1. Interesting news about mechanical kidneys currently being developed in the Economist's technology quarterly-- one model, which is basically a tiny wearable dialysis machine, runs diasylate in a coutercurrent flow across a membrane from blood, and then transfers the waste to a solid sorbent, which can be disposed of. In this way requiring much less fluid than a traditional dialysis machine. Another model being developed utilizes the body's heart rate instead of an internal pump, and involves constructing a filter out of layers of silicon alternating with kidney tubular epithelial cells (harvested from kidneys unsuitable for transplant). The advantage of this system is the ability to recover glucose and electrolytes from the filtered blood. Currently, it is not yet in trials in people, and when it is probably will require immunosuppressants still. But it's easy to imagine seeding these silicon filters with harvested stem or iPS cells from the recipient. (Economist)
2. Using an inhaler without a spacer decreases the efficacy by 40-60%
3. Immediately after an albuterol nebulizer treatment, the user's sats will drop due to a V/Q mismatch. Blood had been shunted away from previously hypoxic/non-aerated parts of the lung, and albuterol affects the b-2 receptors in blood vessels before the b-2 receptors in bronchial smooth muscle-- the reperfusion of blood happens before re-aeration of the same part of the lung.
4. The NNT to prevent acute mastoiditis in uncomplicated AOM (i.e. no fevers, otorrhea) is 4800. Antibiotics do not improve pain at 24 hours; the NNT to improve pain at 2-7 days is 20. Antibiotics do prevent tympanic membrane perforations (NNTB: 33) and contralateral AOM (NNTB: 11). However, the number needed to harm for side effects of antibiotics that otherwise wouldn't have happened (diarrhea, vomiting, rash) was 14. The antibiotics were most beneficial for kids under 2 years with bilateral AOM, or with both b/l AOM and otorrhea. Other kids do not benefit. (cochrane review)
5. If you suspect CHF in a child-- look for S3, S4, hepatic enlargement, edema (can be hard to visualize-- look for recent acute weight changes). CHF due to congenital heart disease will often manifest as failure to thrive, poor weight gain, stressful feeding (sweating, panting, increased work of breathing)
6. For MRSA pneumonia: clinda has much better lung penetration than vanc. And it's delicious! Like drinking sugar water. Linezolid works but is really, really expensive.
7. Hematopoietic stem cell transplant is one of the few treatments that have shown to be of benefit in Krabbe's disease; transplants are from umbilical cord blood, either autologous or matched donors. Transplants do not cure the disease, but they do slow the progression/onset of the neurodegeneration. Of note, transplants are generally regarded as most effective before the onset of symptoms. A 2005 study in the NEJM of 22 infants, half who received transplant and half who didn't, showed that at 3-4 years postop, among those who got a transplant before the onset of symptoms, survival was 100% and nearly all had age-appropriate development of cognitive and language skills, although about half showed delays in motor skills. Among those who got a transplant after the onset of symptoms, survival and outcomes were comparable with untreated controls. (NEJM)
8. Steroids do not affect renal outcomes in patients with HSP. 
9. In the winter, bronchiolitis is usually RSV. In the summer, it's more likely to be parainfluenza, rhino/corona, adeno, or influenza.
10. Someone who is very tachypneic may not be able to take PO meds (i.e. steroids)-- they may aspirate.

1. Exudative pharyngitis in a child, think: group A strep, strep pneumo, EBV, adenovirus. Adenovirus also causes conjunctivitis, otitis, gastroenteritis, and hemorrhagic cystitis. If a child does not have any URI symptoms, its more likely to be strep, but if they have any URI symptoms, its much more likely to be viral, and hence antibiotics would not be indicated. Testing for ASO is not particularly useful, since there is a high carrier rate in the general population.
2. The reason for giving high-dose amoxicillin for acute otitis media is to overcome whatever resistance the bacterial strains may carry.
3. The treatment for scarlet fever is bicilin (pencillin g benzathine) a long-acting injectable penicillin. IM, in the gluteus. If you give this, watch them for 30 minutes for an adverse drug reaction: rigors, nausea. The pills (penicillin V) are large, hard to swallow, and taste bad.
4. Otitis externa is associated with pain upon movement of the pinna, and is common after swimming. Cover for pseudomonas. If you're sure its not a ruptured OM, treat with ciprodex drops: ciprofloaxcin + dexamethasone. You don't want steroids in the inner ear.
5. Ruptured tympanic membrane after AOM is not that uncommon: treat with ofloxacin.
6. For nasal congestion in a child, nasal steroids (flonase) are first-line, oral antihistamines (zyrtec) are second-line. You can also run saline through their nose, and then suction it out with a bulb-- the saline loosens up the mucus.
7. Acute liver failure in pediatric populations: think viral hepatitis, wilson's disease, toxins. To track liver synthetic function, follow coags. For this reason, do not transfuse FFP/cryo or platelets in someone who's coags are down unless they have clinically significant bleeding. Use vitamin K as your main/only treatment. In liver failure, gluconeogenesis is the last synthetic function to go.
8. You cannot diagnose (or rule out) Wilson's disease based on serum Cu or ceruloplasmin levels. Serum Cu is not always elevated, and ceruloplasmin is not always low-- in fact, it is an acute phase reactant, so it may be high or normal. Cu+ is toxic to RBCs, so you will get hemolytic anemia in wilson's.
9. Kayser-Fleischer rings are the best way to diagnose wilson's disease: it will be present in 50% of kids with abdominal signs of wilson's, and nearly 100% of kids with neurological or psychiatric symptoms of wilson's.
10. Serum VMA is not a sensitive test for pheochromocytoma. You want to use serum and urine metanephrines and normetanephrines, which have sensitivities in the 95-100% range. Normetanephrines are more likely to be elevated in extra-adrenal pheo.

1. Insulin requirements in a:
-prepubertal child: 0.5-0.7 units/kg/day: half given as long-acting "baseline" insulin such as lantus, and half given as a short-acting "bolus" insulin before meals such as novalog.
-pubertal child: 1-1.2 u/kg/day. Puberty is a time of growth, and sex-hormones also create a degree of insulin resistance.
2. Goal blood sugar: 80-140 in kids (even though non-diabetic kids run 60-100), 200s in babies. You really don't want kids running hypoglycemic, since its such a critical time for brain development/growth, you'd rather run high sugars than low.
3. 1800 rule: 1800/(total insulin daily dose units) = number of glucose units one unit of insulin will drop your blood sugar, if your sugar is over 150. For example, if you are aiming for a goal sugar of 125, and you are currently at 225, and your normal daily dose is 36 units/day, then 1800/36=50, so one unit of insulin will drop you 50 points, so you need 2 units of insulin-- assuming you are not about to eat a meal, in which case you will also need to correct for the sugars you plan on ingesting. This rule breaks down a little at very high blood sugar levels-- insulin is less effective then, and you will need more.
4. If you have ketones in your blood, that means you do not have enough insulin. 
-small amount of ketones: bolus +5% of your total daily dose of insulin on top of whatever correction
-medium amount of ketones: +10%
-large amount: +15%
5. When correcting blood sugars, assuming you have calculated the correct dose of insulin to give, wait 2 hours before checking your sugars again and giving more correction, if needed. Do not give lots of insulin in a short period of time. With insulin, its always better to start lower and titrate up.
6. For emergency fluid resuscitation, it's good to use a short, fat line-- i.e. a jugular venous line, rather than a longer line like a femoral.
7. Diagnosing wheezing in a child:
-Asthma: +viral trigger, +responds to albuterol, +history of atopy
-VIW/RAD: +viral trigger, +responds to albuterol, no history of atopy
-Bronchiolitis: +viral trigger, doesn't respond to albuterol, no history of atopy
8. Usually asthma is not diagnosed until someone is 3-4 years old, because of the frequency of RAD/VIW in children. Generally, kids who just have VIW will grow out of it by age 4-5 That being said, if a young kid has been hospitalized more than 4 times in the last year for wheezing/difficulty breathing and they have a personal of atopy and a family history of asthma, they need BID inhaled corticosteroids whether you want to call it asthma or not.
9. Most common causes of headache in pediatric populations: migraine/tension headaches, ICP (2/2 tumor/bleed), pesudotumor cerebri
10. Sunscreen needs to be applied 15-60 minutes before sun exposure because it needs time to form a protective film across your skin.

1. 2012 IgNobel prize for neuroscience went to Craig Bennett, Abigail Baird, Michael Miller, and George Wolford [USA], "for demonstrating that brain researchers, by using complicated instruments and simple statistics, can see meaningful brain activity anywhere — even in a dead salmon." From the poster:
Subject. One mature Atlantic Salmon (Salmo salar) participated in the fMRI study. The salmon was approximately 18 inches long, weighed 3.8 lbs, and was not alive at the time of scanning.
Task. The task administered to the salmon involved completing an open-ended mentalizing task. The salmon was shown a series of photographs depicting human individuals in social situations with a specified emotional valence. The salmon was asked to determine what emotion the individual in the photo must have been experiencing.
Analysis. Voxelwise statistics on the salmon data were calculated through an ordinary least-squares estimation of the general linear model (GLM). Predictors of the hemodynamic response were modeled by a boxcar function convolved with a canonical hemodynamic response. A temporal high pass filter of 128 seconds was include to account for low frequency drift. No autocorrelation correction was applied.
Results: A t-contrast was used to test for regions with significant BOLD signal change during the photo condition compared to rest.... Several active voxels were discovered in a cluster located within the salmon’s brain cavity (Figure 1, see above). The size of this cluster was 81 mm3 with a cluster-level significance of p = 0.001.... Out of a search volume of 8064 voxels a total of 16 voxels were significant.... Identical t-contrasts controlling the false discovery rate (FDR) and familywise error rate (FWER) were completed. These contrasts indicated no active voxels, even at relaxed statistical thresholds (p = 0.25).
Moral of the story: when working with fMRI data, generously apply robust statistical methods to reduce false positive findings!
2. There is not enough work for vets-- the current estimate is that supply exceeds demand by the equivalent of over 11,000 full time jobs. (NPR)
3. A meta-analysis in the british medical journal of 72 RCTs (total n>10,000) trying to determine the effects of IV iron vs oral iron/placebo. IV iron more effective in increasing Hgb and reducing risk of transfusions (esp when given with epo or in patients with baseline low ferritin), but also associated with an increased risk of infections. Overall, there was no difference in mortality. I guess anemia of chronic disease really does serve a purpose... evolution wins again. (BMJ)
4. In a dog bite in a child: recently published RCT data shows that given good quality debridement, irrigation, and antibiotic treatment, there is no difference in outcomes between suturing the wound or leaving it to heal by second intention. Cosmetic outcomes are better with primary closing, thus facial wound should be sutured. Time to treatment of <8 hours from bite was associated with a deceased risk of infection. (Injury) Other studies have shown that location on the hand is also associated with an increased risk of infection. Organisms to cover: Pasturella (clinda does not cover, amp does), anaerobes, gram positives from skin flora of victim. First line antibiotic: penicillin+b-lactamase inhibitor (unasyn, zosyn, augmentin). Other options: 3rd gen cephalosporin plus flagyl, floroquinolone plus flagyl, carbapenem monotherapy. Amp/clinda is a good option if you're worried about MRSA, amp covers pasturella and some anaerobes, clinda hits anaerobes gram+ incl MRSA. Don't forget to get clinda sensitivities before you send someone home on it!
5. Cat/human bites in a child: should both be debrided to remove all nidus of infection, irrigated, and left to heal by second intention. Human bites: eikenella is one of the more common organisms that you'll find.
6. Catfact: 89% of cat bites are provoked.
7. Erysipelas vs Cellulitis: Same organisms cause both, treat with amox. Erysipelas are more superficial infections: red, more acute-onset with systemic symptoms. Lesion is less warm, more raised/well-demarcated/clear borders. Often on face, although you can get cellulitis on your face. Cellulitis is deeper, more chronic; in the mid-face area can progress to sinusitis/orbital cellulitis and finally to (rare) cavernous sinus thromboses. Skin infection in an immunocompromised person: think pseudomonas.
8. Neonatal hgb/hct reaches a nadir at 6-8 weeks of life, as lysis of fetal hemoglobin cells begin. At birth, 2/3 of neonatal blood is HgF and 1/3 is HgA. By 4 mos of age, the adult variant predominates.
9. Mammalian bites: 60-90% dogs, 5-20% cats, rest is other animals (raccoon, bats, etc)
10. Increased ICP 2/2 pancytopenia 2/2 lupus: possibly due to microclots decreasing CSF drainage (a-cardiolipin associated with increased risk of clots), or perhaps an increased CSF production in response to severe anemia.

