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235 Cards in this Set

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what causes croup, what causes bronchiolitis? what structures are affected?

treatments?
croup = laryngotrachiobronchitis, it's caused by PIV. this is upper airway inflammation. inspratory stridor and barking cough.

bronchiolitis = RSV. lower airway infection = WHEEZING. mistaken for asthma. kids under 2 at risk can be prophylaxed with PALIIVIZUMAB and treated with RIBIVIRIN.
what are the two diseases that cause leucocytosis with a predominance of lymphocytes?
atypical lymphotyctes seen in primary EBV infection (mononucleosis), and in the ones that mimic it (toxo/CMV)

also in WHOOPING COUGH (bordatella pertussis) - rapid cough followed by inspratory whoop. give ERYTHROMYCIN (to pt and entire family)
what's the random bacteria that causes meningitis that's still considered "aspetic?" how do the symptoms compare to traditional bacterial meningitis?
boriella burgdorferi = lyme disease. onset is 1-2 weeks, instead of near instantenous.

same kind of mild symptoms...low fever, headache, stiff neck, photophobia.

rash = erythema migrans, not petechia/purpura.
what are the CSF findings that differentiate bacterial from viral from lyme meningitis?
1. bacterial: WBC = >1000. Protein high. PMNs dominante. glucose is LOW

2. Viral: WBC = <500, protein normal or high, glucose normal. PMNs = less than 50%.

3. Lyme: WBC = <100, lymphocytes dominate. Protein and glucose is same as viral: protein is normal or high, glucose is normal.
kid with GI infection gets erythema nodosum: what's the likely bug? what's the other random symptom classic for this?
yersenia enterolotica:

also causes PSEUDO-APPENDICITIS.
what are the characteristics of congenital syphilis?
snuffles: bloody, green mucous discharge from the nose.

hepato/spleno megaly, lesions, jaundice.
how do you treat PID?

what are the random rare complications of the causative organisms?
need to cover both neisseria gonorrhea and chlamydia trachomatis:

neisseria killed by single dose third gen cephalosporin (ceftriaxone, ceftazadime).

chlamydia requires longer course of doxy.

could cover both with oral levofloaxcin for 14 days.

neisseria: common cause of septic arthritis.

chlamydia: reiter's syndrome (urethritis, conjuctivitis, arthritis)

fitz hugh curtis syndrome: perihepatitis, caused by both.
what's the risk of vertical HIV transmission?
untreated = 25%.

if mom and baby get AZT, it's 2%
rocky mountain spotted fever: symptoms? treatment? what can it look like?
indistinguishable from meningococcemia: so cover neisseria too.

doxy = treatment of choice.

rash on the wrists, spreading to trunk, involves hands too.

no good test.

ricketcia ricketsia: comes from tick, non-specific flu like symptoms.
major signs of lyme disease? what's the name of the rash?
remember tick has to feed >48 hrs.

facial nerve palsy and heart block are possible.


rash = erythema migrans. this is the targetoid lesion.
what are the 3 major causes of otitis media?
strep pneumo, non-typable H. influenza B, and moraxella cattharals.
what causes scarlet fever? signs?
strep A. think sore throat + sandpaper rash.

don't forget that post-strep glomerulonephritis isn't prevented by antibiotics.
what are the necessary criteria for ADHD?
>6 months
present continuously since age 7
happens at home and at school
poor concentration, hyperactivity, easily distracted.
what's anemia of prematurity? signs? smear shows?
Hb around 7
problem of low RBC production and shortened life span

normochromic/normocytic, low reticulocyte count.
what are the tactile differences in wilms vs. neuroblastoma?
remember that neuroblastoma is in the adrenals above the kidney: it pushes them down and the kidneys aren't palpable.

wilms tumor = kidneys still palpable.
what will make cyanosis more or less evident?
all about Hb saturation:

RIGHT SHIFTING curve makes cyanosis MORE evident. Think that cyanosis shows up in the VENOUS flow, so those things that encourage transfer of O2 into the tissues = more blue.

higher acidity, higher temp, high Hb concentration (competing for fixed o2), less HbF.
what happens to pulmonary vasculature signs on X-ray in L to R vs R to L shunts?
L to R shunts cause increased pulmonary vasculature (forcing more blood through lungs).

R to L shunts diminish vasculature signs.
how can you test pre-ductal vs. post-ductal cyanosis, and what is the significance if difference is detected?
R. arm blood flow is PRE-DUCTAL, lower limbs are POST-DUCTAL.

If pre-ductal has HIGHER O2 sats = 'differential cyanosis' = blue legs - think that de-oxygenated blood is flowing through a PDA...this must be high pressure in the pulm circulation or low pressure in the LV outflow. persistent pulm. HTN of newborn (PPHN), aortic stenosis, coarctation.

opposite: if blue arms, have REVERSE differential cyanosis: this means oxygenated blood is flowing across the PDA into the aorta. TRANSPOSITION
what's a hyperoxia test?
look at preductal ABG (r. arm arterial puncture): give an Fi02 of 100%: if the PaO2 > 250 mmHg, the heart is OK.

if <50, have a heart problem.
why is a PFO needed to survive transposition of the great vessels?
the two cirulcations (pulm/systemic) are in PARALLEL: the left heart pumps blood into the lungs, the blood comes back into the left heart from the lungs. Systemic blood goes into the right heart, pumped back out to the body.

only time you get mixing of oxygenated/deoxygenated blood is through the PFO.
what's total anomalous pulmonary venous connection?
pulmonary veins returning to the right heart don't make it: they hook up to each other or go back to the vena cava, into the RA etc...either way, the only way to get blood from the right heart to the left is through a PFO.
what happens in tricuspid atresia?
no tricuspid valve and no right ventricle. the left heart does pretty much everything: LA collects pulm/systemic blood, and a VSD allows the LV to pump into both the aorta and pulmonary artery. CYANOSIS USUALLY PRESENT EARLY.

also likely to have pulmonary stenosis: this will increase the cyanosis.

left ventricle will HYPERTROPHY because it's doing all the work.
tetraology: what are the 4 defects, what are symptoms in kids?
pulmonary stenosis, VSD, a big aorta, and RV hypertrophy.

kids will squat to increase systemic vascular resistance (drive the R to L shunt the other way, also increase venous return).

also have TET spells: fussy, fast breathing, turn blue.
what's ebstein's anomaly? what's the murmur?
screwed up tricuspid leaflets (downward displacement of tricupsid valve) means that the RV and RA are sort of one unit: TONS of tricuspid regurg = MASSIVELY DILATED RA.

pulmonary artery may not get much blood: depends on a PDA to shunt blood into the lungs.

difficult to treat surgically, if bad, need transplant.

murmur: tricuspid regurg + mid-diastolic murmur PLUS quadrouple rhythm (S3 + S4)
what's hypoplastic left heart?
essentially no blood flow through left heart: any blood getting to systemic circulation comes from RV to pulmonary artery through a PDA.

becomes most obvious as PDA closes in kids: they loose their systemic circulation, get shock.
intusucception: how does it present in kids, and how do you treat and diagnose it?
Colic pain episodes...between these, they're fine. OFTEN feel a mass. usually at the ilio-cecal junction. have red current jelly shit.

use AIR-CONTRAST ENEMA: this diagnoses AND treats most cases.
what about a meckle's diverticulum? what's the signs of this and how do you diagnose?
painless bleeding, usually in kids under 2 years old.

can be SEVERE bleeding, kids can present in shock/anemia.

scan = TECHNETIUM-99m pertechtinate scan = meckle's scan
what are the signs and treatment of iron poisoning?
you can see iron tables on X-ray: they're dense.

nausea/vomiting, low BP due to cytotoxicity and third spacing, liver toxicity.

lactic acidosis = low HCO3-.

