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 +0  (nbme18#34)

The patient walked barefoot on the beach and had cirrhosis, which makes him vulnerable for V. vulnificus bacteremia. V. vulnificus bacteremia has a very poor prognosis.

From Uptodate: "[V. vulnificus] is the leading cause of shellfish-associated deaths in the United States. Infections due to V. vulnificus are most common in individuals who have chronic, underlying illness; individuals with liver disease or hemochromatosis are at greatest risk."

sinforslide  Also see UWORLD ID: 15255

 +0  (nbme21#48)

It seems like Staph aureus UTI's are almost exclusively nosocomial, esp. w/ patients with urinary catheters: "We identified and entered into the study 102 consecutive patients for whom at least 1 urine culture was positive for S. aureus...82% had a urinary catheter of some type in place"

Here's the link to the study


 +2  (nbme21#30)

Male internal genitalia -> Intact SRY , testes, and testosterone.

No female internal genitalia -> Presence of MIF (antimullerian hormone) and intact Sertoli cell function.

Female external genitalia -> No androgen present, which is required for male external genitalia formation.

d_holles  Not sure I understand why T is wrong, but DHT is correct.
d_holles  I thought about this some more -- DHT forms external genitalia while T forms 'male genital ducts'. That's why the correct answer is DHT, not T, since the PT had +ext genitalia, but -internal genitalia. I was thinking that the PT had CAIS, but that would lead to testes only w/o male genital ducts. See FA2019 p608.
d_holles  *I meant -ext genitalia, +int genitalia

 +1  (nbme20#39)

The question stem is asking what features led to the ineffectiveness of pharmacotherapy. Patient's presentation is consistent with Mycoplasma pneumoniae infection, which doesn't have a cell wall and therefore peptidoglycan, which is the site of action for penicillins. It does require sterols for growth, but that wouldn't explain why amoxicillin is ineffective.


 +3  (nbme20#16)

Overview of Saliva production:

  1. Acinar cells secrete initial saliva, which is isotonic to plasma.
  2. Ductal cells modify initial saliva, causing reabsorption of Na+, Cl- and secretion of K+ and HCO-. -> higher K+ and HCO- concentrations, lower Na+ Cl- concentrations in saliva. In this process, MORE NaCl is reabsorbed, meaning that saliva ends up being hypotonic to plasma.

Ductal reabsorption process is hindered in high-flow states, which causes isotonic saliva





Subcomments ...

submitted by sinforslide(12),

The patient walked barefoot on the beach and had cirrhosis, which makes him vulnerable for V. vulnificus bacteremia. V. vulnificus bacteremia has a very poor prognosis.

From Uptodate: "[V. vulnificus] is the leading cause of shellfish-associated deaths in the United States. Infections due to V. vulnificus are most common in individuals who have chronic, underlying illness; individuals with liver disease or hemochromatosis are at greatest risk."

sinforslide  Also see UWORLD ID: 15255 +  


submitted by hmorela(5),

Why is it that the answer isn't also glossopharyngeal since you test CN IX by saying "Ah" also? Please help! Thanks!!

sinforslide  I believe that the arrow pointed to the uvula; uvular deviation would be testing for CN X palsy. CN IX's only motor innervation is the stylopharyngeus. (Not testing for gag reflex!) +1  


submitted by ark110(1),

But what is the difference between option A and option C (132; 4.9; 90; 35)

sympathetikey  K+ shouldn't increase. It's moving into cells due to metabolic alkalosis. +  
home_run_ball  In the parietal cell of the stomach Hydrogen ions are formed from the dissociation of carbonic acid. Water is a very minor source of hydrogen ions in comparison to carbonic acid. Carbonic acid is formed from carbon dioxide and water by carbonic anhydrase. The bicarbonate ion (HCO3−) is exchanged for a chloride ion (Cl−) on the basal side of the cell and the bicarbonate diffuses into the venous blood, leading to an alkaline tide phenomenon. +  
ergogenic22  RAAS increases from volume loss, and thus more aldosterone leads to low K+ +  
sinforslide  Three reasons for hypokalemia. First, some K+ is lost in gastric fluids. Second, H+ shifts out of cells and K+ shifts into cells in metabolic alkalosis. Third, ECF volume contraction has caused increased secretion of aldosterone. +2  


submitted by usmleuser007(136),

Vitamin E deficiency is known to cause similar spinal defects as Vitamin B12 deficiency. However, anemia is not seen.

ergogenic22  Also corticalspinal tract symptoms are not seen, but dorsal column and spinocerebellar tracts are seen +1  
sinforslide  In this case, patient's CF also predisposes fat-soluble vitamin deficiency. +3  
breis  FA pg 70 +  
usmleuser007  Correction: Read more on this Vitamin-E deficiency can in fact cause anemia - hemolytic anemia. This is b/c VitE work as an anti-oxidant; and therefore with reduced anti-oxidation RBCs are more prone to oxidative injuries. +3  


submitted by celeste(38),

Amiodarone, a class III antiarrhythmic drug, has multiple effects on myocardial depolarization and repolarization that make it an extremely effective antiarrhythmic drug. However, amiodarone is associated with a number of side effects, including thyroid dysfunction (both hypo- and hyperthyroidism), which is due to amiodarone's high iodine content and its direct toxic effect on the thyroid. (uptodate.com)

celeste  The "**iod**" part of am**iod**arone reminds me of it's high **iod**ine content. +2  
xxabi  I think of it as the trifecta - gotta monitor LFTs, PFTs, and Ts (thyroid) when on amiodarone! +2  
sinforslide  Also, the patient presented with Afib; this might've been caused by transient hyperthyroidism as a prelude to Hashimoto's. In this case, if you give Amio, you'd cause serious hypothyroidism! +