1. LVAD increases overall survival as well as quality of life in comparison to medical management (MM) in patients with NYHA class IV heart failure (REMATCH trial, n=129). LVAD was associated with a 48% reduction in risk of death from any cause; survival at 1 year was 52% in LVAD vs 25% in MM, at 2 years was 23% and 8%. (NEJM)  Another paper doing sub-group analysis of REMATCH trial data showed clear survival benefit in patients receiving inotropic therapy. In patients not receiving inotropic therapy (n=38), survival for LVAD/MM were 57%/40% at 1 year and 22%/16% at 2 years, but the survival differences were not statistically significant (probably underpowered). (circulation) My interpretation is that the benefits of LVAD are clear among people who are very sick (i.e. NYHA IV and inotrope dependent). Among those who are less sick (NYHA class IV not inotrope dependent), LVAD probably still offers a survival benefit, but it is less clear, and must be weighed against the costs (emotional and financial) of going through a big, painful open heart surgery. Note: all-cause mortality includes mortality from complications of LVAD.
2. ECMO use in neonates is associated with sensorineural hearing loss, with a mean incidence of 7.5% (range 3-21%), compared to an overall rate of 1-3% in NICU survivors. This hearing loss is frequently progressive (70%), and delayed-onset (50%). One study (n=111) found the factors associated with an increased risk of developing SNHL after ECMO are diagnosis of congenital diaphragmatic hernia, extended time on ECMO, and extended use of aminoglycosides. (Pediatrics) My interpretation is that ECMO is probably associated with an overall hypoxia, relative to not being on ECMO (ie. having heart and lungs that work), and perhaps the nerve cells of the cochlea are more sensitive to hypoxia than other cells. CDH is associated with lung hypoplasia and sometimes severe hypoxia, so that fits in well, and aminoglycosides are known ototoxins, so that also fits.
3. Factors associated with congenital/neonatal SNHL: 
-Infection: prenatal CMV infection (most common overall cause of congenital SNHL), toxo, rubella, syphillis, bacterial meningitis (s.pneumo, hib).
-trauma: head trauma, temporal bone fracture
-toxin: aminoglycoside, loop diuretic, lead, arsenic, radiation.
-low birth weight (<1500g), apgar scores less than 4 at 1 min and 6 at 5 min, hyperbilirubinemia requiring exchange transfusion
-hypoxia: mechanical ventilation >5 days, ECMO
-stigmata of conditions associated with SNHL: renal abnormalities, craniofacial abnormalities
4. Waardenburg syndrome: partial albinism (white forelock), SNHL, broad mandible.
5. Sandifer syndrome: GERD, hiatal hernia, hypotonia, spasmodic torticollis and dystonia: spasms last 1-3 minutes and occur multiple times a day, sometimes associated with feeding. Can be mistaken for infantile spasms or epilepsy, esp if the GI symptoms are not clear.
6. Mucopruluent drainage from one eye in a neonate, in the absence of conjuncitivitis, with a history of increased tears in one eye: think nasolacrimal duct obstruction, rather than GC/chlamydia (must have conjunctivitis). These things can also progress to infected cysts that require IV antibiotics.
7. Isolated throbocytopenia in a child with a prodome of viral illness (esp VZV, EBV, CMV), think ITP. CBC with diff will reveal normal morphology of platelets and RBCs, and normal levels of other blood cells. If there is a decrease in WBC/RBCs as well, or LAD/splenomegaly, do a BM biopsy to r/o aplastic anemia or cancer. Among people with ITP, 50% resolve in 1 month, another 30% in 6 months. Treatment is to watch them carefully to prevent injury. Pharmacologic treatment is not shown to improve outcomes, and is only indicated if platelets are <20,000, there are severe bleeding symptoms (intracranial- occurs in 1% of ITP, massive GI bleed) or if a safe home environment cannot be guaranteed. Tx options: IVIg, systemic steroids, splenectomy (need lifelong vaccines against strep pneumo). Platelet transfusion only if there is life-threatening bleeding.
8. Drugs that cause decreased platelets: Heparin (HIT), bactrim, quinine, quinidine, cimetidine, benzos, penicillin.
9. Deep brain stimulators are now incorporating recording as well as stimulating functionality, moving closer to the ultimate goal of a closed-loop, self-adjusting stimulator system. (medgadget)
10. Closed-loop insulin management is finally here! A team at the University of Virginia have linked a blood glucose monitor to an insulin pump via smartphone (bluetooth). The first trial enrolled 20 people with type 1 diabetes for 42 hours, and found the system had a 97% uptime. Paving the way for new trials. (c/o medgadget) (diabetes care) 

1. Human sleep cycles are affected by the phase of the moon, even when they cannot see the light: researchers at the University of Basel re-analyzed old data attained during a sleep study where people were kept inside for long stretches of time, and found that people slept worse on nights when there was a full moon, even when they couldn't have possibly been affected by the light since they were inside for days on end. Quote: "Electroencephalography showed that the volunteers slept, on average, 20 minutes less around the time of the full Moon. It also took them five minutes longer to get to sleep, their delta activity (a measure of how deeply they were sleeping) was 30% lower than at other times, their level of melatonin, a sleep-related hormone, was reduced, and they reported, subjectively, that they had not slept as well as usual. Nor was any of this connected, in female volunteers, with their menstrual cycles." (economist)
2. Hep B immune globulin is expensive, so you don't want to administer it to a neonate unless you have positive Heb B serologies from mom during pregnancy. You don't want to give it to every infant of a mom with unknown Hep B status.
3. To determine whether blood is maternal or fetal, you can use the following tests:
-Apt test: generally a test of secreted blood to see if it is maternal or fetal, i.e. 3rd trimester vaginal bleeding to r/o vasa previa (although if you really suspect previa, don't take the time to do this test, run to surgery) or spit-up from a neonate to figure out if its swallowed maternal blood or infant GI bleed (usually brighter red in color). Technique: put blood into tap water to lyse cells. Spin down, take supernatant (where Hb is), add strong base (KOH, NaOH). Fetal hemoglobin will remain red/pink, but maternal hemoglobin will denature to hematin (turn brown-yellow).
-Kleihauer-Betke: a test of maternal blood to ascertain presence of fetal blood cells. Good to determine extent of maternal-fetal transfusion. Strong acid denatures maternal Hb, but not fetal. So smear the blood on a slide, put it in an acid bath, look under the microscope. Maternal cells will be "ghosted" pale, while fetal red cells will be bright red and normal.
4. Vascular lesions on back/lower back of neonate: blanching suggests vascular malformation (hemangioma). The presence of 2 or more abnormalities on the lower back of a neonate (hair tuft, abnormal/asymmetrical cleft, distorting mass/lipoma, stain, skin tag, dimple) is more suggestive of an occult spinal dysraphism and should be worked up with MRI; single abnormality is overwhelmingly unlikely to be associated with spinal findings and should be worked up with u/s.
5. Caput succedaneum: "boggy" area on baby's head, common finding after delivery, happens from the pressure of baby's head against the dilating cervix (tourniquet effect). Subcutaenous/extraperiosteal collection of serosanguinous fluid, crosses sutures/midline. Resolves spontaenously after a few days.
6. Subgaleal hemorrhage: bleeding under the periosteum, above the skull. Associated with vacuum operative deliveries. Does not cross suture lines. Can lead to increased risk of jaundice. Feels fluctuant upon palpation. Will absorb slowly over weeks-- do not aspirate as it carries a risk of infection/abscess formation. Get imaging if new neuro sx appear. After it absorbs, it may calcify, leaving a relatively softer center and giving the impression of a depressed fracture.
7. The three most common causes of ataxia in a child:
--Postinfectious acute cerebellar ataxia (usu s/p varicella, GI or respiratory infection.)
--Ingestion: barbituates, alcohol, antifreeze, lead, CO, benzos, benadryl
--Guillain-Barre: acute symmetrical ascending demyelinating autoimmune/inflammatory disease. Associated with campylobacter infection.
8. Can't-miss causes of ataxia in a child: 
--Infection (meningitis/encephalitis/sepsis)
--Brain abscess
--Tumor
--Bleed (2/2 trauma, NAT)
--Post-infectious autoimmune (ADEM)
--ICP
--Ischemia (clot, moya moya)
9. Other auses of ataxia in a child:
--Tick paralysis/lyme disease
--Neuromuscular disease (muscular dystrophy, injury, myasthenia)
--Vestibular system disease (labrynthitis- often s/p URI, menieres)
--Basilar migraine
--Seizure, post-ictal
10. Posterior fossa mutism-- happens in 8-38% of children who receive resection of posterior fossa tumors, specifically medulloblastoma. Usually transient, speech returns in 1-15 weeks. Almost always accompanied by cerebellar ataxia.