DEFUROXIME is the chelation treatment of choice.
3 month or younger girl has vaginal bleeding: what's most likely up?
vaginal bleeding of the newborn: comes from maternal hormones that crossed the placenta, she's spotting. do nothing.
B3 deficiency looks like...?
PELLAGRA: dermatitis, dementia, death, diarrhea.
what are the outcomes of septum primum/secundum/sinus venosus ASD's?
septum secundums are typical and, if small, will close spontaneously.

primums/sinus venosus will NOT close spontaneously and must be closed surgically.

note that any of them can lead to RA enlargement over time, SVT, and eventually eisenmenger's.
what are type I and type II second degree heart blocks?
type 1 = progressive lengthening of PR interval until you drop a QRS.

Type 2 = random drop outs of QRS after normal P. No lengthening. problem is below AV (his/purkinje)
third degree heart blocks: how can you tell what structure is generating the escape rhythm?
if it's coming from the AV node, the QRS width will be normal (though the rate is low).

if it's coming from the ventricles, they'll depolarize in a disorganized way and the QRS width will be wider.
what disease presents very much like scarlet fever?
kawasaki's: bright red tongue/throat, sequaminating rash, high fever. almost impossible to tell apart. DIFFERENCE: kawasaki's has CONJUNCTIVITIS and thrombocytosis

remember that group A strep can cause rheumatic fever, while kawasaki's causes coronary artery aneurysms and thrombosis.

treatment for kawasaki's = high dose aspirin and IVIG.
what do you do with a newborn exposed to pertussis?
mom's immunity doesn't help: baby needs erythromycin. only way to prevent for sure.
erythema toxicum? when? what cell inside? mistaken for?

erythema infectiosum = ?

xanthema subitum =?

erythema chronicum migrans?

erythema marginatum?
erythema toxicum does NOT APPEAR IN FIRST 24 hours: usually 2nd/3rd day. full of EOSINOPHILS.

mistaken for staph scalded skin: can appear on day 1, skin sloughs off.


erythema infectosum = fifth disease = parvovirus infection = "slapped cheek"

xanthema subitum = roseola = HHV6 = high fever, goes away, big rash starts on TRUNK moves out

chronicum migrans = lyme disease targetoid rash.

erythema marginatum = rings on trunk/inner arms seen in rheumatic fever
what's a hint that a kid has a STAPH AUREUS pneumonia?
fast onset and lots of bad outcomes: pneumothorax, pneumatocoele, abscesses, etc
what's hand foot mouth disease? aka? signs/symptoms?
herpangina: caused by enteroviruses and coxackie.

high fever, sore throat. little red marks around mouth, hands, feet.
heart block = increased PR interval. what does a SHORTENED PR interval indicate? what symptoms go with it?
wolf parkinson white: an extra pathway from the atria to the ventricles = short PR interval.

get episodes of SVT, which can cause diminished activity due to low cardiac output.
what's TAR syndrome? goes with what heart defects?
thrombocytopenia and absent radius: tiny arms with weird thumbs and almost no platelets. super deadly.

associated with tetragology and ASD.. think T/A.
what's noonan syndrome? associated cardiac defect?
this is the male (or female) turner's: short, kinda fat, webbed neck, cryptorchidism, and PULMONARY STENOSIS. have slanted palpebral fissures and low-set fucked up ears.
inherited prolonged QT syndrome causes what other major defect? signs?
adolescent syncope can be prolonged QT.

seen with CONGENITAL DEAFNESS = jervell lange nielsen syndrome.
neonatal heart block is what until proven otherwise?
maternal SLE. baby can also have rash, THROMBOCYTOPENIA.
PICA can indicate what in relation to hematology?
iron deficiency OR lead poisoning.
what are the basic causes of anemia, how do you think about them? based on size...
rbc destruction, lack of RBC production, RBC loss.

microcytic = Fe++ deficiency, thalasemias, sideroblastic (lead, B6), chronic disease. Problem making HEME (Fe++ deficiency, Pb/B6) or GLOBIN (thalasemias)

macrocytic: folate/B12, orotic aciduria

normocytic: increased destruction (inherent to cell: G6pd, sickle cell, spherocytosis) (outside cell: MAHA, autoimmune). Blood loss.

if retic count is raised, think blood loss/destruction. if not, think lack of production (bone marrow problems).
go through the different kinds of alpha-thalasemia:
4 deletions = HbBart disease: get lots of gamma tetramers (gamma4), this is HbBart and is fatal.

3 deletions = HbH disease: gamma production happens in utero and are born with SOME HbBart. Eventually, as beta production comes online, get HbH (beta tetramers) appear by several months.

Alpha thal trait = 2 deletions. Mild anemia. NORMAL ELECTROPHORESIS.

1 deletion = silent carriers.
describe the 2 kinds of beta thalasemia:
major = two gene problems (not usually deletions, problems with transcription/translation).

No HbA can be made. Lots of HbF when born.

Without therapy, get frontal bossing, extramedullary hematopoesis, severe anemia/splenic destruction, death within a couple years.

support with transfusions = get iron overload.

one deletion = trait, mild anemia. Increase in HbA2 (2 alpha, 2 delta). and HbF.
what does TEC stand for? what might be mistaken for it?
Transient erythroblastopenia of childhood: random failure of bone marrow to make RBC's. usually post viral infection.

normocytic anemia with DECREASED RETIC COUNT.

like diamond-blackfann syndrome, but happens >1 yr old.
compare IgG and IgM autoimmune hemnolysis:
IgG is warm, cannot agglutinate, can't complete complement through C9 so no intravascular hemolysis (but will cause extravascular hemolysis).

IgM is cold, can turn on complement through C9 and does intravascular hemolysis so you'll see dropped haptoglobin, and does cause agglutination.
if you have hemolysis that isn't due to intrinsic RBC membrane problems, what's the though process?
non-immune: microangiopathic = HUS/TTP/DIC. Macroangiopathic = synthetic valves, burns, AV malformations.

isoimmune = Ab's against someone else's RBCs. ABO incompatability.

Autoimmune: IgM or IgG, sometimes post-infections or post drugs (alpha methyl dopa, quinidine, penicillin).
osmotic fragility test diagnoses what?
spherocytosis. remember that these kids DO GET APLASTIC CRISES from parvovirus B19 infections.
what can cause sickling in sickle cell patients?

what do you see on electrophoresis of sickle cell trait and disease?
low o2 concentration, temperature changes, acidosis, and dehydration.

trait electrophoresis: less than 40% HbS, 60% HbA

HbSS electrophoresis: ZERO percent HbA, >80% HbS, HbA2 and HbF.

don't forget that sickle kids have DELAYED DEVELOPMENT/puberty.
in sickle cell patients, what kinds of vaso-occlusive crises do they get at what age?
at months old to a few years, get DACTYLITIS = hand/foot syndrome = avascular necrosis of metacarpal/tarsal bones.

children get long bone/sternum pain.

teenagers get avascular necrosis of the femoral head.
what happens in the hearts and abdomens of sickle cell patients?
heart gets chronic microvascular damage and hypertrophies...adults often die of CHF.

