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 +0  (nbme21#35)

Diarrhea causes loss of water, Na and Bicarb. Remember that diarrhea is a cause of non anion gap metabolic acidosis because the loss of bicarbonate is compensated by increasing Chloride reabsorption. So she can have hyperchloremia or hyponatremia due to intake of only free water for 24 hours. But she has SEIZURES so hyponatremia is most likely


 +2  (nbme21#35)

Diarrhea causes loss of water, Na and Bicarb. Remember that diarrhea is a cause of non anion gap metabolic acidosis because the loss of bicarbonate is compensated by increasing Chloride reabsorption. So she can have hyperchloremia or hyponatremia due to intake of only free water for 24 hours. But she has SEIZURES so hyponatremia is most likely


 +1  (nbme20#3)

This is a keloid. In normal wound healing type 3 collagen is first synthesized and then degraded by Matrix metalloproteinase (a collagenase which uses Zinc as a cofactor) and replaced by Type 1. In a Keloid an excessive amount of disorganized Type 3 collagen persists. Therefore the defect is in Collagen synthesis (Type 1 synthesis)

dulxy071  Wouldn't Granulation tissue be the (more correct) answer since the initial collagen laid down for wound healing is Type III collagen which is consistent of granulation tissue? Collagen is a vast for so many types of itself as we know




Subcomments ...

submitted by hungrybox(256),

Loperamide: Agonist at u-opioid receptors. Slows gut motility (remember, constipation is a common side effect for all opioids).

quiz yourself:

Q: Would a junkie want to use Loperamide?

A: No, it has poor CNS penetration (which is why it has a low addictive potential).

Q: Would a junkie rather have morphine or buprenorphine?

A: Morphine. Both are u-opioid agonists, but morphine is a full agonist while buprenorphine is only a partial agonist.

Q: What about morphine vs. codeine?

A: Trick question, both are partial agonists.

cienfuegos  Thanks for passing off the knowledge. Regarding the last part, aren't morphine and codeine full agonists? +3  
champagnesupernova3  Yes they are +1  


submitted by hungrybox(256),

Following a stroke, this patient had weakness of her left face and body, so the stroke must have affected the right side of her brain. B was the only choice on the right side of her brain.

Still confused? Read on...

The voluntary motor fibers (corticospinal tract) descend from the primary motor cortex, cross (decussate) at the medullary pyramids, and then synapse at the anterior motor horn of the spinal level.

Because of decussation at the medullary pyramids, you should make a note of where any stroke occurs. Is it above the medullary pyramids? Then it will affect the side opposite the stroke (contralateral). Is it below the medullary pyramids? Then it will affect the same side as the stroke (ipsilateral).

hungrybox  Woops, E is also on the right side (also remember that imaging is looking up at someone, feet first). But a cerebellar stroke would have caused ataxia. +  
mnemonia  Very nice!! +  
usmleuser007  What gets me is that they mention that Left 2/3 of face is affected. This should indicate a non cortical innervation as most of the cranial nuclei are bilaterally innervated from the left and right hemisphere. If left 2/3 of the face is affected then it should also mean that the lesion is after CN5 nuclei. +1  
yotsubato  @hungrybox Thats not the cerebellum thats the occipital lobe. You would see leftsided homonymous hemianopsia in that lesion +1  
mrsmac  To my mind, it is simpler to consider the question first in terms of blood supply distribution. Left sided hemiparesis and weakness of lower 2/3 of face are both indicative of a MCA rupture/stroke (First Aid 2018 pg. 498). Furthermore, since the injury has affected motor function we would be considering the descending tract i.e. lateral corticospinal which courses through the ipsilateral posterior limb of the internal capsule then decussates in the caudal medulla. +1  
mrsmac  You're considering the wrong CN here. CN5 motor function involves muscles of mastication and lower 2/3 of tongue. The nerve in question in this case is CN7/VII Facial n. CNVII UMN injury affects the contralateral side, whereas LMN injury affects ipsilateral (First Aid 2018 pg. 516). i.e. before and after the nucleus in pons respectively. I hope this helps. +1  
nala_ula  Spastic means UMN lesion, since they also don't specify if there is arm or leg weakness, I didn't assume it was MCA stroke. I went with the reasoning that for there to be spastic hemiparesis, there must be damaged to the UMNs and therefore the internal capsule is where these tracts are. +  
champagnesupernova3  Omg this whole discussion is confusing. Internal capsule contains ALL corticospinal and corticobulbar fibers = contralateral hemiparesis and UMN facial lesion +1  


submitted by hungrybox(256),

The 2 commandments of ethics questions:

  1. Don't ever pick an answer where you sound like a dick
  2. Don't ever consult the ethics committee

Served me well on this question.