1. Flocks of migratory birds avoid crashing into each other upon landing by always landing in alignment with earth's magnetic field. Quote: "The latest research suggests that birds detect magnetic fields in two ways. One relies on small pieces of magnetite (a magnetic iron oxide) lodged in their beaks, or inner ears, or both. The other employs a magnetism-sensitive chemical reaction in their eyes, allowing them to “see” the Earth’s magnetic field, probably as bright and dark spots superimposed on their visual fields" (Economist)
2. Fascinating show from radiolab about Emergence, the property of order emerging spontaneously from a large group of disorganized individuals (i.e. acting without central leadership). Emergence is addressed in the context of swarm animals (ants, fireflies) and in neurons in the brain. A theory is proposed that brain cells of different senses firing at the same time/rate is the foundation for coherent, integrated ideas-- i.e. the smell, appearance, feel, taste of coffee are integrated to make the concept of "coffee" (Radiolab)
3. GDM leads to organomegaly as well as macrosomia: hepatosplenomegaly and enlargement of the interventricular septum. The latter reverses upon reduction of insulin levels. At birth, IDM will have hypoglycemia, as well as certain electrolyte abnormalities: hypomagnesemia and hypocalcemia (present 10-50% of the time, depending on the study, often associated with hyperphosphatemia-- possibly a function of polycythemia and cell lysis? possibly a function of decreased PTH from increased Ca in utero?). Finally, the polycythemia (hi glucose -> hi metabolism -> hypoxia -> polycythemia) leads to paradoxical iron deficiency elsewhere in the body as iron is shunted into RBC synthesis.
4. Ceftriaxone displaces bilirubin from albumin, increasing blood [UCB] and leading to gallstones and biliary sludging.
5. Red cell factors that will lead to increased hemolysis in a neonate, and thus more jaundice: 
-Structural: spherocytosis
-Enzyme: G6PD, pyruvate dehydrogenase def.
-Immune: ABO/Rh
6. GI factors that will lead to decreased excretion of UCB: meconium ileus, duodenal atresia
7. Physiological (i.e. nonpathological) causes of jaundice: 
-Race (see previous post)
-Physiologic: infants have b-glucoronidase, their RBCs have shorter lifespans, more ineffective hematopoesis takes place, liver function is not as good, UGT1A1 activity is not as good.
-Breastfeeding (early jaundice): the low amount of breastmilk/colostrum made in the first days post-partum mean that exclusively breastfed babies will be slightly food/drink deprived in the early days of life. Less albumin/protein, and increased hepato-GI cycling of GI contents, leading to increased b-glucorindase activity.
-Breastmilk: (later jaundice) some substance in the breast milk increases UCB in the blood. Perhaps there's something that inhibits UGT1A1, or has b-glucorinidase activity (or is b-glucoronidase)
7. Jaundice due to increased CB is rarer than UCB, and merits an extensive workup for biliary obstruction (choledochal cyst, progressive familial intrahepatic cholestasis, biliary atresia) or genetic diseases (dubin-johnson, rotor)
8. Catfact: cats can jump up to 5x their height in a leap.
9. Insects must beat their wings hundreds of times a second in order to stay aloft, which is far too fast to be explained by calcium-regulated myosin-actin mechanisms. A new paper out in Nature examining bumblebees flying by x-ray scattering found data to support a theory that bee muscles act via oscillatory stretch activation, where stretching of one muscle by a counterpoint/yoked muscle flexing leads to increased myosin head affinity, leading to reflexive contraction. This process is Ca independent. (Nature)
10. Significant steps were made in figuring out why anti-EGFR drugs cause those awful pruritic rashes, published this week in Science. From the abstract: "We established a parallel mouse model by ablating EGFR in the epidermis. These mice developed skin lesions similar to the human rash. Before lesion development, we detected increased mRNA expression of chemokines in the skin associated with early infiltration of macrophages and mast cells and later infiltration of eosinophils, T cells, and neutrophils. As the skin phenotype evolved, changes in blood counts and circulating chemokines reproduced those seen in the gefitinib-treated patients. Crossing the mutant mice with mice deficient for tumor necrosis factor–α (TNF-α) receptors, MyD88, NOS2, CCR2, T cells, or B cells failed to reverse the skin phenotype. However, local depletion of macrophages provided partial resolution..." (Science)

1. Catfact: cats can squeeze through any opening the size of their head, because their collarbones are not connected to other bones in their body, only to muscles.
2. Catfact 2: Cats have over 30 muscles that control their outer ear, and can rotate each one independently 180 degrees. They can also hear up to 65 kHz (humans can only hear up to 20 kHz)
3. Moyamoya syndrome is a disease of vascular wall thickening in the internal carotid artery and its branches (MCA, ACA), that leads to progressive stenosis and increased risk of ischemia and stroke. In the early stages, collateral arteries form in an attempt to increase perfusion, but these collaterals are friable and prone to hemorrhage (proved by something as small as sneezing), aneurysm, and thrombosis. On MRA, first the collaterals will appear, then eventually disappear as the stenosis progresses so far as to lead to nearly complete ischemia. At this point, other vessels such as the basilar and external carotid will begin to spawn collaterals, and hypoxia to the brain will become severe.
4. Treatment for moyamoya involves anti-platelet agents to prevent stroke (aspirin); there are also surgical procedures that involve either bypass grafts of external carotid or superficial temporal artery directly onto MCA, or putting burr holes in the skull/placing temporalis muscle over it with the idea that the hypoxic brain will form new collaterals. Moyamoya is common among people with NF1 and trisomy 21.
5. People with trisomy 21 have an increased likelihood developing seizures. The distribution for seizure development is bimodal: in childhood (infantile spasms) and in the 30s-40s. Seizure development in adult life is associated with increased risk of dementia later on. 18% of people with trisomy 21 also have a concurrent autism-spectrum disorder, a rate which is 10x higher than the general population. Additionally, due to ligamentous laxity (including in posterior longitudinal ligament), there is an increased risk of atlanto-axial instability. Check echo (EF) and cspine xray before sedation, which is necessary for MRI/MRA in a young kid.
6. Risk factors for the development of neonatal jaundice: 
-Prematurity
-Polycythemia/IDM
-Race: Asian, Native American, Hispanic most likely. African american and white less likely.
-Hemolytic diseases (SCA, G6PD)
-ABO/Rh incompatibility
-Family Hx of jaundice.
7. In neonates at risk for hypoglycemia, do accuchecks at 2 hours of life (after feeding) and q3-6 afterwards. IDM/LGA: check for 12 hours after birth, preterm/SGA: check for 24 hours after birth.
8. Management of stroke in pediatric patients:
-No fibrinolytics in anyone under 18 years old, data is currently inadequate re: benefits and harms. Trials are currently undergoing to evaluate further.
-Keep the head of the bed level to increase perfusion to brain if at all possible (i.e. not in imminent danger from cardiorespiratory concerns)
-Do not treat HTN, again to increase brain perfusion, unless there is clear HTN-related end-organ damage going on.
-Big IVs, 10mg/kg bolus, maintenance fluids.
9. Subdural vs epidural hemorrhage in peds: 
-Age: Subdural is more common in kids <1 year old, epidural more common in older kids and adults.  
-Skull fracture: 1/3 of subdurals are assoc w skull fracture, 2/3 of epidurals are.
-Seizures: accompany 60-90% of subdural hematoma, <25% of epidural patients
-Retinal hemorrhage: subdural (common), epidural (uncommon)
-Blood source: subdural- venous, epidural-arterial
-Laterality: subdural usu b/l, epidural usu u/l
-Symptoms: subdural- emesis, seizures, increased tone, irritability, personality changes, inattention, FTT, fever, anemia. epidural- altered mental status, then lucid period, then sx of increased ICP- LOC, bradycardia, irregular respirations,
-Outcomes: Mortality is greater with epidural, but morbidity greater with subdural (touches brain parenchyma, headaches, fatigue, nausea, sleep problems)
10. Hyenas are not just scavengers; they are pack hunters that have a developed system of communication. They decide what kind of prey to hunt before they set off hunting: you can predict what kind of prey they are going for by the size of the hunting pack, and they will bypass other kinds of prey on their way to the target species.

1. Interesting article on neuromorphic computing in this week's Economist. Essentially, various groups are trying to build a computer system that behaves like the human brain does. Their techniques vary, but resemble each other in that instead of having a central processor following a written program, they're making systems of decentralized, highly-interconnected groups of individual processors that sum the signals they receive and use that information to decide whether or not to fire in an all-or-nothing manner (electronic action potentials) and are able to strengthen and prune connections without outside input. Seems like the engineers are going to figure out how the brain works before the life scientists do. Not surprising, they're definitely smarter than us.
2. Baby Derm: 
-To tell eczema vs seborrehic dermatitis: eczema is itchy, SD is not. Eczema: short lukewarm baths, vaseline on the body, topical steroids if you need it. Nothing stronger than 2.5% hydrocortisone on the face.
-Diaper dermatitis vs candidaisis: diaper dermatitis spares skin folds. Treatment for both is naked time, avoid baby wipes (use wet towels). Dermatitis: use desitin or any other barrier cream, don't rub it in the point is to act as a barrier. for candidiasis, topical nystatin.
-Tinea capitis: treat with PO griseofulvin for 6 weeks, 20-20ug/kg/day with fatty food. The associated liver damage is probably not as big a concern as it was once believed.
-Scabies: 5% permetherin lotion all over, cover it with more lotion, go to sleep leave it on 8 hours, wash it off the next day. Wait a week, if you still have sx do it again. Treat everyone in the family even if only one has sx, launder everything in really hot water.
-Impetigo: topical mupirocin (binds a t-RNA synthetase in staph and strep), IV clinda if its really bad.
3. Parvo is most dangerous in:
-Patients with sickle cell anemia, in which it can precipitate an aplastic crisis. Hydroxyurea, being essentially a chemotherapy agent that increases HbF, can also drop someone's WBC, but rarely drops their platelets. To check for aplastic crisis, check platelets.
-Pregnant women/fetuses: causes hydrops.
-Dogs, especially puppies: causes respiratory and cardiac failure.
Parvo in adults: acute symmetric polyarthritis.
4. Colic: rule of 3s: disappears before 3 mos, 3 hours a day (sum total) of inconsolable crying, at least 3 days a week.
5. Tylenol dosing: 
Fever/Pain for infants/children 10-15 mg/kg/dose q4-6 hours. (neonates: q6-8). max dose 3g/day.
"old infants tylenol" now off the market, 80mg/0.8 cc (100mg/cc).
Children's tylenol: 160mg/5cc (32mg/cc)
Chewable: 80 or 160 mg/tab
Adult: 325, 500, 1000.
6. If you suspect tylenol overdose: draw levels at 4 hours after ingestion, if >200 probable hepatic damage, go to PICU. If <150, probably ok.
Treatment: N-acetylcysteine, gastric lavage, activated charcoal. If they took it in pill form recently, make them throw it up: the pills take a while to absorb in the stomach.
7. If a kid comes in with recurrent nosebleeds, ask him about bleeding elsewhere: GI tract, easy bruising, blood from teeth brushing, difficulty stopping bleeding after injury. FHx of bleeding diathesis.
8. Hydrocarbon toxicity (gasoline, turpentine, mineral oil, kerosene): main worry is aspiration pneumonitis, which occurs in 30-40% of kids with hydrocarbon tox; risk increases with higher volatility/low viscosity compounds. The hydrocarbons penetrate deeply into the lung parenchyma, causing bronchospasm, inflammation, necrosis. Can lead the kid to go into fulminant ARDS. Hydrocarbons also collect in various other lipid-rich parts of the body and wreck havoc, including brain, liver, kidney, etc.
9. Kiddie ID clinical pearls: 
-Coughing fits leading to apnea in a child [ALTE]: chlamydia pneumnoia vs pertussis (absolute leukocytosis, cleaved leukocytes on diff. Kids' cartilage is not developed enough for whoop).
-Toddler with wheezes and crackles but excellent sats, is pink and happy: RSV bronchiolitis. No tx, admit if sats<90 or for hydration issues.
-Few months old, afebrile, stigmata of pneumonia: chlamydia.
-BPD vs Bronchiolitis: in BPD, lungs are little scarred up from lack of surfactant+ventilator, bronchospasms come easy, responds to neb treatments. In bronchiolitis, the problem is edema and they won't respond to nebs.
-Really bad airway edema (ie. croup): steroids and racemic epinephrine (a-agonism will drop edema from the inside)
-Weeks of cold symptoms and night cough that is progressively worsening plus halitosis: sinusitis.
-Older kid with stigmata of pneumonia, but low fever and looks ok, with a CXR full of diffuse interstitial findings: atypicals, likely mycoplasma.
-Fever in a newborn: culture everything, amp/cefotaxime. Cover for e.coli, GBS, s.pneumo, staph, listeria (in rough order of prevalence). Gent causes hearing damage, ceftriaxone biliary sludging.
-Suspected meningitis: LP and ceftriaxone/vanc asap. If you're worried about increased ICP (focal neuro signs, extreme altered mental status, cushing's triad HTN+low HR/RR), you can get a stat CT in ~20 mins, will not affect outcome. Don't let them herniate.
-High fever for 3-5 days, rash, seizures: roseola.
-5 days of high fevers + rash of any kind + LAD>1.5cm + edema of hands/feet + bulbar conjunctivitis (spares avascular part around iris) + buccal/tongue mucosa reddening = kawasaki. Without treatment, 27% aneurysm. Hit with high dose aspirin for 2-3 days, then low dose for 4-6 weeks til you've got a clear echo. IVIg day 5-7 only.
10. Supraclavicular nodes: R side drains mediastinum, lungs; L side drains abdomen. These nodes are never normal, with malignancy high on the differential even in the absence of other symptoms. Refer for biopsy.