abdomen is similar, but pain mimics acute abdomen: hard to rule out apendicitis, etc.
what does G6pd deficiency do and how is it different in greeks vs. blacks?

how do you test for it?
no G6pd = no NADPH = no reducted glutathione = oxidative damage.

blacks have an isoenyme that decays in 13 days.

greeks have a worse condition with an isozenzyme that lasts only a few hours.

don't forget heinz bodies (precipitated globin) and bite cells. `

g6pd assays may be falsely negative during crises (the crappy cells already died out) - may need to wait for them to recover or test their moms (it's x-linked recessive, so had to come from mom).
what do kids given goat milk get?
folate deficiency
what's diamond blackfan syndrome? risks? treatment?
a pure-red cell aplasia. like TEC, but happens in 1st year.

differentiate from TEC by age of onset AND in diamond, RBC ADA is elevated (normal in TEC).

often have physical defects and increased risk of leukemia later.

treatment is life long high dose steroids or transfusions.
what happens in fanconi anemia? associated conditions?
PANcytopenia, due to mutation in DNA repair.

goes with lots of developmental abnormalities (microcephaly, absent thumbs, cafe au lait spots, weird kidneys). risk of leukemia. hyperpigmentation.
what's neonatal isoimmune thrombocytopenic purpura?
when baby platelet ends up in mom's circulation, she makes IgG against it, that crosses placenta and kills baby's platelets.
what causes TTP and what are the signs?
lack of von wilibrand factor cleaving protein (ADAMTS 13). big multimeric vWF cause platelet aggregation and a MAHA syndrome. Get fever/renal/NEURO findings.
what happens to PT and PTT in hemophelia A and B? what about vWF deficiency? treatment options?
PT is normal, PTT is prolonged.

vWF deficiency can have normal or prolonged PTT (it supports factor 8).

there are no phenotypical differences between hemophelia A and B.

DDAVP (desmopressin) will increase release of factor 8 AND vWF from endothelial cells and 4x increase concentration, but does NOTHING FOR FACTOR 9 deficiency.
what's the triad of tumor lysis syndrome? why are these bad?

what's hyperleukocytosis?
hyperPHOSPHATEMIA = bind calcium, precipitate out as crystals that damage kidney tubules, AND cause hypocalcemia (tetany)

hyperURICEMIA - precipitate in renal tubules = renal failure.

hyperKALEMIA = arrhythmia

all stuff that normally lives inside cells escaping.

>200,000 wbc's = hyperleukocytosis: causes sludging and backup into the lungs (hypoxemia) and into the brain (strokes): happens in both ALL and AML.

need to pull out WBCs before starting chemo.

also remember that ALL tends to have mediastinal mases which can mess with the lungs and cause superior vena cava syndrome.
what are the 5 parts of beckwith widemann syndrome?
1. big tongue (macroglossia)

2. big baby (macrosomia)

3. big insulin (hypoglycemia)

4. omphalocoele

5. ear pitting

6. GU abnormalities?
what conditions is wilms tumor associated with?
beckwith widemann

WAGR: wilms tumor, aniridia, genitourinatry abnormlaities, retardation.

pearlman syndrome (weird face, islet cell hypertrophy, macrosomia, hamartoma).
compare osteosarcoma and ewing's sarcoma:
both appear in adolescents. both appear as pain/localized swelling, and are often misdiagnosed as trauma

ewing's = 11:22 translocation, onion skinning. can happen in EITHER long or flat bones. probably a neuroendocrine tumor. usually in EPHYSIS (middle of bone) and has SYSTEMIC SYMPTOMS (weight loss/fever)

osteosarcoma (osteogenic sarcoma) = only long bones at the metaphysis = proximal/distal bones. comes from bone producing mesenchymal stem cells. Less likely to have systemic symptoms.
isolated thrombocytopenia post viral infection = ? treatment?
ITP.

generally no treatment: if platelets get below 30,000 or severe bleeding happens, can treat with STEROIDS (giving more platelets may not be helpful, as the antibodies that shred them are still present).
if erythrocyte protoporphyrin (EP) is increased, what might be wrong?
problem making heme: either Fe++ deficiency (common) or lead poisoning (uncommon).

only a lead level can tell the difference: if it's below 10, it's normal.
what's kasabach merritt syndrome?
think big vessel tumor that sequesters platelets, RBCs, drives up d-dimers/fibrinogen. goes with kaposiform hemangioepithelioma.
what's phaces syndrome?
posterior fossa abnormality
facial hemangioma
arterial abnormalities
coarctation of aorta
eye abnormalities
sternal abnormalities.
physiologic anemia of the newborn occurs when?
6 to 8 weeks, when fetal Hb drops off and EPO drops.
what's a kleinhauer betke stain?
done on new mom's blood, looking for HbF: if it's there, assume a feto-maternal transfusion occurred at birth and is responsible for any fetal anemia.
in DIC, what coagulation factors are consumed?
2, 5, and 8. think hemophelia A plus the first two parts of the final common pathway.

also, PT tests 2, 5, 10, and 7.
what are the common test used to evaluate development and IQ?
development:
Denver II and CAT/CLAMS. Looks at gross motor, fine motor, language, personal/social. Note that language is the best predictor of future intellect.

IQ:
Wechsler = pre school
Stanford-Binet = school age.

IQ between 50 and 70 = mildly retarded. 30 to 50 = moderately around 20 = profoundly retarded.
Development: go through the milestones to know in the first year:
2 mo: social smile, recognizes parents. track with eyes but not past midline.

4 mo: back to front/front to back rolling

6 mo: sit unsupported, rake, pass objects back and forth. Begin STRANGER ANXIETY (peaks around 1 year), BABBLES

9mo: crawl, words with no meaning

12 mo: understand 2 word commands, use mama dad right, walk alone
2nd year through childhood developments to know?
18mo: 3 block tower. 20 words. parallel play

24 mo: kick/throw, 4-6 block tower, draw a straight line, 2-3 word sentences, stairs without help, 50% of words understandable to stranger

3 years: tricycle, draw circle, 75% of words understandable to stranger

4 years: draw a cross, catch
a fall onto an arm with "anterior displacement of the fat pad" is what and causes what bad side effect?
suprachondrylar humerous fracture.

causes volkman's contracture: tense forearm skin. it's a COMPARTMENT SYNDROME and requires immediate FASCIOTOMY surgery to relieve pressure. comes from VASCULAR COMPROMISE and may be present even if a radial pulse is present
how do you treat clavicular fractures in newborns who were big and had birth trauma?
don't need to - they're green stick and will repair on their own.
describe asperger's:
difficulty relating to other people, don't uderstand sarcasm/metaphors, and usually develop very specific and intense interests.

still have good communication, no repeatitve movement stuff.
what's a rash that makes you think you should look for HepB infection?
Giannoti-Crosti syndrome: = "acrodermatitis" = rashes on extensor surfaces of arms and legs, but NOT ON THE TRUNK.

can be a sign of HepB, but also known to go with EBV, varicella.
what's molluscum contagiosum?
little papules caused by a poxvirus. , usually in sweaty places. seen in wrestlers, sauna goers.

can last for years - often burned off.
what are the jaundices that go with breast milk?
breast feeding jaundice happens in the first couple days, breast milk happens at about 2 weeks.

breast feeding comes from lack of nutrients in the breast milk that fail to suppress the 'entero-hepatic circulation' : so bile's being hyper-reabsorbed.

breast milk hyperbilirubinemia is of unknown origin. probably a hormone.
3 causes of floppy babies?
werding-hoffman: degeneration of anterior horn LMN's

infant botulism.

early onset of PRADER WILI (hyperphagia is later on)
what conditions/drugs cause SIADH and how can you treat it?
brain tumors/surgery, lisinopril/carbamazapine/tricyclics can all cause SIADH.

treat with DEMECLOCYCLINE: this can induce a kind of nephrogenic DI that will be less sensitive to the increased ADH.
constitutional vs. familial short stature:
familial starts off short, ends up as short as the rest of the family. bone age is normal.

constitutional can have delayed puberty = delayed bone age, eventually catch up to the rest of the expected family height.
in failure to thrive, what happens to height, weight, and head circumfrence?
head circumference maintains normal size, while height and weight don't increase at normal rates.
what are the general classes of endocrine disorders that can cause growth retardation?
GH insufficency: screened for by looking for IGF-1 (and binding protein). Idiopathic associated with midline defects, birth asphyxia, hypoglycemia, cleft pallate, Can come from physically/mentally abusive environments.

