HY lecture notes:
Congenital hip dysplasia –> Dx with “clicking/clunking” of hip (Ortolani + Barlow maneuvers) –> if (+), do ortho referral next. Sounds incredibly wrong, since referral is supposed to notoriously be a wrong answer, but it’s what the USMLE wants (this is even assessed a couple times in UWorld for Step 3).
If ortho referral is not listed, go straight to imaging. Do ultrasound if under 6 months; do x-ray if over 6 months. The 4-6 month-range is borderline, but don’t worry about it. Essentially if ultrasound is negative or equivocal between 4-6 months of age, x-ray may have some utility if done subsequently, but the USMLE highly likely won’t go there. Just choose ultrasound if under 6 months and x-ray of hip if over 6 months.
Tx = Pavlik harness, but on the USMLE, they’ll say “abduction harness.” It’s a frog-leg-looking harness.
Slipped capital femoral epiphysis (SCFE) –> 11-13-year-old (preadolescent) overweight boy with a painful limp. X-ray will show slippage of the epiphyseal plate of the hip. Tx with surgical pinning.
Idiopathic avascular necrosis of the hip (Legg-Calve-Perthes) will be a kid 5-8 years old who has a painful hip. It’s the fact that it’s idiopathic that makes the Dx LCP disease. If there’s a known cause, e.g., sickle cell or chronic / high-dose corticosteroid use, the Dx isn’t LCP, and is instead just “avascular necrosis.”
So, e.g., random kid with avascular necrosis of hip –> Dx = LCP disease
Kid with sickle cell has avascular necrosis of hip –> Dx = avascular necrosis.
The femoral head will classically be “contracted” on x-ray. This is really really HY. This word overrides pretty much any other descriptor you can get in a question stem. For example, there’s a Q on one of the NBME forms where they say it’s a kid who’s 8 years old with a painful limp, and they tell you the x-ray shows a “contracted femoral epiphysis.” So immediately you’re like, “Oh that sounds like SCFE bc of the ‘femoral epiphysis’ part.” But the Dx is Legg-Calve-Perthes because the word “contracted” wins.
X-ray can be negative in the first few weeks of the avascular necrosis, but it’s the next best step in diagnosis regardless. If they tell you the x-ray is negative, do a bone scan or MRI to diagnose. There’s a Q on one of the newer peds forms where they say a bone scan (bone scintigraphy) was performed on a young kid with hip pain –> what’s the Dx? –> answer was LCP disease. So if you only thought x-ray was used, you’d be wildly confused.
For non-atrial fibrillation patients with TIA / stroke / retinal artery occlusion, if they blindly ask you which lifestyle change will best decrease risk of recurrence, the answer is hypertension control, not smoking cessation. Hypertension control is more important than smoking cessation for decreasing risk of embolic phenomenon from the carotid arteries. If the patient has atrial fibrillation as the etiology, that’s entirely different.
So guy who’s middle age has elevated blood pressure and is heavy smoker; he has a TIA –> how to best decrease recurrence? –> answer = lisinopril, not smoking cessation.
Hypertension causes endothelial damage notably at the carotids bc of the systolic impulse pounding on the endothelial cells there due to their proximity to the heart. Current guidelines want carotid endarterectomy as the Tx if carotid occlusion on duplex ultrasound being > 70% when symptomatic (sympomatic = TIA, stoke, or retinal artery occlusion), or >80% when asymptomatic. A bruit isn’t a symptom; it’s a sign.
If under those thresholds, do medical therapy with statin + clopidogrel, OR statin + dypridamole + aspirin.
USMLE also wants you to know rhabdomyolysis –> false (+) blood on urine dipstick. So you’ll see 2+ blood on dipstick but 0-4 RBCs/HPF on light microscopy.
Rhabdo is seen in alcoholics, electrical burns, McArdle, drugs such as statins + fibrates combo.
Rhabdo is nephrotoxic –> can cause acute tubular necrosis + hyperkalemia.
Tx for acute gout = indomethacin, steroids, or colchicine. All are equally acceptable according to current literature, but USMLE favors indomethacin first as standard Tx.
If indomethacin + steroids are not listed, colchicine will be the answer.
Steroids are the answer in patients with renal insufficiency or Hx of renal transplant.
Chronic gout Tx with allopurinol or febuxostat (xanthine oxidase inhibitors). Never give these in acute gout as they can make it worse.
Uricosurics such as probenecid are not first-line for chronic gout and should not be used in those with uric acid overproduction because of risk of precipitating renal stones. Probenecid can also be used to maintain beta-lactam levels in the blood.
Two biggest risk factors for pseudogout (Calcium pyrophosphate deposition disease; CPPD) are hemochromatosis and primary hyperparathyroidism.
Will present as monoarthritis of a large joint, such as the knee, or as an osteoarthritis-like presentation in someone with hemochromatosis or primary hyperparathyroidism. Tx acutely same as gout. For chronic, Tx underlying cause, since xanthine oxidase inhibitors clearly are unrelated.
Tx of osteoarthritis (OA) = weight loss (if overweight) + acetaminophen. NSAIDs can also be used first-line for Sx, but acetaminophen is superior bc it won’t affect the kidney. USMLE wants acetaminophen as the answer; this on on the family medicine forms.
They might tell you in a vignette that an older woman is taking high doses of naproxen (an NSAID) to Tx her OA (clearly not what someone should be doing, but then they go on to explain that she has renal pathology because of it). They say she has peripheral edema. –> Why does she have edema –> answer = decreased renal excretion of sodium / increased renal retention of sodium.
Basically NSAIDs knock out prostaglandin synthesis –> decreased afferent arteriolar dilatation –> decreased renal blood flow –> pre-renal insufficiency ensues –> kidney tries to increase fluid retention because it thinks blood volume is low –> upregulation of RAAS –> AT II causes increased PCT reabsorption of sodium –> increased sodium retention through PCT –> water follows sodium –> edema.
This also explains why fractional excretion of sodium (FeNa) is low in pre-renal etiologies of renal failure –> kidney tries to reabsorb sodium as the mechanism for increasing fluid retention.