1. There is some data that during REM sleep, there is an interruption between the hippocampus and the neocortex, which interrupts our ability to form strong memories; this is one explanation for why dreams seem to escape us so quickly. This connection is also necessary to synthesize sensory elements of memories into one coherent experience, which is why our REM dreams, although highly vivid and emotional, are often fragmented and nonsensical. c/o Penelope Lewis (neuroscientist) in an interview with NPR:  http://www.npr.org/templates/transcript/transcript.php?storyId=212276021
2. EKG tips: 
-check top L corner for scale of measurement/recording
-sinus rhythm? check if every QRS is preceded by a P, PR intervals symmetric, P wave is not too large (suspect atrial hypertrophy)
-check axis: lead 1 is at 3 o'clock, aVF at 6 o'clock.
-RVH: right-axis deviation (except endocardial cushion defect), R>S wave in V1, S>R wave in V6.
-LVH: L axis deviation, S in V1 and R in V6 add up to >5mm.
3. Sedation options in peds: 
-Fentanyl/Midazolam: tried and true. Good pain control. Warnings: narcotics in kids can lead to resp suppression, midazolam works great most of the time but rarely can cause a paradoxical opposite effect and lead to anxiety, involuntary movements, aggressive/violent behavior.
-Precedex/Propofol: Precedex offers adequate pain control for most procedures, is long-acting and is good for long procedures/studies (i.e. MRI). Flipside is it takes a while to wear off (45-60 min), and as all kids under sedation must be constantly monitored, you need a lot of nurses. Propofol is non-opiate non-barbituate sedative that offers no pain control. Fast on, fast off, safe in good hands.
-Ketamine/Propofol: Ketamine is an NMDA antagonist and disassociative anesthetic. It causes sedation without respiratory depression or airway loss-- people totally breathe on their own. Causes slight HTN/tachycardia. In adults can lead to hallucinations, but rarer in kids. Contraindicated in patients with ICP, IOP, psychosis, in critical condition. Good for stable, healthy patients undergoing short procedures.
4. Indications for intubation for sedation: facial trauma/malformations that may may emergent intubation difficult, severe lung disease, significant cardiovascular disease
5. The sound of a PDA in a newborn is not like that of older kids. Because of increased pulmonary resistance in neonates, there is only flow across the PDA during systole, resulting in more of a mid-systolic ejection murmur than the continuous machine-like murmur of older children.
6. Things that cause hyperkalemia: 
-Cell injury (burns, rhabdo, tumor lysis synd, ischemia, hemolysis)
-Acidosis, low insulin, DKA
-Transfusion of old blood 2/2 hemolysis. People who really need fresh blood: cardiac/cardiac surgery patients, renal failure)
-Muscle injury 2/2 tourniquet left on too long, or squeezing small feet for blood.
-Hyperosmolar state.
-RTA 4/hypoaldosterone
-Other: beta-blockers, digitalis (causes K to shift out), low Mg causes K wasting.
-not diet: you can't eat enough bananas to make yourself hyperkalemic.
7. When to treat K imbalances:
-In adults, who often have subpar cardiac health, you really want to keep their K above 4. Babies and kids (not teenagers) who have very healthy hearts can tolerate much lower levels of K (down to 2s). IV potassium is associated with some bad outcomes, so use it only if you really need to. Indications for K replenishment: K<2-2.5, K<3.5-4 with hypokalemic symptoms (cardiac symptoms, profound weakness or respiratory changes), someone with a history of cardiac disease. If you treat, give 0.5-1 mEq/kg (0.5 for no sx, 1 if +cardiac sx) top out at 40 mEq IV, 60 mEq PO. PO is better, if they can take it.
-Hyperkalemia is very dangerous! Someone can go from a normal EKG to ventricular arrhythmias very quickly, bypassing the peaked T waves and prolonged PR and QRS widening and such. Treat anyone with a K over 6, or close to 6 and trending up. Treat at even lower levels if they have symptoms.
-If you suspect K imbalances, recheck with an arterial stick.
8. Treatment for hyperkalemia: 
-Calcium to protect myocardium. 1 dose buys you 20 mins. Ca causes cutaneous burns, so try to give it in a central line. If you don't have time and all you have is a peripheral IV, CaGluconate is thought to have less of a burn effect. Dose: 50-100mg/kg. 100 if someone is in extremis. CaChloride: central line only, 10-20mg/kg. Max 2g.
-Kayexylate: slurry, give rectally with a catheter. At first, give with sorbitol (osmotic agent that will help pull things out). Works in 10 mins. You may need more than one dose-- if you need more than 2 doses, ask for kayexylate without sorbitol. It can be given PO (and should be in someone who is neutropenic and immunocompromised) but it tastes bad and your patients may not tolerate. If there is a g-tube or you suspect good cooperativity, PO is ok.
-Albuterol
-Insulin+Glucose: Insulin dose, 0.1uL/kg. Glucose: 2-5mL/kg of D10 or D25. If they are a big person (i.e. teenager, almost adult) you can give an amp of D50. Don't do that in a child. Check sugars q10-15 minutes.
-Sodium Bicarb, 1-2 mEq/kg. One amp is 50 mEq.
9. When your treatment is not working: K keeps rising, EKG changes keep progressing, then put in a quinton cathether and get ready to go to dialysis.
10. Things that cause hypokalemia: 
-Drugs: diuretics, aminoglycosides, amphotericin.
-Vomiting (via alkalosis), diarrhea
-Alkalosis, increased insulin,
-Hyperaldosterone
-Beta agonists,
-Plasmapharesis.

1. Salmonella gastroenteritis is usually self-limited and will resolve in a day or two. It requires a large inoculum and is rarely transmitted person to person. In addition to the gastroenteritis symptoms, it can be associated with neurological symptoms (headaches, seizures, drowsiness, confusion). It can cause transient bacteremia (1-5%) and seed distant sites, causing osteomyelitis, meningitis, pneumonia, arthritis; this is more likely in people who are immunocompromised/asplenic and infants. Except in these vulnerable groups, we don't use antibiotics. Do not use anti-motility agents. It is ubiquitous in the animal kingdom, including notably in many reptiles, like iguanas and turtles.
2. Shigella gastroenteritis will resolve without treatment, but it takes 1-2 weeks, so we usually treat it to speed up resolution. It requires a small inoculum, and is usually transmitted person to person. WBC will be low, but have a significant left shift. Can also be associated with neurological symptoms (headaches, confusion, seizure, hallucinations). Rarely associated with complications: HUS (with strains that make shigatoxin), meningitis, cholestatic hepatitis, toxic megacolon, rectal prolapse, cystitis, Ekiri syndrome (toxic, fever, seizures, rapidly progressive brain edema/death within 8-48 hours of symptom onset, extremely rare), arthritis/conjunctivitis/urethritis 2-5 weeks after especially in HLA-B27.
3. Gibert's syndrome is associated with at 66% ARR of heart disease (determined using Framingham heart study data). Apparently UCB is an anti-oxidant. (credit: SMG)
4. Use of walkers in children should be strongly discouraged. They do not make any difference in the age kids learn to walk, and in fact, age of walking is not an indication of intelligence. The age of first walking in 95% of kids is 9-17 mos. Walkers are dangerous because if a kid falls off the stairs in a walker, he'll sustain significant injury to his neck--- whereas if a kid falls off the stairs not in a walker, they rarely hurt their c-spines. Kids' c-spines (up to 8 years) are much more elastic than that of adults. Experiments in cadavers show that the vertebral column can stretch up to 2 inches without disruption. Additionally, the facet joints are shallower and more horizontal, the ligaments of the neck are more elastic, the neck muscles are weaker-- all of which decrease the incidence of fracture/serious injury. (http://www.medscape.com/viewarticle/527718_3)
5. Questions to evaluate language development in an toddler: 
--General: Concerns about hearing? Does he try to imitate speech? Is he interested in people?
--Receptive language: Can he understand commands (give it to me), name body parts you point to, make sounds of animals you name
--Expressive language: Does he gesture/point/shake or nod head? How does he express himself? What words does he say, and does he use them correctly?
Language Milestones:
--7 days: can differentiate mom's voice from other females
--2 weeks: can differentiate dad's voice from other males
--6 mos: coos
--9 mos: nonspecific mama/dada
--1 year: specific mama/dada, one-step commands
--15 mos: ~10 words
--18 mos: knows nouns (cup, ball), and names. Can follow two-step commands.
--2 years: making 2-3 word sentences.
6. CP: non-progressive disorders of movement and posture
=Spastic quadriplegia: spasticity in all 4 limbs, due to global cerebral injury
=Spastic diplegia: spasticity worse in LE than UE, due to perivernticular white matter damage (i.e. hemorrhage), often seen in premature infants
=Dyskinetic (athetoid: constant motion of head/eyes/limbs, dystonic: fixed posture): damage to BG, thalamus, cerebellum. Assoc with kernicterus, perinatal asphyxia.
=Spastic Hemiplegic: stroke, dmg to UMN.
=Ataxic: damage to cerebellum.
7. Risk factors for CP identified in a case-series (n=213) in Australia: Prematurity (78%), IUGR (34%), intrauterine infection (28%), perinatal hypoxia (10%).
8. APGAR scores are predictive of neonatal survival, but not of development later on in the child's life.
9. Interesting research about near-death experiences in rats. EEG data of high-frequency activity in the 30 seconds immediately following cardiac arrest suggest a "hyperconscious" state, which would mesh with humans who claim they experience vivid hallucinations/visions that "feel more real than reality". http://www.pnas.org/content/early/2013/08/08/1308285110 (c/o NPR shots blog)
10. A great TED talk about self-assembling materials on a human scale http://www.ted.com/talks/skylar_tibbits_the_emergence_of_4d_printing.html