Cushing's

Hypothyroidism

Chronic cyanotic diseases, sickle cells, CF...chronic infectious states that increase metabolic demand.
how do you treat 21 hydroxylase deficiency?
cortisol - doses of florinef will cause ACTH production to decrease.

ACTH is driving the increased production of sex steroids.

remember that 21 hydroxylase is necessary to make aldosterone and cortisol, and the precursors have no mineralcorticoid activity.
what are the conditions like precocious puberty, how are they classified, and what are the significance?
precocious puberty = puberty in boys before 9 and in girls before 7. usually Gonadotopin-dependent (GDPP) and in girls = idiopathic, in boys = CNS problem (tumor).

GIPP = indepednent = mccune-albright, familial testitoxicosis, leyding tumors, ectopic HCG production.

Thelarche = early breast buds, usually isolated condition with no increase in hormones, no worries.

Andrenarche = sex hair early, can be due to increased sex hormones/gonadotropins, need to evaluate.

GDPP test: given GnRH, should bump up gonadotropins (LH/FSH) into puberty levels.

GIPP (independent) = no increase when GnRH given.
how do you treat GDPP
long-acting GnRH injections: remember that it's the 'pulsatile' action that increases LH/FSH,but when given in continuous strong doses it suppresses gonadotropin release.
vitamin D deficiency vs. hypoparathyroidism vs. pseudohypoparathyroidism: what happens to Ca++ and phos?
in both hypoparathyroidism and pseudohypoparathyroidism, the Ca++ is low and the phos is high (phos trashing hormone).

in vitamin D deficiency, PTH gets cranked up to save Ca++: this leads to low phos. Probably have low Ca++ too.
a hyperthyroid mom: what's the risk to the baby?
if it's due to grave's disease, then the antibodies can cross the placenta and cause the baby to mainfest grave's disease too: this can cause HEART FAILURE.

if the mom has really high TSH for some reason or really high t3/t4, these do NOT cross the placenta and the baby is at no risk.
what are the signs of pseudohyperparathyroidism? plasma concentrations of Ca++ and phos?
high PTH circulating. DENSE bones, mental retardation, brachydactily (short fingers), and calcifications all over.

have the same serum chemistries as people with normal hypoparathyroidism: low Ca++, high phos.
what electrolyte imbalance becomes important in kids immobilized with long bone fracutres?
hypercalcemia. imagine the bone breaking and spreading calcium all over. end up with GI pain, groans, STONES = hematuria, HYPERTENSIVE ENCEPHALOPATHY.

need to look at the calcium to creatinine ratio: if it's >0.2 = hypercalcuria.
compare wilson's vs. meinke's vs. A1ATd:
wilson's will have CNS/behavior changes which can be seen later in life. Increased LFTs/portal hypertension possible. also the copper screws with the renal tubules (fanconi's anemia) = amino acids, glucose, protein in pee.

Meinke's: shows up in first couple months, depigmented/fryable hair, mental retardation, hypothermia/hypotonia, myoclonic seizures.

a1atd: cirrhosis/high LFTs early in life, CNS bleeds possible, cholestasis. don't always see lung problems.
what does presence/absence of C peptide mean?
you should find C peptide: it's packaged with the insulin in the pancreas.

if NO C peptide, someone's injecting exogenous insulin.
nutritional rickets: what do you expect to find in regards to Ca++, phos, and alk phos in the urine/blood?
low vitamin D will cause low Ca++: this will increase PTH secretion to resorb Ca++ from the bones and urine.

serum Ca++ concentration is probably normal due to PTH compensation: serum phos is probably low (also PTH), and alk phos high (remodeling).

urinary Ca++ is low (got resorbed).

blood test = high alk phos, low phos.
urine = low Ca++
acanthosis nigricans in a kid is probably...?
type 2 diabetes.
lawrence moon bidel disease = ?
obesity retardation little balls and NIGHT BLINDNESS (retinosa pigmentosum)
what's holt-oram syndrome?
usually missing radii, screwed up thumbs (hands attached to elbow), heart defects
newborn physiologic jaundice usually appears when? when should you worry about even mild jaundice?
physiologic jaundice is on days 2 or 3:

born with juandice or in the first day, worry about erythroblastalis fetalis.

if it shows up in the first week but after day 3, worry about SEPSIS (jaundice can be a sign of sepsis).

a 7 day old with basic lethargic symptoms and jaundice should get a spinal tap, blood cultures.
when can you use pharmacology to help with enuresis? what drugs?
normal until age 5. after age 5, work with the family to wake up in the middle of the night, use bed wetting alarms, etc.

if still having problems, use DDAVP (desmopressin = ADH) or imipramine
kids with HSP (henoch schonlein)/IgA nephropathy: what GI complication are they predisposed to?
for some reason, HSP kids are known to get INTUSCUCSEPTION.
a young teenage boy/girl athlete has lots of pain at the top of the tibia where the patellar tendon inserts - what's wrong?
osgod-schlatler: aka traction apophysitis. the quadracept grows fast and pulls on the tibial tubericle, pulling it off/damaging it.
what are the 2 kinds of cellulitis around the eye you worry about, and how do you tell them apart?
preseptal and orbital cellulitis.

any report of lack of extra ocular movement, changes in vision, proptosis = orbital cellulitis.

eyelid discoloration is more likely seen in pre-septal
aside from simply being premature, what factors increase the risk for RDS?
hayline membrane disease can be made worse by

1. being male
2. gestational diabetes (high insulin kills surfactant)
3. c-section (no stress hormones)
4. perinatal asphyxia
compare conduct disorder, oppositional defiant disorder, and antisocial personality disorder:
conduct disorder = teenagers who do things that violate basic norms of society like continuously stealing, beating people up, etc

oppositional defiant disorder is in children who act out against authority figures.

antisocial personality disorder is the outcome of conduct disorder, you just can't diagnose personality disorders before age 18.
a young boy with gout has?
lesch nyhann syndrome: self mutilation! deficiency in HGPRT (hypoxanthine guanine phosphoribosyl transferase). High uric acid levels.
cephalohematoma and caput secundum: which crosses suture lines?
cephalohematoma is a SUB-PERIOSTEAL hemorrhage that does NOT cross suture lines

caput secundum is a tissue hemorrhage
if they give you a history of a kid who falls with a pencil/stick in their mouth, what do you have to worry about?
damage to the carotid artery that later thromboses and sends emboli into the brain to cause strokes.

side note: S3 sounds are NORMAL in kids.
edwards syndrome: which chromosome, signs/symptoms, and heart defect?
VSD = #1 in edward's. John Edwards has vd

think john edwards: voting age is 18.

small head, small jaw, rocker bottom feet, overlapping fingers with no palmar creases
when does tetraology vs. transposition present?
tetraology can present years after birth (or months).

transposition shows up in the first few hours. remember that with transposition, there are parallel flows that depend on shunts for systemic circulation: as the PDA closes, the cyanosis will worsen.
a baby has probable meningitis and signs of high ICP. (bulging fontanelle, etc). what are the first couple steps to manage?
1. give 3rd gen cephalosporin.