linwanrun1357  If there is a choice about asking what the patient is worried about. Is this right? It does not sound like a dick :) +1  
champagnesupernova3  If this were about a treatment asking why hes worried would be right but hes kind of doing the hospital a favor so I dont think you're supposed to try to convince or pressure him +  


submitted by nwinkelmann(111),

In case anyone is a dense as I am and just didn't understand/remember what exactly expiratory flow is = FEV1. In restrictive conditions, FEV1 is normal or increased due to decreased FVC. Interstitial fibrosis = increased airway parenchyma scaffold around the airways, which is what provides radial traction. The greater the radial traction, the lower the collapsing force, and so expiratory flow is increased.

champagnesupernova3  FEV1 is increased due to greater recoil of the lung tissue. FEV1/FVC is increased bc of that and bc of decrease in FVC +  


submitted by nbmeans(0),

I wasnt sure of this one, it said thrombin time was normal

champagnesupernova3  A normal thrombin time indicates fibrongoen is functioning normally +  


submitted by yotsubato(312),

Well thats a really crude way to screen for depression...

champagnesupernova3  There's really no other way to say it without using euphemisms +  


submitted by kimcharito(4),

well...in FA2018 said misoprostol increase production of GASTRIC mucosa and the question said ESOPHAGUS mucosa....maaaay be is that reason

champagnesupernova3  Reducing acid production helps mucosa heal alot more than increasing prostaglandins. We learn about misoprostol because it can be used if you dont have anything else but you're never gonna choose it over a PPI +  


submitted by hayayah(447),

A big thing here too is noticing that the ALP is decreased. Osteoblast activity is measured by bone ALP. I think that was the main focus here and not that you necessarily need to know the CBFA1 gene mutation.

sympathetikey  Exactly. That's the only way I got to the answer. +  
pakimd  isnt increased alk phos consistent with increased osteoblastic activity? +  
champagnesupernova3  A defect with chondrocytes would cause an short limbs like in achondroplasia so those are ruled out +  


submitted by usmleuser007(135),

https://www.ncbi.nlm.nih.gov/pubmed/301658

Relief of intractable pain was produced in six human patients by stimulation of electrodes permanently implanted in the periventricular and periaqueductal gray matter. The level of stimulation sufficient to induce pain relief seems not to alter the acute pain threshold. Indiscriminate repetitive stimulation produced tolerance to both stimulation-produced pain relief and the analgesic action of narcotic medication; this process could be reversed by abstinence from stimulation. Stimulation-produced relief of pain was reversed by naloxone in five out of six patients. These results suggest that satisfactory alleviation of persistent pain in humans may be obtained by electronic stimulation.

usmleuser007  These questions seem unfair to test because they are based on experimental data. Guess they are there to limit a perfect score. +  
xxabi  I just read it as patients take opioids to blunt or control pain. So if the electrode does the same thing (decrease pain), then an antagonist of opioids (naloxone) would bring the pain back? Idk if that reasoning is sound but that's the logic I used, I didn't even think of it as experimental. +7  
xxabi  Also its the only one that's an opioid antagonist from the list! +1  
redvelvet  they are writing these questions in an evidence-based manner because the questions in medicine cannot be produced by a self imagination or logic. But that doesn't mean that we have to know their exact evidence like this question. we can use our own basic knowledge and adjust it with logic. so opioids have an analgesic effect in the body and naloxone can revert it. +3  
champagnesupernova3  Anything that reduces pain by brain stimulation is increasing endogenous opiods like endorphins and encephalitis. +  
champagnesupernova3  Enkephalins* not encephalitis +  


submitted by usmleuser007(135),

https://www.ncbi.nlm.nih.gov/pubmed/301658

Relief of intractable pain was produced in six human patients by stimulation of electrodes permanently implanted in the periventricular and periaqueductal gray matter. The level of stimulation sufficient to induce pain relief seems not to alter the acute pain threshold. Indiscriminate repetitive stimulation produced tolerance to both stimulation-produced pain relief and the analgesic action of narcotic medication; this process could be reversed by abstinence from stimulation. Stimulation-produced relief of pain was reversed by naloxone in five out of six patients. These results suggest that satisfactory alleviation of persistent pain in humans may be obtained by electronic stimulation.