1. Still's murmur: a type of functional, benign murmur. Very common in children. Heard best at LLSB, louder when the kid is supine. Less than 3/6. Musical in quality (i.e. higher pitched than a rumbling, low-pitched murmur, and lower-pitched than a high-pitched, harsh blowing murmur). Generally have an ejection-type sound, crescendo-decrescendo. Thought to be due to vibrations of valve attachements/chordae.
2. Systolic murmurs are present in up to 60% of people, up to 90% of which are associated with normal findings on echo. A mid-systolic murmur should be regarded as innocent not based on the loudness or duration of the murmur, but on the presence of other signs-- additional heart sounds, abnormalities in S2, clinical symptoms-- SOB, dizziness, syncope, cyanosis, family history of structural heart conditions.
3. Physiologic pulmonary artery stenosis: another functional murmur. Usually II/VI, mid-systolic, best heard at ULSB, can radiate to axilla or back or entire precordium. Common benign finding in infants 2 weeks to 6 months of age, more common in low-birthweight kids since they have smaller pulmonary arteries. Caused by physiological small size of pulmonary arteries leading to increased turbulence of blood flow leading to murmur. Totally benign, the kids grow out of it. A study done in Japan (1996) compared 25 term, low-birthweight infants with PPS and 25 term, low-birthweight without and found no difference in main pulmonary artery velocities, but a significant difference (like twice as high) in the pulmonary branches.  http://www.ncbi.nlm.nih.gov/pubmed/8724652
4. Beckwith-Wiedemann Syndrome: overgrowth syndrome, commonly associated with hemihyperplasia, abdominal wall defects, transient hypoglycemia in newborns that resolves on its own, ear pits/creases, and increased risk of malignancy. Annual screens should be done to monitor for the development of tumors: blood AFP/HCG (germ cell), urine VMA/HVA (neuroblastoma), and u/s (wilms).
5. Prader-Willi: an imprinting disorder of chromosome 15. Loss of paternal or uniparental disomy of maternal chromosomes. Kids are born with severe hypotonia (more so than in trisomy 21) leading to poor suck and failure to thrive; they might need a g-tube for feeding. Around age 1, the hyperphagia sets in (can last until age 8-10) leading to obesity. Associated mild-moderate intellectual disability, brachydactyly, hypogondadism.
6. Angelman Syndrome: imprinting disorder of chromosome 15, loss of maternal or UPD of paternal. Associated with seizure disorders (80-90% prevalence), laughing, stereotyped/jerky movements, moderate-severe intellectual disability. Fair hair, macrognathia.
7. Patau Syndrome/Trisomy 13: midline defects. Holoprosencephaly, micrognathia, b/l cleft lip/palate, omphalocele. Polydactyly, deafness, cubis aplasia. 80% mortality in first month.
8. Edwards Syndrome/Trisomy 18: associated with hypertonia at birth (CP presents later), polydactyly, overlapping fingers, micrognathia, cardiac defects (VSD, PDA), horseshoe kidney, ectopic pancreatic tissue, rocker-bottom feet, prominent occiput. 90% mortality in first year. More common in girls than boys, 4:1.
9. Down's Syndrome/Trisomy 21: associated with hypotonia (90%), brushfield spots ("diamonds in their eyes"), sandal-gap toes, simian crease, heart defects ~50% (VSD, ASD, endocardial cushion defect), GI defects (hirschprungs, duodenal atresia), increased risk of ALL, cataracts, strabismus, hypothyroid, atlanto-axial instability, clinodactaly/brachydactyly, moyamoya leading to stroke. Follow up: echocardiogram in neonatal period, optho evaluation before 6 mos and eye exams every year, including vision screening. Annual TSH/T4, c-spine x-ray between age 3-5.
10. Herbal Medicine in kids: 
--St.John's Wort: Wort is an old English word for plant. Used to treat depression. Most studies show equivocal data compared to SSRIs or placebo, due to the presence of a strong placebo effect in RCTs for depression. Many, many drug interactions (it's a CYP inducer). Other side effects: GI, photosensitivity. Contraindicated in bipolar patients-- like SSRI, it can push someone into mania.
--Feverfew: used to treat migraines. Has anti-serotonin, anti-platelet effects.
--Peppermint: anti-spasmodic, in tea form may be effective in IBS. In oil form, can be topically applied for headaches.
--Chamomile: anti-inflammatory, possibly slows peristalsis, can help with colic. As a concentrated tea swish, can help with mucositis associated with chemo.
--Black licorice: anti-spasmodic, anti-inflammatory, good for dyspepsia/gastritis. Naturally contains Glycyrrhizin, which is a sweetener but also seems to cause hypertension and hypokalemia. Because of this, whole licorice will interact with many antihypertensives, and thus should not be taken for longer than 2-3 weeks. If you buy licorice that has been de-glycyrrhizined, it is safer for continual use.
(c/o University of Arizona pediatrics podcast.)

1. To r/o dehydration in a toddler: check for tears, slobber, at least 3 wet diapers a day. If a toddler is sick, its ok if he doesn't eat (as long as he has enough body fat and isn't a real skinny minny kid), but he needs to drink.
2. Pneumovax (23-valent s.pneumo vaccine, covers 90% of all disease causing variates) is a polysaccharide vaccine and thus is not immunogenic enough to have any response in children under the age of 2. It's indicated in people over 65 and in children 2 years+ who have an increased risk of s.pneumo (i.e. asplenics/sickle cell, acquired immunodeficiency including HIV/chemo/radiation/transplant recipients, congenital immunodeficiency including complement deficiency and phagocytic disorders, heart/lung/renal failure/diabetes).
In kids under 2 years, we use prevnar, which is a 13-valent, protein vaccine-- each antigen conjugated to CRM-197 which is a non-toxic mutated diptheria toxin protein (single AA mutated glu->gly)
3. Vaccines!!
Rota: 2/4/6
Hib: 2/4/6, 1 year (or 15 mos)
Prevnar: 2/4/6, then 1 year.
DTaP: 2/4/6 mos, 1 year (or 15 mos), then 4 years
Polio (salk): 2/4/6, then 4 years
Hep B: birth, 2 mos, 6 mos.
Hep A: 1 year, dose #2 given 6 mos after dose #1
MMR: 1 year, 4 years
VZV: 1 year, 4 years
Gardasil: 9-11 years, and then dose #2 (2 mos after dose #1), dose #3 (6 mos after dose #1)
Flu shot: 6  mos for attenuated vaccine, 2 years for live (nasal spray). 2 doses 4 weeks apart for kids <9 getting the shot for the first time, or if their last year's shot was the first time and they only got 1 then.
4. Catch up vaccinations... too complex to memorize. Important points:
-once they hit 5 years, they're too old for prevnar/HiB.
-once they hit 15 weeks, they're too old to start rota
You're never too old for the other ones! Sorry kids.
5. Differential for ALTE:
-Neuro: seizure/post-ictal, increased ICP (bleed/fluid/mass), breath-holding spells-- can be cyanotic (due to tantrum) or pallid/non-cyanotic (due to pain/trauma/fall). 6 mos to 6 years is age range.
-Pulm: RSV, pneumonia, pertussis
-Cardio: bradycardia (congenital long QT), ductal-dependent congential heart defects can decomp really fast, tet spells.
-GI: GERD-- unclear whether GERD -> choke -> apnea, or apnea -> LES relax --> GERD, congenital swallowing problems/TEF.
-Gen: sepsis, toxin (CO poisoning, botulism toxin, opiates), inborn errors of metabolism
6. Tricuspid valve atresia: congenital absence of the tricuspid valve. Most of the time (80%) there is muscle where there should be valve, most of the rest of time time it's membranous; rarely, there will be a valve with fused cusps. The real problem is that nearly 100% of the time there's concomitant hypoplastic R heart, so you're essentially facing a kid with only one ventricle. ASD and VSD are mandatory for survival. There's lots of mixing and the neonate will be cyanotic. 75% of the time, there is also inadequate blood flow to the lungs 2/2 pulm artery stenosis or outflow tract obstruction or VSD being small.
7. Surgery to fix TVA:
--(1, done in neonate) Make sure there is blood flow to the lungs.Connect the aorta directly to the pulmonary artery (Blalock-Taussig shunt). Other surgery you may need to do: make sure VSD/ASD stay open, fix any pulmonary artery stenosis/obstruction. In the case where there is too much flow to the lungs, you may need to band the pulmonary artery to prevent pHTN/high-resistance pulm circuit. The final surgery to fix TVA depends on there being a pressure gradient from SVC to pulmonary arteries.
--(2, done @ 3-6 mos) Connect SVC to pulmonary artery (glenn procedure), remove your old aortic-pumonary shunt. At this point, blood from IVC is still going to R atria through the ASD to the left side, where it is mixing with freshly oxygenated blood. The kid will still be cyanotic.
--(3, done @ 2-3 years) You shunt blood from IVC to pulmonary artery (fontan procedue). You can either connect the R atria to the pulm artery, or you can do an extracardiac fontan and directly plug IVC to pulm artery with a tube. If the systemic pressure is higher than pulmonary artery pressure, great! Sometimes you can have too much flow into the lungs and cause edema-- you can put a hole between IVC and atria to relieve it. The problem is that if there is high resistance in the pulmonary circuit, blood from VC may not be able to enter. Kids with a mean pulm artery >15 are not candidates for Fontan procedures. Don't forget that going on bypass causes increased resistance in the pulmonary circuit.
8. Long term problems of Fontan procedures:
-People do great until about 20-30 years out, there is a significant increase in mortality.
-CV: arrhythmias, sudden death
-Pulm: Restrictive lung disease
-Coags: hypercoagulability, 41% incidence of atrial mural throbmi, although most are silent. ASA and well-monitored coumadin have comparable outcomes, both better than badly-monitored coumadin.
-Chronic venous stasis
-Renal failure (50% of people have at least mild renal failure)
-Hepatic dysfunction.
9. Transplant is not a great solution for people with TVA-- too few hearts, and lots of early mortality compared to Fontan, where early mortality is ~5%.
10. You don't get pulmonary edema in cases of hypoalbuminemia because the lung epithelium are permeable to albumin, so its hard to create an oncotic pressure gradient with changes in albumin concentration. Perhaps this evolved so that our lungs wouldn't flood every time we went through a period of starvation? Food for thought... (source: SMG)