2. get scan of the head

3. LP.

don't forget to scan the head before getting an LP if there are signs of ICP
what can you screen for to look for celiac's disease?
anti-tissue transglutaminase (IgA) or anti-endomysial antibodies (IgA)
lots of vomiting: what changes to electrolytes/pH is expected?
tossing up blie acid leaves you ALKALOTIC.

also throw up potassium-rich fluid = hypOkalemia, hypOchloremia.

severe dehydration can lead to hypernatremia?
what's a big cause of volvolus, what causes it, and how can you diagnose?
volvulus is intestine twisting on itself: this is often the result of MALROTATION with mesentery being in the wrong place.

X-ray will show air in the stomach but not much in the intestines, the ligament of tritz/cecum are in the wrong place usually. CURLY Q SIGN

symptoms usually include BILIOUS VOMITING (small intestine blockage usually does this). bloody vomit/poop possible. colicy pain?
phenytoin and valproate: what birth defects do they cause?
phenytoin causes funny nails, IGUR, and CLEFT PALATE (Phenytoin = Palate, Funny nails)

Valproate = spina biffida
what are the signs of homocystinuria? treatment? enzyme deficiency?
problem converting methionine to cysteine/serine. Enyzme = cystathione synthetase deficiency

problems are NOT IN INTFANCY: see in the first couple years. look MARFANOID and have THROMBOSES (homocystine = thrombotic)

mild retardation possible

treat with B6 administration.
someone who has GERD symptoms or food getting stuck/pain who also has lots of allergies/asthma might have...?

treatment?
eosinophilic esophagitis: biopsy shows tons of eosinophils.

treatment = steroids.

looks like GERD presentation but PPI/H2R receptor blockers don't help.
what antibodies are sometimes positive in crohn's and UC?
crohn's = ASCA + in 55% of cases (anti-saccharomyces cervisae antibodies)

UC: p-ANCA is positive in 70% of UC.
constipated 3 year old: is fecal soiling worrying or reassuring?
reassuring: if there's no fecal soiling, poop is not getting around the impacted stool and can be a sign of HIRSCHPRUNG's.

if there is soiling, it's probably "functional" - need to catch it early, as it's a re-inforcing condition that's harder to treat later on.

kid probably passed meconium late.
reflux in kids can cause what bad outcomes?
think bradycardia and reflux-induced apnea. chronic lung disease too if the contents are aspirated.

barrett's is possible in older kids who have had GERD for awhile.
what are the first teeth to erupt?

what do you see in people who bottle feet juices for a long time?
mandibular before maxillary.

middle incisors (man/max), lateral inscisors (man/max), then molars.

bottles with juice lead to maxillary frontal teeth (inscisors) to decay, with normal mandibular teeth.
for what things does activated charcoal NOT work?
strong acids or bases

alcohols (ethanol, methanol, ethyline glycol...)

iron, potassium, cyanide, lithium.

good for psych med OD's, though
how is thalasmia trait diagnosed?
usually asymptomatic anemia with normal iron studies.

note that the RDW will be normal in thalasemia: it's pretty specific for iron deficiency anemia.
weight doubles by 5 mo, triples by 1 year. what happens to height?
goes up by 50% in 1st year.

doubles by 4 years

triples by 13 years
someone with mcccune albright syndrome has what symptoms?
precocious puberty, cafe au lait spots, bone abnormalities. can go with other endocrine things (like cushing's).
a downsy kid starts walking funny and having upper motor neuron problems. what is it?
atlanto-axial instability: the joint is hyper mobile and can compress the spinal cord.
how does vitamin C deficiency show up in a child?
scurvy is different:
trouble with wound healing
bleeding (petechae). bones with epiphyseal separation.
go over the fluid requirements or kids:

over what time are deficits replaced?
per day:
first 10 kg: 100/kg/day
next 10kg: 50/kg/day
all other: 25/kg/day

per hour
4, 2, 1.

note that for each 100cc of water, need 3meq of NaCl and 2MeQ of K

Defiticts:
replace half the deficit in the first 8 hours, give the rest over the next 16.

unless it's hypernatremic dehydration (DI?) - replace over 48-72 hours to prevent cerebral edema.
what are the really fast ways to treat hyperkalemia? slow ways?
#1: CALCIUM GLUCONATE: stabilizes heart myocyte membrane

high hyperkalemia that has to be rapidly corrected:
insulin + glucose
making the blood alkalotic: NaHCO3-, hyperventilation (blow off Co2)

long acting:
Kayexylate/dialysis
what's the first sign of dehydration in children?

mudpiles?
tachycardia = first sign of dehydration in children

methanol, uremia, DKA, paraaldehydes, INH/IRON/Inborn errors of metabolism, lactic acidosis, ethanol, salicylates
when do you expect antibody levels to be lowest in intfancy, and what if they don't increase?
physiologic hypogammaglobinulemia happens 6-12 weeks, then the baby starts to make their own.

some kids take longer = transient hypogammaglobulinemia of infancy. some later get diagnosed with bruton's/CVID, most are fine.
quick review of wiscot aldrich:

also, in CGD, what bugs typically infect?
Mostly B cell dysfunction (low IgM, high IgA?), atopic dermatitis, THROMBOCYTOPENIA.

usually die in teens from bleeds/infections.

CGD: bugs that make catalayse are typical infectors: think STAPH AUREUS, ASPIRGILLUS, and candida.
what's the allergic triad?
allergic rhinitis (allergies), atopic dermatitis (eczema), and asthma. AAA.

somebody with one is likely to have the others.
go over the different kinds of juvenile arthritis:
JIA - juvenile idiopathic arthritis. Oligoarticular (<5 joints) = most common.

If it's RH+, it's likely late-onset teenager POLYARTICULAR JIA.

also have a version with daily high fevers + acute phase reactants (SYSTEMIC JIA)

ERA: enthesitis related arthritis = saccro-iliac joints where tendons insert. HLA-b27 associated.
dermato/polymyositis: what are the classic signs?
VIOLACEOUS DERMATITIS OF EYELIDS (heliotrope rash)

high CK (dermatomyositis affects muscles).

proximal muscle weakness: situps, climbing stairs difficult.

grotton papules on the MCP joints.
what kind of jaundice does galactosemia cause? what's the other bug that does same thing?
CONJUGATED - remember that conjugated jaundice = pathologic, and this is super-pathologic

CMV can also present as CONjugated.
how can you tell between a pituitary adenoma and a crainopharyngioma?
crainopharyngioma is more common in BOYS and is often CALCIFIED.

pituitary adenomas are often prolactinomas with their associated symptoms and are usually found in women.
a baby that turns blue while feeding and then pink while crying has...?
choanal atresia - you also can't pass a catheter up the nose into the pharynx.

