could be due to Hirschsprung's disease, or it could be due to meconium ileus. In Hirschsprung's, you diagnose via a rectal suction biopsy. in her springs, remember that there is an association with which genetic condition that is going to be down syndrome. Now, meconium ileus is going to be related to cystic fibrosis. You have this mucus, thick, thick mucus that is going to be at the terminal ileal junction.
And you're going to be thinking of doing an air or gastrograph and enema, which could be diagnostic and therapeutic. Also, what's another cause of failure to pass meconium? Well, If you have anal atresia and that anal atresia or imperfect anus could be associated with other congenital genetic disorders, such as bacterial syndrome.
All right, let's go through this NBME style question. An infant presents for routine examination. Exam is notable for a raised red 2.5 centimeter lesion on the scalp with.
fine telangiectasia surrounding the lesion. The patient is afebrile and the lesion is painless. What is the next best response to the family?
Excellent. I'm seeing a lot of great answers. And if you're saying reassurance, you are absolutely correct.
Typically the next best response, and these could be quotes in your answer choices, is that for the strawberry hemangiomas, this is a benign rash. and the rash will actually grow before it spontaneously involutes. In some cases where it's cosmetically challenging or there's true obstruction to the vision, you may use topical or systemic beta blockers.
All right. So I do want to kind of close with some of the neonatal skin rashes. One of them is erythema toxicum neonatorum.
This is going to be small red macules and papules with. surrounding erythema at the base. They are going to be located on the trunk as well as proximal extremities.
You could also get a congenital dermal melanocytosis. This is characteristically known as Mongolian spots. And Mongolian spots are basically going to be due to melanocytes that are entrapped in the dermis and causing you to have hyperpigmentation in, for example, the buttocks region. Now, you're...
differential diagnosis, whenever you see bruising in the rear end, is going to be non-accidental trauma or child abuse. So documentation is so key here. And then if you have a port wine stain and a trigeminal distribution, you're going to be thinking of nevus flemius.
And they typically say sharp demarcated port wine rash. This is associated with Sturge-Weber syndrome. So you may need to get a skull. x-ray that shows the tram track calcification.
You may also be worried about other airway vascular lesions, such as a vascular ring or a hemangioma of the airway, which we talked about when we were talking about stridor. So the test-taking tip for a majority of these neonatal rashes is that the next best step in management is usually going to be reassurance. We're going to end today by talking about developmental milestones.
Now, rather than me just putting up a table of developmental milestones and just reading it to you, what I'm going to do is I'm actually going to be thinking about it as a continuum or a timeline, and we're going to be covering gross... and fine motor. And I'm going to tell you what are the ones that they actually like for you to know for your exam. So here is a timeline and you can see two months all the way to five years. And what we're going to be covering are the gross motor.
And think about this as, okay, they're going to walk before they run. They're going to think about it as a continuum. Okay.
All right. So what we're going to be covering now are developmental milestones, gross motor from two months to five years. All right, here we go.
So number one, around two months to four months, you're going to start lifting your head. You're going to get really good head control at around four months. The baby is going to start to roll.
Remember premature rolling may be due to hemhypertrophy or increased hypertonia say in, for example, a cerebral palsy, or you can have Beckwith-Weidman syndrome. Afterwards. At around six months, the baby sits up. So I remember six months sits up.
At around nine months, the baby is going to start to crawl. And then 10 to 11 months, they're going to start to cruise furniture. Before at one year old, they're going to take their first steps independently.
Eventually, the baby at around 18 months or so is going to be able to run. And then. you are going to be thinking around two years old, they are going to slowly start going up the stairs. At around three years old, you're going to be thinking of the baby being able to ride a tricycle, so three and tricycle. And then at four to six years of age, they're going to be able to hop and skip and do a little bit more of the advanced gross motor tasks.
Let's- change the timeline a little bit and talk about fine motor development. So in fine motor development at two months, you're going to track past the midline, whether it's the head or the, the hands by four months, they're going to bring the hands to the midline at six months. They're going to start to reach for things, but it's going to be very primitive. It's going to be nonspecific. So a raking grip, and then eventually they're going to start getting.
better find motor control. They can hold sippy cups. At one year of age, they're eating those small little cereals or rice puffs with a fine pincer grasp. At two years old, they're going to start drawing a line. So I like to say two points to a line.