usmleuser007  These questions seem unfair to test because they are based on experimental data. Guess they are there to limit a perfect score. +  
xxabi  I just read it as patients take opioids to blunt or control pain. So if the electrode does the same thing (decrease pain), then an antagonist of opioids (naloxone) would bring the pain back? Idk if that reasoning is sound but that's the logic I used, I didn't even think of it as experimental. +7  
xxabi  Also its the only one that's an opioid antagonist from the list! +1  
redvelvet  they are writing these questions in an evidence-based manner because the questions in medicine cannot be produced by a self imagination or logic. But that doesn't mean that we have to know their exact evidence like this question. we can use our own basic knowledge and adjust it with logic. so opioids have an analgesic effect in the body and naloxone can revert it. +3  
champagnesupernova3  Anything that reduces pain by brain stimulation is increasing endogenous opiods like endorphins and encephalitis. +  
champagnesupernova3  Enkephalins* not encephalitis +  


submitted by strugglebus(75),

Hydrocodone/Methadone can lead to dependence--you avoid in long term use. NSAIDs you also avoid due to partial ineffectiveness in neuropathic pain as well as ulcer risk. TCA's are known to treat neuropathic pain very well (i.e. diabetes, ART therapy)

champagnesupernova3  Drugs for neuropathic pain: TCAs, gabapentin and pregabalin +  


submitted by ergogenic22(55),

Pt has signs and Sx of hypercortisol. Low/normal ACTH favors elevated cortisol independent of ACTH, confirmed by lack of response to dexamethasone suppression. Zona fasciculata is origin of cortisol production.

champagnesupernova3  They tried to confuse us saying both low dose and high dose dexamethasone didnt suppress it. But when ACTH is low you dont even need to do high dose dexamethasone test. The high dose is only to differentiate between Pituitary adenoma and ectopic ACTH production +  


submitted by hayayah(447),

A fractured cribriform plate (anterior skull trauma) can result in leaking of cerebrospinal fluid into the nose and loss of sense of smell. Smell plays a large role in the perception of taste. So, in practice, a patient may complain of loss of taste rather than of smell.

brownielove79  can it be a facial nerve??? with lateral head trauma (injury during passage through middle ear, or external auditory canal??) doubt!!! +  
doodimoodi  Olfaction is actually more important that tongue sensation in terms of food taste (think of how food tastes bland when you have a cold) +  
doodimoodi  than* +  
champagnesupernova3  If taste is completely lost then it's an olfactory issue. If its lost only on a part of the tongue then the nerve that provides taste to that area is suspected. +  


submitted by hayayah(447),

Clinical use of K-sparing diuretics:

  • Hyperaldosteronism
  • K+ depletion
  • HF
  • hepatic ascites (spironolactone)
  • nephrogenic DI (amiloride)
  • antiandrogen
redvelvet  Patients with hepatic ascites have hyperaldosteronism; because the intravascular volume is escaped to third space(ascites). So adding spironolactone is a good choice. +1  
champagnesupernova3  Always combine a K+ losing diuretic with a K+ sparing diuretic +2  


submitted by dickass(15),

Nonmaleficence: “Do no harm.”

Even if the patient wants to die, I guess.

champagnesupernova3  FA says you cant assist suicide but you can prescribe pain medication which they can conveniently overdose on +  
dickass  "Physicians may, however, prescribe medically appropriate analgesics even if they shorten the patient's life." (wink, wink) It's vague, but I guess the main point is to let the patient have relief, side effects no longer important. I still don't think you can just give the patient a bottle of benzos though. +  


submitted by strugglebus(75),

Ok, so you can reason this by drawing out REIT (sorry I can't draw it here). Anywho, you know its a restrictive disorder and will have a decreased RV, so automatically you know that RV is a component of FRC (FRC= RV+ERV). Thus, FRC should also be decreased. You also know that restrictive diseases are characterized by a steady decrease in FEV1/FVC since both components are decreasing. This leaves you with VC decreasing since FVC= forced vital capacity.

champagnesupernova3  FEV1 and FVC both decrease but FEV1/FVC actually increases because FVC decreases more than FEV1 so the ratio increases +  
fluentinwhale  Excuse my stupidity but what is REIT? +  
eliassam1  REIT, Residual volume, ERV, IRV, TV R E = FRC E I T = VC I T = IC REIT = TLC total lung capci I +  
eliassam1  Residual volume, ERV, IRV, TV R E = FRC E I T = VC I T = IC REIT = TLC total lung capci +  


submitted by celeste(38),

While the lifetime risk in the general population is just below 1%, it is 6.5% in first-degree relatives of patients and it rises to more than 40% in monozygotic twins of affected people. Analyzing classic studies of the genetics of schizophrenia done as early as in 1930s, Fischer concludes that a concordance rate for psychosis of about 50% in monozygotic twins seems to be a realistic estimate, which is significantly higher than that in dizygotic twins of about 10–19% (ncbi.nlm.nih.gov/pmc/articles/PMC4623659/#ref3)

imnotarobotbut  How is one supposed to know this before having read this article? +4  
imgdoc  This question falls under the either you know it or you dont category. It isnt in FA or Uworld +  
jaxx  So why would these A-holes put it on there as if prepping for this exam isn't stressful enough :-| +1  
doodimoodi  Lol just why seriously +1  
champagnesupernova3  This was mentioned in the Kaplan behavioral videos +  
usmlecrasher  and there's so much unnecessarily BS instead of real questions +