needs to be corrected.
what are the cystic diseases of newborn kidneys to know?
autosomal recessive polycystic kidney disease: recessive, both kidneys affected, also get DILATED /FIBROTIC BILE DUCTS. need transplant.

multicystic dysplastic kidney: lots of cysts in ONE kidney that usually involutes (or gets removed so you don't get wilms tumor).
what's the most common cause of hydronephrosis in the newborn?
UP-JO (up yo urethra):

ureter-pelvic juntion obstruction: often primary (narrowing, weird angle, interaction with a vessel).
what's PUV?
posterior urethral valves: happens only in BOYS and prevents ouflow of urine from the bladder.

causes trabeculated bladder, HYDRONEPHROSIS,bladder distension.

note that it can lead to vesico-urethral reflux (VUR) and infections - anybody with VUR needs to be on antibiotic prophylaxis.
hydrocoeles and varicocoeles: what do they look like, how do you treat?
hydrocoeles are remnants of the process vaginalis - if they COMMUNICATE with the peritoneal cavity, they can INCARCERATE and need to be repaired.

non-communicating hydrocoeles can be left alone.

vericoclcles usually appear on STANDING and have bag-of-worm sign. repair surgically (increased risk of infertility).
how is pyelonephritis in infants and older children different?
infant fever is most often due to pyelo and comes from HEMATOGENOUS SEEDING

older kids have ascending infections with enteric flora.
how do you treat minimal change disease, and what's the most common complication?
steroids: these are immunosuppressive.

spontaneous bacterial peritonitis is the most common complication.

don't forget that nephrotic syndrome raises triglycerides/cholesterol, this can be dangerous and persistent.
what's a blood test that might help differentiate post-strep glomerulonephritis from IgA nephropathy?
post strep glomerulonephritis always HAS LOW C3. don't forget that both throat/skin infections can cause and giving antibiotics early in the infection does NOT prevent kidney disease.

IgA nephropathy has normal C3. this progresses to chronic glomerulonephritis in 25% of cases.
what's thin membrane disease?
aka benign familial hematuria: can be microscopic/gross hematuria, and it's DOMINANT (so see one parent with it).

nothing to worry about.
5 month old has tuberous sclerosis and little weird seizures. what drug to use?
these are INFANTILE SPASMS and should be treated with intramuscular ACTH.
CNS and R to L shunts: what do you have to watch for?
R to L shunt means you're skipping the lungs: things in the venous circulation end up in the arterial circulation.

this means that INFECTIONS and ABSCESSES are really easy to find in the brain.
when does iron deficiency normally show up? what does the retic count show?
6-12 months, or after. at birth have 6 mo of iron stores.

kids who breast feed 'till 12 mo, drink lots of cows milk (causes occult bleeding and doesn't have much iron).
what might be a sign during pregnancy that the kid has a congenital diaphragmatic hernia, and how is it managed?
polyhydramnios - the stomach doesn't work for some reason.

#1 priority is keeping the bowel loops from dilating: PLACE AN OG TUBE immediately, then get them on a ventilator, confirm with X ray, etc.
fredreich's ataxia: what's the inheritance, disease course, typical findings, risk of recurrence?
trinucleotide repeat that is RECESSIVE.

involves cord/peripheral nerves with atrophy. ataxic gait begins in late childhood

most kids dead by 30, after being wheel chair bound.

note that they get necrosis of heart fibers = myocarditis and inverted T waves.
when do you repair an umbilical hernia?
>3cm, >3 years old
what predisposes to neural tube defects?

what are the major NTD'S?
maternal MALNUTRITION
valproate/carbamazapine
hyperthermia
infections

note that a mom who's already had one has a 4% chance of having another.

NTDs:
anencephaly
encephalocoele (head contents exposed)
spina biffida

for the survivable ones (spina biffida), major cause of death is UTI: they loose sphincter control from lower CNS destruction.
in communicating hydrocephalus, which ventricles are dilated?
all ventricles. this comes from impared absorption at the arachnoid granulations (meningitis, subarachnoid hemorrhage, leukemia).

can sometimes come from overproduction (choroid plexus papilloma)

non-communicating = obstructive, and ventricles proximal to the blockage dilate
what are the kinds of febrile seizures, and what do you do with a patient who has their first?

complications?
simple = generalized seizure, short duration.

complex: focal, long duration.

rarely, first sign of meningitis is a seizure: for 1st febrile seizure, probably get an LP to R/O.

kids with febrile seizures have INCREASED RISK OF DEVELOPING EPILEPSY
briefly go over the different kinds of seizures:
general vs. partial:

partial starts in one hemisphere. can be simple (stays local) or complex (move, cross hemisphere)

generalized = both hemispheres at the same time, always complex. this can include tonic/clonic AND ABSENCE SEIZURES (3 hz).

don't forget todd's paralysis: post-ictal hemi/total paralysis. sometimes if a seizures happens during sleep, this is the only sign.
what's the equation about ICP that you need to remember?
cerebral perfusion pressure = MAP - ICP.

generally want to maintain the cerebral perfusion pressure.
who gets pseudotumor cerebri, signs, and course?
overweight teenage girls.

there's increased ICP: you'll see papiledema.

probably comes from impared resorption of CSF.

CT scan is normal.

treatment = repetative LP's to relieve pressure. self-limited, resolves.
opthamology - what is the #1 cause of leukocoria in kids? what's the eye screen that should be done at every visit?

tearing up in a neonate is probably...?
#1 leucocoria cause = cataracts. note that galactosemia doesn't have to be responsible.

check for strabismus at every visit - this is the #1 cause of amylopia (dim vision through a healthy eye) - if one eye looks a little off, it'll miss its critical development period and never catch up.


tearing up in a neonate is probably nasolacramal duct obstruction
what are the buzz words for the phankomatoses? NF1/Nf2, VHL, sturge webber, tuberous sclerosis.
NF1 = risk of optic nerve gliomas. cafe au lait spots, lots of gliomas possible.

NF2 = bilateral acustic neuromas. meningomas, etc.

tuberous sclerosis: ash leaf spots (hypopigmented, find with woods lamp), shaygreen patches (thick epidermis. SEGA's. CARDIAC RHABDOMYOMAS.

sturge-webber: V1 distribution port-wine stain, mental retardation, glaucomas.

Von-hippel-lindau: retinal angiomas, cerebellar hemangioblastomas, renal cell carcinomas
difference between ataxia telangectasia and fredreich's ataxia?
ataxia telangectasia = ATM = DNA repair = immune deficiency, show up early in childhood, cerebellar ataxia, cerebellar changes, recessive.


fredreich's ataxia = recessive trinucleotide repeats. later in childhood, peripheral nerves, muscle atrophy, CARDIOMYOPATHY.
when it comes to inherited brain diseases, divide into gray/white/systemic. what are the major ones in each category?
gray: things that kill cell bodies: nieman pick, tay sachs, gaucher's.

white: adrenoleukodystrophy (demyelination and ADRENAL INSUFFICEINCY, PERIVASCULAR INFLAMMATION, UMN signs, death).

systemic: includes rett syndrome here. X linked, males die in utero, affeted femals regress and have HAND WRINGING>
pseudotumor cerebri: signs, associations, who's typically affected?
young fat ladies. goes with thyroid dysfunction.

positive papiledema, but no signs of increased ICP on CT. self limited, probably problem with CSF resporption.
what are the signs/symptoms of slipped capital femoris ephysis (SCFE)?
usually an OBEESE boy, shorter limb that's internally rotated at the hip, pain referred to the KNEE.