1. The cutoff between epi-pen (0.3 mg) and epi-pen JR (0.15 mg) is 30 kg body weight. Epi-pen Jr goes to kids 15-30 kg.
2. Pediatric shock protocol:
-Make sure you have an airway, intubate if needed. Infants: towel under shoulders, head in sniff position. Young kids: towel under head, neutral position. Older kids/adolescents: the older they are, the more you hyperflex the neck back. Inbutation tube size: (age+4)/4. Intubation tube depth (cm): tube size * 3. In patients where you're worried about increased ICP, do not use ketamine (worsens ICP).
-Determine if you need fluids (cap refill, pulses, HR, UO). If so, get IV access: if you can't get a line in 90 seconds or 3 tries, go to IO line. Best place to put it: antero-medial proximal tibia, where it's flat. In older kids, you can do distal tibia a few cm above medial malleolus). Lidocaine to periosteum if you have time. Put needle in, when you get to bone, push/twist until you get to marrow. Aspirate to check you're in marrow-- you can use the marrow to do labs (T&S, etc). You will need to put pressure on the bag to get fluids in, and keep pressure to prevent the line from clogging up. Put in some heparinated saline, check for extravasation into tissues-- if you're in subQ tissue, you can cause compartment syndrome.
-Resuscitate with 20mL/kg isotonic NS boluses, as fast as you can. Can repeat twice, up to a total of 60mL/kg. If they are still in shock, consider pressors/inotropes if they are in distributive or cardiogenic shock, and blood if they are in hemorrhagic shock.
3. Prophylactic treatment for contacts of neisseria meningitis/sepsis patients: rifampin or IM ceftriaxone for kids, cipro for adults.
4. Absence seizures can be triggered in office by ~2 mins of hyperventilation. Useful for confirmation of diagnosis, in the office or during an EEG.
5. DDx for seizure in a 2 y/o:
--Gen: fever, trauma, pseudoseizure.
--Tox: diabetes meds, b-blockers, cocaine, alcohol (withdrawal), AED, tricyclics, INH (B6 deficiency), lithium
--ID: meningitis/encephalitism, brain abscess
--Neuro: epilepsy, tumor, hemorrhage, increased ICP, tuberous sclerosis, stereotyped mvmt assoc with autism
--Endo/Met: hypoglycemia, DKA, hypocalcemia, hyper/hypoNa, vitamin A excess, vit B6 deficiency
6. Management of febrile seizures:
--LP: <6mos: indicated. 6-12 mos: indicated in the absence of clinical sx suggestive of meningitis only if HiB/S.pneumo (PNV13) vaccines are incomplete or they are on antibiotics that could mask meningitis symptoms,  >12 mos: indicated only in the presence of clinical sx suggestive of meningitis
--Imaging: not indicated, unless there is a hx of trauma, an enlarging/very large head suggestive of hydrocephalus, focal neuro deficits, abnl neuro exam, or signs of increased ICP.
--Labs: not helpful in the setting of febrile seizures. Indicated only if there is reason to suspect electrolyte abnormalities as the cause (i.e. lots of diarrhea/vomiting, excessive water intake e.g. over-dilute formula)
--EEG: not indicated, especially hours after the seizure is over. Most likely to find abnl findings right after seizure, does not influence treatment.
--Treatment for febrile status epilepticus: Diastat (rectal suppository of diazepam, give 5 minutes after seizure begins).
7. Anticipatory guidance about febrile seizures/status:
--don't let the child be unsupervised in any activity where if he seized, he'd be in danger (i.e. in the pool/tub, riding a bike/monkey bars, don't let him sleep in upper bunk, etc)
--no spoon in the mouth. Clear the area around, don't try to stop the movements just let them seize.
--incidence of epilepsy in kids with febrile seizures is about 2% vs that of the general population at 1%.
8. In evaluating septic joints in kids, think Kingella. More common in kids less than 4, but can happen in other age groups. Most often affects knee and hip. Other pathogens to consider: staph aureus, neisseria, salmonella in kids with sickle cell.
9. It used to be believed that HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) organisms were the most common cause of culture-negative endocarditis, presumably because they were difficult to culture, but studies have found that they are in fact easily cultured with current techniques as long as you wait for at least 5 days. A large, multicenter trial (n=407) of presumed culture-neg endo found 0 cases of HACEK organsims. Another trial (n=348) of presumed culture-neg endo in France managed to get a positive culture in 79% of cases, and the top etiologies were: coxiella burnetti (48%), bartonella (28%), strep (4%), t.whippli (2%), However, it should be noted that Q fever is much more common in France than in other countries.
10. "Idiopathic pulmonary hemosiderosis is a rare disease found primarily in children that causes recurrent episodes of diffuse alveolar hemorrhage. Recurrent alveolar bleeding may eventually produce pulmonary hemosiderosis and fibrosis. Diffuse alveolar hemorrhage is characterized by hemoptysis, dyspnea, alveolar opacities on chest radiographs, and anemia and can result from a variety of underlying conditions.... When no underlying cause for repeated episodes of diffuse alveolar hemorrhage is apparent, the entity is referred to as idiopathic pulmonary hemosiderosis (IPH)" -uptodate

1. In a kid with tears/clear mucus coming out of one eye, think obstructed nasolacrimal duct (aka dacryostenosis). Presents in 6% of neonates, usually clears up on its own by 9-12 months. Parents can help by massaging the medial eye: pressure on lacrimal sac (proximal to duct) can push fluid distal, using hydrostatic pressure to open blockage. If it doesn't clear on its own, optho can put in a thin cathether or probe and open it up.
2. Night terrors are parasomnias, like sleepwalking. The pathophysiology is unclear, but some believe that it's a product of incomplete arousal from deep/NREM sleep. Corroborative with this, parasomnias are often triggered by things that cause nighttime waking, like OSA, GERD, restless legs. Kids are difficult to arouse during night terrors, and they should not be woken up. Night terrors are common after anaesthesia. Kids usually grow out of them by adolescence.
3. In a kid with progressive macrocephaly, think bleeding, tumors, hydrocephalus. In a kid with progressive microcephaly, think premature suture closure, TORCH infections (CMV).
4. Daily weight gain by age: From 0-4 months, expect on average a 30g/day, 4-6 months 15-20g/day, 6-12 mos 10-15 g/day. Before you diagnose failure to thrive, look at the kid. Infants store their fat in their abdomen, butt, thighs so if he looks big and healthy, and he appears active and alert, he is probably not failing to thrive.
5. Incomplete/inevitable/missed abortions can be managed expectantly, medically (miso) or surgically (d&c). Surgical procedures are most likely to have led to complete evacuation by 48 hours, and expectant least likely. Rates of infection (2-3%) are the same in all 3.
-Medical management: 800mcg miso vaginally: vaginal has better success rates than PO miso. Misoprostol (E1) is cheaper than E2s. In one large trial (n=652), 71% had complete explusion by day 3, 84% by day 8. Overall expulsion rate for missed ab (81%) vs inevitable/incomplete (93%). RCT data has shown no difference in miso alone vs miso+mifepristone, as there is already a low-progesterone state.
-Surgical management: indicated for women who don't want to wait and who are experiencing heavy bleeding or signs of infection. Give 100 mg doxycycline PO 12 hours apart on the day of the procedure.
6. Pregnancy termination:
0-9 weeks: medical
0-13 weeks: D&C
13+: D&E
Ectopic:
-Methotrexate: 35% of all patients are eligible for MTX therapy: subject must be unruptured, hemodynamically stable, mass <4 cm, can follow up, and b-hcg<5000. A systematic review (n=1300) found 4 dose MTX was slightly more effective than one dose (93 vs 88%) but carried significantly more side effects.
-Otherwise, either salpingostomy (don't suture, leave it open to heal) or salpingectomy. The data (cohort studies, with many confounders including tube status influencing choice of surgery) doesn't seem to show a major difference in fertility post-op, but a higher risk of repeat ectopic in salpingostomy.
7. Eye inflammation!
-Blepharitis: inflammation of whole eyelid. Treat with warm compress.
-Hordeolum/stye: infection of sebaceous or apocrine glands, often inside the eye. Can affect upper or lower lid, painful, acute onset. Treat with warm compress, wash with baby shampoo. Check visual acuity, ROM. If suspicion for/progression to cellulitis, then antibiotics.
-Chalazion: meboian gland cyst, only upper lid.
8. Eye cellulitis:
-Orbital/septal: inside eye cavity, can lead to proptosis (eval from above), changes in vision, loss of ROM, abscess formation. Usually from sinuses. Usually s.pneumo and staph. Treat: IV antibiotics: ceftriaxone to cover s.pneumo, clinda for staph. Can sub amp or unasyn (amp/sulbactam) if you feel like ceftriaxone is overkill for s.pneumo. Clinda has great tissue penetration, is a good drug for cellulitis.
-Preseptal/periorbital cellulitis: outside of the eye cavity, on the lids, less worrisome. Usually just staph. Treat with PO clinda. Differentitate from blepharitis: blepharitis is along the rim of the eye, usually just the upper lid, a little swelling; pre-septal cellulitis is the whole eyelid, upper and lower, often swelling the whole eye shut.
-DDx of swollen eye: insect bites, trauma. If its B/L think nephrotic syndrome, neuroblastoma, CHF.
9. Conjunctivitis:
-Within 24-48 hrs of birth: think chemical
-2-4 days: gonorrhea
-5-12 days: chlamydia
In older kids:
-Bacterial: mucopurulent discharge. Tx with erythromycin eye drops. If its otitis-conjuctivitis, think non-typeable H flu. This will not respond to amox alone, you need augmentin (amox+clavaluate).
-Viral: adenovirus. Clearer mucus discharge.
-Allergic: itchy, minimal drainage. Eye drop/systemic antihistamines.
10. Abdominal pain tips:
-colicky/crampy: suggests obstruction of peristaltic organ (ureter, bowel)
-insidious onset: suggests visceral peritoneum inflamm, or well-contained (abscess)
-in the absence of diarrhea, think outside of GI tract

