welcome redditors!to snoo-finity ... and beyond!
Welcome to laminin's page.
Contributor score: 9

Comments ...

 +6  (nbme20#33)

Tetracyclines have a high affinity to form chelates with polyvalent metallic cations such as Fe+++, Fe++, Al+++, Mg++ and Ca++. Many of these tetracycline-metal complexes are either insoluble or otherwise poorly absorbable from the gastro-intestinal tract. Milk and other dairy products, antacids containing polyvalent cations, as well as various iron salts ingested simultaneously with tetracycline derivatives, might interfere with their absorption by 50 to 90% or even more. source: https://www.ncbi.nlm.nih.gov/pubmed/946598

almondbreeze  FA 2019 pg. 192: Do not take tetracyclines with milk (Ca2+), antacids (eg. Ca2+ or Mg2+), or iron-containing preparations b/c divalent cations inhibit drugs' absorption in the gut

 +2  (nbme20#7)

can someone explain why it says he has an 'intact' PTH concentration...is it to let us know that the PTH concentration is a result of pathology? and what's his dx? thanks!

yotsubato  I swear they make up some of this stuff. Like whats up with the thirst, urination, and peptic ulcer diseases.
redvelvet  hypercalcemia can cause nephrogenic diabetes inspidus; so thirst, urination. hypercalcemia can also cause peptic ulcer disease. His symptoms are all about hypercalcemia due to hyperparathyroidism.
namira  "Hypercalcemia can cause renal dysfunction such as nephrogenic diabetes insipidus (NDI), but the mechanisms underlying hypercalcemia-induced NDI are not well understood." https://www.kidney-international.org/article/S0085-2538(16)30704-9/fulltext
dulxy071  Why can't the correct answer be C) which points towards renal failure, which may lead to secondary hyperparathyroidism having the same results I believe
pmofmalasia  The secondary hyperparathyroidism in renal failure is due to loss of calcium in the non-functioning kidney. In this question the calcium was elevated, so you can rule out renal failure.

 -1  (nbme20#46)

also maybe could do process of elimination...the 'costophrenic angle tenderness' clues us in to it being a renal problem, and the only renal answer choice is obstructive uropathy

spdrwmn  glomerulonephritis was an answer choice

Subcomments ...

submitted by sympathetikey(606),

Source: https://en.wikipedia.org/wiki/Myelin

"myelin speeds the transmission of electrical impulses called action potentials along myelinated axons by insulating the axon and reducing axonal membrane capacitance"

littletreetrunk  I think this makes total sense, but how does it not ALSO stop fast axonal transport? +2  
laminin  axonal transport is transport of organelles bidirectionally along the axon in the cytoplasm since myelin is on the outside of the axon demyelination doesn't affect this process. source: https://en.wikipedia.org/wiki/Axonal_transport "Axonal transport, also called axoplasmic transport or axoplasmic flow, is a cellular process responsible for movement of mitochondria, lipids, synaptic vesicles, proteins, and other cell parts to and from a neuron's cell body, through the cytoplasm of its axon." +2  
yotsubato  axonal transport is mediated by kinesin and dynein. Microtubule toxins like vincristine block these +3  
drdoom  @littletreetrunk "axonal transport" is movement of bulk goods via microtubules (which run from soma to terminus); ions, on the other hand, move in an "electrical wave" that we call an action potential! no axonal (microtubular) transport required! in other words, de-myelination will have no effect on the transport of bulk goods; but it will really mess up how fast "electrical waves" traverse the neuron! +