probably needs a pin in it.

this is in contrast to avascular necrosis (legg calvae) - usually normal kid, no issues, mild hip/knee pain.
what's the treatment for congenital hip dysplasia?
pavlik harness. think pavlov.
what's toxic synovitis?
not too sure - happens post viral infection. unlike infectious (septic) arthritis, range of motion is in tact.

septic arthritis has limited range of motion and happens in neonates, usually in the hips, and can be gbs/e.coli

osteomyelitis tends to have normal range of motion.
weird feet when a kid is born: what are the 2 possibilities and how are they diagnosed/treated?
metatarsus aductus (MA) - plantar/dorsiflexion are normal. foot can be molded by hand into the normal shape.

talipes equinovarus: the hindfoot is stuck in plantar flexion. this is club foot and has to be treated.
kid with a URI who, several weeks later, has weird CNS findings and enhancing white matter lesions on MRI has what?
ADEM: acute disseminated encephalomyelitis. like a really fast MS in kids <10yo.
what are the signs of myotonic dystrophy? inheritance?
rare because it has DISTAL muscle weakness and breakdown (high CPK - but not MD).

goes with baldness, small balls, and cataracts.

DOMINANT - trinucleotide repeat.

note that myotonic part means they CAN'T RELEASE THINGS (hand shakes, door knobs, etc).
tourettes has whats?

what does a kid who just got phenergan with body twitches have? cure?
tourettes = vocal and physical tick - often goes with OCD.

dystonic ticks happen after phernergan - cure is IV diphenhydramine. common side effect.
kid with a URI who, several weeks later, has weird CNS findings and enhancing white matter lesions on MRI has what?
ADEM: acute disseminated encephalomyelitis. like a really fast MS in kids <10yo.
what are the signs of myotonic dystrophy?
rare because it has DISTAL muscle weakness and breakdown (high CPK - but not MD).

goes with baldness, small balls, and cataracts.
tourettes has whats?

what does a kid who just got phenergan with body twitches have? cure?
tourettes = vocal and physical tick - often goes with OCD.

dystonic ticks happen after phernergan - cure is IV diphenhydramine. common side effect.
kid with a URI who, several weeks later, has weird CNS findings and enhancing white matter lesions on MRI has what?
ADEM: acute disseminated encephalomyelitis. like a really fast MS in kids <10yo.
what are the signs of myotonic dystrophy?
rare because it has DISTAL muscle weakness and breakdown (high CPK - but not MD).

goes with baldness, small balls, and cataracts.
tourettes has whats?

what does a kid who just got phenergan with body twitches have? cure?
tourettes = vocal and physical tick - often goes with OCD.

dystonic ticks happen after phernergan - cure is IV diphenhydramine. common side effect.
what is poland syndrome?
amastia and missing pectoralis. obvious chest deformity. also have webbed fingers sometimes.
what's the heart defect that goes with diabetic moms?

what are the general conditions to look out to infants of diabetic moms?
babies can get hypertrophic cardiomyopathy, but it's usually transient. think transposition of great vessels.

anencephaly
NTDs
caudal regression.
what drug do you treat lyme disease with?
<9 = amoxicillin
>9 yrs old = doxy.

this is for stage 1 disease.

if it's disseminated and you have CNS involvement/heart problems, use ceftriaxone or PenG
neonatal sepsis: how is it divided, what's the #1 cause?

treatment?
early onset = first week, late onset = >7 days.

GBS = #1

remember that newborns can present with hypOthermia instead of fever.

amp + 3rd generation cephalosporin, or amp + aminoglycoside.
what forms of HSV infections do neonates get?
local lesions - skin, eyes, mouth. 1 to 2 weeks.

disseminated disease: 1 week, shock/hypotension/hepatitis/pneumonia

CNS - 1 mo, seizures/meningitis
what's laryngomalacia, what happens to it, and how do you deal with it?
most common cause of loud inspratory noise in newborns - appears by 1 month, goes away by 2 years.

floppy soft palate/epiglottis.

keep baby upright for 1/2 hour after feeding.

airway kinda collapses on inhalation.

it runs in families.
when does celiac's show up in a kid? signs?
around 12 months when parents start giving gluten.

dermatitis herpetiformans (extensors of arms/legs) + malabsorption shits.
how do you treat septic arthritis in a kid, and where does it usually come from?
hematogenous spread - most kids have a history of a URI recently. staph aureus is the #1.

needs IMMEDIATE SURGICAL DRAINAGE and IV antibiotics (nafacillin + 3rd generation cephalosporin).
how do iron deficiency anemia and thalasemia get told apart?
iron deficiency: low retic count (can't make new RBCs), high RDW

thalasemia: high retic, normal RDW.

note that high RDW = >20%
a 2 year old who had URI kinda symptoms a week ago and how has a hoarse voice, fever, and neck pain might have...
retropharyngeal ABSCESS - probably see a protrusion in the back of the throat.

likely made up of lots of bacteria including anerobes, so broad abx coverage is required.
what vitamin should you give to people with measles infection? what blood abnormalities are common here?
vitamin A.

note that measles goes along with low WBCs and low platelets.
what has a shortened PR interval and narrow QRS complex?
wolf parkinson white - accessory pathway from the atria to the ventricles that lets some signal skip the AV node and get to the ventricles faster

some will depolarize before other, takes less time, and has a delta wave.
what does neonatal tetanus look like? comes from?
unimmunized moms + untrained birth helpers w/ unsterile clamping of cord.

get spasms/tetany in the first 2 weeks. die of apnea/sepsis
small for gestational age newborns are at risk for what?
hypoxia (and induced polycythemia), hypoglycemia (no fat stores), hypocalcemia, hypothermia
what's spondylolisthesis? signs/symptoms?
seen in kids, "step off' in the lumbar spine: anterior slipping of L5/S1.

kids will have back pain and loose some nervous control (bed wetting).
how do iron deficiency anemia and thalasemia get told apart?
iron deficiency: low retic count (can't make new RBCs), high RDW

thalasemia: high retic, normal RDW.

note that high RDW = >20%
a 2 year old who had URI kinda symptoms a week ago and how has a hoarse voice, fever, and neck pain might have...
retropharyngeal ABSCESS - probably see a protrusion in the back of the throat.

likely made up of lots of bacteria including anerobes, so broad abx coverage is required.
what's laryngomalacia, what happens to it, and how do you deal with it?
most common cause of loud inspratory noise in newborns - appears by 1 month, goes away by 2 years.

floppy soft palate/epiglottis.

keep baby upright for 1/2 hour after feeding.

airway kinda collapses on inhalation.

it runs in families.
when does celiac's show up in a kid? signs?
around 12 months when parents start giving gluten.

dermatitis herpetiformans (extensors of arms/legs) + malabsorption shits.
how do you treat septic arthritis in a kid, and where does it usually come from?
hematogenous spread - most kids have a history of a URI recently. staph aureus is the #1.

needs IMMEDIATE SURGICAL DRAINAGE and IV antibiotics (nafacillin + 3rd generation cephalosporin).
how do you know if it's a bad VSD and if it needs to be surgically closed?

what's the murmur you hear?
loud, harsh sound = MILD VSD:
VSDs heard on the left lower sternal border. like tricuspid valve.

most close by 1 year, nearly all by 10 years. small hole = big sound.

soft VSD's are suspicious and might have to be treated.

if symptomatic, it's probably bad. note that you can also have a diastolic murmur at the apex = mitral sound from TOO MUCH BLOOD COMING BACK (L to R shunt, the blood comes back).
young kid who had wheezing from birth still wheezes, relieved by extending neck. what is it?
vascular ring compressing the airway.

can come from double aortic arch, right sided aorta, lots of crap. bronchodilators don't help much.
what happens if you don't clamp a cord fast enough, and what are the symptoms?
polycythemia: too much blood gets into the baby. crit >65% = polycytemia.
blood gets too thick and doesn't enter the brain well = CNS symptoms (lethargy).

also can't make it into the pulmonary vasculature = respiratory distress.
axillary hair, pubic hair, breast developent: if a girl has one or more of these early (7 years), which are worrying?
only pubic hair (pubarche) is worrying = 50% of cases have CNS cause.

thelearche (boobs) and andrenarche (axillary hair) are not pathological.

