Hopefully this helps some of you. Short HY clip here. And here are the HY notes to go with it:

Hopefully this helps some of you. Short HY clip here. And here are the HY notes to go with it:

Do colonoscopy starting age 50 and do every ten years. If first degree relative (parent or sibling) has Hx of colon cancer, start at age 40 or 10 yrs before that family member was diagnoses, whichever is earlier, then do every 5, not 10 years.

In patients diagnosed with IBD (Crohn or UC), do colonoscopy 8 years after Dx is made, followed by every 1-2 years thereafter. Sounds outrageously often, but it’s what the literature says.

In patients with Peutz-Jeghers syndrome, although the hamartomatous polyps are non-cancerous, there is still increased risk of multi-system malignancy in PJS, including CRC. Do colonoscopy at age 8. If positive, continue every three years. If negative at age 8, repeat at age 18, then do every 3 years.

For BPH, always insert a catheter first, even if he has bacteriuria.

So for instance, if 72-year-old male with suprapubic mass (bladder), fever 100F, and 1+ bacteria in the urine, insert catheter before giving antibiotics.

Calcified pleural / supra-diaphragmatic plaques = asbestosis.

Causes restrictive lung disease. Normal or increased FEV1/FVC.

FEV1 and FVC are both, as independent variables, decreased. But the ratio is normal or increased.

There’s a Q on a newer NBME for Step 1 that forces you into a corner to choose normal FEV1 as an independent variable, but it was the only answer that made sense. So just be aware it’s never hard-and-fast rule for the variables.

Radial traction in restrictive lung disease = “stickiness” of fibrosis on the outside of the airways, decreasing their ability to close --> FEV1 is greater than expected --> FEV1/FVC is greater than expected. In contrast, obstructive lung disease the ratio is decreased because radial traction isn’t involved.

Systemic inflammatory response syndrome = at least 2 out of 4 of the following:

  • Temp <36 or >38
  • RR >20
  • HR >90
  • WBCs <4,000 or >16,000 cells per mm3

Sepsis = SIRS + source of infection.

Septic shock = sepsis + low BP.

Treat community acquired sepsis with third-generation cephalosporin. Ceftriaxone is most frequently used.

In pediatrics, cefotaxime is often chosen. There’s a Q on one of the IM forms that says there’s an 11-month-old with sickle cell who missed a dose of penicillin prophylaxis (for Strep pneumo) and now has septic shock. How do you treat? Wrong answer was penicillin. Correct answer was cefotaxime. Ceftriaxone was not listed.

Cefotaxime apparently causes less displacement of bilirubin from albumin, so there’s less chance of jaundice in peds.

But then there was a different question on NBME8 where it was a slightly older child who had sepsis, and the answer was ceftriaxone. Cefotaxime wasn’t listed. So the bottom line is, be aware that cefotaxime is frequently chosen in peds, and if you’re given it as an answer choice next to ceftriaxone, choose cefotaxime. But if either drug is the only third-gen ceph listed, just go with whichever they list.

Empiric Tx for meningitis = vancomycin + ceftriaxone (+/- steroids).

Do lumbar puncture BEFORE antibiotics, the same way all blood cultures are done before giving antibiotics.

Indications for doing a head CT before an LP in suspected meningitis:

  • Seizure
  • Focal neurologic signs (e.g., motor or sensory dysfunction)
  • Papilledema or if the optic fundi cannot be visualized
  • Confusion that interferes with the neurologic exam / decreased Glasgow score

If confirmed Neisseria meningitidis meningitis, give rifampin to close contacts --> decreases nasopharyngeal colonization.

Rifampin upregulates P-450. If on hormonal contraception, give ciprofloxacin instead (inhibits P-450).

N. meningitidis classically causes non-blanching rash; that’s how you know it’s the causal organism in the vignette, versus, e.g., S. pneumo, which doesn’t cause non-blanching rash.

Low blood pressure in someone with meningococcal septicemia = Waterhouse-Friderichsen syndrome = hemorrhagic necrosis of the adrenal glands.

Give normal saline (0.9% NaCl) first. But if that’s insufficient, give hydrocortisone. The adrenal necrosis means decreased cortisol, so you need to replace glucocorticoid.

Cortisol normally maintains BP by upregulating alpha-1 expression on vascular endothelium so that NE and E can bind and constrict. It is permissive of the effects of catecholamines, meaning without its presence, NE and E cannot do their job. So even though NE is classically given in septic shock as a pressor agent, in the setting of WFS, give hydrocortisone.

Fludrocortisone is the treatment for Addison disease (primary adrenal insufficiency, where aldosterone and cortisol are both low).

All glucocorticoids have varying degree of mineralocorticoid effect, meaning they can very marginally act similar to aldosterone in the kidney.

Glucocorticoids like prednisone, hydrocortisone, and dexamethasone have very little mineralocorticoid effect. That is, they are very similar to cortisol and dissimilar to aldosterone.

Fludrocortisone has very high mineralocorticoid effect, meaning it can function like cortisol AND aldosterone, and is therefore appropriate in Addison.

Cushing syndrome can sometimes cause an isolated decrease in potassium because chronically elevated cortisol levels can lead to enough mineralocorticoid effect at the kidney to cause potassium wasting. But it requires very high, and chronic, glucocorticoid / cortisol levels to achieve this. But that’s a heads up, because you might get a patient with Cushing syndrome who has a K of 3.0, and that’s why.