1. DDx of constipation in a child:
--GI: hirschprungs (no stool in rectal vault, trisomy 21), anal stenosis/anterior anus, IBS, IBD, small L colon (IDM), meconium ileus (on imaging look for bubble sign, underdevelopment of distal colon) or DIOS (same as mec ileus, in older kid)
--Neuro: spinal cord trauma, dysraphism (tethering/MMS), compression. Hypotonia (trisomy 13), neurofibromatosis, CP
--Drugs/toxins: anticholinergics, opiates, iron, lead, laxative abuse, botulism, antidepressants
--Endocrine: hypothyroid, hyperCA/hyperparathyroid, pregnancy
--Heme/Onc: neuroblastoma, pelvic cancer
--GU: over-full bladder, UTI
--Resp: CF
--Diet: anorexia, no fiber in diet, cows milk intolerance
--functional (can be associated with intro of solid foods, toilet training, starting school)
--with-holding (painful defecation leads to withholding--> loss of sphincter tone--> loses sensation of urgency--> worse constipation). Look for kid on toes.
2. NEXUS criteria for clearing C-spine in people of all ages (mnemonic "nsaid"). Little data on children <2 years, but still used by some practicioners.
--No focal Neuro deficits
--No Spinal tenderness (palpate down c-spine)
--No Altered consciousness
--No Intoxication
--No Distracting injuries
Shown to be sensitive in picking up spinal cord injury. Protip: if the kid is flailing his arms and legs all about and crying loudly, his spinal cord is fine.
3. Every peds trauma patient gets O2, regardless of their sat.
4. If you think you may have to intubate a trauma patient, think about drawing up meds (etomidate/succinycholine) beforehand, as you have to calculate doses and volume to draw by weight of kid, and it takes a while. Also, consider gathering fiber optic intubation equipment to the trauma room.
5. In a kid with chest trauma who acutely decompensates, suspect cardiac tamponade. To prepare for chest trauma kid: chest tubes, decompression needles. PS Respiratory symptoms + tachycardia + chest trauma are suggestive of tension pneumothorax, even in the absence of tracheal deviation.
6. A kid with head trauma may have brain bleeds, and thus may seize at inopportune moments: draw up ativan ahead of time in case you need to emergently administer it.
7. Weight loss in newborns: It's normal to lose up to 10% of birthweight in their first week or so of life: you expect a full return to birthweight by the time they're 2 weeks old.
8. Hyperbilirubemia criteria are highly dependent on age (measured in hours). Use http://bilitool.org/ to determine if baby is at risk. Transcutaneous bilirubin measurements are less accurate than serum-- if suspicion is high, do the blood test. Jaundice goes from head to toe, and a rough measure of blood level is possible based how far down the jaundice is seen.
Face 4-8
Upper trunk 5-12
Lower trunk & thighs 8-16
Arms & lower legs 11-18
Palms & soles >15
9. Cri du Chat is associated with many physical and neurological findings, among which are severe developmental delay, largyngeal abnormalities (problems sucking/swallowing, laryngeal stenosis-- may necessitate g-tube feeding) and cardiac anomalies, like ASD, VSD and tetralogy of fallot: if the pulmonic stenosis is repaired, it may be associated with pulmonic insufficiency. The murmur may be a whooshing sound, with a loud systolic and a much quieter diastolic, louder in the pulmonic window.
10. Brain tumors in children come in multiple histological subtypes: meduloblastoma (small round blue cells, may have drop mets), ependymoma (usually in 4th ventricle), pylocytic astrocytoma (grade 1 astrocytoma, solid and cystic components, good prognosis), low grade astrocytoma (grade II), and high-grade astrocytoma (grade III/IV). Prognosis highly dependent on location and diffuse vs focal. Try to avoid radiation, as irradiating children leads to growth stunting and neuro-cognitive delay-- the younger the kid, the worse the consequences.

1. Febrile seizures come in 2 types: simple and complex.
-simple: generalized, <15 min, one in 24 hours, rare
-complex: partial, >15 min, more than 1 in 24 hours, common
2. Chronic treatment for febrile seizures is generally not indicated because many AEDs have limited effectiveness and carry significant side effects (i.e hepatic failure with valproate). Acetaminophen/NSAIDs treat fever but do not decrease incidence of febrile seizures. Diazepam can decrease incidence of seizures if given at the beginning of a cold, but seizures can often be the first presenting symptom of a viral illness, so practically it's not very useful.
3. Acute otitis media occurs in up to 75% of all children by age 1. Kids' eustachian tubes are shorter and more horizontal, more prone to be obstructed with mucus/swollen adenoids. Otitis media is common a few days after the start of a viral infection, and is usually caused by s.pneumo, moraxella, or HiB. Diagnosis criteria: (1) Effusion (impaired movement on insufflation) (2) inflammation (bulging/color change of tympanic membrane to hemorrhagic, grey, yellow) and (3) acute onset of symptoms, such as pain.
4. Treatment for AOM: Most (90%) of kids over 2 years old do not require antibiotic treatment, as acute otitis media is self-limiting and will resolve in 2-3 days. Criteria for treatment: age<2 years, toxic-appearing kid >2, hx of recurrent complex AOM, immunodeficiency or abnormal cranial anatomy, AOM that fails to improve after 48 hours. First line treatment is amoxicillin (high dose: 75-90 mg/kg/day divided into 2 doses for 5 days). If pt fails to improve after another 48 hours, consider resistance and add clavulanate to the amoxicillin, if pt still fail to improve, try IM ceftriaxone and call for ID consult. And ENT consult.
5. If someone comes into your ER, 3 days after a 2 week hospital stay for open abdominal surgery, spiking 40 degree fevers with a 30 cm incision that appears to be dehiscing and leaking obviously purulent serosanguinous fluid, PO bactrim and discharge to home is not an appropriate management plan. Bactrim is for 20 year old women with UTIs, and that woman needs to be admitted for surgical debridement. You'll want to provide broad-spectrum coverage of gram positives (+MRSA), gram negatives, and anaerobes (abscess/GI tract organisms). Consider vanc+ 3rd gen cephalosporin/aminoglycoside + metronidazole, until your cultures (of tissue) grow out a specific organism with sensitivities.
6. Weight gain in pregnancy:
BMI <18 = 30-40 lb
BMI 18-25 = 25-35 lbs
BMI 25-30 =  15-25 lbs
BMI 30+ =10-20 lbs
7. First trimester screen: HCG and PAPP-A+ nuchal translucency (85% sensitivity)
Second trimester screen: AFP, b-HCG, unconjugated estriol  (triple screen) + Inhibin A (quad screen)
8. Adults can tolerate 3-4 minutes of apnea before they become hypoxic. In premature neonates, its closer to 15-20 seconds. School age kids: 1-2 mins, etc. It's a function of how much lung capacity they have and how much oxygen reserve they have therein.
9. Glucose & Dementia: A big (n=2067) cohort study in NEJM showed higher glucose levels are associated with an increased risk of dementia: glucose of 115 vs 100, HR 1.18 (95% CI 1.04-1.33). http://www.nejm.org/doi/full/10.1056/NEJMoa1215740
10. Beta agonists and steroids cause leukocytosis.

1. Chronic NBNB vomiting (w/ weight loss) in an infant:
--Refuses food: likely GERD (esp younger than 3-4 months) since kids’ abdominal/diaphragm muscles are weak and can’t keep food down. At >3-4 months, think other causes. An inflammatory malabsorption (esp with diarrhea), intussuception (esp with blood in stool

--Doesn’t refuse food: think obstruction vs milk allergy.  In a neonate or young infant, think congenital obstruction, in an older kid, think constipation. R/o with abd x-ray to look for fecal impaction, u/s to look for pyloric stenosis. Think cow’s milk allergy if the kid has recently been weaned from breast milk (unless the mom drank a ton of cow’s milk, there will have been little cow milk protein in her milk). Change to very hydrolyzed formula (nutramigen) and see if it resolves. 

2. Bartter’s syndrome (NKCC2 R mutation): it’s like they’re on Lasix all the time. Shutting down the receptor means greater volume of more dilute urine- you can’t remove salt at TALH, so you can’t remove water in collecting ducts. You lose the cycling of K (K comes in through NKCC, goes out through K channel), so you lose the net positive charge in kidney tubule lumen, which is the driving force for the reabsorption of divalent cations. This leads to kidney wasting of Ca & Mg. You don’t waste Na, since your kidneys ramp up reabsorption of Na at the DCT and CD, at the price of losing K and H. Additionally, the loss of Cl at NKCC means that your body will also reclaim bicarbonate to make up the charge balance, worsening the alkalosis. Treatment is to figure out which electrolytes are low, and to replenish.

3. Gittleman’s syndrome: NaCl R mutation: its like you’re on a thiazide diuretic all the time. Gordon’s syndrome: mutation in the regulation of NaCl, leading to increased expression, the opposite of being on a thiazide: you retain water and salt, and become hypertensive. Tx with a thiazide diuretic (now isn’t that convenient?

4. Lasix tolerance: starting Lasix diureses great at first, but over time the kidneys compensate. I.e. upregulation of Na-Cl receptors in the DCT. This compensatory process is driven in part by hypochloremia. Replenishing chloride will often cause diuresis to resume, as will adding a thiazide diuretic (which will possibly worsen the hypochloremia

5. Complete asthma history:

--Age of dx, +eczema/allergies, previous classification: symptoms/week (wheezing, coughing, SOB), nighttime symptoms/month (waking up to cough

--History: number of ER/hospital visits in the last year/lifetime. Lifetime ICU/intubation/bipap. How often do you miss school/work or does asthma interfere with activities.

--Medication: rescue inhaler/nebs, controller medicine, allergy medicine. Ask: how often are each used/using a spacer?

--Triggers: smoke, weather, exercise, pets, scents, mold, colds.

--Family Hx of atopy

6. Rolandic epilepsy: a benign epilepsy of childhood, peak incidence at 7-9 years of age, usually resolves by 13 on its own. Associated with centro-temporal spikes on EEG. A partial simple epilepsy that involves the face muscles, occurs generally at night (can be missed). Can generalize to tonic-clonic seizures. Generally not managed with AED: meds decrease generalization, but don’t decrease incidence of partial seizures. 

7. DDx of hemoptysis in a child:

--Infectious: TB, lung abscess (strep/staph), bronchiectasis (CF)

--Mechanical: foreign object, tracheal erosion from suctioning someone on a ventilator, trauma

--Rheum: Wegener’s (GPA), goodpasture, sarcoidosis, churg-strauss

--Vascular/Blood: AVM, PE

--Other: diffuse alveolar damage (precursor to ARDS), malignancy

--Cardiac: diastolic failure => backup of blood in lungs => pulmonary hypertension & blood leaking into alveoli. Think mitral stenosis, diastolic heart failure (amyloid/sarcoid), pulmonary hypertension. 

--Differentiate from hematemesis: pH (hematemesis will be acidic, hemoptysis will be alkaline), appearance (hemoptysis will be frothy) 

8. Babies fed exclusively goat's milk or who are vegan/fed with breastmilk from a vegan woman can suffer from B12 or folate deficiency and end up with megaloblastic anemia, or worse, methylmalonic acidemia --- inability to convert MMA to succinyl-CoA, MMA accumulates in myelin and can lead to seizures, neurodevelopmental consequences. 

9. The only indications for soy formula are galactosemia, or strict vegetarian diet. Babies that are allergic to milk have a 10-15% cross-allergy with soy, so it's better to put them on hydrolyzed cow's milk formula. 

10. Review of hypersensitivities: 

--type 1: anaphylaxis, IgE mediated

--type 2: autoantibodies against fixed structure (i.e. basement membrane-- goodpastures)

--type 3: autoantibodies against non-fixed antigen (i..e. IgM against IgG)

--type 4: cell-mediated, delayed.