Pubarche is a Problem.
what complication should you associate with superchondylar arm fractures?
adults don't get these, kids do.

brachial artery entrapment - so make sure to check a radial pulse
hyper IgM syndrome (HIM) - what sets it apart?
HIM will have high IgM, low IgG and IgA.

DECREASED B and neutrophils.

OPPORTUNISTIC INFECTIONS (PCP pneumonia common)
what component of the DTaP vaccine can be problamatic, what happens, and what do you do in the future?
Pertussis: if encephalopathy/high fever/anaphylaxis happens, don't give anymore:

give only DT in the future.
newborn has red eyes - what is it based on time? treatment?
just a day old = reaction to silver nitrate.

<1 week = gonoccous. treat with ceftriaxone.

>1 week = chlamydia. treat with oral erythromycin.
joint pain post URI w/ decreased range of motion, mildly elevated WBCs, high ESR?
transient sinovitis - nothing to worry about. it'll go away. rest and nsaids.
a few weeks old, has hyponatremia, hyperkalemia, hypoglycemia, low BP. what to do?
high dose corticosteroids - has congenital adrenal hyperplasia and is in adrenal crisis. needs bolus too.
what kind of non-musculoskeletal exam is required in kids with JIA over the long term?
slit lamp - they get anterior uveitis (non-granulomatous). can go blind.
what's the likely diagnosis if baby has presentation kinda like diaphragmatic hernia, but the stomach is where it's supposed to be?
CCAM - congenital cystic adanomatous malformation - cyst forms in the chest during week 20 and collapses the lung, it gets hypoplastic.

affected lobe has to be resected.

small risk of future cancer.
though you don't have to treat croup, what can you do?
inhaled racemic epinephrine and steroids.
steeple sign = ?

thumb sign = ?
steeple = croup

thumb = epiglottitis
what's idiopathic pulmonary hemosiderosis?
a long standing pulmonary hemorrhage, kids cough up and swallow. sometimes gets into the lungs = very short term pneumonia.

do a bronchoaveolar lavage to see the hemosiderin macrophages.

also might find digested blood in poop.
when should you give a baby varicella Ig?
if mom had onset 5 days prior to delivery or 2 days after. other than that, leave alone.
what does neonatal hypothyroidism look like?
subtle - bradycardia, big head, distended abdomen (constipation), hypothermia, jaundice, edema (genitals especially).
what's the test of choice to screen for a suspected hirschprung's?
anal manometry. if it's normal (relaxed internal sphincter, dilated colon) = rule out hirschprung's.

next test is a barium enema.

then full thickness biopsy to confirm.
childhood hemangiomas are the most common tumors of childhood. what do you have to look out for?
they generally involute and are no big deal. they can be anywhere, on any organ.

if they're big, they're essentially big AVM's and can cause platelet sequestration and heart failure.
first step in epiglottitis? assume the patient's still breathing but having the typical "dog sniffing" and wheezing/stridor
intubate. don't do antibiotics, LP, scans. low threshold for intubation.
what infantile reflexes disappear first?
palmar grasp and rooting should be gone in the first couple months.

moro lasts 'till six.

parachute is last to develop, sticks around for life.
neonate with meningitis is found to have lots of brain abscesses. what bug did it, what do you do?
this is vertically-transmitted citrobacter. typical CSF findings are of normal bacterial meningitis.

ceftriaxone and gent...it's usually resistant to amp, though you'd probably include it anyway.

often need to be drained.
what are the hints that a newborn has cocaine vs. opiate addiction?
cocaine = high pitched cry and excessive sucking. note they also can get white matter lesions like little strokes, be small.

opiates = GI complaints, resp. distress, tremors.
healthy marfanoid kid - what murmur do you expect?
aortic regurg. they have this murmur even before they fully disect.
what are the birth defects you can get with gestational diabetes?
hypoglycemia and lots of RBCs common in fat gestational diabetic kids. also hypocalcemia

left colon dysgenesis.
hypertrophic cardiomyopathy (can go away)
renal vein thrombosis
caudal dysgenesis
kid inhales something but is pretty stable. what do you do?
if they're clearly not in the process of actively coughing it up, go after it with a RIGID BRONCH.

in adults, it'd be flexible.
what do you see in fanconi anemia?
anemia doesn't usually show up 'till around 5, and it's aplastic.

hypermpigmented, they're short, have little heads, little balls, weird hands (screwed up thumbs or radii)
What's chedaki hegashi syndrome?
microtubule problem = immune deficiency. OCCULO/cutaneous ALBINISM. giant cells 'cause they can't phagocotyze properly.
what are the major dominant inherited disorders?
NF1/2, tuberous sclerosis, von wili, spherocytosis, Marfan's, Huntington's, FAP, cholesterolemia,
what are the X linked diseases?
fabray's and hunter's. G6pd. Lesch nyhan. Wiscott aldrich.
What's Barter syndrome?
essentially being born taking lasix. Thick ascending tubule Na/K/2cl transport doesn't work - so vol. depleted, hyponatremic, hypokalemia.

Crank up aldosterone = makes it worse, alkalotic, hypokalemia.

The polyuria in utero can cause polyhydramnios.
What are the inherited disorders of platelets? tests that tell apart?
Von Wili - most common = normal # of platelets, Ristocetan assay = 0, CORRECTS with normal plasma, normal Epi/ADP/Collagen tests. Dominant.

Bernard Soulier: Big, crappy platelets. # decreased. Ristocetan test 0, does NOT correct.

Glanzmann's: IIB/IIIa failure. Plt # normal. Ristocetan test NORMAL. ADP/EPI/collagen tests ABnormal.
Strabismus and pseudo-strabismus - how can you tell apart?
these will both have wonky eyes.

pseudostrabismus has a NORMAL CORNEAL LIGHT REFLEX - and you don't have to do anything (it'll get better on its own)
what's the treatment for neonatal eye gonorrhea/chlamydia?
for gonorrhea = IM ceftriaxone.

for chlamydia = PO erythromycin.
excessive unilateral tearing in an relatively newborn = what, what do you do about it?
blocked tear duct = dacrostenosis. up to 1 year, cure by massage/lid cleaning.

after 1 year, get an optho to probe it.
what's the treatment for impentiago?
topical mupirocen (covers s. aureus and strep a).

oral erythromycin will do.
by what mechanism are asplenics more likely to get infections?
lack of phagocytosis. spleen has dendridic cells which activate T-helpers, which in turn present antigens to B-cells to make antibodies.

Few antibodies in asplenics.
What's the hallmark of LAD?
leukocyte adhesion deficiency = PMNs can't chemotax to where they're supposed to be - delayed umbilical stump falling off, infections with no pus...