And then they're going to start drawing some shapes. So at three years old, they'll start drawing a circle. At around four years old, they'll start drawing an X. At four and a half or so, they're going to start drawing a square with their last shape that they can draw that takes a little bit more finesse is a triangle. So the mnemonic that I like to use is this PlayStation mnemonic.
So if you've heard of a PlayStation controller or seen one, you note that they have different shapes. So if you're going to start at the three o'clock position, pretend it's a clock and go clockwise. At three years old, circle. At four years old, across.
At. four and a half, you're going to be thinking about a square. And then at five years old, you're going to be thinking about a triangle. This mnemonic is really helpful. And remember, the USMLE makes it very obvious developmental abnormalities.
So when it's like kind of a gray zone, think about just reassurance, unless it's egregiously incorrect. All right. This is going to be our final question for today. A six-year-old girl is brought to the office by her parents due to concern about her speech.
She is talkative and has an expansive vocabulary. However, she consistently mispronounced words and greater than 25% of her words are unable to be deciphered. She was hospitalized as an infant with strep pneumo meningitis, but otherwise is healthy.
Height and weight have been consistent at the 30th percentile. When given a crayon and paper, the patient confidently climbs into the examination table and writes her first name. Tympanic membranes are clear bilaterally.
the remainder of the physical exam is normal. Which of the following is the best next step in evaluating this patient? What do you think is the best answer here? Excellent.
And if you are going to be saying, get a hearing test, you're absolutely correct. Remember, hearing test is key in patients who have a history with bacterial meningitis. as well as patients who are going to have recurrent otitis media.
And we talked about that. And this was just a little bit of a space repetition. All right, everyone.
Well, I just want to say from the bottom of my heart, thank you so much for attending. And if you don't mind sticking around for a couple minutes, I'm going to give you guys some exciting announcements. Don't forget, I'm going to put it in the chat box.
Please don't forget for... signing up for the comprehensive webinar. The comprehensive webinar is going to have a very unique curriculum that's different than the topics that we went through today.
It's going to go a little bit deeper, a lot more test-taking strategies, a lot more topics in a more active recall way with diagnostic schemas. So please feel free to sign up. I'm going to keep it a very, very small class so we can learn all together in a small group setting.
In this class, we are going to really dive deep into every single organ system so that you can integrate the highest yield vignettes for shelf, step 2CK, as well as even comp exams. I'm going to be in future sessions going through clerkship by clerkship, the highest yield vignettes that you will see on your exam, as well as on your practice assessments. So please stay tuned.
This is a true passion project, and I'm so glad you're here with me on this journey. Finally, I am going to be placing, and I would love for you guys to just spend just two minutes writing a review. If you are writing a review, I'm going to be putting your name into a raffle, and I will be selecting one student to complimentary be a part of my... comprehensive pediatric rapid review session on May 13th.
So I would love your honest feedback. The link to write a review and be considered for the raffle and the scholarship is going to be in the chat box right now. You can also Google High Guru Trust Pilot, especially if you're watching this at a later time, feel free to just write a review. Give me what you liked and what I can do to optimize your learning even more. I would love for each of you all to connect with me in any way.
You know, High Guru is all about you. You as a student, developing clinician, developing physician. And so tag High Guru on Instagram, subscribe to my YouTube, share it with your friends, post on Reddit, whatever can get the word out would be so, so humbling to me because I hope that it is helping your learning as you go throughout these videos. If you have not already, I am going to be growing my YouTube Step 2CK playlist.
It's not just rote reading slides. As you can see, I put a lot of effort into this because I want to construct your knowledge in a very unique way. So I have approached to labs and radiology thus far, but make sure you favorite this.
Make sure you share it with your classmates. And with that, I'm going to end today. Thank you all so much.
And before you leave, just type in one thing you learned or any questions you have. I'm going to stick around for some questions that you may have in the chat box. And I will see you in the next session.
Happy studying.