1. Most infants will drink 2-6 oz of formula/breast milk per meal, and will drink every 1-3 hours. The baby will decide how much is enough-- don't deny an infant food. If s/he eats more, she will likely spit up more, that's ok. Don't let a neonate go >4 hours without food.
2. "wry neck" aka congenital torticollis, can be due to in-utero malposition or birth trauma, due to shortening of one of the SCM muscles. SCM is shortened, resulting in head being turned towards unaffected side and tilted towards the affected side, and sometimes well feel tight/have a calcified portion. Since the baby tends to turn its head one way, it may result in asymmetric head shape from lying preferentially on one side/in one way. Tx is to stretch it for by purposefully turning towards unaffected side and massaging the muscle for 30-60 seconds, multiple times a day (i.e. every time you change the diaper).
3. At 9 months, a child should be able to clap its hands/wave bye bye, have a pincer grasp, sit up on its own, crawl, say mama/dada, and is beginning to become afraid of strangers. This can make the exam more difficult, because baby is afraid of you: sit them in parents' lap for exam. They should be sleeping through the night; if baby is waking up wanting to be fed in the night, tell parents not to feed til morning. Put baby back to sleep in crib when it's tired but not yet asleep, that way baby will learn to fall asleep on its own (i.e wont be dependent on being rocked to sleep by parent).
You draw blood for:
-CBC to check for anemia, since 6-9 months is when their iron stores from mom run out). If breast feeding, should start supplementing iron at 4-6 months 1mg/kg/day.
-Lead results. No level of lead is "ok" but we aim for a blood lead level <5. If it's over 10, then the state will send people to examine the house. BLL>45 can be associated wtih lethargy, anorexia, decreased activity, vomiting, abd pain, constipation, anemia. BLL>70: acute encephalopathy, comna, seizures, ataxia, behavioral changes. Over 30s-40s, treat with succimer (DMSA). Over 70, treat with EDTA/dimercaprol. If a kid comes in with a high lead level, x-ray them to look for lead in their GI tract. If there are paint chips in their belly, chelation is pointless and will only encourage greater absorption. Most common sources of lead: paint chips, window frames, soil (from leaded gasoline and demolition of old buildings), pipes. Lead poisoning more common in kids with iron deficiency.
4. At 2 months, baby should be able to hold its head up off the table, follow an object past midline (eyes don't focus til ~4 months), coo, recognize faces and have a social smile. Infants can see black, white and red but not other colors well. At 2 month visit, they should be vaccinated with: oral polio, DTaP, Prevnar (13-valent pneumococcus), hep B, HiB. No flu shots. No water since that can lead to hyponatremia.
5. When doing a well-baby checkup, ask about
(1) developmental milestones  (2) eating (breast vs formula, how much, how frequent) (3) wet diapers - should be >6/day (strength of urination), BM- should be >1-4/day (color, consistency-- tell them to call docs if poo is black, red, or clay-beige colored). (4) home safety (car seats, smoke detectors, pets, cigarette smoke in the home)
When doing an infant exam, check fontanelles, red reflex, ears, neck for LN, clavicle, abdomen for masses, femoral pulses, testicular descent (boys), diaper rash, spine, reflexes- moro, babinksy.
6. Car safety for kids:
Infant-2 years: rear facing carseat in back,\
Age 2-4 years/up to 40 lbs: forward-carseat, \
Age 4-8 years/til 4'9": booster seat, age 8+/4'9"+: seat belt.
Can't sit in the front until age 13.
7. Obesity leads to type 2 DM in children, sleep deprivation may compound the risk. In children younger than 10, most DM is type 1 with type 2 being rare, but the ratio of type 2 gradually increases as you go up in age from 10-19
8. Rashes in kids: often eczema or contact dermatitis. Treat with topical steroids: high- and low-potency depending on the severity of the breakout. No high-potency steroids on face or groin: skin is thinner and more sensitive. Higher systemic absorption, darkening. Psoriasis is rare in children, usually presents as guttate after strep. Seborrheic keratosis common in infancy (cradle cap) but rare afterwards.
0. Causes of childhood rash:
First disease: measles
Second disease: scarlet fever
Third disease: rubella
Fourth disease: n/a
Fifth Disease: parvo- erythema infectiosum
Sixth disease: roseola (HHV-6/7)-- assoc with high fever (38.5-40.5) for 3-5 days, followed by maculopapular blanching rash. Assoc with bulging fontanelles and febrile seizures (assoc with 20-30% of first febrile seizures in children)
Others: RMSF, VZV/chickenpox, mumps, rhinovirus, allergic rxn to pencillins
10. Small umbilical hernias are common in children of color (up to 80%).

1. Child presents with fatigue, easy bruising. CBC comes up with a WBC of 100K, 98% blasts, hb 5 and platelets 5k. You suspect ALL.
Workup:
-BMP: ALL kids often have high K/Phos (since cells are lysing) and low Ca (since phos is high).
---Tx hyperK: shift K intracellularly (albuterol neb, insulin+glucose, bicarb if they're acidotic) and excrete it (lasix, kayexylate). Give kayexylate PO, not rectally, b/c kids with ALL are often effectively neutropenic. Even if their counts are high, their neutrophils suck/are blasts.
---To prevent Ca-Phos crystals, do not supplement Ca unless they are symptomatic, aim for a Ca*Phos<60, and do not alkalinize beyond 8.
---Keep an eye on BUN/Cr since crystal precipitation (urate/ca-phos) and tumor invasion/compression of GU system can cause renal failure.
-Uric Acid & LDH: both will give you a sense of tumor burden and of tumor lysis syndrome. To prevent uric acid crystals from forming, alkalinize slightly with bicarbonate.
-CXR: look for mediastinal mass
-Immunophenotyping: figure out if its acute vs chronic, lymphocytes vs monocytes, T-cell vs B-cell.
-Coag studies: PT/PTT & d-dimer/fibrinogen to r/o DIC
 2. Preventing tumor lysis syndrome: give allopurinol with chemotherapy. If someone is symptomatic, you can give a uricase, which directly breaks down urate. However, it is very expensive and thus not indicated for broad use in everyone. Steroids can help lower tumor burden in a slightly slower, more controlled way.
3. DDx of anterior mediastinal mass: lymphoma (hogkins/non-hodgkins), T-cell ALL (esp in teenager), thymoma, germ cell, thyroid. Posterior mediastinal mass: neuroblastoma (check urine/serum VMA/HVA)
4. It's hard/potentially dangerous to sedate someone with a mediastinal mass: they often have diminished respiratory capacity; in sedation, you lose negative intrathoracic pressure and respiratory muscle tone, further reducing ease of breathing (and also of mechanical ventilation). This can cause the mass to fall onto the mediastinum and compress either the respiratory structures (even a trach wouldn't help you then) or the major vessels, leading to a precipitous fall in preload and then to cardiac arrest.If you're going to sedate someone with a mediastinal mass, load them up with IV fluids beforehand and have an ECMO on standby.
5. Hyperleukocytosis can lead to leukostasis (sludging of WBC) esp if white count is in the hundreds of thousands. Sludging of capillaries in lungs (leading to respiratory insufficiency) and brain (leading to neurological deficits ranging from fatigue or behavior changes to ataxia, seizures, stroke) are most concerning. Kidneys can also take a hit.
6. In terms of leukostasis, myeloblasts are the worst because they are big, least deformable, and trap plasma between them. Lymphoblasts are slightly better (i.e. you need a higher "leukocrit" to have the same clinical sequelae) and mature lymphocytes are the best. The body will often decrease the hematocrit in an attempt to reduce blood viscosity-- thus, in someone with leukostasis, do not transfuse unless absolutely necessary, even if their hb is very low.
7. Spinal cord compression can happen in neuroblastomas, adrenal tumors, spinal  osteosarcoma. First sx is pain, then paresthesias, final loss is bladder/bowel. Tx is with high-dose steroids and laminectomy.
8. Any temperature over 100.4 F/38 C in a newborn (measured rectally) requires emergent hospitalization for at least 48 hours, with blood and urine cultures and a LP (neonate BBB is less developed). Most common bugs causing infection in a neonate: listeria, e.coli/GNR, enterococcus, GBS. (Slightly older neonate: HiB, S.pneumo, Neisseria). Treat empirically with Amp+Gent, or Amp+Cefotaxime in places with widespread gent resistance. Amp covers listeria, e.coli and other easy GNR (hib, kleb, proteus etc), and easy gram pos like strep and non-b-lactamase-staph. Cefotaxime is a 3rd generation cephalosporin like ceftriaxone, and has excellent gram negative coverage-- hits everything except pseudomonas.
9. Constipation is a common occurrence in kids. Treat with stool softeners first (PEG, like miralax): titrate up the dose if its not working at first. Go to stimulant laxatives (like senna) only after the stool softeners have failed. If you do give a stimulant, you must also concomitantly give a stool softener.
10. Treat a penicillin-induced allergic rash with benadryl (children: 1-2 mg/kg q6 hours)

1. Type 1 RTA: distal tubule, error with H-K transporter in a-intercalated cells. Associated with severe acidosis due to inability to excrete H, and hypokalemia due to inability to re-absorb K. Easily treated with bicarbonate, children will often "outgrow" it. In adults, often due to autoimmune disease (sjogren's lupus) and can often be a presenting feature of the disease. In children, can be due to genetics (mutated transporter) or nephrotoxic drugs (ifosfamide).
2. Type 2 RTA: proximal tubule, error with Na-Bicarbonate transporter. Kidneys waste bicarbonate; Treatment is bicarbonate supplementation, but it's like filling a bucket with a leak in the bottom. Difficult to treat, often associated with significantly damaged tubules, often requires lifelong treatment. Sometimes associated with Fanconi's syndrome. In adults, often due to accumulation of immunoglobulin light chains (multiple myeloma), which are resistant to degradation by lysosomal enzymes of prox tubule cells and will thus accumulate there.
3. Type 4 RTA: distal tubule, error with aldosterone action; either aldosterone deficiency or resistance. Results in hyperkalemia (aldosterone causes loss of K). Treat with aldosterone-mimetic.
4. All cases of RTA will cause non-anion gap acidosis, since "the kidneys compensate for NaHCO3 loss by retaining NaCl in an attempt to preserve volume, with the net effect being a mEq-for-mEq exchange of chloride for bicarbonate and no change in the AG." -uptodate
5. Common presenting symptoms of RTA in children: failure to thrive, kidney stones, paralysis/weakness (from electrolyte abnormalities), tachypnea.
6. Giving maintenance fluids: if you give isotonic maintenance fluids, people will eventually become edematous. People with normal kidneys will naturally pull back the vast majority of the sodium in their urine, leading water to go with it. Water follows salt, so the more salt you give the more water you give. Additionally, the stress response (2/2 pain, stress from being in the hospital) leads to ADH secretion, which pulls back more water and leads patients to become volume overloaded. If you want to avoid this, you give hypotonic maintenance fluids, so that there is less salt in their system. However, when you do this, you risk diluting out their serum and giving them hyponatremia.
-In adults, who often are suffering from some degree of heart or renal failure, you don't want to volume overload them, so you tend to give more hypotonic solutions (0.5NS, for example)
-In children, who have healthier hearts, you're more worried about hyponatremia, so you give isotonic solutions (0.9 NS, or LR).
7. Insensible fluid losses: 400-600 ml/m2/day. Max Na replenishment rate: 10 mEq/day
8. if you're really worried about edema/third spacing, you can give someone albumin to pull all the fluid out of their third spaces, and then chase them with lasix.
9. Most common cause of congenital blindness in utero: CMV, then rubella. Most common cause of preventable blindness in infants: chlamydia. Erythromycin eye drops cover GC, but not chlamydia well. if you're worried about chlamydia, do systemic erythromycin.
10. Treatment for moms with GBS: first line penicillin (0% resistance). Next line clinda (15% resistance). If resistant to clinda, give vanc. Side effects of ceftriaxone (biliary sludging/cholecystitis), erythromycin (pyloric stenosis), doxycycline (stained teeth/bones since it's a Ca chelator)